Ultimate Renal Path Review

Front 1

Nephrotic sx in addition to massive proteinuria (6)

Back 1

1) anasarca (generalized pitting edema) + ascites, 2) HTN in some types 2/2 Na+ retention, 3) hypercoagulable state (2/2 loss of antithrombin III; can cause renal vein thrombosis), 4) hypercholesterolemia (caused by hypoalbuminemia - unknown mech), 5) hypogammaglobulinemia (2/2 loss of gammaglobulins in urine), 6) fatty casts with maltese crosses and oval fat bodies

Front 2

___ is kidney of essential hypertension, due to hyaline arteriolosclerosis.

Back 2

Benign nephrosclerosis

Front 3

_____ has a negative charge; it is repelled by negatively charged GBM.

Back 3

Albumin

Front 4

_____ is a yellow tumor with renal vein invasion

Back 4

Renal cell carcinoma

Front 5

1-alpha hydroxylase: synthesis + action site, function

Back 5

synthesized in proximal renal tubule cells. Catalyzes 2nd hydroxylation of vitamin D in kidney

Front 6

2 damaging effects of cytokines in glomerular dz

Back 6

1) cause GBM to lose (-) charge
2) damage to podocytes, causing fusion

Front 7

2 key findings - nephrotic syndrome

Back 7

massive proteinuria, fatty casts

Front 8

2 types of hereditary glomerular dz

Back 8

1. Alport's syndrome 2. benign familial hematuria

Front 9

2 types of submicroscopic defects seen in EM on renal biopsy

Back 9

1) podocyte fusion in nephrotic syndrome
2) damage to VEC (visceral epithelial cells)

Front 10

3 causes of hematuria: lower urinary tract

Back 10

Infection, 2) transitional cell carcinoma, BPH

Front 11

3 causes of hematuria: upper urinary tract

Back 11

1) renal stone, 2) GN, 3) RCC

Front 12

3 clinical manifestations of glomerular dz

Back 12

1. nephritic
2. nephrotic
3. chronic GN

Front 13

3 key findings - nephritic syndrome

Back 13

moderate proteinuria, dysmorphic RBCs, RBC casts

Front 14

3 mechanisms producing glomerular disease

Back 14

1) IC deposition
2) anti-GBM Ab
3) T-cell production of cytokines

Front 15

3 types ARF

Back 15

prerenal, instrinsic, postrenal

Front 16

4 functions of vitamin D

Back 16

1) increases GI absorption of Ca++ and phosphorus, 2) promotes bone mineralization, 3) maintains serum [Ca++], 4) stimulates monocytic stem cells to become osteoclasts

Front 17

4 sites of glomerular IC deposition

Back 17

1) subendothelial - b/w endothelial cell and GBM
2) subepithelial - passed through GBM but caught beneath podocytes
3) intramembranous - within GBM
4) mesangial

Front 18

6 causes of chronic GN in decreasing order of incidence

Back 18

1. RPGN (90%) 2. Focal segmental (80%) 3. MPGN type I (40%) 4. Membranous glomerulonephropathy (20-30%) 5. Type IV diffuse proliferative GN in SLE (20%) 6. IgA glomerulonephropathy (10%)

Front 19

Abuse of what can cause calcium kidney stones?

Back 19

ethylene glycol (antifreeze) or vitamin C

Front 20

ACE inhibitors

Back 20

Captopril, enalapril, lisinopril

Inhibit ACE (in lung) so no production of AT II and preventing inactivation of bradykinin a potent vasodilator - increase renin b/c of loss of feedback
uses: HTN, CHF, diabetic renal disease
toxicity: CAPTOPRIL
Cough, angioedema, proteinuria, taste changes, hypotension, pregancy problems (fetal renal damage), rash, increased renin, lower AT II - ALSO hyperkalemia
avoid with bilateral renal artery stenosis - because ACE inhibitors significantly decrease GFR by preventing constriction of efferent arterioles

Front 21

Acetazolamide

Back 21

inhibits carbonic anhydrase - causes HCO3- diuresis and reduced stores of HCO3- also inhibits formation of aqueous humor
uses: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
toxicity: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
*acetazolamide causes acidosis

Front 22

actue pyelonephritis

Back 22

affects cortex with relative sparing of glomeruli/vessels. White cell casts in urine are classic. presents with fever, CVA tenderness, nausea and vomiting

Front 23

acute interstitial renal inflammation with fever, rash, eosinophilia and hematuria beginning 2 weeks after taking what drugs?

Back 23

Drug-induced interstitial nephritis; penicillins, NSAIDS, diuretics

Front 24

acute poststreptococcal glomerulonephritis

Back 24

nephritic syndrome
LM - glomeruli enlarged and hypercellular, PMNs, lumpy-bumpy appearance
EM - subepithelial immune complex humps
IF - granular
*commonly in children post streptococcal infection - peripheral and periorbital edema. Resolves spontaneously

Front 25

Acute renal failure (acute kindey injury) causes

Back 25

1) prerenal azotemia
2) intrinisc renal
3) postrenal

Front 26

Acute Renal Failure (ARF)

Back 26

rapid onset (days) azotemia PLUS oliguria/anuria

Front 27

Acute tubular necrosis

Back 27

most common cause of acute renal failure in hospital. self-reversible, but fatal if left untreated (provide supportive dialysis). Associated with renal ischemia (shock, sepsis), crush injuries (myoglobinuria), toxins. Death most often occurs during initial oliguric phase

Front 28

ADPKD

Back 28

multiple, large, bilateral cysts that ultimately destory the parenchyma. Enlarged kidneys. presents with flank pain, hematuria, HTN, urinary infection, progressive renal failure.
AD mutation in APKD1 and APKD2
death from complications of chronic kidney disease or HTN (due to increased renin production). Associated with polycystic liver disease, berry aneurysms, mitral valve prolapse

Front 29

Alk phos effects on bone mineralization

Back 29

promotes it by hydrolyzing (blocking) inhibitors of Ca++-phosphate crystallization like pyrophosphate

Front 30

Alport's syndrome

Back 30

nephritic syndrome - mutation in type IV collagen - split basement membrane
KEEN! Ears (deafness), Eyes, Kidneys and nerve disorders

Front 31

Amyloidosis is associated with what conditions?

Back 31

multiple myeloma, chronic conditions, TB, rheumatoid arithritis

Front 32

Analgesic nephropathy occurs from chornic use of _____

Back 32

acetaminophen + aspirin (causes renal papillary necrosis)

Front 33

anasarca in some nephritic dz mech

Back 33

Na+ retention --> increased plasma hydrostatic pressure

Front 34

Ang II vascular effects

Back 34

VASOCONSTRICTION: systemic arterioles (PVR), renal efferent arterioles

Front 35

APN occurs more in ______

Back 35

females

Front 36

ARPKD

Back 36

infantile presentation in parenchma - AR. associated with congential hepatic fibrosis. significant renal failure in utero can lead to potters; concern beyond neonatal peroid are HTN, portal HTN, and progressive renal insufficiency

Front 37

Azotemia

Back 37

elevated [BUN] and [Cr]

Front 38

benign familial hematuria

Back 38

Auto dominant dz that causes extremely thin GBM. Renal function normal (benign). Sx: mild proteinuria + persistent microscopic hematuria

Front 39

BJ proteinuria

Back 39

BJ = bence jones, seen in multiple myeloma

Front 40

BPH: hyperplasia or hypertrophy?

Back 40

hyperplasia

Front 41

bug causing spontaneous peritonitis in nephrotic syndrome

Back 41

strep pneump

Front 42

C5a

Back 42

neutrophil chemotactic

Front 43

Calcium kidney stones

Back 43

most common kidney stone (75-85%). made of calcium oxylate or calcium phosphate or both
increased risk in conditions that cause increased calcium: PTH, vitamin D, cancer, milk-alkali syndrome) - lead to hypercalciuria and stones - tend to recur

Front 44

c-ANCA

Back 44

wegners can cause crescentric glomerulonephritis

Front 45

cause of Potter's syndrome?

Back 45

malformation of ureteric bud

Front 46

CCr normally decreases with ____

Back 46

age

Front 47

child aged 2-4 presents with huge, palpable flank mass, hemihypertrophy. The mass contains embryonic glomerular structures. What is the tumor?

Back 47

Wilms' tumor

Front 48

chronic pyelonephritis clinical manifestations?

Back 48

coarse, asymmetric corticomedullary scarring and blunted calyces; tubules can contain eosinophilic casts (thyroidization of the kidney)

Front 49

Chronic Renal Faiure produces renal osteodystrophy due to?

Back 49

- secondary HPTH
- osteomalacia
- osteoporosis

Front 50

cyclophosphamide toxicity (2) in lower urinary tract

Back 50

1. hemorrhagic cystitis, 2. risk factor for TCC

Front 51

Cystine kidney stone

Back 51

often secondary to cystinuria. Hexagonal shape. rarely, may form cystine stagohrn claculi

Front 52

Diabetic glomerulopathy is more common in type ___ diabetes

Back 52

type 1 diabetes

Front 53

dialysis cysts

Back 53

cortical and medullary cysts resulting from long standing dialysis

Front 54

diffuse cortical necrosis

Back 54

acute generalized infarction of cortices of both kidneys. Likely due to vasospasm and DIC. Associated with obstetric catastrophics (abrupito placentae) and septic shock

Front 55

do you see casts in bladder cancer or kidney stones?

Back 55

NO - could see RBCs but no casts

Front 56

Does pitting edema distinguish nephritic from nephrotic syndrome?

Back 56

NO

Front 57

drug induced intersitital nephritis

Back 57

actue intersitial renal inflammation. pyuria (usually eosinophils) and azotemia occurring 1-2 weeks after administration. Associated with fever, rash, hematuria and CVA tenderness

drugs: diuretics, NSAIDs, penicilin derivatives, sulfonamides, rifampin act as haptens, inducing hypersensitivity

Front 58

drugs implicated in the pathogenesis of acute interstitial nephritis?

Back 58

NSAIDs, beta-lactam antibiotics (penicillins and cephalosporins), sulfonamides, diuretics (furosemide and thiazides), phenytoin, cimetidine, methyldopa

Front 59

drugs that can cause hematuria (2)

Back 59

1. anticoagulants (warfarin, heparin) = MC, 2. cyclophosphamide

Front 60

dysmorphic RBCs in glomerular disease

Back 60

nephritic syndrome

Front 61

EM use in renal biopsy specimen

Back 61

1) detect submicro defects in glomerulus
2) detect SITE of IC deposition

Front 62

EM: subendothelial humps, mesangial proliferation (splits BM)

Back 62

membranoproliferative glomerulonephritis

Front 63

erythropoietin synthesized where?

Back 63

KIDNEY: made in renal cortex by interstitial cells in peritubular capillary bed

Front 64

Ethacrynic acid

Back 64

same as ferosemide - but given to those with sulfa allergy - loop diuretic

Front 65

fatty casts

Back 65

nephrotic syndrome

Front 66

Ferosemide

Back 66

loop diuretic - works on ascending loop of henle on the Na+/K+/2Cl- channel (inhibits it) - abolishes hypertonicity of the medulla - so urine cannot be concentrated - Loops Loose Calcium!
uses: edematous states (CHF, cirrhosis, nephrotic syndrome, pul edema), HTN, hypercalcemia
toxicity: OH DANG
ototoxicity, hypokalemia, dehydration, allergy (sulfa), Nephritis (interstitial), gout

Front 67

finding on immunofluorescence in Goodpasture's?

Back 67

linear pattern, anti-GBM IgG Abs

Front 68

findings in diabetic nephropathy

Back 68

LM: Kimmelstiel-Wilson lesions, basement membrane thickening, glomeruli appear like golf balls

Front 69

findings in membranous glomeruloneprhitis in SLE

Back 69

wire-loop lesion with subepithelial deposits

Front 70

findings in minimal change disease/lipoid nephrosis?

Back 70

LM: normal glomeruli; EM: foot process effacement

Front 71

findings in nephrotic syndrome

Back 71

massive proteinuria, hypoalbuminemia, peripheral and periorbital edema, hyperlipidemia

Front 72

Focal segmental glomerulosclerosis

Back 72

type of primary nephrotic syndrome
LM - segmental sclerosis and hyalinosis
similar to minimal change disease but seen in adults
most common glomerular disease in HIV patients - more severe in these patients too

Front 73

Fusion of podocytes is a sign of :

Back 73

nephrotic syndrome

Front 74

gene association with renal cell carcinoma?

Back 74

deletion of VHL gene on chromosome 3

Front 75

gene association with Wilm's tumor?

Back 75

deletion of tumor suppressor WT1 on chromosome 11

Front 76

generalized infarction of both cortices of kidneys

Back 76

diffuse cortical necrosis - likely due to DIC and vasospasm. Associated with obstetric catastrophies (abrupito placentae) and septic shock

Front 77

granular casts in urine

Back 77

acute tubular necrosis

Front 78

Granular pattern on IF

Back 78

IC deposition in glomerulus

Front 79

Granular pattern on Immunofluorescence indicates:

Back 79

immunocomplex type of glomerulonephritis

Front 80

gross path of chronic GN

Back 80

shrunken kidneys

Front 81

hematuria cause in nephritic syndrome

Back 81

inflamed glomeruli from IC deposition

Front 82

hematuria, hypertension, oliguria, azotemia

Back 82

nephritic syndrome

Front 83

high serum Ca causes what?

Back 83

delirium, renal stones, abdominal pain, not necessarily calciuria

Front 84

high serum chloride concentration is secondary to what?

Back 84

non-anion gap acidosis

Front 85

high serum K causes what?

Back 85

peaked T waves, wide QRS, arrhythmias

Front 86

high serum Mg causes what?

Back 86

delirium, decreased DTRs, cardiopulmonary arrest

Front 87

high serum Na+

Back 87

neurologic; irritabiltity, delirum, coma

Front 88

high serum PO4-

Back 88

high-mineral ion product causes renal stones, metastatic calcifications

Front 89

histopath of chronic GN (2)

Back 89

1. glomerular sclerosis and tubular atrophy

Front 90

Horseshoe kidney is associated with:

Back 90

Turner's Syndrome

Front 91

How do you prevent urate nephropathy?

Back 91

allopurinol BEFORE aggressive cancer therapy

Front 92

How do you treat the condition commonly seen in kids that presents with peripheral and periorbital edema?

Back 92

resolves spontaneously
acute poststreptococcal glomerulonephritis
from immune complex deposition

Front 93

How does renal cell carcinoma present clinically?

Back 93

hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss

Front 94

HTN in nephritic syndrome due to

Back 94

Na+ retention

Front 95

hyaline casts in urine

Back 95

nonspecific

Front 96

Hydrochlorothiazide

Back 96

Works on distal convoluted tubules - inhibits Na+/Cl- reabsorption - reducing the diluting capacity of the nephron - decreased Ca2+ excretion
uses: HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus
toxicity: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC). sulfa allergy

Front 97

IC in SLE

Back 97

DNA-anti-DNA

Front 98

IF and EM findings in Berger's disease?

Back 98

mesangial IgA deposits (Berger's also known as IgA nephropathy)

Front 99

If someone needs a loop diuretic for edema and they have a sulfa allergy what can you use?

Back 99

Ethacrynic acid

Front 100

IF stain on renal biopsy

Back 100

identifies patterns and types of protein deposition

Front 101

If you have acute cystitis what can you see in the urine?

Back 101

WBCs but no casts

Front 102

If you have renal failure what can't you do? What are the 2 types?

Back 102

create urine and excrete nitrogenous wastes
2 types:
1) acute (ATN)
2) chronic (hypertension and diabetes)

Front 103

IgA nephropathy

Back 103

(Berger's disease) type of nephritic syndrome - deposition of IgA in mesangium
* usually presents/flares with URI or acute gastroenteritis

Front 104

Immunofluorescent congo red stain of glomeruli show apple-green birefringence. What is the diagnosis?

Back 104

Amyloidosis

Front 105

In acute tubular necrosis when does death usually occur?

Back 105

during the initial oliguric phase

Front 106

In nonenzymatic glycosylation, there is a _______ to protein

Back 106

high vessel/tubular permeability

Front 107

In order for second hydroxylation of vitamin D to occur, what enzyme is required?

Back 107

1-alpha-hydroxylase in proximal tubule

Front 108

In plain film, 80% stones are ____

Back 108

radioplaque

Front 109

Increased CCr is seen in:

Back 109

- normal pregnancy
- early diabetic glomerulopathy

Front 110

increased incidence of renal cell carcinoma if what?

Back 110

smoke or obese

Front 111

infection with what type of organism leads to struvite kidney stones?

Back 111

urease-positive bugs - proteus vlugaris, staph, klebsiella

Front 112

Inheritance patterns in Alport's

Back 112

MC = X-linked recessive. Also auto dom/recessive types.

Front 113

intrinsic renal: acute renal failure

Back 113

usually due to ATN or ischemia/toxins; less commonly due to actue glomerulonephritis (RPGN). Patchy necrosis leads to debris obstructing tubule and fluid blackflow across necrotic tubule - decreased GFR. urine has epithelial cases. BUN resorption is impaired - decreases BUN/creatinine ratio

Front 114

K+ sparing diuretics

Back 114

K+ STAEys
Spironolactone, Triamterene, Amiloride, explerenone

Spirnoolactone is a competitive aldosterone receptor antagonists in the cortical collecting tubule
Triameterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT
uses: hyperaldosteronism, K+ depletion, CHF
toxicities: hyperkalemia (can lead to arrhythmias), endocrine effects with aldosterone antagonists (spironolactone causes gynecomastia, antiandrogen effects)

Front 115

key finding in nephrotic syndrome

Back 115

proteinuria > 3.5 g/day

Front 116

Kidney stones complications and how to treat?

Back 116

Complications: hydronephrosis and pyelonephritis
Treatment: encourage fluid intake

Front 117

kidney stones often seen as a result of diseases with increased cell turnover, such as leukemia and myeloproliferative disorders

Back 117

uric acid

Front 118

Kimmelstiel-Wilson nodules

Back 118

seen in diabetic glomerulonephropathy - GBM thickening, nodular glomerulosclerosis

Front 119

Linear ImmunoFluorescence indicates:

Back 119

anti-GBM disease (Goodpasture Syndrome)

Front 120

Linear pattern on IF

Back 120

anti-GBM dz
(Goodpasture's)

linear b/c antigen (GBM) evenly distributed

Front 121

LM and IF: crescent moon shape

Back 121

rapidly progressive (crescentic) glomerulonephritis

Front 122

LM in Alport's

Back 122

FOAM CELLS = lipid accumulation in VECs

Front 123

LM: diffuse capillary and BM thickening; IF: granular pattern; EM: spike and dome

Back 123

membranous glomerulonephritis

Front 124

LM: glomeruli enlarged and hypercellular, neutrophils, lumpy-bumpy; EM: subepithelial humps; IF: granular pattern

Back 124

acute postreptococcal glomerulonephritis

Front 125

LM: segmental sclerosis and hyalinosis

Back 125

focal segmental glomerular sclerosis - most severe disease in HIV patients

Front 126

loop diuretic indicated for the treatment of edema associated with CHF, cirrhosis, and renal disease?

Back 126

furosemide (also HTN and hypercalcemia)

Front 127

low serum Ca causes what?

Back 127

tetany, neuromuscular irritability

Front 128

low serum chloride concentration is caused by what?

Back 128

is secondary to metabolic alkalosis, hypokalemia, hypovolemia, increased aldosterone

Front 129

low serum K causes what?

Back 129

U waves on ECG, flattened T waves, arrhythmias, paralysis

Front 130

low serum Mg causes what?

Back 130

neuromuscular irritability, arrhythmias

Front 131

low serum Na causes what?

Back 131

disorientation, stupor, coma

Front 132

low serum PO4 causes what?

Back 132

low-mineral ion product causes bone loss, osteomalacia

Front 133

lower urinary tract

Back 133

bladder, urethra, prostate

Front 134

Lumpy-bumpy pattern on IF

Back 134

granular pattern

Front 135

major toxicities of ACE inhibitors?

Back 135

cough, increased renin, hyperkalemia

Front 136

major toxicity of acetazolamide?

Back 136

hyperchloremic metabolic acidosis

Front 137

major toxicity of ethacrynic acid

Back 137

gout

Front 138

major toxicity of furosemide?

Back 138

OH DANG!
Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

Front 139

mannitol

Back 139

osmotic diuretic that acts in the proximal tubules - increases the osmolality of the tubular fluid - producing increased renal flow
used for: increased intracranial pressure, drug overdose, shock
toxicity: plumonary edema, dehydration
don't use in anuria and CHF

Front 140

mannitol contraindications?

Back 140

anuria, CHF

Front 141

MC mech (2): renal tubules or interstitium

Back 141

infectious or toxic

Front 142

MC mech causing glomerulonephritis (GN)

Back 142

IC deposition

circulate + deposit there or develop in situ

Front 143

MC mech: glomerular disease

Back 143

immunologic

Front 144

MCC gross hematuria in absence of infection

Back 144

transitional cell carcinoma

Front 145

MCC hematuria: lower urinary tract

Back 145

infection

Front 146

MCC hematuria: upper urinary tract

Back 146

renal stone

Front 147

MCC microscopic hematuria in men

Back 147

BPH

Front 148

mech of glomerular injury in nephrotic syndrome

Back 148

cytokines

Front 149

mech of periorbital edema in nephritic syndrome

Back 149

salt retention in loose periorbital skin

Front 150

mech of renal regulation of Ca++ homeostasis

Back 150

2nd hydroxylation of vitamin D --> 1-alpha-hydroxylase converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol

Front 151

mechanism of ACE inhibitors?

Back 151

inhibit ACE, reducing angiotensin II and preventing inactivation of bradykinin. Results in increased renin release

Front 152

mechanism of acetazolamide?

Back 152

Carbonic anhydrase inhibitor. Acts in PCT. depletion of HCO3

Front 153

mechanism of ethacrynic acid

Back 153

loop diuretic blocks Na/K/Cl cotransporter, reduces ability to concentrate urine

Front 154

mechanism of furosemide?

Back 154

loop diuretic. inhibits Na/K/Cl cotransport in thick ascending limb. reduces hypertonicity of medulla preventing concentration of urine in the collecting tubule. also promotes loss of Ca due to decreased electrochemical gradient

Front 155

mechanism of hydrochlorothiazide

Back 155

thiazide diuretic. inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of nephron. decreases Ca excretion

Front 156

mechanism of IC deposition damage to glomeruli

Back 156

Ics activate complement system. Produce C5a (chemotactic to neutrophils) --> neutrophils damage glomeruli

Front 157

mechanism of Losartan

Back 157

angiotensin II receptor inhibitor (does not produce cough)

Front 158

mechanism of mannitol?

Back 158

osmotic diuretic, increased tubular fluid osmolarity, producing increased urine flow. works in PCT

Front 159

Mechanism of spironolactone?

Back 159

competitive aldosterone receptor antagonist in cortical collecting tubule

Front 160

mechanism of Triamterene and amiloride?

Back 160

block Na channels in CCT

Front 161

Medullary cystic disease

Back 161

megullary cysts sometimes leads to fibrosis and progressive renal insufficiency with urinay concentrating defects. Ultrasound shows small kidneys - poor prognosis

Front 162

Membranoproliferative glomerulonephritis

Back 162

Subendothelial ICs with granular IF.
Type I EM: "tram-track" appearance due to GBM splitting caused by mesangial ingrowth - associated with C3 nephritic factor
type II EM: "dense deposits" - associated with HBV>HCV

*usually progresses slowly to CRF

Front 163

Membranous glomerulonephritis

Back 163

LM - diffuse capillary and GBV thickening; EM - spike (basement membrane material) and dome (immune complex deposition) appearance with sub epithelial deposits; IF - granular
SLE's nephrotic presentation

Front 164

metabolic consequences seen in renal failure?

Back 164

1. Anemia (decreased EPO)
2. Renal osteodystrophy (failure of active vitamin D production)
3. Hyperkalemia
4. metabolic acidosis due to decreased acid secretion and decreased HCO3- generation
5. Uremic encephalopathy
6. Sodium and H2O excess --> CHF and pulmonary edema
7. Chronic pyelonephritis
8. Hypertension

Front 165

Minimal change disease

Back 165

Type of primary nephrotic syndrome - commonly seen in young children - on LM everything looks normal on; on EM loss of podocyte foot processes - loose albumin not Ig's - may be triggered by infection or immune stimulus - responds to corticosteroids

Front 166

most common cause of acute renal failure in hospital? What do you do?

Back 166

acute tubular necrosis - self reversible - get them through it via dialysis

Front 167

most common cause of acute renal failure?

Back 167

acute tubular necrosis

Front 168

most common cause of nephrotic syndrome in adults?

Back 168

membranous glomerulonephritis

Front 169

most common tumor of the urinary tract system?

Back 169

transitional cell carcinoma

Front 170

most common type of kidney stones?

Back 170

calciium oxalate, calcium phosphate, or both

Front 171

Mutation in Alport's

Back 171

mutations in alpha-chains (3,4,5) of type IV collagen in GBM

Front 172

mutation in Alport's? characteristic findings?

Back 172

collagen IV; nerve deafness and ocular disorders

Front 173

Nephritic syndrome - symptoms and causes

Back 173

Inflammatory process - hematuria and RBC casts in the urine. Associated with azotemia, hypertension. oliguira, and proteinuria (<3.5 g/day)

Front 174

Nephritic syndrome is a _____-related injury to glomeruli

Back 174

neutrophil

Front 175

Nephritic syndrome SX

Back 175

HTN
periorbital edema +/- anasarca
azotemia
oliguria
Hematuria
Proteinuria
RBC casts
neutrophils in sediment

Front 176

Nephritic syndrome: mech

Back 176

neutrophil-related injury to glomeruli

Front 177

nephritic syndrome: sediment contains what cell types?

Back 177

neutrophils

Front 178

nephrotic syndrome in IV drug user or HIV nephropathy

Back 178

focal segmental glomerulosclerosis

Front 179

nephrotic syndrome increases risk of what type of infection

Back 179

hyperplasia

Front 180

nephrotic syndrome increases risk of what type of infection

Back 180

spontaneous peritonitis 2/2 strep pneumo

Front 181

Nephrotic Syndrome is a _____ injury to podocytes, leading to loss of negative charge on GBM

Back 181

cytokine

Front 182

non-glomerular renal dz associated with DM (2)

Back 182

renal papillary necrosis, pyelonephritis (acute + chronic)

Front 183

normal serum BUN

Back 183

7/18/2011

Front 184

Obese male aged 50-70 years, smoker, with hematuria and palpable mass, fever, weight loss. what is diagnosis?

Back 184

Renal cell carcinoma

Front 185

oliguria definition

Back 185

< 400 mL/day

Front 186

oliguria in nephritic syndrome

Back 186

due to decreased GFR from inflamed glomeruli

tubular function intact

Front 187

Outcome of Membranoproliferative glomerulonephritis?

Back 187

slowly progresses to renal failure

Front 188

outcome of Rapidly progressive glomerulonephritis?

Back 188

rapid course to renal failure. number of crescents indicates prognosis

Front 189

ovoid, PAS-positive hyaline masses

Back 189

Kimmelstiel-Wilson nodule - most specific lesion of diabetic glomerulosclerosis

Front 190

Painless hematuria is sign of what?

Back 190

bladder cancer

Front 191

p-ANCA

Back 191

microscopic polyarteritis - can cause crescentric glomerulonephritis

Front 192

Patient presents with acute renal failure. labs show Urine osmolality <350, Urine Na >20, Fe(Na) >2% and BUN/Cr <15. Where is the problem

Back 192

Renal

Front 193

Patient presents with acute renal failure. labs show Urine osmolality <350, Urine Na >40%, BUN/Cr >15. What is the cause?

Back 193

post-renal; generally outflow obstruction due to stones, BPH or neoplasia

Front 194

Patient presents with acute renal failure. labs show Urine osmolality >500, Urine Na <10, Fe(Na) <1% and BUN/Cr >20. Where is the problem

Back 194

Prerenal

Front 195

patient presents with flank pain, hematuria, hypertension, urinary infection and progressive renal failure. US shows multiple, large, bilateral renal cysts. What is the underlying cause?

Back 195

APKD from AD mutation in APKD1 gene

Front 196

persistent proteinuria typically indicates

Back 196

intrinsic renal dz

Front 197

postrenal acute renal failure

Back 197

outflow obstruction (stones, BPH, neoplasia, congenital anomalies). develops only with bilateral obstruction

Front 198

Potter's syndrome?

Back 198

bilateral renal agenesis - oligohydraminos, limb & facial deformities,pulmonary hypoplasia

Front 199

Prerenal azotemia

Back 199

acute renal failure from decrased RBF (hypotension) - decreased GFR. Na+/H20 and urea reabsorbed by kidneys so BUN/creatinine ratio increase (usually greater than 15) in attempt to conserve volume

Front 200

proteinuria definition

Back 200

> 150mg/24 hrs or > 30 mg/dL (dipstick)

Front 201

proteinuria in nephritic syndrome

Back 201

between 1.5-3.5 g/day

Front 202

pyrophosphate

Back 202

inhibits Ca++-phosphorus crystallization, decreasing bone mineralization

Front 203

pyuria, azotemia, fever, rash, hematuria, CVA tenderness 2 weeks after starting a drug

Back 203

drug-induced interstitial nephritis
drugs that can cause it are: diuretics, NSAIDs, penicillin derivatives, sulfonamides, rifampin

*act as haptens, inducing hypersensitivity

Front 204

qualitative detection of protein in urine - 2 tests and specificities

Back 204

dipstick (albumin only), SSA (albumin + globulins)

Front 205

Rapidly progressive (crescentic) glomerulonephritis (RPGN)

Back 205

LM and IF - crescent-moon shape. crescent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages. Several disease processes can cause this pattern:
1) goodpastures - type II hypersensitivity; antibodies to GBM; male dominant disease - hematuria/hemoptysis (lung involvement)
2) Wegner's granulomatosis; c-ANCA
3) Microscopic polyarteritis; p-ANCA

Front 206

RBC casts

Back 206

nephritic syndrome

Front 207

RBC casts in urine

Back 207

glomerular inflammation (nephritic syndromes), ischemia, or malignant hypertension

Front 208

Renal cell carcinoma

Back 208

most common renal malignancy - invades IVC and can travel up it and metastasize hemotogenously; lung and bone
most common in men 50-70
increased incidence with smoking and obesity. associated with von hippel-lindau and gene deletion in chromsome 3, originates in renal tubule cells - polygonal clear cells

Front 209

Renal cell carcinoma derives from ____ cell

Back 209

proximal tubule cell

Front 210

Renal cell carcinoma has ectopic secretion of:

Back 210

- EPO
- PTH-related peptide

Front 211

Renal cell carcinoma invades ___

Back 211

renal vein

Front 212

renal cell carcinoma is associated with what genetic condition?

Back 212

von hippel-lindau gene deletion in chromosome 3

Front 213

renal cell carcinoma is associated with what syndromes?

Back 213

paraneoplastic (ectopic EPO, ACTH, PTHrP, and prolactin)

Front 214

renal cell carcinoma most commonly affects who?

Back 214

men ages 50-70

Front 215

renal disease of amyloidosis

Back 215

LM - congo red stain, apple-green birefrigence (under polarized light)
associated with multiple myeloma, chronic conditions, TB, and RA.

Front 216

renal papillary necrosis

Back 216

sloughing of renal papillae - gross hematuria, proteinuria. May be triggered by a recent infection or immune stimulus
associated with:
1)DM 2) acute pyelonephritis 3) chronic phenacetin use (acetaminophen is a phenacetin derivative) 4) sickle cell anemia

Front 217

renal pathology associated with DIC?

Back 217

diffuse cortical necrosis

Front 218

renal regulation of acid-base homeostasis

Back 218

controls synthesis + excretion of H+ and bicarb

Front 219

renal regulation of Na+

Back 219

controls reabsorption in prox and distal collecting tubules

Front 220

renal regulation of vascular tone (2)

Back 220

Ang II and renal-derived PGE2

Front 221

renal regulation of water

Back 221

by concentrating + diluting urine

Front 222

second most common type of kidney stone; can form staghorn calculi that can be nidus for UTIs

Back 222

ammonium magnesium phosphate (struvite)

Front 223

simple cysts

Back 223

benign, incidental finding. cortex only

Front 224

small kidneys on ultrasound

Back 224

medullary cystic disease - poor prognosis

Front 225

Specific IF + EM findings in Alport's

Back 225

none

Front 226

split basement membrane with nerve deafness and lens dislocation or cataracts

Back 226

Alport's syndrome

Front 227

Struvite kidney stones (ammonium magnesium phosphate) NHPO4)

Back 227

second most common type of kidney stone. caused by infection with urease positive bug: staphylococcus, Proteus, Klebsiella - can form staghorn calculi that can be a nidus for UTIs

Front 228

the diuretic used in edema?

Back 228

Ferosemide - loop diuretic - works on ascending loop of henle - inhibits Na+/K+/2Cl- channel

Front 229

The renal _____ is relatively ischemic

Back 229

medulla

Front 230

There is increase in what in osmotic damage to glomerular capillary endothelial cells?

Back 230

sorbitol

Front 231

this is a common cause of recurrent hematuria in young patients

Back 231

IgA nephropathy (Berger's disease)

Front 232

This nephritic syndrome is most frequently seen in children and presents with peripheral and periorbital edema

Back 232

Acute poststreptococcal glomerulonephritis. resolves spontaneously

Front 233

thyroxidization of the follicles

Back 233

occurs in chronic pyelonephritis - becuase of eosinophilic casts in the tubules - looks like follicles of the thyroid

Front 234

toxicities of hydrochlorothiazide

Back 234

hypokalemic metabolic acidosis, hypercalcemia, sulfa allergy

Front 235

toxicity of K-sparing diuretics?

Back 235

hyperkalemia, antiandrogenic effects

Front 236

Transitional cell carcinoma

Back 236

most common tumor of urinary tract system (can occur in the renal calyces, renal pelvis, urters, and bladder). Painless hematuria is suggestive of bladder cancer. Associated problems in your Pee SAC: Phenacetin, Smoking, Aniline dyes, Cyclophosphamide

Front 237

transitional cell carcinoma is associated with what?

Back 237

problems in your Pee SAC:
phenacetin, smoking, analine dyes, and cyclophosphamide

Front 238

tubular function in nephritic syndrome

Back 238

intact

Front 239

two principal causes of rapidly progressive glomerulonephritis?

Back 239

anti-glomerular basement membrane and primary systemic vasculitis

Front 240

Types of nephritic syndrome

Back 240

PAST HAM
Poststreptococcal
IgA nephropathy (Berger's disease)
SLE
TTP/HUS

Henoch-Schonlein purpura
Alport's syndrome
Membranoproliferative glomerulonephritis
RPGN (rapidly progressing glomerulonephtritis)
Anti-GBM: Goodpasture's
Immune Complex: Henoch-Schonlein purpra, Hypersensitivity vasculitis, Cryoglobulinemia, SLE
Pauci-immune: Wegner's, Churg Strauss, Microscopic polyarteritis, PAN

Front 241

types of radiolucent kidney stones?

Back 241

uric acid and cystine

Front 242

Under an Electron microscope, immunocomplex deposits are _____

Back 242

electron-dense

Front 243

upper urinary tract

Back 243

kidneys, ureters

Front 244

ureter crosses anterior to the origin of what artery to enter the pelvis?

Back 244

external iliac

Front 245

Uric acid kidney stone

Back 245

strong association with hyperuricemia (eg. gout). often seen in diseases with increased cell turn over (leukemia, myeloproliferative disorders)

Front 246

urinary tests for protein

Back 246

qualitative: dipstick, sulfosalicylic acid (SSA) quant: 24-hr urine collection

Front 247

VEC

Back 247

visceral epithelial cell

Front 248

Vit D effects on bone

Back 248

stimulate bone mineralization by stimulating release of alk phos from osteoblasts

Front 249

WAGR complex?

Back 249

Wilm's tumor, Aniridia, genitourinary malformation, and mental-motor retardation

Front 250

waxy casts in urine

Back 250

advanced renal disease/CRF

Front 251

WBC casts in urine

Back 251

tubulointerstitial disease, acute pyelonephritis, glomerular disorders

Front 252

What acute renal injury if urine osmalality <350, urine Na+>40, FeNa>4%, Serum BUN/Cr>15?

Back 252

postrenal cause

Front 253

what acute renal injury if urine osmolality <350, urine Na>20, FeNa>2%, serum BUN/Cr<15

Back 253

renal cause

Front 254

What acute renal injury if urine osmolality > 500, urine Na < 10, FeNa < 1%, and serum BUN/Cr > 20

Back 254

prerenal cause

Front 255

What anemia does Chronic Renal Failure produce?

Back 255

normocytic anemia (qualitative platelet defect)

Front 256

What are acute drug-induced TIN?

Back 256

- methicillin
- NSAID
- rifampin
- sulfonamides

Front 257

What are causes of Chronic Pyelonephritis (CPN)?

Back 257

- VUR in young girls
- chronic hydronephrosis

Front 258

What are crescents?

Back 258

proliferations of parietal epithelial cells

Front 259

What are features of acute drug-induced TIN?

Back 259

- abrupt onset fever
- oliguria
- rash

Front 260

What are features of Alport's syndrome?

Back 260

- hereditary nephritis
- sensorineural hearing loss
- ocular defects

Front 261

What are features of ATN?

Back 261

- BUN:Cr ratio <15
- hyperkalemia
- metabolic acidosis

Front 262

What are features of Chronic lead poisoning?

Back 262

proximal tubules with nuclear acid-fast inclusions

Front 263

What are features of CPN?

Back 263

- glomerular scarring
- tubular atrophy (thyroidization)

Front 264

What are features of CRF?

Back 264

- high anion gap metabolic acidosis
- high serum phosphorus/potassium
- low serum calcium

Front 265

What are features of diffuse cortical necrosis?

Back 265

#NAME?

Front 266

What are features of malignant hypertension?

Back 266

- >210/120 mm Hg
- encephalopathy
- renal failure

Front 267

What are features of nephritic syndrome?

Back 267

- moderate proteinuria (<3.5)
- dysmorphic RBC
- RBC cast

Front 268

What are features of nephrotic syndrome?

Back 268

- proteinuria >3.5
- fatty casts

Front 269

What are features of renal infarction?

Back 269

- hematuria
- flank pain

Front 270

What are features of renal stones?

Back 270

- ipsilateral colicky pain in flank radiating to the groin
- hematuria

Front 271

What are features of sickle cell nephropathy?

Back 271

- loss concentration
- hematuria
- renal papillary necrosis
- APN

Front 272

What are features of Wilm's tumor?

Back 272

- child with unilateral flank mass
- hypertension

Front 273

What are findings in APN and not lower UTIs?

Back 273

- fever
- flank pain
- WBC casts in urine

Front 274

What are key findings in postrenal azotemia?

Back 274

- obstruction behind kidney
- initial ratio >15
- If obstruction persists, <15

Front 275

What are key findings in prerenal azotemia?

Back 275

- decreased Cardiac Output
- decreased GFR
- ratio > 15

Front 276

What are key findings in renal azotemia?

Back 276

- intrinsic renal disease
- extrarenal loss of urea
- ratio <15

Front 277

What are renal stones?

Back 277

- calcium oxalate
- calcium phosphate

Front 278

What are struvite stones?

Back 278

- Magnesium ammonium phosphate (MAP)
- urease producers
- alkaline urine pH

Front 279

What are the 4 types of kidney stones?

Back 279

1) calcium
2) ammonium magnesium phosphate
3) Uric acid
4) Cystine

Front 280

What are the ACE inhibitors?

Back 280

Captopril, Enalapril, Lisinopril

Front 281

What are the consequences of renal failure?

Back 281

1) Na+/H20 retention (CHF, pulmonary edema, hypertension)
2) Hyperkalemia
3) Metabolic acidosis
4) Uremia (clinical syndrome marked by increased BUN and creatinine): nausea, pericarditis, asterixis, encephalopathy, platelet dysfunction
5)anemia (can't make EPO)
6) renal osteodystrophy (can't make active form of vitamin D)
7) dyslipidemia (especially increase in triglycerides)
8) growth retardation and developmental delay in children

Front 282

What are the K sparing diuretics?

Back 282

Spironolactone, Triamterene, Amiloride, eplerenone

Front 283

What are the things that cause primary nephrotic syndrome?

Back 283

FMMMM
Focal segmental glomerulosclerosis, Minimal change disease, Membranous glomerulonephritis, Membranoproliferative golmerulonephritis, mesangial proliferation

Front 284

What are the things that cause secondary nephrotic syndrome?

Back 284

SAD
SLE
Amyloidosis
Diabetic nephropathy

Front 285

What can expired tetracycline cause?

Back 285

fanconi's syndrome

Front 286

What can you give a person if they have a cough from an ACE inhibitor?

Back 286

angiotensin II receptor blocker (ARB) - does not cause cough!

Front 287

What cast is seen in ATN?

Back 287

Renal tubular cell cast

Front 288

What casts are sign of CRF?

Back 288

waxy casts

Front 289

What casts does Bence Jones Protein produce?

Back 289

tubular casts with foreign body giant cell reaction

Front 290

What causes diffuse cortical necrosis?

Back 290

likely due to a combination of vasospasm and DIC. Associated with obstetric catastrophes and sepsis

Front 291

What causes membranous glomerulonephritis?

Back 291

drugs infections, SLE, and solid tumors - most common cause of adult nephrotic syndrome

Front 292

What causes nephrotic syndrome? What do you see in those with nephrotic syndrome?

Back 292

loss of charge barrier - fused basement membrane
see proteinuria (>3.5 g/day; frothy urine), hyperlipidemia (increased lipoprotein synthesis because of low proteins and the liver is trying to make more), hypoalbuminema, edema, fatty casts. Increased risk of infection and thromboembolism

Front 293

What condition do you see hyaline casts?

Back 293

nonspecific

Front 294

What conditions do you see granular (muddy brown) casts?

Back 294

ATN - acute tubular necrosis

Front 295

what conditions do you see RBC casts?

Back 295

nephritic syndomres (glomuerulonephritis), ischemia, malignant hypertension

Front 296

What conditions do you see waxy casts?

Back 296

advanced renal disease - chronic renal failure

Front 297

What conditions do you see WBC casts?

Back 297

acute pyeonephritis, tubulointerstitial inflammation, transplant rejection

Front 298

What detects hydronephrosis, not stones?

Back 298

ultrasound

Front 299

What determines protein filtration?

Back 299

GBM's
- size
- charge

Front 300

What do calcium kidney stones look like?

Back 300

radiopaque. oxalate crystals can result from ethylene glycol (antifreeze) or vitamin C abuse

Front 301

What do cystine kidney stones look like? What do you treat them with?

Back 301

faintly radiopaque. treat with alkalinzation of the urine

Front 302

What do loop diuretics and thiazides do to blood pH?

Back 302

increase it (alkalosis)
1) volume contraction - loose water - so low blood volume - AT II - increased Na/H exchange in proximal tubules - more H+ into urine - which gets reabsorbed and HCO3- diffuses into the blood
2) K+ loss leads to K+ exiting cellls (H+/K+ exchanger) in exchange for H+ entering cells
3) in low K+ states, H+ (rather than K+) is exchanged for Na+ in the collecting duct leading to alkalosis and paradoxical aciduria

Front 303

What do loop diuretics do to Ca+?

Back 303

Loops Loose Calcium - abolish lumen positive potential in thick ascending limb of henle - decreased paracellular Ca+ resorption - hypocalcemia, increased urinary Ca+

Front 304

What do RBCs in urine with no casts indicate?

Back 304

Bladder cancer

Front 305

What do struvite stones look like?

Back 305

radiopaque or radiolucent
worsened by alkaluira

Front 306

What do thiazide diuretics do to Ca+?

Back 306

volume depletion - upregulation of Na+ reabsorption - enhanced paracellular Ca2+ in proximal tubul and loop of henle. thiazides block luminal Na+/Cl- cotransport in distal convoluted tubule - increase Na+ gradient - increase interstitial Na+/Ca2+ exchange - hypercalcemia

Front 307

What do you give to treat minimal change disease?

Back 307

corticosteroids

Front 308

What do you see in someone with fanconi's syndrome?

Back 308

defect with: early Na+ resorption, decrease phosphate reabsorption, decrease HCO3- reabsorption

complications: ricketts, metabolic acidosis (loose HCO3- type 2 RTA)
increase distal Na+ reabsorption - hypokalemia

Front 309

What do you use to treat nephrogenic diabetes insipidus?

Back 309

Hydrochlorothiazide

Front 310

What does a uric acid kidney stone look like?

Back 310

radiolucent

Front 311

What does CA inhibitors and K+ sparing diuretics do to the blood pH?

Back 311

decrease it - causing acidemia -
CA inhibitors - inhibit reabsorption of HCO3-
K+ sparing - aldosterone blockade prevents K+ secretion and H+ secretion. also hyperkalemia leads to K+ entering cells and H+ exiting cells

Front 312

What does Chronic renal failure produce?

Back 312

- hypertension
- pericarditis
- CHF
- atherosclerosis

Front 313

What does creatine supplements increase?

Back 313

serum creatinine

Front 314

What does diuretics do to urine K+?

Back 314

All of them except K+ sparing (spirnolactone, triamterene, amiloride, eplerenone) increase urine K+ (because by inhibiting Na+ reabsorption more Na+ is delivered to distal convoluted tubule which stimulates aldosterone - and Na+ reabsorbed and K+

Front 315

What does diuretics do to urine NaCl?

Back 315

all of them increase it - and water follows - serum NaCl may decrease as a result

Front 316

What does hyaline arteriolosclerosis of efferent arteriole increase?

Back 316

GFR, producing hyperfiltration injury

Front 317

What does immunocomplexes do?

Back 317

1. activate complement
2. C5a produced
3. attract neutrophils

Front 318

What does seeing casts mean?

Back 318

That the cause of hematuria/pyuria is of renal orgin

Front 319

What does the presence of casts in the urine indicate?

Back 319

hematuria/pyuria is of renal origin

Front 320

What does WBCs in urine with no casts inddicate?

Back 320

Acute cystitis

Front 321

What drugs can cause fanconi's syndrome?

Back 321

cisplatin, expired tetracycline

Front 322

What happens in diabetic glomerulonephropathy?

Back 322

Nonenzymatic glycosylation (NEG) of GBM - increase premeability, thickening. NEG of efferent arterioles - increased GFR - mesangial expansion. LM - mesangial expansion, GBM thickenign, nodular glomerulosclerosis (kimmelstiel-Wilson nodules)

Front 323

what happens in WAGR complex?

Back 323

deletion of tumor suppressor gene WT1 on chromosome 11

Front 324

what happens to BUN and creatinine in a normal nephron

Back 324

BUN is reabsorbed for countercurrent multiplication, but creatinine is not

Front 325

What happens to the cells during ATN?

Back 325

loss of cell polarity, epithelial cell detachment, necrosis, granular (muddy brown) casts. 3 stages
1) inciting event - maintenace (low urine) - recovery (2-3 weeks)

Front 326

What increases in microangiopathy?

Back 326

deposition type IV collagen

Front 327

What increases reabsorption of calcium out of urine?

Back 327

thiazides

Front 328

What is a biomarker of kidney function?

Back 328

Cystatin C

Front 329

What is a cause of hypertension in children?

Back 329

Reflux nephropathy

Front 330

what is acute tubular necrosis associated with?

Back 330

renal ischemia (e.g. shock), crush injury (myoglobinuria), toxins

Front 331

What is amyloidosis associated with?

Back 331

multiple myeloma, chronic disease, RB, and RA

Front 332

What is associated with renal ischemia (shock, sepsis), crush injury (myoglblinuria), and toxins?

Back 332

acute tubular necrosis

Front 333

What is end-product of creatine metabolism?

Back 333

Creatinine

Front 334

What is Fanconi's syndrome? What are its complications?

Back 334

Defect in proximal tubule transport. Complications include rickets, osteomalacia, hypokalemia, metabolic acidosis

Front 335

What is filtered, but partly reabsorbed?

Back 335

Urea

Front 336

What is free water clearance in CRF?

Back 336

zero

Front 337

What is hamartoma associated with tuberous sclerosis?

Back 337

Angiomyolipoma

Front 338

what is initial treatment for malignant hypertension?

Back 338

nitroprusside

Front 339

what is renal papillary necrosis associated with?

Back 339

diabetes, acute pyelonephritis, chronic phenacitin use, sickle cell anemia

Front 340

What is SLE's nephrotic presentation?

Back 340

membranous glomerulonephritis (diffuse membranous glomerulopathy)

Front 341

What is the best overall sensitivity and specificity in renal stones?

Back 341

spiral CT

Front 342

What is the damage seen in focal segmental glomerulosclerosis?

Back 342

involves parts of some of the glomeruli

Front 343

What is the first sign of diabetic glomerulopathy?

Back 343

microalbuminuria

Front 344

What is the gold standard test to evaluate renal disease?

Back 344

Urinalysis

Front 345

What is the most common cause o fupper urinary tract obstruction?

Back 345

Renal stone

Front 346

What is the most common cause of Acute Renal failure?

Back 346

Acute Tubular Necrosis (ATN)

Front 347

What is the most common cause of adult nephrotic syndrome?

Back 347

membranous glomerulonephritis (diffuse membranous glomerulopathy)

Front 348

What is the most common cause of APN?

Back 348

E. Coli

Front 349

What is the most common cause of chronic glomerulonephritis?

Back 349

Rapidly progressive glomerulonephritis (RPGN)

Front 350

what is the most common cause of death in patients with SLE?

Back 350

diffuse proliferative glomerulonephritis (due to SLE or MPGN)

see subendothelial DNA-anti-DNA immune complexes - wire looping of capillaries

granular IF

SLE can also present as nephrotic syndrome

Front 351

What is the most common cause of diabetic glomerulopathy?

Back 351

poor glycemic control

Front 352

What is the most common cause of increased serum BUN?

Back 352

CHF

Front 353

What is the most common cause of ischemic ATN?

Back 353

prerenal azotemia

Front 354

What is the most common cause of malignant hypertension?

Back 354

pre-existing Benign Nephrosclerosis

Front 355

What is the most common cause of nephrotoxic ATN?

Back 355

aminoglycosides

Front 356

What is the most common cause of renal infarction?

Back 356

emboli

Front 357

What is the most common cause of transitional cell carcinoma (TCC)?

Back 357

smoking

Front 358

What is the most common cause of Tubulointerstitial nephritis (TIN)

Back 358

Acute pyelonephritis (APN)

Front 359

What is the most common complication of upper urinary tract obstruction?

Back 359

hydronephrosis

Front 360

What is the most common cystic disease in children?

Back 360

Renal dysplasia

Front 361

What is the most common glomerular disease in HIV patients?

Back 361

Focal segmental glomerulosclerosis

Front 362

What is the most common mechanism causing glomerulonephritis?

Back 362

immunocomplex

Front 363

What is the most common mechanism for upper/lower UTIs in females?

Back 363

Ascending infections

Front 364

What is the most common metabolic abnormality causing calcium stones?

Back 364

hypercalciuria

Front 365

what is the most common renal malignancy of childhood (ages 2-4)?

Back 365

Whilms' tumor (nephroblatoma)

Front 366

What is the most common renal malignancy?

Back 366

Renal cell carcinoma

Front 367

What is the most common renal stone?

Back 367

calcium oxalate

Front 368

What is the most common tumor of the urinary tract system?

Back 368

transitional cell carcinoma

Front 369

What is the most common type of Acute Tubular Necrosis (ATN)?

Back 369

Ischemic Acute Tubular Necrosis

Front 370

What is the most common type of kidney stone?

Back 370

Calcium stones - make of calcium oxylate or calcium phosphate

Front 371

What is the msot common cause of renal cell carcinoma?

Back 371

smoking

Front 372

What is the msot common primary renal tumor in children?

Back 372

Wilm's tumor

Front 373

What is the nephrotic syndrome that present as nephritic syndrome?

Back 373

Membranoproliferative glomerulonephritis

Front 374

What is the Rx for calcium stones?

Back 374

hydrochlorothiazide

Front 375

What is the triad for renal cell carcinoma?

Back 375

- hematuria
- flank pain
- abdominal mass

Front 376

what is uremia?

Back 376

clinical syndrome marked by increased BUN and creatinine and associated symptoms

Front 377

What is very important to prevent stones?

Back 377

hydration

Front 378

What is Vesicoureteral reflux?

Back 378

urine refluxes into the ureters during micturition

Front 379

What is visible with IVP in CPN?

Back 379

cortical scars that overlie blunt calyces

Front 380

What is visibly seen on IVP of Renal Papillary necrosis?

Back 380

'ring defect' from sloughing of papilla

Front 381

What is wrong in fanconi's syndrome?

Back 381

problem with proximal tubules - cannot transport amino acids, glucose, phosphate, uric acid, protein, and electrolytes. Can be congenital or acquired. causes include wilson's disease, glycogen storage diseases, and drugs (cisplatin, expired tetracycline)

Front 382

What nephritic syndrome presents/flares with an URI or acute gastroenteritis?

Back 382

IgA nephropathy - Berger's disease

Front 383

What occurs in thin basement membrane disease?

Back 383

persistant hematuria

Front 384

What paraneoplastic syndromes is renal cell carcinoma associated with/

Back 384

ectopic EPO, ACTH, PTH related peptide, and prolactin

Front 385

what regulates Ca++ homeostasis?

Back 385

kidney

Front 386

what regulates Ca++ homeostasis?

Back 386

kidney

Front 387

what regulates Ca++ homeostasis?

Back 387

kidney

Front 388

What slows progression of nephropathy in type 1/type 2 diabetes?

Back 388

ACE inhibitor/receptor blockers

Front 389

what stone is worsened by alkaluria?

Back 389

Struvite`

Front 390

What things are associated with transitional cell carcinoma?

Back 390

Pee SAC
Phenacetin, Smoking, Analine dyes, Cyclophosphamide

Front 391

What tumor contains embyronic glomerular structures?

Back 391

whilms' tumor - most common tumor of children (age 2-4)

Front 392

What tumor originates from polyclonal clear cells?

Back 392

renal cell carcinoma

Front 393

what type of hypersentivity rxn in IC deposition?

Back 393

type III

Front 394

What vasoconstricts efferent arteriole?

Back 394

ATII

Front 395

What vasodilates afferent arteriole?

Back 395

Renal PGE2

Front 396

when does death most often occur in ATN?

Back 396

during initial oliguric stage

Front 397

When is mannitol contraindicated?

Back 397

anuria and CHF

Front 398

where does renal cell carcinoma originate?

Back 398

renal tubule cells (polygonal clear cells)

Front 399

Which conditions may lead to hypercalciuria and stones?

Back 399

hypercalcemic conditions: cancer, increased PTH, increased vitamin D, milk-alkali syndrome

Front 400

Which syndrome has less glomerular inflammation?

Back 400

Nephrotic syndrome

Front 401

Whilms' tumor (nephroblastoma)

Back 401

most common renal malignancy in children. presents with huge palpable flank mass and/or hematuria. may be associated with hemihypertorophy syndromes. Contains embryonic glomerular structures. Deletion of tumor suppressor gene WT1 on chromosome 11. Can be part of WAGR complex: whilms' tumor, aniridia (absent iris), GU malformation, mental-motor retardation

Front 402

white cell casts in urine are pathognomonic for what?

Back 402

acute pyelonephritis

Front 403

why do kidneys stay low in abdomen in horseshoe kidney?

Back 403

get trapped under IMA

Front 404

Why is creatinine an excellent metabolite for renal clearance testing?

Back 404

Filtered; not reabsorbed or secreted

Front 405

Wilm's tumor causes hypertension how?

Back 405

Hypertension due to renin secretion

Front 406

wire looping of capillaries in kidney

Back 406

diffuse proliferative glomerulonephritis
from SLE - most common cause of death

Front 407

2 differences in proteinuria b/w nephritic and nephrotic

Back 407

more/less than 3.5g/day AND nephritic proteinuria = nonselective (vs. nephrotic proteinuria loses albumin but not globulins)

Front 408

functional proteinuria: definition

Back 408

< 2 g/24 hrs
not associated with renal dz

Front 409

4 causes functional proteinuria

Back 409

fever, exercise, CHF, orthostatic proteinuria upon standing

not associated with renal dz

Front 410

4 types proteinuria

Back 410

1. functional, 2. overflow, 3. glomerular, 4. tubular

Front 411

overflow proteinuria

Back 411

variable amt. LMW proteinuria

amt. filtered > tubular reabsorption

Front 412

3 causes of overflow proteinuria

Back 412

1) multiple myeloma w/ BJ protein
2) hemoglobinuria (e.g., intravascular hemolysis)
3) myoglobinuria (crush injuries, McArdle's, increased serum creatine kinase)

Front 413

tubular proteinuria

Back 413

< 2 g/day

defect in proximal tubule reabsorption of LMW proteins (ex: AA at normal filtered loads)

Front 414

3 causes of tubular proteinuria

Back 414

1) heavy metal poisoning (lead, mercury)
2) Fanconi syndrome
3) Hartnup dz

Front 415

Fanconi syndrome

Back 415

inability to reabsorb glucose, AA, uric acid, phosphate, bicarb

Front 416

Hartnup dz

Back 416

defect in reabsorption of neutral AA (e.g., tryptophan) in GI tract and kidneys

Front 417

Question

Back 417

Answer

Front 418

Which arteriole does ATII preferentially constrict: afferent or efferent? What does this do to GFR and FF?

Back 418

Efferent. This increases GFR, but not RPF, so it increases FF.

Front 419

What part of the kidneys are responsible for producing erythropoetin?

Back 419

The endothelial cells of the peritubular capillaries of the kidney are responsible for producing erythropoetin.

Front 420

How does the kidney help maintain calcium homeostasis? What are the functions of Vitamin D?

Back 420

The kidney helps to maintain calcium homeostasis through second hydroxylation of Vitamin D. The functions of Vitamin D include increases in GI reabsorption of calcium and phosphorus, bone mineralization by stimulation of the release of alkaline phosphatase from osteoblasts, increases in production of osteoclasts from macrophage stem cells.

Front 421

How does the kidney make the second hydroxylation of Vitamin D? Where is the enzyme found?

Back 421

1-alpha-Hydroxylase is synthesized in the proximal tubule cells. 1AH converts 25-(OH)2 to 1,25-(OH)2.

Front 422

What hormone upregulates the production of Vitamin D in the kidney?

Back 422

Parathyroid Hormone (PTH)

Front 423

Describe the structures that define the Upper Urinary Tract. What is the most common Upper Urinary Tract cause of Hematuria? What are other causes?

Back 423

The kidneys and ureters define the Upper Urinary Tract. Renal stones are the most common cause of upper renal tract hematuria. Other causes include Glomerulonephritis, and Renal cell carcinoma.

Front 424

Describe the structures that define the Lower Urinary Tract. What is the most common Lower Urinary Tract cause of Hematuria? What are other causes?

Back 424

The bladder, urethra and prostate define the Lower Urinary Tract. The most common cause of Lower Urinary Tract hematuria is Infection. Other causes include Transitional cell carcinoma (most common cause of gross hematuria in the absence of infection) and Prostatic hyperplasia (most common cause of microscopic hematuria in adult males).

Front 425

Which drugs are most commonly associated with Hematuria? Which are most commonly the cause?

Back 425

Anticoagulants such as Warfarin and Heparin, and Cyclophosphamide which causes Hemorrhagic cystitis and is a risk factor for transitional cell carcinoma. Anticoagulants though, are the most common drugs responsible for causing Hematuria.

Front 426

What are the diptstick and 24hr definitions of Proteinuria? What does persistent proteinuria usually indicate?

Back 426

>30mg/dL (dipstick) and >150mg/24hrs is defined as the presence of proteinuria. Persistent proteinuria usually indicates intrinsic renal disease.

Front 427

What protein(s) is the Dipstick test testing for specifically?

Back 427

Dipstick tests are specific for albumin.

Front 428

What protein(s) is the Sulfosalycilic Acid (SSA) test testing for?

Back 428

SSA detects albumin and globulins

Front 429

What is the definition of Functional Proteinuria. What type of conditions or activities may lead to this? Is there progression to renal disease with this type of proteinuria?

Back 429

This is defined as the presence of protein in the urine, but not more than 2g/24hrs, and it is not associated with renal disease. Causes of Functional Proteinuria can include exercise, fever, CHF, orthostatic posture as opposed to recumbent posture. There is NO progression to renal disease.

Front 430

Define overflow proteinuria. What are some of its possible causes?

Back 430

In overflow proteinura, the protein loss is variable and typically consists of a low molecular weight proteinuria. The amount of protein filtered is simply greater than that which can be reabsorbed by the tubules. Some of the possible causes for this include multiple myeloma with Bence Jones proteinuria, hemoglobinuria (e.g. intravascular hemolysis), Myoglobinuria: (crush injuries), MacArdel's glycogenosis (deficient muscle phosphorylase) with increase in creatinine kinase

Front 431

Define the Glomerular proteinuria associated with Nephritic Syndrome. Explain the cause of this syndrome that leads to proteinuria. Give an example of a Nephritic syndrome.

Back 431

Proteinuria associated with Nephritic Syndrome is defined as protein 150mg<3500mg/24hrs. Damage to the Glomerular Basement Membrane GBM is the cause of this NON-SELECTIVE proteinuria with loss of albumin and globulins. Post-streptoccocal glomerulonephritits is an example of this.

Front 432

Define the Glomerular proteinuria associated with Nephrotic Syndrome. Explain the cause of this syndrome that leads to proteinuria. Give an example of a Nephrotic syndrome.

Back 432

Proteinuria associated with Nephrotic Syndrome is defined as protein >3500mg/24hrs. Loss of the negative charge on the GBM is the cause of this SELECTIVE proteinuria with the loss of albumin, but NOT globulins. An example of a Nephrotic Syndrome is minimal change disease.

Front 433

What is the difference in the type of proteinuria associated with Nephrotic Syndrome vs. Nephritic Syndrome?

Back 433

Nephrotic Syndrome is associated with massive proteinura whereas Nephritic Syndrome is generally associated with much less. The protein loss in Nephrotic Syndrome is also a selective loss of Albumin, but not Globulins. In contrast Nephritic Syndrome involves a Non-selective loss of both albumin and globulins.

Front 434

Define the proteinuria associated with Tubular defects. How much protein is lost in 24hrs? What is the cause? Describe some specific syndromes and poisonings that might cause this.

Back 434

The proteinuria associated with Tubular defects is generally <2g/24hrs. The defect is often in proximal reabsorption of low-molecular-weight proteins (e.g. amino acids) at normal filtered loads. Heavy metal poisoning (lead and mercury), Fanconi Syndrome, and Hartnup's disease are all examples of Tubular defects that lead to proteinuria.

Front 435

What malabsorptions take place in the kidney with Fanconi Syndrome?

Back 435

Fanconi syndrome is the inability to reabsorb glucose, amino acids, uric acid, phosphate, and bicarbonate.

Front 436

Describe the malabsorptions that take place in the kidney with Hartnup disease.

Back 436

Hartnup disease is a defect in reabsorption of the neutral amino acids (e.g. tryptophan) in the GI tract and Kidneys.

Front 437

Describe the normal range for BUN. Where does the urea nitrogen come from? What produces it? How is it filtered and reabsorbed by the kidney?

Back 437

8-17mg/dL. BUN is produced as the end product of amino acid and pyrimidine metabolism produced by the urea cycle in the liver. The urea nitrogen is filtered by the kidneys and is partially reabsorbed by the proximal tubule.

Front 438

Describe the factors that determine serum levels of BUN.

Back 438

Serum levels of BUN depend on the following: -GFR -Protein content in diet -Proximal Tubule reabsorption -Functional status of the urea cycle

Front 439

Describe the conditions that lead to increased levels of BUN. Explain the mechanisms that lead to the increases in BUN in these states.

Back 439

Decreased cardiac output, Increased Protein intake, Increased Tissue catabolism, Acute glomerulonenphritis, Acute or Chronic renal failure, and Postrenal disease (e.g. urinary tract obstruction). All of these conditions either contribute to a lowered GFR (which allows for more time for proximal tubule reabsorption or leads to back-diffusion of urea), or increased amino acid degredation, both of which lead to increasing the BUN.

Front 440

Describe the conditions that lead to decreased levels of BUN. Explain the mechanisms that lead to the decreases in BUN in these states.

Back 440

Increased plasma volume (e.g. normal pregnancy, SIADH), Decreased urea synthesis (e.g. Cirrhosis, Reye syndrome, fulminant liver failure), Decreased protein intake (Kwashiorkor, starvation). These conditions contribute to the decreases in BUN through increases in GFR, dysfunctional urea cycles, or decreases in amino acid availability/degredation.

Front 441

What is the most common cause of increased BUN?

Back 441

Congestive Heart Failure.

Front 442

Describe a normal serum creatinine level. How does creatinine get produced?

Back 442

Normal Serum Creatinine is 0.6mg-1.2mg/dL. Creatinine is the normal metabolic end product of creatine in muscle (creatine binds phosphate in muscle for ATP synthesis).

Front 443

How is creatinine treated by the kidneys and why does is serve as and approximate measure for GFR? How much does it over estimate by?

Back 443

Creatinin is filtered, but neither secreted nor reabsorbed (...much), by the kidneys, thus it is a good measure of GFR. Creatinine excretion over-estimates GFR by ~10%.

Front 444

How does serum concentration of creatinine vary with age and muscle mass?

Back 444

It is increases with age, and decreases with muscle wasting.

Front 445

What nutritional supplement will increase a patients serum creatinine?

Back 445

Creatine.

Front 446

What is Azotemia?

Back 446

Azotemia is a medical condition characterized by abnormal levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood.

Front 447

Define Pre-Renal Azotemia. Describe some of the condition(s) that would cause Pre-Renal Azotemia. What is the mechanism by which this happens?

Back 447

Pre-Renal Azotemia is caused a decrease is cardiac output. Some of the conditions that lead to this state include blood loss, congestive heart failure, and shock. This happens because there is hypoperfusion of the kidneys which results in a decrease in GFR. The decreased GFR causes creatine and urea to back up in the the blood. In addition the filtrate is slower to move through the tubules so that there is more time for reabsorbtion of urea than usual.

Front 448

Describe the Cardiac Output, GFR and BUN:creatinine ratio associated with Pre-Renal Azotemia.

Back 448

Pre-Renal Azotemia is associated with decreased cardiac output, decreased GFR, and a BUN:creatinine ratio >15

Front 449

Describe a normal BUN:Creatinine Ratio.

Back 449

A normal BUN:Creatinine ratio is describe as 15 or less.

Front 450

What is another name for Renal Azotemia? What type of kidney disease does is indicate?

Back 450

Uremia. This normally indicates intrinsic kidney disease.

Front 451

Describe the damage is occuring in the kidney in Renal Azotemia. What are some examples of conditions when this occurs? What is the associated BUN:Cr ratio?

Back 451

In Renal Azotemia the problems are occurring because of parenchymal damage in the kidney. Acute Tubular Necrosis (ATN) and Chronic Renal Failure are examples of conditions that cause Renal Azotemia. In Renal Azotemia the serum BUN:Cr ratio is maintained (i.e. <15 or =15)

Front 452

Explain the pathophysiologic mechanism behind Renal Azotemia. Why is a normal to low BUN:Cr ratio maintained?

Back 452

In Renal Azotemia there is a decreased GFR, which causes creatinine and urea to back up in the blood, but in contrast to the other Azotemias, here there is extrarenal loss of the urea and so the BUN:Cr ratio remains the same or slightly decreased. Additionally, after filtration both urea and creatinine are lost in the urine because proximal tube cells are sloughed off in renal failure.

Front 453

Describe the cause of Post-Renal Azotemia. What are some examples of conditions that cause this?

Back 453

Post-Renal Azotemia is caused by urinary tract obstruction below the kidneys, with NO intrinsic parenchymal disease. Examples of this are prostate hyperplasia, blockage of ureters by stones/cancer.

Front 454

Describe the BUN:Cr ratio associated with Post-Renal Azotemia. Explain the mechanism behind this. What other type of Azotemia could this develop into if left untreated?

Back 454

The BUN:Cr ratio associated with Post-Renal Azotemia is usually >15. This happens because obstruction of urine flow decreases GFR. There is a subsequent back up of both urea and creatinine in the blood. Increased tubular pressure also causes the extra back-diffusion of urea, BUT NOT creatinine into the blood and thus contributes to a BUN:Cr ratio greater than 15. Persistent obstruction will cause Renal Azotemia with a BUN;Cr ratio

Front 455

How does Creatinine clearance correlate with age: does it increase or decrease as one ages?

Back 455

Creatinine clearance decreases with age.

Front 456

What is the standard decrease in Creatinine Clearance as you progress past the age of 50yrs?

Back 456

There is an annual decrease in CCr of 1mL/min beyond age 50.

Front 457

Describe two particular conditions where observe and INCREASE in a patient's Creatinine Clearance.

Back 457

Two conditions in which patients exhibit an increase in Creatinine Clearance are normal pregnancy and early diabetic glomerulonephropathy.

Front 458

What is a normal CCr in an adult? What is considered abnormally low? What rate indicates Renal Failure?

Back 458

A normal adult CCr is 97-137mL/min. In general, a CCr below 100mL/min is abnormally low. CCr below 10ml/min indicates renal failure.

Front 459

Explain why CCr increases with normal pregnancy.

Back 459

In pregnancy there is a increase in plasma volume that causes an increase in the GFR leading to an increase in CCr; this clearance is the highest at the end of the first semester.

Front 460

Explain why CCr increases in Early Diabetic Glomerulopathy.

Back 460

The efferent arteriole becomes constricted due to hyaline arteriolosclerosis causing an increase in the GFR and CCr. Increased GFR damages the glomerulus which leads to what is called hyperfiltration injury.

Front 461

If you see red or pink urine what could the indicate the possible presence of?

Back 461

Hematuria, hemoglobinuria, or myoglobinuria.

Front 462

Infection with what bacteria will produce alkaline urine? Why?

Back 462

Proteus infections will produce alkaline urine because the bacteria make a urease that convert urea to ammonia.

Front 463

What is the pH of the urine most often controlled by?

Back 463

The pH of the urine is determined by the diet and acid-base status of the patient.

Front 464

In what conditions are we likely to see Ketonuria? What molecules does it test for?

Back 464

Diabetic ketoacidosis, starvation, ketogenic diets, pregnancy. The dipstick ketone test only detects Acetone and AcAc, but NOT B-OHB (Hydroxybutryic Acid)

Front 465

Name a condition that would cause Hemoglobinuria.

Back 465

Intravascular Hemolytic Anemia.

Front 466

Name a condition that would lead to Myoglobinuria.

Back 466

Crush injuries.

Front 467

Name some conditions that would lead to Hematuria (RBCs in the urine).

Back 467

Renal calculus (stone), infection, cancer (renal cell carcinoma, transitional cell carcinoma), glomerulonephritis (RBCs are dysmorphic), BPH, Sterile Pyuria

Front 468

Give an example of a pathogen that might invade the urinary system an increase the concentration of Nitrites.

Back 468

This happens during a urinary tract infection with an organism such as E.Coli that is a Nitrate-reducing pathogen.

Front 469

Define Pyuria. What is Sterile Pyuria and which two pathogens/conditions can cause it?

Back 469

Pyuria is defined as the presence of neutrophils in the urine. Sterile Pyuria is the presence of neutyrophils in the urine but NEGATIVE standard urine culture. Two organisms and associated conditions that can cause a sterile Pyuria are Chlamydia trachomatis urethritis and renal tuberculosis

Front 470

When do we see Ova Fat Bodies/Lipid Casts in the urine?

Back 470

These are Renal Tubluar Cells with lipid that are found in Nephrotic Syndrome (e.g Minimal Change Disease) and can also be seen in Acute Tubular Necrosis.

Front 471

Describe the significance of Red Blood Cell Casts in the urine.

Back 471

RBC casts in the urine most often signify Nephritic type of glomerulonephritis (e.g.poststreptococcal glomerulonephritis).

Front 472

Describe the significance of White Blood Cell Casts in the urine.

Back 472

White blood cell casts in the urine often signify Acute Pyelonephritis or Acute Tubulointerstitial Nephritis (drugs).

Front 473

Describe the significance of Waxy and Broad Casts in the urine.

Back 473

The significance of Waxy and Broad casts in the urine is that they are signs of Chronic Renal failure. They often have a large diameter due to tubular atrophy.

Front 474

Describe some of the more common causes of finding Calcium Oxalate Crystals in the urine.

Back 474

A pure vegan diet, ethylene glycol poisoning, calcium oxolate caliculi.

Front 475

Describe some of the more common causes of finding Uric Acid Crystals in the urine.

Back 475

Hyperuricemia associated with Gout or Massive Destruction of Cells after Chemotherapy

Front 476

Describe some of the more common causes of finding Cystine Crystals in the urine.

Back 476

Cystinuria.

Front 477

What receives a larger proportion of the blood supply to the kidney: cortex or medulla? Which one is considered tobe relatively ischemic compared to the blood supply?

Back 477

The Cortex receives ~90% of the blood supply that goes to the kidney. The Medulla is considered to be relatively ischemic compared to the blood supply.

Front 478

The Renal arteries are considered to be end arteries. Do they have any collateral circulation feeding the kidneys? What will happen to one of the kidneys if there is an occlusion of any branch of a renal artery?

Back 478

The Renal Vessels are considered end arteries, which means there is NO COLLATERAL circulation. Occlusion of anybranch of a renal artery produces infarction.

Front 479

Which vessel contains the Juxtaglomerular apparatus? What is this collection of cells responsible for producing?

Back 479

The JG apparatus is found in the afferent arterioles of nephrons. It is responsible for the production of Renin in response to decreased perfusion pressure.

Front 480

When do we see Ova Fat Bodies/Lipid Casts in the urine?

Back 480

These are Renal Tubluar Cells with lipid that are found in Nephrotic Syndrome (e.g Minimal Change Disease) and can also be seen in Acute Tubular Necrosis.

Front 481

Describe the significance of Red Blood Cell Casts in the urine.

Back 481

RBC casts in the urine most often signify Nephritic type of glomerulonephritis (e.g.poststreptococcal glomerulonephritis).

Front 482

Describe the significance of White Blood Cell Casts in the urine.

Back 482

White blood cell casts in the urine often signify Acute Pyelonephritis or Acute Tubulointerstitial Nephritis (drugs).

Front 483

Describe the significance of Waxy and Broad Casts in the urine.

Back 483

The significance of Waxy and Broad casts in the urine is that they are signs of Chronic Renal failure. They often have a large diameter due to tubular atrophy.

Front 484

Describe some of the more common causes of finding Calcium Oxalate Crystals in the urine.

Back 484

A pure vegan diet, ethylene glycol poisoning, calcium oxolate caliculi.

Front 485

Describe some of the more common causes of finding Uric Acid Crystals in the urine.

Back 485

Hyperuricemia associated with Gout or Massive Destruction of Cells after Chemotherapy

Front 486

Describe some of the more common causes of finding Cystine Crystals in the urine.

Back 486

Cystinuria.

Front 487

What receives a larger proportion of the blood supply to the kidney: cortex or medulla? Which one is considered tobe relatively ischemic compared to the blood supply?

Back 487

The Cortex receives ~90% of the blood supply that goes to the kidney. The Medulla is considered to be relatively ischemic compared to the blood supply.

Front 488

The Renal arteries are considered to be end arteries. Do they have any collateral circulation feeding the kidneys? What will happen to one of the kidneys if there is an occlusion of any branch of a renal artery?

Back 488

The Renal Vessels are considered end arteries, which means there is NO COLLATERAL circulation. Occlusion of anybranch of a renal artery produces infarction.

Front 489

Which vessel contains the Juxtaglomerular apparatus? What is this collection of cells responsible for producing?

Back 489

The JG apparatus is found in the afferent arterioles of nephrons. It is responsible for the production of Renin in response to decreased perfusion pressure.

Front 490

What Renal-derived arachiodonic acid mediator is responsible for controlling blood flow in to the nephrons in the afferent arteriole?

Back 490

Blood flow in the afferent arterioles is controlled by PGE2 (vasodilator).

Front 491

What mediator is responsible for controlling blood flow out of nephrons in the efferent arteriole? What do the efferent arterioles eventually become?

Back 491

Blood flow in the efferent arterioles is controlled by ATII (vasoconstrictor). The efferent arterioles eventually become the peritubular capillaries.

Front 492

NSAIDs inhibit the production of PGE2 in the afferent arterioles of nephrons. Explain how this increases the risk of ischemic damage to the medulla.

Back 492

When PGE2 production is inhibited it leaves intrarenal blood flow to be completely managed by the efferent arterioles, whose blood flow is maintained by ATII, a vasoconstrictor. This puts the medulla at risk because the efferent arterioles turn into the peritubular capillaries, which dive down into the medulla and feed the tissue.

Front 493

What type of material is the Glomerular Basement Membrane made out of? What factors are the primary determinants of protein filtration through the GBM?

Back 493

Type IV collagen. The primary determinants of protein filtration are Size and Charge.

Front 494

What is the glycosaminglycan responsible for the charge of the GBM? Does it confere a positive or negative charge to the membrane? What type of proteins are permeable to the Glomerular Basement Membrane and which are not?

Back 494

Heparan sulfate is the molecule that conferes a negative charge to the GBM. Cationic proteins low molecular weight (<70,000) e.g. amino acids are permeable to the membrane. Albumin, which has a strong negative charge is NOT permeable to the membrane.

Front 495

What allows albumin to get through the GBM and pass into the urine?

Back 495

Loss of the negative charge of the membrane allows albumin to enter into and be lost in the urine.

Front 496

Describe the two main causes of GBM thickening. Provide examples of conditions that generate this.

Back 496

1) Deposition of immune complexes (e.g. Membranous glomerulonephropathy) 2) Increased synthesis of Type IV collagen (e.g. Diabetes mellitus)

Front 497

Which cells in the glomerulus are responsible for creating the Glomerular Basement Membrane?

Back 497

The Visceral Epithelial Cells with podocytes lining the glomerular capillaries are primarily responsible for production of the GBM.

Front 498

What happens to the Podocytes of the Visceral Epithelium during the Nephrotic Syndrome?

Back 498

There is fusion or effacement of the podocytes which is a sign that is present in any of the causes of the nephrotic syndrome.

Front 499

Which cells of the Glomerulus are responsible for secreting inflammatory mediators and proliferative damage in IgA Glomerulonephritis? What is the normal job of these cells?

Back 499

The cells partially responsible for releasing inflammatory mediators and causing proliferative damage in IgA glomerulonephritis are the Mesangial Cells. The normal function of the mesangial cells is to provide support to the glomerular capillaries.

Front 500

Proliferation of what cells lining Bowman's capsule causes "crescents" that destroy the glomerulus?

Back 500

The Parietal Epithelial Cells.

Front 501

What is the most common renal cystic disease seen inchildren?

Back 501

Renal Dysplasia.

Front 502

What is the most common congenital kidney disorder? Which blood vessel causes problems? What other conditions is this disorder associatedwith?

Back 502

The most common congenital kidney disorder is Horseshoe kidney (90% are fused at the lower pole). The kidney is trapped behind the root of the INFERIOR MESENTERIC ARTERY and that is what has kept it from migrating properly. With Horseshoe kidney there is an increased incidence with Turner's syndrome and danger of infection with stone formation.

Front 503

Describe the first functional change in the kidney that appears when Renal failure is occurring? (*this occurs before the BUN and creatinine begin increasing and before the appearance of any cellular casts)

Back 503

The very first function to be lost in the kidney in the setting of Renal failure is the ability to concentrate urine.

Front 504

What is a simple test that can be used to evaluate the kidney's ability to concentrate urine? What measure tells you that this ability is intact?

Back 504

First thing in the morning, after an overnight sleep (when the urine should be concentrated), obtain a urine sample from a patient and do a specific gravity test. If the specific gravity is over 1.023 the ability to concentrate urine is intact. If it is lower than this, the kidney's is may be going into failure.

Front 505

What is Urate Nephropathy? What does the pH of the urine have to be in order for this disorder to take place? How can you correct for this disorder with medication to make sure that it does not develop?

Back 505

Urate Nephropathy is the formation of Uric acid crystals in the urine. The pH of the urine must be acidic in order for these crystals to form. In order to stop the formation of these crystals in the urine you can raise the pH (alkalinization) by using carbonic anhydrase inhibitor and excreting bicarbonate.

Front 506

What restricts the movement of a horseshoe kidney? What keeps it in place? What keeps it from descending or ascending?

Back 506

The Inferior Mesenteric Artery.

Front 507

What in utero condition and what sign is infantile polycystic kidney disease associated with? Why?

Back 507

Oligohydramnios and Potter's facies. This happens because there could never be a recycling of amniotic fluid back into the womb through the kidneys. The polycystic kidneys cannot produce urine, so the fluid that is ingested by the fetus cannot be excreted an builds up in the body of the fetus. This fluid produces swelling, the oligohydramnios (lack of fluid in placenta) and Potter's facies. This is incompatible with life

Front 508

What is the genetic difference between infantile and adult polycystic kidney disease?

Back 508

Infantile polycystic kidney disease is autosomal recessive and adult polycystic kidney disease is autosomal dominant.

Front 509

What signs and injuries due to problems of blood pressure and problems of the heart will be present in someone with polycystic kidney disease? What condition might be seen in the colon?

Back 509

Hypertension that can lead to berry aneurysm and mitral valve prolapse can present in patients with polycystic kidney disease. Diverticulosis might also be present in the colon.

Front 510

What is electrochemial properties are responsible for keeping albumin out of our urine normally? What molecule is specific does this job?

Back 510

The strong negative charge of the glomerular basement membrane. The Glyscosaminoglycan Heparan Sulfate is responsible for supplying this negative charge.

Front 511

Describe the inheritance pattern of Renal Dysplasia, the most common congenital cystic disease in children. Describe the morphology of the kidney.

Back 511

There is NO inheritance pattern for Renal Dysplasia, despite it being the most common cystic disease in children. In this disease there is generally abnormal development of one or both kidneys, and abnormal structures persist in the kidneys (e.g. cartilage, immature collecting ductules). On exam, or grossly, these kidneys present as an enlarged, irregular, cystic, unilateral ( or bilateral) flank mass.

Front 512

Explain the mode of inheritance of Juvenile Polycystic Kidney Disease. Where are cysts found in the kidney and which kidney does it generally affect? What other organ does this disease affect?

Back 512

The mode of inheritance of Juvenile Polycystic Kidney Disease is Autosomal Recessive. This is a bilateral kidney disease, thus it affects both kidneys. The cysts appear in both the cortex and medulla of the kidneys. Cysts also occur in the liver, and there is an association with congenital hepatic fibrosis leading to portal hypertension. There

Front 513

Explain the mechanism of the Maternal Oligohydramnios found in Juvenile Polycystic Kidney Disease. Describe some of the deformations of the newborn that are associated with this condition.

Back 513

Patients with Juvenile Polycystic Kidney disease can prodcue Maternal Oligohydramnios because the kidneys are not able to process the amniotic fluid that the fetus ingests. The amniotic fluid cannot be recycled through the fetus and thus backs and stays in the fetus and decreases in the womb. Newborns had Potter's facies, which includes low-set ears, parrot beak nose, and lung hypoplasia.

Front 514

Describe the mode of inheritance of Adult Polycystic kidney disease. How early is the onset of this disease? At what age does Chronic Renal Failure (CRF) set in?

Back 514

The mode of inheritance of Adult Polycystic kidney disease is autosomal dominant, with bilateral cystic disease developing by age 20-25. CRF begins at age 40-60, due to destruction of kidneys by slowly expanding cysts.

Front 515

Describe the structures affected in Adult Polycystic Kidney disease. Which two other organs are commonly involved? What types of brain injury are these patients at risk for suffering and why?

Back 515

In Adult Polycystic Kidney disease cysts involve all parts of the nephron in the cortex and medulla. There are also cysts commonly present in both the liver and the pancreas. Patients with Adult Polycystic Kidney disease are at risk for stroke due to rupture of berry aneurisms or for intracerebral hemorrage due to the hypertension that is associated with 80% of cases.

Front 516

What other findings are associated with Adult Polycystic Kidney disease?

Back 516

Other findings in patients with Adult Polycystic Kidney Disease include sigmoid diverticuolsis, hematuria, mitral valve prolapse, and a risk for developing renal cell carcinoma.

Front 517

What is the inheritance pattern associated with Medullary Sponge Kidney? Describe where cysts form in the kidney with this disease and describe the appearance of key structures that are associated. What recurrent problems are associated.

Back 517

There is no inheritance pattern associated with Medullary Sponge kidney. In this disease there are often multiple cysts that appear in the collecting ducts in the medulla. Striations are present in the papillary ducts of the medulla, with a characteristic "Swiss cheese" appearance. Recurrent UTIs, hematuria, and renal stones are associated with Medullary Sponge Kidney.

Front 518

What is the most common cause of Acquired Polycystic Kidney Disease? What leads to obstruction of renal tubules? Is there a risk for the development of a particular cancer?

Back 518

The most common cause is renal dialysis and this occurs in ~50% of patients on long-term dialysis. Tubules become obstructed by interstitial fibrosis or oxalate crystals. There is a small increased risk for developing Renal Cell Carcinoma.

Front 519

What are Simple Retention Cysts of the kidney? Do children or adults get them? What findings may be in the urine? What other disease can this sometimes be confused with and how does one test to evaluate the difference?

Back 519

Simple Retention Cysts of the kidney are the most common renal cysts in adults, and they are derived from tubular obstruction. This disease may produce hematuria and may require needle aspiration to distinguish it from Renal Cell Carcinoma.

Front 520

Explain what the term Focal glomerulonephritis means.

Back 520

This designates that only a few glomeruli are abnormal in the disease.

Front 521

Explain what the term Diffuse Glomerulonephritis means.

Back 521

This term designates that all glomeruli in the kidney are found to be abnormal.

Front 522

Explain what the term Proliferative Glomerulonephritis means.

Back 522

This term designates, that in affected glomeruli, there are found to be >100 nuclei.

Front 523

Explain what the term Membranous Glomerulopathy means.

Back 523

This means that in the glomeruli you will find thick Glomerular Basement Membranes, but no proliferative change.

Front 524

Explain what the term Membranoproliferative Glomerulonephropathy means.

Back 524

This means that you will find thick Glomerular Basement Membranes and hypercellular glomeruli

Front 525

Explain what the term Focal Segmental Glomerulosclerosis means.

Back 525

This designates that there is fibrosis involving only a segment of the involved glomerulus.

Front 526

Explain what the term Crescentic Glomerulonephritis means.

Back 526

This describes the proliferation of parietal epithelial cells around the glomerulus.

Front 527

Explain what the term Primary Glomerular Disease means. Provide an example.

Back 527

This means that the disease involves only glomeruli and NO other target organs. (e.g. Minimal Change disease)

Front 528

Explain what the term Secondary Glomerular Disease means. Provide an example.

Back 528

This means that the disease involves only glomeruli and other target organs. (e.g. SLE).

Front 529

What type of Hypersensitivity Reaction is associated with a linear patter of Immunofluorescent staining of the glomeruli?

Back 529

Type II Hypersensitivity- Autoantibody deposition.

Front 530

What type of Hypersensitivity Reaction is associated with a granular patter of Immunofluorescent staining of the glomeruli?

Back 530

Type III Hypersensitivity- Immune complex deposition.

Front 531

What are the sites of immune complex depostion in the found in the glomerulus?

Back 531

Subepithlial, Subendothelial, and Intramembranous/Mesangial.

Front 532

Explain the mechanism by which immune complex deposition in the glomeruli leads to damage of the tissue.

Back 532

The immune complexes seem to activate the compliment system. C5a is produced, which is chemotactic to neutrophils. Neutrophils in turn, damage the glomeruli.

Front 533

What are the three mechanisms known to cause glomerular disease?

Back 533

1) Autoantibodies directed against the GBM (Type II Hypersensitivity- Goodpasture's syndrome) 2) Immune complex deposition (Type III Hypersensitivity- poststreptococcal glomerulonephritis) 3) T-cell production of cytokines

Front 534

How does the T-cell production of cytokines lead to damaging of the glomeruli? What is an example of a disease that does this?

Back 534

The cytokines cause the GBM to lose its negative charge. An example of a disease that does this is Minimal Change Disease.

Front 535

What are the three types of the clinical manifestations of glomerular diseases?

Back 535

Nephritic Syndrome, Nephrotic Syndrome, and Chronic Glomerulonephritis.

Front 536

What is the most common mechanism causing glomerulonephritis?

Back 536

Immune complex deposition is the most common mechanism causing glomerulonephritis.

Front 537

Describe the clinical and laboratory findings associated with Nephritic syndrome.

Back 537

Hypertension (Na+ retension), Periorbital swelling, Oliguria (<400mL urine/day), Hematuria (dysmorphic RBCs with irregular membranes), Neutrophils in the sediment (particular in IC types), RBC casts are a key finding, proteinuria <3.5g/day, and Azotemia with BUN:Cr >15.

Front 538

What are the two key findings that indicate Nephritic Syndrome.

Back 538

Moderate proteinuria (0.150g-3.5g/day) and RBC casts.

Front 539

What are the common examples of primarily Nephritic types of glomerular disease.

Back 539

IgA Glomerular Nephropathy (Berger's disease), Poststreptococcal glomerulonephritis, Diffuse Proliferative glomerulonephritis (SLE), Rapidly Progressive glomerulonephritis.

Front 540

Describe the most common type of glomerulonephritis. What is this due to? Where in the glomerulus does the problem occur?

Back 540

The most common type if glomerulonephritis is IgA Glomerulopathy (Berger's disease). This disease is due to the increased mucosal synthesis and decreased clearance of IgA (There is an increased serum IgA associated with ~50% of cases). The IgA Immunocomplexes (Type III Hypersensitivity) deposit amongst the mesangial cells and then activate the complement pathway to cause damage to the glomeruli.

Front 541

What other disease might IgA glomerulonephropathy have overlapping features with? What signs might you find in the urine? What type of sickness does this usually follow? Can this condition progress to CRF (Chronic Renal Failure)?

Back 541

IgA Glomerulonephropathy may have overlapping features of disease shared with Henoch-Schonlein purpura. There may also be episodic bouts of hematuria (either microscopic or gross), which usually follows an upper respiratory infection. IgA Glomerulonephropathy has a 40-50% chance of slowly progressing to CRF.

Front 542

What is the most common type of postinfectious glomerulonephropathy? Where are the deposits found in the glomerui?

Back 542

Poststreptococcal Glomerulonephritis. This usually follows Group A streptococcal infections of the skin (e.g. Scarlet Fever) or pharynx. Subepithelial IC deposits are found upon inspection of the glomeruli.

Front 543

Describe the pathogenesis of Poststreptococccal Glomerulonephritis. Titers of what antibodies are increased in the serum? Does this PS Glomerulonephritis usually progress to CRF?

Back 543

Poststreptococcal glomerulonephritis is caused by Subepithelial IC deposits. ICs activate the Alternative Compliment Pathway and there is also a diffuse proliferative pattern with neutrophil infiltration. There are increased titers of anti-DNAase B and hematuria may show up 1-3 weeks post infection. This disease usually resolves and it is uncommon for it to progress to CRF.

Front 544

What disease is most often the cause of Diffuse Proliferative Glomerulonephritis? What type of deposits are seen in the glomeruli and what are they made of? What is a key descriptive feature of this disease and what is being describe?

Back 544

Diffuse Proliferative GN is the most common subtype of glomerular disease in SLE. Subendothelial deposits of DNA-anti-DNA ICs activate the classical compliment pathway. In this disease there is seen to be "wire looping" of the capillaries, which are indicative of subendothelial ICs. There is also neutrophil infiltration with hyaline thrombi in capillary lumens.

Front 545

Kidneys are the major target organ for what autoimmune disease that presents with a malar rash; what type of syndrome is produced? What does a serum ANA test showing rim patterns correspond to the presence of? Can this possibly progress to CRF?

Back 545

Kidneys are the major target organ in SLE (~90% of cases) and is responsible for producing Diffuse Porliferative Glomerulonephritis. Serum ANA test showing a rim pattern correspond to the presence of anti-dsDNA antibodies. Diffuse Proliferative Glomerulonephritis due to SLE usually evolves into CRF and is a common cause of death in patients with SLE.

Front 546

What are three clinical diseases associated with Rapidly Progressive Glomerulonephritis? What does this normally progress to and over what time course? Is this a syndrome due to primary or secondary types of glomerular disease?

Back 546

Rapidly Progressive glomerulonephritis is associated with Goodpasture syndrome, microscopic polyarteritis (p-ANCA), and Wegener's granulomatosis (c-ANCA). This syndrome usually leads to the rapid loss of renal function and progresses to ARF over days to weeks (very poor prognosis). This syndrome can be due to both primary and secondary types of glomerular disease.

Front 547

What renal syndrome is Goodpasture syndrome associated with? What type of hypersenstivity is it and what are titers do we look for in the serum? What is the IF pattern? Are the EM electron dense deposits? When does crescentic GN begin?

Back 547

Goodpasture is associated with Rapidly Progressive Glomerulonephritis. This is associated with Type II Hypersensitivity, in which we look for anti-Glomerular Basement Membrane antibodies. The IF looks linear and there are NO electron dense deposits seen with EM. Crescentic GN begins with hemoptysis and ends with renal failure.

Front 548

Which has more glomerular inflammation: nephritic or nephrotic syndrome?

Back 548

Nephritic Syndrome.

Front 549

What is the key proteinuria finding in Nephrotic Syndrome? Which clinical features can it share with liver failure and why? What condition is there an increased risk of developing and with from what organism (in adults vs. children).

Back 549

The key finding in Nephrotic syndrome is proteinuria greater than 3.5g/24hrs. Two clinical features that Nephrotic syndrome shares with liver failure are pitting edema and ascites due to hypoalbuminemia. With this there is an increased risk of developing spontaneous peritonitis; with adults the organism responsible is usually E.coli, and with children usually Strep.pneumo.

Front 550

Besides massive proteinuria, pitting edema, and ascites associated with the Nephrotic syndrome, what other laboratory and clinical findings are often associated?

Back 550

Hypertension in some types (due to salt retention), Hypercoagulabe state due to loss of antithrombin III (potential for renal vein thrombosis), Hypercholesterolemia (hypoalbuminemia increases cholesterol synthesis through an unknown mechanism), Hypogammaglobulinemia (due to loss in the urine), and Fatty Casts (Maltese Crosses and oval fat bodies).

Front 551

What are the two most indicative findings associated with the Nephrotic syndrome?

Back 551

Proteinuria greater than 3.5g/day and Fatty Casts with Maltese cross and oval fat bodies. The Maltese crosses are due to cholesterol, which is always increased in nephrotic syndrome.

Front 552

What is the most common type of postinfectious glomerulonephropathy? Where are the deposits found in the glomerui?

Back 552

Poststreptococcal Glomerulonephritis. This usually follows Group A streptococcal infections of the skin (e.g. Scarlet Fever) or pharynx. Subepithelial IC deposits are found upon inspection of the glomeruli.

Front 553

Describe the pathogenesis of Poststreptococccal Glomerulonephritis. Titers of what antibodies are increased in the serum? Does this PS Glomerulonephritis usually progress to CRF?

Back 553

Poststreptococcal glomerulonephritis is caused by Subepithelial IC deposits. ICs activate the Alternative Compliment Pathway and there is also a diffuse proliferative pattern with neutrophil infiltration. There are increased titers of anti-DNAase B and hematuria may show up 1-3 weeks post infection. This disease usually resolves and it is uncommon for it to progress to CRF.

Front 554

What disease is most often the cause of Diffuse Proliferative Glomerulonephritis? What type of deposits are seen in the glomeruli and what are they made of? What is a key descriptive feature of this disease and what is being describe?

Back 554

Diffuse Proliferative GN is the most common subtype of glomerular disease in SLE. Subendothelial deposits of DNA-anti-DNA ICs activate the classical compliment pathway. In this disease there is seen to be "wire looping" of the capillaries, which are indicative of subendothelial ICs. There is also neutrophil infiltration with hyaline thrombi in capillary lumens.

Front 555

Kidneys are the major target organ for what autoimmune disease that presents with a malar rash; what type of syndrome is produced? What does a serum ANA test showing rim patterns correspond to the presence of? Can this possibly progress to CRF?

Back 555

Kidneys are the major target organ in SLE (~90% of cases) and is responsible for producing Diffuse Porliferative Glomerulonephritis. Serum ANA test showing a rim pattern correspond to the presence of anti-dsDNA antibodies. Diffuse Proliferative Glomerulonephritis due to SLE usually evolves into CRF and is a common cause of death in patients with SLE.

Front 556

What are three clinical diseases associated with Rapidly Progressive Glomerulonephritis? What does this normally progress to and over what time course? Is this a syndrome due to primary or secondary types of glomerular disease?

Back 556

Rapidly Progressive glomerulonephritis is associated with Goodpasture syndrome, microscopic polyarteritis (p-ANCA), and Wegener's granulomatosis (c-ANCA). This syndrome usually leads to the rapid loss of renal function and progresses to ARF over days to weeks (very poor prognosis). This syndrome can be due to both primary and secondary types of glomerular disease.

Front 557

Describe the most common cause of Nephrotic Syndrome in children. Who gets it more often, girls or boys? `

Back 557

The most common cause of Nephrotic syndrome in children is Minimal Change disease. This occurs more commonly in girls than in boys and in ~15% of adults with nephrotic syndrome.

Front 558

Describe the pathophysiology associated with the nephrotic syndrome, Minimal Change disease. What are some of the secondary causes of this disease? What do the glomeruli look like? What is seen on IF and EM?

Back 558

Minimal change disease is associated with T-Cell cytokines causeing damage to the GBM. This damage causes the GBM to lose its negative charge and allow the SELECTIVE PASSAGE OF ALBUMIN, but not globulins into the urine (Selective Proteinuria). Some secondary causes of Minimal Change Disease include NSAIDs and Hodgkin's Lymphoma. The glomeruli are structurally normal, but there will be postive fat stains in the glomerulus and tubules. There will be a negative IF and EM will show fusion of podocytes and NO deposits.

Front 559

What often precedes the nephrotic syndrome Minimal Change disease in children? Describe the type of therapy for this disease and how patients respond.

Back 559

Minimal Change disease is often preceeded by respiratory infection or routine immunization. The therapy for this disease most often consists of steroid therapy because the pathophysiology lies in productions of cytokines by T-cells. Patients generally respond well to this therapy and progression into CRF is rare.

Front 560

What is a key separating feature of Minimal change disease from other nephrotic syndromes with regard to blood pressure?

Back 560

A key feature of Minimal change disease that separates it from other nephrotic syndromes is that patients are often Normotensive.

Front 561

Focal Segmental Glomerularsclerosis can be either a primary or secondary disease. Describe two of the most common secondary causes. What are the laboratory findings on IF and EM? What type of proteinuria and hemtauria are seen? Prognosis?

Back 561

Focal segmental glomerulosclerosis is often secondarily cause by HIV and Intravenous Heroin abuse. IF findings are negative, but EM will show focal damage of the Visceral Epithelial Cells. Non-selective proteinuria and microhematuria are present are common. This disease has a poor prognosis and commonly progresses to CRF.

Front 562

What is the most common glomerular disease found in HIV patients?

Back 562

Focal Segmental Glomerulosclerosis.

Front 563

Diffuse Membranous Glomerulopathy is the most common cause of nephrotic syndrome in adults and has both primary and secondary causes. What are some of its secondary causes?

Back 563

Drugs: e.g. Captopril Infections: HBV, Plasmodium malariae, syphilis Malignancy: carcinomas, non-Hodgkins lymphoma Autoimmune disease: SLE (nephrotic presentation)

Front 564

Describe the microscopic characteristics that are seen in a patient with Diffuse Membranous Glomerulopathy.

Back 564

In Diffuse Membranous Glomerulopathy we see diffuse thickening of membranes; silver stains show "spike and dome" pattern beneath visceral epithelial cells (subepithelial deposits). We also see subepithelial ICs with granular IF.

Front 565

What is the most common type of Membranoproliferative Glomerulonephritis (is nephrotic syndrome the only way it presents)? What other conditions is it associated with?

Back 565

The most common type of MPGN is Type I MPGN. Though usually a nephrotic syndrome this can sometimes present as a nephritic syndrome. Type I MPGN is most commonly associated with HBV, HCV, or Cryoglobulinemia.

Front 566

What type of glomerular deposits do we see with Type I MPGN. Explain the pathophysiology behind this disease. Desribe the characteristic signs we see on EM. Does this progress to CRF?

Back 566

In Type I MPGN we see Subendothelial IC deposits with a granular IF. ICs activate the classical and alternative complement pathways that then cause damage. EM shows tram tracks caused by splitting of the GBM by an ingrowth of mesangium. The majority of these cases progress to Chronic Renal Failure.

Front 567

Describe the special "factor" that Type II MPGN (Dense Deposit Disease) is associated with and how is contributes to the pathophysiology of this disease. What does the EM show? Does this disease progress to CRF?

Back 567

Type II MPGN is associated with the C3 Nephritic Factor (C3NeF), an autoantibody that binds to C3 convertase (C3bBb) and prevents the degradation of C3 convertase causing sustained activation of C3 and resulting in very low levels of C3. EM shows diffuse intramembranous deposits ("Dense Deposit Disease") with "tram tacks". This disease is seen more often with renal transplant patients and has a poor prognosis with most peopl progressing to CRF.

Front 568

What are the other two names that Diabetic Glomerulosclerosis goes by? Does this occur with both types of Diabetes? Describe the risk factors associated with the development of this disease.

Back 568

Nodular Glomerulosclerosis and Kimmelstiel-Wilson Disease. This can occur in both Type I and Type II diabetes, but more often is seen associated with Type I. The risk factors associated with Diabetic Glomerulosclerosis are Poor glycemic control, Hypertension, and Diabetic Retinopathy (there is a high correlation with coexisting glomerulonephropathy).

Front 569

What is the most common cause of renal failure in the U.S.?

Back 569

The most common cause of renal failure in the U.S. is poorly controlled Diabetes.

Front 570

Describe the pathogenesis of Diabetic Glomerulonephropathy with respect to NEG (Nonenzymatic Glycosylation), Osmotic damage, Hyperfiltration, and Collagen deposition.

Back 570

NEG, which is the attaching of glucose to amino acids, of the GBM and tubule basement membranes increases vessel and tubular permeability to proteins. NEG of the afferent and efferent arterioles produces hyaline arteriolosclerosis and generally involves the efferent arteriole before the afferent. This leads to constriction in the efferent arteriole that increases GFR and leads Hyperfiltration injury of the mesangium. Osmotic damage occurs to the glomerular capilary endothelial cells when glucose is converted to sorbitol inside the cells and water follows. Diabetic microangiopathy leads to increased collagen deposition of Type IV collagen in the GBM, tubular basement membranes, and mesangium.

Front 571

What effect does Diabetic Glomerulosclerosis have on podocytes?

Back 571

The EM of a glomerulus from a patient with Diabetic Glomerulonephropathy will show fusion of podocytes.

Front 572

What are the nodular masses seen in the glomeruli of patients with Diabetic Glomerulosclerosis representative of?

Back 572

These nodular masses are representative of increased type IV collagen synthesis and trapped proteins in the mesangial matrix.

Front 573

How long does it take for microalbuminuria to develop in a patient with diabetic glomerulosclerosis? How do we test for it?

Back 573

It usually takes ~10 years of poor glycemic control for the manifestation of microalbuminuria. This is detected with a microalbuminuria dipstick which detects levels of 1.5-8mg/dL protein in the urine.

Front 574

What are other diseases associated with diabetes other than diabetic glomerulosclerosis?

Back 574

Renal papillary necrosis, acute and chronic pyelonephritis.

Front 575

What is the rational behind treating Diabetic Glomerulosclerosis with an ACE inhibitor?

Back 575

ACEi's are prescribed when microalbuminuria is first detected. It slows the progression of diabetic glomerulopathy by decreasing pressure in the glomerular capillaries by decreasing ATII vasoconstriction of the hyalinized efferent arterioles.

Front 576

What is the mode of inheritance associated with Alport's syndrome? Explain the pathophysiologic mechanism behind this syndrome. Describe the microscopic findings. Are there any other effects that occur outside the kidneys?

Back 576

Alport's syndrome is an X-linked dominant disease 85% of the time. This disease comes from a defect in the synthesis of alpha-5-subtype type IV collagen in the GBM. The microscopic findings include lipid accumulation in VECs producing foam cells. Sensorineural hearing loss and ocular abnormalities are also commonly present.

Front 577

What are the big three symptoms associated with the hereditary glomerular disease, Alport's syndrome?

Back 577

Hereditary nephritis, sensorineural hearing loss, and ocular defects.

Front 578

What are the findings seen in Thin Basement Membrane Disease? Describe the mode of inheritance.

Back 578

Thin Basement Membrane Disease is a "benign familial hematuria" with an autosomal dominant mode of inheritance. The GBMs are extremely thin and there is mild proteinuria and persistent microscopic hematuria, but there is still normal renal function

Front 579

Name the four major causes of Chronic glomerulonephritis in descending order of incidence.

Back 579

1) Rapidly progressive glomerulonephritis (RPGN) 2) Focal segmental glomerulosclerosis 3) Type I Membranoproliferative glomerulonephritis 4) IgA glomerulonephritis

Front 580

Describe the gross and microscopic findings associated Chronic glomerulonephritis.

Back 580

Shrunken kidneys, glomerular sclerosis and tubular atrophy.

Front 581

What is the most common cause of acute renal failure?

Back 581

The most common cause of acute renal failure (ARF) is Acute Tubular Necrosis, which is further subdivided into ischemic and nephrotoxic subtypes.

Front 582

What are two definitional clinical findings that are associated with Acute Renal Failure?

Back 582

Acute Renal Failure is seen to be accompanied by acute suppression of renal function developing in 24hrs. It is also characterized by anuria or oliguria (<400mL/24hrs)

Front 583

Besides Acute Tubular Necrosis, what are some other causes of acute renal failure? Provide examples.

Back 583

Postrenal obstruction: e.g. prostate hyperplasia, invasive cervical cancer Vascular disease: e.g. malignant hypertension Other: RPGN, drugs, DIC, urate nephropathy

Front 584

What is the most common subtype of Acute Tubular Necrosis? Describe the most common cause of this subtype.

Back 584

The most common subtype of Acute Tubular Necrosis is Ischemic Acute Tubular Necrosis. This is most commonly caused by prerenal azotemia due to hypovolemia.

Front 585

Describe the effects of ischemic damage to the endothelial cells associated with Ischemic ATN.

Back 585

Ischemic damage to endothelial cells causes decreases in vasodilators (e.g. NO, PGi2), increase in vasoconstrictors (e.g. endothelin), with the overall net effect of vasoconstriction of afferent arterioles, which decreases GFR.

Front 586

What is a key cellular cast of Acute Tubular Necrosis?

Back 586

The Renal tubular cell cast is a key cast of ATN.

Front 587

Describe the ischemic damage of tubule cells associated with Ischemic Acute Tubular Necrosis.

Back 587

The ischemic damage of tubule cells associated with Ischemic Acute Tubular Necrosis causes detachment of tubular cells into the lumen causing obstruction, and production of pigmented renal tubular cell casts. These casts also obstruct the lumen causing and increase in intratubular pressure, which decreases GFR, pushes fluid into the interstitium, and has the net effect of oliguria.

Front 588

Where is the site of tubular damage associated with Ischemic ATN?

Back 588

1) Straight Segment of Proximal tubule (part of the nephron most susceptible to hypoxia) 2) Medullary segment of the thick ascending limb (TAL) 3) Tubular Basement Membranes are disrupted at these sites (this prevents renal tubular cell regeneration)

Front 589

What is the most common cause of Nephrotoxic ATN? Describe some other causes. What are some of the microscopic findings associated?

Back 589

Aminoglycosides are the most common cause (e.g. gentamycin) of Nephrotoxic ATN. Some of the other causes include radiocontrast agents, and heavy metal agents (e.g. lead and mercury). Microscopic findings include primarily damages in the proximal tubule cells, with the tubular basement membrane remaining intact.

Front 590

Describe the clinical and laboratory findings associated with ATN.

Back 590

Oliguria is present in most cases, although some cases have polyuria (>800mL/24hrs), there are pigmented renal tubular cell casts present in the urine, hyperkalemia and increased anion gap metabolic acidosis, increased serum BUN and creatinine with a ratio

Front 591

Describe the urine outputs that define Oliguria. What are the major causes of Oliguria?

Back 591

Oliguria is defined as a urine output <400mL/day or <20mL/hr. The major causes of oliguria include: -Prerenal azotemia (most common cause) -Acute Glomerulonephritis (nephritic type) -Acute Tubular Necrosis (renal azotemia) P -Postrenal azotemia.

Front 592

What are the four tests that we use to differentiate the types of oliguria? What are they evaluating in order to give us insight as to the etiology of a patients oliguria

Back 592

-Urine Osmolarity (UOsm) -Fractional Excretion of Na+ (FENa+) -Random Urine Na+ (UNa+) -Serum BUN:Cr Ratio These tests are evaluating tubular function.

Front 593

When using the Urine Osmolarity (UOsm) to evaluate the cause of Oliguria, what do the results indicated based on the defined parameters?

Back 593

A UOsm >500 mOsm/kg indicates good concentrating ability and intact tubular function, while a UOsm <350 mOsm/kg indicates poor concentrating ability and tubular dysfunction.

Front 594

When using the Fractional Excretion of Na+ (FENa+) to evaluate the cause of Oliguria, what do the results indicated based on the defined parameters?

Back 594

The FENa+ represents that amount of Na+ excreted by the urine divided by the amount of Na+ filtered by the kidneys. An FENa+ <1% indicates good tubular function and >2% indicates tubular renal dysfunction (and for this test is highly predictive of ATN as the cause of Oliguria).

Front 595

When using the Random Urine Na+ (UNa+) to evaluate the cause of Oliguria, what do the results indicated based on the defined parameters?

Back 595

A random UNa+ <20mEq/L indicates intact tubular function, and a random UNa+ >40mEq/L indicates tubular dysfunction.

Front 596

When using the Serum BUN:Cr Ratio to evaluate the cause of Oliguria, what do the results indicated based on the defined parameters?

Back 596

A serum BUN:Cr ratio >15 indicates intact tubular function, and a serum BUN:Cr ratio =/<15 indicates tubular dysfunction.

Front 597

Prerenal Azotemia and Acute Glomerulonephritis are both possible causes for Oliguria. Of the four tests we use to evaluate tubular function we see that both these test come back with preserved tubular function. So, how do we differentiate between these two diseases?

Back 597

To distinguish between Prerenal Azotemia and Acute Glomerulonephritis Urine Sediment Examination is most useful. In Prerenal Azotemia the sediment has NO abnormal findings, or may have a few hyaline casts. The sediment in Acute Glomerulonephritis (nephritic type) has hematuria and RBC casts.

Front 598

Postrenal Azotemia and Acute Tubular Necrosis are both possible causes for Oliguria. Of the four tests we use to evaluate tubular function we see that both these test come back with tubular dysfunction. So, how do we differentiate between these two diseases?

Back 598

To distinguish ATN from Postrenal Azotemia as a cause of tubular dysfunction and oliguria urine sedimentation is most useful. ATN will have a sediment with pigmented renal tubular cell casts, while Postrenal Azotemia will have a normal sediment and a history of obstruction.

Front 599

What do the four tests for causes of Oliguria show for Prerenal Azotemia and AGN? What are the sedimentation findings that differentiate the two?

Back 599

(FNa+)- <1% (BUN:Cr)- >15 (UNa+)- <20 (UOsm)- >500 Sedimentation for Prerenal Azotemia is normal (or maybe hyaline casts), but AGN shows hematuria and RBC casts.

Front 600

What do the four tests for causes of Oliguria show for Postrenal Azotemia and ATN? What are the sedimentation findings that differentiate the two?

Back 600

(FNa+)- >1% (BUN:Cr)- 20 (UOsm)- <350 Sedimentation for Postrenal Azotemia shows normal sediment, but ATN shows Renal Tubular Casts.

Front 601

What is the most common cause of Tubulointerstitial Nephritis (TIN)? Name two other causes.

Back 601

The most common cause of Tubulointerstitial Nephritis is Acute pyelonephritis. Other causes include drugs, less common infections such as Legionella and Leptospirosis, SLE, leadpoisoning, urate nephropathy and multiple myeloma.

Front 602

Describe some of the risk factors associated with Acute Pyelonephritis (APN)?

Back 602

Some of the risk factors for APN include urinary tract obstruction, medullary sponge kidney, diabetes mellitus, pregnancy, and sickle cell trait/disease.

Front 603

Describe the most common etiology behind Acute Pyelonephritis and explain the mechanism.

Back 603

The most common pathogenic process leading to APN is Vesiculoureteral Reflux (VUR) with ascending infection. In VUR the intravesicular portion of the ureter is NOT compressed during micturation as it normally should be and urine refluxes into the ureter.

Front 604

What abnormality in function must be present in order for an ascending infection of the lower urinary tract to cause APN?

Back 604

If Vesiculo ureteral reflux (normally reflux is blocked during micturation) is present infected urine ascends to the renal pelvis and renal parenchyma and causes APN.

Front 605

Describe the gross and microscopic findings associated with APN.

Back 605

Grossly, grayish white areas of abscess formation are in the cortex and medulla. Microscopically, microabscess formation occurs in the tubular lumens and the interstitium.

Front 606

Describe the clinical findings associated with APN. What is a key laboratoty finding?

Back 606

APN presents with spiking fever, flank pain, increased frequency of urination, and painful urination (dysuria). WBC casts are a key laboratory finding. Pyuria, bacteriuria, and hematuria are common.

Front 607

Describe the clinical findings that are present with APN, but not lower UTIs.

Back 607

APNs, and not lower UTIs, present with flank pain, and WBC casts in the urine.

Front 608

Explain some of the complications associated with APN.

Back 608

Some of the complications of APN include Chronic pyelonephritis, Perinephric abscess, Renal papillary necrosis, Septicemia with endotoxic shock.

Front 609

What are the two causes of Chronic Pyelonephritis?

Back 609

CPN is most likely to be cause by either VUR starting in young girls or Lower urinary tract obstruction (produces hydronephrosis- e.g. prostatic hyperplasia, renal stones)

Front 610

Describe the difference of the gross findings associated with Reflux type CPN vs. Obstructive type CPN.

Back 610

In the Reflux type CPN we see U-shaped cortical scars overlying a blunt calyx whereas in the Obstructive type we see Uniform Dilation of the calyces (like in bronchiectasis in the lungs), with diffuse cortical tissue.

Front 611

Describe the microscopic findings associated with CPN.

Back 611

Because of the chronic inflammation associated with CPN, we see secondary scarring of the glomeruli. There is tubular atrophy and the tubules contain eosinophilic material resembling thyroid tissue ("thyroidization").

Front 612

What are the clinical findings associted with CPN?

Back 612

When a patient presents with CPN there is usually a history of recurrent APN. CPN may cause hypertension (as refluxnephropathy is a cause of hypertension in children), and it may cause CRF.

Front 613

What are the common drugs that can cause Tubulointerstitial Nephritis?

Back 613

Penicillin (particularly methicillin), Rifampin, Sulfonamides, NSAIDs, and Diuretics

Front 614

Explain the pathogenesis of Acute Drug-induced Tubulointerstitial Nephritis (TIN). What type of hypersensitivities are involved? How long does it take for symptoms to show up? Describe the clinical findings associated.

Back 614

Acute drug-induced TIN occurs through a combination of Type I and Type IV hypersensitivity about 2 weeks after begin a new course of treatment. The clinical and laboratory findings associated with drug-induced TIN include the abrupt onset of fever, oliguria, and rash, with eosinophilia and eosinophiluria (highly predeictive). BUN:Cr ratio is

Front 615

Which two drugs are the cause of Analgesic Nephropathy? What type of nephritis does it cause? Explain the pathogenesis of these two drugs and what complications can occur as a result of this disorder. Who experiences this more often, men or women?

Back 615

The drugs responsible for inducing Analgesic Nephropathy are Acetaminophen and Aspirin. They cause a type of Tubulointerstitial Nephritis (TIN). The chronic use of Acetaminophen for more than 3 years causes free radical damage to the renal tubules in the medulla and Aspirin inhibits renal synthesis of PGE2 leaving ATII unopposed and inhibits blood flow to the renal medulla. This occurs more often in women than in men and complications can include Renal papillary necrosis, Hypertension, CRF, and Renal Pelvic and Bladder Transitional cell carcinomas.

Front 616

What is a key finding/complication associated with Analgesic Nephropathy? How does it present? Describe what it looks like on histopathology. What are other causes of this complication?

Back 616

A key finding in Analgesic Nephropathy is Renal Papillary Necrosis. This is a sloughing off of the renal papillae that produces gross hematuria, proteinuria, and colicky flank pain. An IVP shows a "ring defect" where one or more papillae used to reside. Other causes of renal papillary necrosis include Diabetes, Sickel Cell trait/disease, and APN.

Front 617

Analgesic Nephropathy is a combination of what drugs leading to what key finding?

Back 617

Acetaminophen + Aspirin => Renal Papillary Necrosis

Front 618

Urate Nephropathy is most commonly due to what type of treatment? How can Urate Nephropathy be avoided in this setting? What are other causes of Urate Nephropathy?

Back 618

Urate Nephropathy occurs due to the massive release of purines such as that associated with the aggressive treatment of disseminated cancer (e.g. Leukemia). This can be prevented with the use of Allopurinol before treatment. Lead poisoning and Gout can also cause Urate Nephropathy.

Front 619

What are effects are produced in the kidney as a result of Chronic Lead Poisoning? Describe the characteristic inclusions that signify lead poisoning.

Back 619

As a result of Chronic Lead Poisoning, the kidney decreases the secretion of uric acid (which leads to Urate Nephropathy). The lead also has a direct toxic effect that produces TIN. In the proximal tubule cells there will likely be characteristic acid-fast inclusions seen.

Front 620

How does Multiple Myeloma cause problems with proteinuria in the kidney? What are the special protein casts we see with this disease? What is the characteristic "reaction" and what parts of the nephron does it involve?

Back 620

Multiple Myeloma causes a particular type of proteinuria called Bence-Jones (BJ) proteinuria. BJ proteinuria produces tubular casts from light chain proteins that are toxic to the renal tubular epithelium. Casts obstruct the lumen and incite a foreign body giant cell reaction. This reaction involves the tubules and interstitium leading to renal failure.

Front 621

What are the two conditions, other than BJ proteinuria, that affect the kidney due to Multiple Myeloma?

Back 621

Two other conditions that Multiple Myeloma produces in the kidneys are Nephrocalcinosis and Primary Amyloidosis.

Front 622

Describe how Nephrocalcinosis due to Multiple Myeloma affects the kidney.

Back 622

Nephrocalcinosis is due to hypercalcemia and involves the metastatic calcification of the basement membrane of the collecting tubules. This ultimately causes polyuria and renal failure.

Front 623

Describe how Amyloidosis due to Multiple Myeloma affects the kidney.

Back 623

Primary Amyloidosis produces nephrotic syndrome as the BJ light chain proteins are converted to amyloid.

Front 624

Describe the epidemiology and pathogenesis of Chronic Renal Failure. How long does it take to develop? What is the GFR associated? What are the main primary causes?

Back 624

CRF involves progressive, irreversible azotemia that develops over months to years. The kidney no longer functions well enough to sustain life and the GFR drops to below 10mL/min. The primary causes of CRF in descending order are Diabetes, Hypertension Glomerulonephritis (RPGN and FSGS particularly), and Cystic Renal disease (Renal dysplasia in children and Adult Polycystic Kidney disease).

Front 625

Describe the gross appearance of the kidneys seen in patients with CRF. What are the hematologic findings associated?

Back 625

Upon gross examination of Kidneys that suffered CRF, bilaterally they appear small and shrunken. Hematologic findings in the patient might include Normocytic anemia (primarily due to decreased erythropoetin production) and qualitative platelet defects.

Front 626

Name the conditions that contribute to the Renal Osteodystrophy found in Chronic Renal Failure.

Back 626

Osteitis fibrosa cystica, Osteomalacia, and Osteoporosis.

Front 627

Explain how CRF can lead to Osteitis cystica. What role does Vit. D and PTH play?

Back 627

Osteitis cystica of CRF is due to Hypovitaminosis D. Alpha-1 Hydroxylase cannot make Vit D and this leads to hypocalcemia. Hypocalcemia in turn stimulates the production of PTH (2ndary HPTH). 2ndary HPTH increases bone resorption and causes lytic lesions in the bone (e.g. jaw). Hemorrhage into cysts causes brown discoloration.

Front 628

Explain how CRF can lead to Osteomalacia. What role does Vit. D play?

Back 628

Hypovitaminosis D associtated with CRF leads hypocalcemia which leads to decreased bone mineralization (Osteomalacia). This produces fractures and bone pain in the patient.

Front 629

Explain how CRF can lead to Osteoporosis. What role does PTH and metabolic acidosis play?

Back 629

Osteoporosis is the loss of bone matrix (osteoid) and minerals, which causes an overall reduction in bone mass. In CRF it is due to chronic metabolic acidosis and high levels of PTH. Excess H+ ions are buffered by bone. This also produces fractures and bone pain.

Front 630

Describe the Cardiovascular findings associated with CRF and why they happen.

Back 630

Hypertension from salt retension, Hemorrhagic fibrinous pericarditis from high uremic levels, and CHF with accelerated atherosclerosis (likely from hypertension).

Front 631

Hemorrhagic gastritis and Uremic frost (urea crystals that deposit on the skin) are both associated with what end-stage kidney disease?

Back 631

Chronic Renal Failure (CRF).

Front 632

Describe the Acid-Base and electrolyte abnormalities associated with CRF.

Back 632

Hyperkalemia and increased ion gap metabolic acidosis are included. Sodium is usually normal except in salt losing types of CRF.

Front 633

Describe the two causes of Hypocalcemia seen in CRF.

Back 633

Hypovitaminosis D due to decreased synthesis of 1-alpha-hydroxylase leads to decreased reabsorption of calcium from the small intestine. Hyperphosphatemia precipitates calcium into bone and soft tissue, which pulls calcium out of serum and leads to metastatic calcification.

Front 634

Which type of casts are seen to be a sign of CRF?

Back 634

Waxy and broad casts.

Front 635

What is the most common disease of essential hypertension? Explain the pathogenesis. Describe the gross appearance of the kidney and what can be found on lab results.

Back 635

Benign Nephrosclerosis is the most common renal disease of essential hypertension. Hyaline arteriolosclerosis of arterioles in the renal cortex leads to increased intrarenal pressures and inflammation and causes tubular atrophy, interstitial fibrosis, and glomerularsclerosis. Grossly, the kidneys present with a finely granular cortical surface. Lab results show mild proteinuria, hematuria without RBC casts, and renal azotemia.

Front 636

Explain the epidemiology of Malignant Hypertension. What is the underlying background of disease that it is seen most in? What are risk factors for its development?

Back 636

Malignanat hypertension is the sudden onset of elevated hypertension that is most often seen on a background of Benign nephrosclerosis (BNS). It may also occur in normal individuals and as a complication of many other disorders. Risk factors include pre-existing BNS (most common), Hemolytic uremic syndrome, Thrombocytopenic purpura, and Systemic sclerosis.

Front 637

Explain the pathogenesis of Malignant Hypertension. Describe what is found upon gross and microscopic inspection.

Back 637

The pathogenesis in Malignant hypertension is due to the vascular damage of arterioles and small arteries. Upon gross and microscopic inspection we see fibrinoid necrosis, necrotizing ateriolitis, and glomerulitis. Pinpoint hemorrhages on the cortical surface give a classic "flea bitten" appearance. Hyperplastic arteriolosclerosis or "onion skinning" lesions are seen as a result of smooth muscle hyperplasia and reduplication of basement membranes.

Front 638

What is the definition of Malignant Hypertension? Describe some of the laboratory findings associated with Malignant Hypertension. How do you treat malignant hypertension?

Back 638

The clinical definition of Malignant Hypertension is a rapid increase in blood pressure equal to or greater than 210/120 mmHg. The laboratory findings associated include azotemia with a BUN:Cr ratio

Front 639

What are the clinical findings associated with Malignant Hypertension with regard to the brain and the kidney?

Back 639

In Malignant Hypertension there is a risk of Hypertensive encephalopathy. This can lead to cerebral edema, papilledema (loss of the normal optic disc margin), Retinopathy (flame hemorrhages, exudates), and the potential for intracerebral bleed. If left untreated oliguric acute renal failure will ensue.

Front 640

What are the most common causes of Renal infarction?

Back 640

Embolization from the left side of the heart (most common), Atheroembolic renal disease, vasculitis (particularly polyarteritis nodosum.

Front 641

Describe the clinical symptoms associated with Renal Infarction. What will the gross and microscopic images look like?

Back 641

Renal Infarction presents with the sudden onset of flank pain and hematuria. Upon gross and microscopic inspection we find irregular wedge-shaped pale infarctions in the cortex. Old infarcts have a V-shaped appearance due to scar tissue.

Front 642

Describe the presentations of Sickle Cell Nephropathy.

Back 642

Asymptomatic hematuria (most common) due to infarctions in the medulla, loss of concentrating ability, renal papillary necrosis, and pyelonephritis.

Front 643

Diffuse cortical necrosis is a complication of emergencies in what class of patients? What are examples of conditions that this can be a complication of? What is the cause of Diffuse Cortical Necrosis?

Back 643

Diffuse Cortical Necrosis is a complication of an obstetric emergency such as Preeclampsia, and Abruptio placentae. It is due to DIC limited to the renal cortex. There are fibrin clots in arterioles and glomerular capilaries. We see bilateral, diffuse, pale infarct of the renal cortex. There is anuria in a pregnant woman followed by ARF.

Front 644

Describe the most common cause of Hydronephrosis. What are other causes? Explain the gross findings and lab symptoms.

Back 644

The most common cause of an Hydronephrosis in the kidney is Renal Stoned. Next is Retroperitoneal fibrosis, then cervical cancer, and benign prostatic hyperplasia. Upon inspection, gross findings reveal dilated ureters and renal pelvis. There is compression atrophy of the renal medulla and cortex. Hydronephrosis obstruction may produce postrenal azotemia.

Front 645

What is the most common complication of Upper Urinary Tract Obstruction?

Back 645

Hydronephrosis.

Front 646

What is Urolithiasis? What are the risk factors associated with it? What is the most common metabolic abnormality associated with it?

Back 646

Urolithiasis is renal stones. Risk factors include Hypercalciuria in the absence of Hypercalcemia (most common metabolic abnormality). This usually due to increased GI absorption of calcium.

Front 647

Besides Hypercaliuria, what are other risk factors associated with Urolithiasis?

Back 647

Decreased urine volume which concentrates the urine, reduced urine citrate (which normally chelates) calcium, Primary hyperparathyroidism, diets high in dairy products (contains phosphates) or oxalates, and urinary infections due to urease producers (e.g. Proteus).

Front 648

What are the main types of renal stones that may be responsible for Urolithiasis?

Back 648

Calcium Oxalate, Calcium Phosphate, Magnesium ammonium phophate, Uric acid and Cystine.

Front 649

What is the most common type of kidney stone in adults. This also type also has an increased incidence in pure vegans and Crohn's disease.

Back 649

Calcium Oxalate stones.

Front 650

What is the most common type of kidney stone in children. This is also associated with dairy products and distal renal tubule acidosis.

Back 650

Calcium Phosphated stones.

Front 651

What type of kidney stone is referred to as a "Staghorn Calculus" or a struvite stone? This is associated with urease producers (e.g. Proteus) and alkaline urine (smells like ammonia).

Back 651

Magnesium ammonium phosphate stones.

Front 652

Describe the clinical findings associated with Urolithiasis. How do you detect stones that do not visualize?

Back 652

Clinical findings will often include ipsilateral colicky pain in the flank with radiation to the groin. There may be either gross hematuria or microscopic hematuria. Renal ultrasound and IVP detect stones that DO NOT visualize.

Front 653

Describe Angiomyolipoma. What type of tumor is associated with and what type of conditions?

Back 653

This is a Angiomyolipoma is a Hamartoma composed of blood vessels, smooth muscle, and adipose cells. It is associated with Tuberous sclerosis, which involves mental retardation and multisystem hamartomas.

Front 654

What do Alias Grawitz tumor, clear cell carcinoma, and hypernephroma all describe? Describe the Cytogenic abnormalites that are involved in the both the sporadic and hereditary versions of this cancer. Which cells does it derive from? What are its risk factors?

Back 654

Renal Cell Carcinoma. This cancer whether sporadic or hereditary usually includes translocations with loss of the von Hippel-Lindau (VHL) suppressor gene. These cancers are derived from the proximal tubule cells. Risk factors include smoking (most common), VHL (hemangioblastomas of cerebellum, and retina, and bilateral renal cell carcinoma), and Adult Polycystic Kidney disease.

Front 655

What is the most common type of Renal cell carcinoma? Is it usually sporadic or hereditary? Where does it occur in the kidney and what does it look like? Does it metastasize?

Back 655

Clear cell carcinoma. Most casess are sporadic and the remainder are associated with VHL. Theses masses are usually located on the upper poles with cysts and hemorrhage. The tumor is a bright yellow mass larger than 3 cm most cases. It is composed of clear cells that contain lipid and glycogen. There is a tendency for renal vein invasion (may invade vena cava and extend to the right side of the heart). Metastases is most common to the lung.

Front 656

What are the most common extrarenal involvements of clear cell Renal cell carcinoma?

Back 656

Metastasis to the lung is the most common site. These lung lesions are often hemorrhagic, with a "cannonball" appearance on radiographs. Bone lytic lesions are common, and hemorrhagic nodules on the skin due to increased vascularity in the tumor.

Front 657

Describe the clinical findings associated with Renal Cell Carcinoma. What is the classical triad? What ectopic hormones may be secreted?

Back 657

Here we see the triad of hematuria, flank mass, and costovertebral angle pain (fever may also occur). Renal cell carcinoma may also produce a left-sided varicoele if the left renal vein is invaded. The ectopic secretion of Erythropoetin (secondary polycythemia) and PTH (hypercalcemia) may occur.

Front 658

What are the prognoses associated with Renal Cell Carcinoma?

Back 658

Recurrence decades later is common. Most cases don't have metastases, but if there is the 5 year survival rate is less than 50%. Extension into the renal or through the renal capsule has the worst prognosis, with very low survival rates.

Front 659

What is the most common cancer of the renal pelvis?

Back 659

The most common cancer of the renal pelvis is Transitional Cell Carcinoma (and approx 50% of these have associated tumors elsewhere in the urinary tract).

Front 660

Describe the risk factors associated with Transitional Cell Carcinoma.

Back 660

Smoking (most common), Phenacetin abuse, Aromatic amines (aniline dyes), Cyclophosphamide.

Front 661

What is the second most common cancer of the renal pelvis? What are risk factors?

Back 661

Squamous cell carcinoma. Risk factors include renal stones and chronic infection.

Front 662

Describe the most common primary renal tumor in children. Is it more commonly sporadic or hereditary? What is the mode of inheritance in the hereditary version?

Back 662

The most common primary tumor in children is Wilm's Tumor (occurs between ages 2-5). Sporadic is the most common form, and the hereditary form is an autosomal dominant mutation on Chromosome 11.

Front 663

What is WAGR syndrome?

Back 663

Wilm's tumor, aniridia (absent iris), genital abnormalties, retardation.

Front 664

What is Beckwith-Wiedemann syndrome?

Back 664

Wilm's tumor, enlarged body organs, hemihypertrophy of extremities.

Front 665

Describe a Wilm's tumor and where it is derived from.

Back 665

Wilm's tumors are large, necrotic, gray-tan tumors. They are derived from mesonehpric mesoderm and contain abortive glomeruli and tubules, primtive blastemal cells and rhabdomyoblasts.

Front 666

Describe the clinical findings on a child with a Wilm's tumor.

Back 666

Unilateral paplable mass in a chile with hypertension. The hypertension is secondary to renin secretion. Lungs are the most common site of metastsis.

Front 667

Which two type of renal stones are radiolucent and tend to form in acidic urine?

Back 667

Uric acid and Cystine stones.

Front 668

What is another name for triple phosphate stones, and in what setting are they most commonly seen?

Back 668

Another name for triple phosphate stones is Magnesium ammonium phosphate stones. These most commonly occur in urinary tract infections with agents that alkalinize the urine with urease (e.g. Proteus)

Front 669

Epithelial crescents are a key feature of what process? What is an example of a disease that can lead to this process?

Back 669

Epithelial crescents are morphologic correlates of of rapidly progressive glomerulonephritis. Patients with this condition rapidly develop renal failure. One example of a disease that can lead to this process is Goodpasture syndrome

Front 670

Is Focal Segmental GS generally responsive or unresponsive to corticosteroid therapy?

Back 670

FSGS is typically unresponsive.

Front 671

In which nephrotic syndrome do patients respond very well to corticosteroid treatment?

Back 671

Minimal Change Disease.

Front 672

Lens dislocation is a feature of what hereditary renal disease? What are other features of this disease?

Back 672

Alport Syndrome. Other features include nephritis accompanied by nerve deafness, and other eye disorders such as posterior cataracts, and corneal dystrophy.

Front 673

Although they are the less common variety, what type of urethral tumors tend to occur in older women and be locally aggressive?

Back 673

Squamous cell carcinoma.

Front 674

What structures in urogenital tract can potentially become dilated as a result of long standing obstruction?

Back 674

There ureteral, pelvic and calyceal dilation leading to hydroureter and hydronephosis.

Front 675

What gross changes to the kidney occur as a result of nephrosclerosis?

Back 675

The kidneys become smaller and develop granular surfaces.

Front 676

IgA nephropathy occurs with increased frequency in patients with what other underlying condition? What other condition is this thought to be a variant of? Why does it also occur with increased frequency in patients with liver disease?

Back 676

Celiac Sprue. This is thought to be a possible variant of Henoch-Schonlein purpura. IgA GNitis occurs in patients with liver disease because there is defective hepatobiliary clearance of IgA complexes (secondary IgA nephropathy).

Front 677

Membranoproliferative glomerulonephritis involves the depostion of what two factors in the glomeruli.

Back 677

Membranoproliferative glomerulonephritis involves the deposition of IgG and C3

Front 678

Glomerular capillary thrombosis is a typical complication of what syndrome associated with infections of certain E.Coli strains and Shilgella?

Back 678

Hemalytic-uremic syndrome can cause glomerular capillary thrombosis.

Front 679

5-10% of Renal cell carcinoma tumors can secrete erythropoeitin and lead to what condition of the blood?

Back 679

Polycythemia.

Front 680

Why are serum levels of creatinine and urea not usually affected in patients with Renal cell carcinoma?

Back 680

This is because Renal cell carcinomas are usually unilateral and do not destroy all of the kidney. Thus, there no significant loss of renal function and the urea nitrogen and creatinine are not elevated.

Front 681

About how long does it take for drug induced interstitial nephritis to show symptoms? What type of hypersensitivity reactions are involved?

Back 681

It usually takes about 2 weeks. Elements of Type I and Type IV hypersensitivity reactions are involved.

Front 682

What type of renal necrosis can CHF lead to?

Back 682

CHF can lead to ATN, or Acute Tubular Necrosis.

Front 683

Maculopapular rash, fever, elevated blood pressure, hematuria, pyuria, proteinuria, elevated BUN and SCr, and eosinophiuria are all associated with what type of TIN (tubulointerstitial nephritis)?

Back 683

Drug-induced TIN.

Front 684

Explain the mechanism of how Hemolytic Uremic Syndrome (HUS) due to infection can cause glomerular capillary thrombosis and ARF.

Back 684

The verotoxin produced by E.coli or Shigella damages renal endothelium, which reduces NO and promotes vasoconstriction and necrosis, which in turn promotes thrombosis.

Front 685

Post-infectious glomerulonephritis presents with what type of glomerular deposits on Electron Microscopy?

Back 685

Subepithelial deposits.

Front 686

Alport syndrome is most commonly inherited by what means? Is this the only way? What is the defect? How does this affect the basement membrane of tubules?

Back 686

Alport syndrome is most commonly and X-linked disease, although is can show up as an autosomal recessive or dominant disease. The defect is most often in the synthesis of alpha5 Type IV collagen which leads to defective basement membranes in the tubules. There is variability of basement membrane thickening as a result.

Front 687

Amyloidosis and membranous glomerulonephritis mainly produce proteinuria without what?

Back 687

Hematuria.

Front 688

Diabetes mellitus involves what kind of glomerular changes?

Back 688

Nodular and diffuse glomerular sclerosis are characteristic of what Diabetes mellitus

Front 689

What are the most common complications of Autosomal dominant polycystic kidney disease?

Back 689

Hypertension and infection.

Front 690

Persons with dialysis acquired cysts are at increased risk for what disease?

Back 690

Renal Cell Carcinoma.

Front 691

Fibrinoid necrosis is a feature of what condition?

Back 691

Malignant nephrosclerosis.

Front 692

What does painless hematuria in older adults suggest? If there is the additional presence of constitutional symptoms such as fever and weakness?

Back 692

A renal neoplasm. If fever and weakness are involved the suspicion of renal cell carcinoma should be raised.

Front 693

A patient with nephrotic syndrome, granular immunofluorescence with IgG and C3 deposits likely, and uniform thickening of glomerular capillary basement membranes has what disease? Where type of deposits are they?

Back 693

This is membranous glomerulonephritis. On EM it will show subepithelial electron-dense deposits.

Front 694

What type of deposits does Type I MPGN show? Describe the characteristic finding of the basement membranes in this disease.

Back 694

Type I MPGN has subendothelial electron-dense deposits. In this disease there is seen to be a characteristic doubling of the basement membrane.

Front 695

If there is podocyte effusion on EM with few other findings clinically, what process is taking place?

Back 695

Minimal change disease (Lipoid nephrosis).

Front 696

The presence of overt proteinuria in a diabetic patient that had microalbuminuria suggest what will happen in the near future?

Back 696

This finding suggests that there has been progressive loss of renal function with continuing progression to end-stage renal disease with-in 5 years.

Front 697

C3 nephritic factor with decreased compliment in the serum is characteristic of what type of disease?

Back 697

C3 nephritic factor and decreased levels of compliment in the serum are found in Type II MPGN (Dense Deposit Disease).

Front 698

What other organ does Autosomal Recessive Polycystic Kidney Disease typically involve?

Back 698

The Liver. If the patients survive beyond infancy they develop congenital hepatic fibrosis.

Front 699

Compare to the symmetrically enlarged kidneys composed of small radially arranged cysts of RPKD (and possibly a liver showing multiple epithelium-lined cysts and proliferation of bile ducts), describe the appearance of the kidneys in DPKD.

Back 699

In DPKD we see bilaterally enlarged kidneys replaced by 1-4cm fluid filled cysts.

Front 700

What is the most common renal cystic disease seen in fetuses and infants? Describe the appearance of the kidneys and cysts. Does this happen bilaterally? Is there hepatic invovlment?

Back 700

The most common renal cystic disease affecting fetuses and infants is Multicystic Renal Dysplasia (Multicystic Dysplastic Kidney). Here the cysts and kidneys are variably sized. This disease can be focal, unilateral, or bilateral. Congenital hepatic fibrosis, however, is not present. That is a feature of RPKD.

Front 701

Irregular cortical scars with pelvicaliceal dilation may represent what process? (can be somewhat correlated to bronchiectatsis). What is this process caused by?

Back 701

Hydronephrosis complicated by infection in chronic pyelonephritis. This process is most often possible due to reflux nephropathy.

Front 702

What are the typical features found in kidneys scarred from Chronic Pyelonephritis? Is the involvement usually symmetric or asymmetric?

Back 702

Typical features include coarse and irregular scarring resulting from ascending infection, blunting and deformity of the calyces, and asymmetric involvement of the kidneys.

Front 703

What type of cancer is a Wilm's tumor? Microscopically, what does this tumor look like?

Back 703

Wilm's tumor is a nephroblastoma and its microscopic pattern resembles the fetal kidney nephrogenic zone.

Front 704

Diffuse basement membrane thickening, in the absence of proliferative changes, and granular deposits of IgG and C3 are typical of this condition. It is caused by the deposition of immune complexes on the basement membrane (intramembranous), which activates compliment.

Back 704

This describes membranous glomerulopathy

Front 705

Explain the symptoms and findings present in Medullary Sponge Kidney. What are the changes that are dfound inside the kidney?

Back 705

In MSK, cystic dilation of 1-5mm is present in the inner medullary and papillary collecting ducts. MSK is bilateral in 70% of cases. Not all papillae are affected equally, although caliculi are often present in dilated collecting ducts. Patients usually develop kidney stones, infection, or recurrent hematuria in the third to fourth decade. More than 50% of patients have stones.

Front 706

Necrotizing papillitis with papillary necrosis can be a complication of actue pyelonephritis. What type of chronic disease patients are particularly prone to the development of this condition? What about obstruction? What type of long term use of medication can also lead to this?

Back 706

Diabetic patients are particularly prone to this. Papillary necrosis develops when acute pyelonephritis occurs in combination with urinary tract obstruction. Papillary necrosis can also occur with the chronic use of analgesics.

Front 707

Renal biopsy of a patient with Alport syndrome will show what type of characteristic cell and basement membrane changes?

Back 707

Prominent tubular foam cells are present along with glomerular basement membrane thickening and thinning.

Front 708

Exposure to analine dyes and B-Napthylamine (arylamines) increases the risk of what type of cancer?

Back 708

Urothelial Carcinoma.

Front 709

Radiation and cytotoxic drugs such as Cyclophosphamide are risk factors for what type of condition?

Back 709

Hemorrhagic cystitis.

Front 710

What kidney disease puts you at risk for a berry aneurysm? How many people with this disease actually have a berry aneurism?

Back 710

ADPKD puts you at risk for a berry aneurism. About 10-30% of patients with ADPKD actually have an intracranial berry aneurysm, which can rupture at any time.

Front 711

Does Amyloidosis cause your kidney size to increase or decrease?

Back 711

Amyloidosis causes your kidney size to increase.

Front 712

Patients with multiple myeloma may present with high total serum protein, and back pain. Explain these symptoms.

Back 712

The high serum protein comes from high globulin levels from the presence of monoclonal protein. Back pain can be indicative of lytic bone lesions that occur in, but are not limited to, the spine. The ribs are a common spot for these lesions as well.

Front 713

Necrotizing arteriolitis (fibrinoid necrosis of the arterioles) and hyperplastic areriolosclerosis are distinctive vascular lesions of what disease?

Back 713

Malignant hypertension.

Front 714

In crush injuries, large amounts of myoglobin can be released and turned into toxic metabolites in the kidney. What condition can this cause?

Back 714

Toxic Acute Tubular Necrosis (ATN).

Front 715

Segmental tubular necrosis is a finding associated with what injury to the kidney caused by ischemia?

Back 715

Ischemic ATN.

Front 716

Schistomiasis is a risk factor for what type of bladder cancer: Transitional cell carcinoma or Squamous cell carcinoma?

Back 716

Squamous cell carcinoma.

Front 717

Approximately 80% of sporadic clear cell carcinomas show loss of both alleles of what gene?

Back 717

The von Hipple Lindau (VHL) gene. This leads to Renal cell carcinoma that presents in the 6th-7th decade of life.

Front 718

In Renal cell carcinoma which gene is abnormal on which chromosome? Where else do defects in this gene produce disease? What other organ systems? Can there be other tumors?

Back 718

Renal cell carcinoma is a feature of von Hippel-Lindau disease and is caused by an abnormality in chromosome 3. Other features include cerebellar and spinal hemangioblastomas, renal and pancreatic cysts, retinal angiomas, and pheochromocytomas.

Front 719

Are the initial clinical symptoms of Renal cell carcinoma more often caused by the tumor itself or metastases?

Back 719

Initial clinical symptoms are frequently caused by the metastases and not by the renal carcinoma itself. The classic clinical manifestation of renal cell carcinoma - a triad of hematuria, flank pain, and palpable flank mass - is seen in only about 10% of affected patients.

Front 720

The Denys-Drash syndrome is associated with what tumor of the Kidney?

Back 720

This is associated with increased incidence of a Wilm's Tumor.

Front 721

Urothelial Carcinoma of the renal pelvis is associated with use of what type of drugs to treat chronic pain? What other condition and process is associated with these drugs that likely leads to this increased incidence of cancer?

Back 721

Analgesic (NSAID) abuse nephropathy is characterized by chronic tubulointerstitial nephritis (TIN) with papillary necrosis. It is associated with urothelial carcinoma of the renal pelvis.

Front 722

Amyloidosis of the kidney is associated with what malignant condition? (think bence-jones bodies)

Back 722

Multiple Myeloma.

Front 723

Do simple renal cysts cause life threatening disease?

Back 723

No. Simple renal cysts are usually benign, although they may cause symptoms if hemorrhage into them causes sudden distention and pain.

Front 724

Urinary VMA (vanillylmandelic acid) will be positive in children with what condition?

Back 724

Wilm's Tumor.

Front 725

How would you describe the tissue found in a Wilm's tumor?

Back 725

Tri-phasic nephrogenic process with epithelial, stromal and blastemic cell types. A tumor that is reminiscent of fetal kidney

Front 726

Features which differentiate Stage I from Stage II Wilm’s tumor include what two main characteristics?

Back 726

Absence of renal capsular penetration and absence of renal sinus invasion.

Front 727

Name 5 risk factors associated with Bladder Cancer.

Back 727

Cigarette smoking, Aniline dyes, 2-naphthylamine, Analgesic Nephropathy, Hemorrhagic cystitis secondary to cyclophosphamide, and Schistosoma haematobium bladder infections.

Front 728

PSA can be elevated in prostatic carcinoma, but also in what other condtions?

Back 728

Prostatic adenocarcinoma, BPH, Prostatitis, and Prior GU instrumentation and/or prostatic manual exam.

Front 729

The most common location of Prostatic adenocarcinoma is anterior or posterior lobe?

Back 729

Posterior lobe.

Front 730

Gleason's grading system of adenocarcinoma is based on what parameters?

Back 730

Is based on the microscopic architectural pattern of the gland. The Gleason system scores malignant glands from 1 to 10. A Gleason system low grade carcinoma is composed of small uniform glands. A high grade carcinoma shows solid tumor infiltration with only occasional glands. An intermediate grade tumor shows intermediate histologic characteristics.

Front 731

Paraneoplastic syndromes which may occur in patients with prostatic adenocarcinoma include what?

Back 731

Thrombosis, coagulopathies, nonbacterial thrombotic endocarditis.

Front 732

What are the four so-called, pulmonary renal syndromes?

Back 732

Goodpasture's syndrome, SLE, Wegener's granulomatosis, and Microscopic polyangitis.

Front 733

What are two environmental triggers that seem to have an association with development of Goodpature's syndrome?

Back 733

Cigarette smoking and exposure to solvents (hydrocarbons).

Front 734

What diseases are in the differential diagnosis of something that presents with both nephritic urinary sediment and nephrotic-range proteinuria?

Back 734

The list is limited: MPGN, Wegener's granulomatosis, and SLE.

Front 735

What process may be mistaken for renal cell carcinoma clinically, radiographically and grossly ?

Back 735

Xanthogranulomatous pyelonephritis.

Front 736

Who gets renal stones more often, men or women? What is the peak age of onset for urolithiasis? Can large renal stones within the pelvis remain clinically silent?

Back 736

Men. The peak age of onset is the third decade of life. Yes, large stones can form, even in the renal pelvis and remain clinically silent.

Front 737

Hyperparathyroidism and Sarcoidosis may lead to what type of renal stone development?

Back 737

Calcium stone.

Front 738

Consumption of what type of foods containing what compund, can cause renal calcium stone formation?

Back 738

May form in persons who consume excessive oxalate-containing foods such as tea, colas, citrus juices, spinach, and peanuts

Front 739

Can calcium renal stones form in patients if they do not have hypercalcemia?

Back 739

Yes.

Front 740

What are the types of problems that can lead to Hydronephrosis?

Back 740

Hydronephrosis is a dilation of the collecting system of the kidney secondary to chronic obstruction, which may be caused by congenital malformation, prostatic hyperplasia, lithiasis, urinary tract neoplasia, genital tract neoplasia, etc.

Front 741

Hyperplasia of the prostate gland results from the effect of growth factors produced when what molecule binds to nuclear androgen receptors of epithelial and stromal cells?

Back 741

DHT (dihydrotestosterone).

Front 742

Histologic features seen in a biopsy of benign prostatic hyperplasia include what two main findings?

Back 742

Nodular growth of abundant stroma and an increase in number of glands.

Front 743

What are some of the complications of BPH (Benign Prostatic Hyperplasia)? Are prostatic adenocarcinoma or urothelial squamous cell carcinoma complications of BPH?

Back 743

Hydronephrosis, pyelonephritis, prostatic calculi, hypertrophy of the bladder wall, bladder diverticula, and cystitis. Cancer is not a complication of BPH.

Front 744

Striate appearance of the cortex and medulla of the kidney on CT imaging is characteristic of what condition?

Back 744

This is characteristic for pyelonephritis.

Front 745

Name some of the predisposing risk factors for UTI and pyelonephritis.

Back 745

Pregnancy, Female sex, Urinary catheterization, Diabetes mellitus, and Immunosuppression

Front 746

Non-steroidal anti-inflammatory drug (NSAID) associated renal syndromes include what two conditions?

Back 746

Minimal change disease (lipoid nephrosis), and Hypersensitivity interstitial glomerulonephritis and acute renal failure.

Front 747

What is a common condition that diabetic patients, sickle cell patients, and patients with UTI's, or urinary obstruction may have in common?

Back 747

Papillary necrosis.

Front 748

Explain the probable explanations of the pathogenesis of papillary necrosis in analgesic abuse.

Back 748

The pathogenesis most likely works through the inhibition of prostaglandin synthesis resulting in reduction in papilla blood flow and ASA glutathione depletion with subsequent production of lipid peroxides by acetaminophen leading to tissue damage in papilla.

Front 749

What is the most common symptom of Renal Dysplasia?

Back 749

Frequuent Urinary tract infection.

Front 750

Desccribe ADPKD. Is it a rare disease? Which chromosome contains the genetic mutation? What are the symptoms that it will present with? Does it evolve to chronic renal failure?

Back 750

ADPKD is not a rare disease, it occurs in 1/1000 people. The most common genetic mutation is found on Chromosome 16. This most manifests in adult life with flank pain, hematuria, elevated creatinine, and hypertension. It eventually evolves into chronic renal failure.

Front 751

What are some of the examples of Systemic Diseases that cause Nephrotic Syndrome?

Back 751

Diabetes, Amyloidosis and multiple myeloma, Systemic lupus erythematosus (WHO class 5), Membranous glomerulopathy (infectious diseases), Membranoproliferative GN (infectious diseases), can also present as nephritic syndrome.

Front 752

What are the causes of Primary low compliment nephritic syndromes?

Back 752

Post-infectious (Post-streptococcal) glomerulonephritis, and MPGN (idiopathic).

Front 753

What are the causes of Systemic low compliment nephritic syndromes?

Back 753

Infectious endocarditis, SLE (WHO class 3, and 4), MPGN (infectious)

Front 754

What are the causes of Primary normal compliment nephritic syndromes?

Back 754

IgA Nephropathy, Hereditary Nephritis (Alport syndrome), Crescentic Rapidly progressive ANCA positive GN (can also present as acute renal failure)

Front 755

What are the causes of Systemic normal compliment nephritic syndromes?

Back 755

Anti-basement membrane disease (Goodpasture's disease, can also present as acute renal failure), Systemic vasculitis, ANCA positive, can also present as acute renal failure.

Front 756

What are the diseases that can lead to Thrombotic Micoangiopathy and be a Systemic cause of Nephritic Syndrome? (there are 4)

Back 756

Thrombotic Microangiopathy (TMA or MAHA) - presents as Nephritic syndrome or acute renal failure accompanied by hemolytic anemia, hemorrhages, and purpura. It has multiple clinical presentations and names: when it is associated with predominantly neurologic symptoms it is called thrombotic thrombocytopenic purpura (TTP). With diarrhea: hemolytic uremic syndrome (HUS); As a complication of hypertension: malignant hypertension; As a complication of pregnancy: eclampsia. Most frequent presentations are TTP & HUS. Many cases respond to treatment.

Front 757

What are some of the medications that can lead to Membranous Glomerulopathy?

Back 757

Gold, Penicillamine, Mercury, and Captopril.

Front 758

Thyroiditis can lead to what type of Nephrotic syndrome?

Back 758

Membranous Glomerulopathy.

Front 759

What is the suspected mechanism of diabetic nephropathy?

Back 759

Hyperfiltration and increased glomerular capillary pressure lead to changes in the collagen composition, resulting in thick GBM and increased mesangium.

Front 760

What are the two conditions that can be caused from exposure to analine dyes and napthalyine?

Back 760

Bladder cancer and Acute Tubular Necrosis.

Front 761

How does Thrombotic Microangiopathy damage the kidenys? Describe the pathogenesis.

Back 761

Endothelial damage leads to aggregation of platelets followed by thrombocytopenia. Microthrombi contain fibrin filaments. These fibrin filaments damage RBCs causing hemolysis.

Front 762

What is the greatest side effect of hyponatremia?

Back 762

Cerebral edema.