Path 20 Kidney

Front 1

Prerenal azotemia is seen in what conditions?

What diseases cause this?

Back 1

hypoperfusion of kidneys

d/t hemorrhage, shock, volume depletion, CHF

Front 2

Postrenal azotemia is seen in what conditions?

Back 2

when urine flow is obstructed beyond the level of the kidney

Front 3

Which syndrome is caused by glomerular disease and is characterized by visible hematuria, mild proteinuria, HTN?

Back 3

Nephritic syndrome

Front 4

Nephritic syndrome with rapid decline (hours to days) in GFR?

Back 4

Rapidly progressive glomerulonephritis

Front 5

Syndrome caused by glomerular disease, w/ heavy proteinuria, hypoalbuminemia, severe edema, hyperlipidemia, lipiduria?

Back 5

Nephrotic syndrome

Front 6

Oliguria/anuria + recent onset of azotemia?

Back 6

Acute renal failure

Front 7

What are the predominant characteristics of diseases with renal tubular defects?

Back 7

polyuria, nocturia, electrolyte disorders (metabolic acidosis)

Front 8

Bacteriuria + pyuria?

Back 8

UTI

Front 9

Severe spasms of pain (colic) + hematuria?

Back 9

nephrolithiasis

Front 10

One of the most common causes of renal failure?

Back 10

chronic GN

Front 11

what forms the physical barrier of the glomerulus?

Back 11

type IV collagen (lamina densa)

Front 12

what forms the electrical barriers of the glomerulus?

Back 12

Heparan sulfate in lamina rara externa and interna

Front 13

What is the predominant cause of glomerular injury?

Back 13

immune mechanisms

Front 14

What processes lead to focal segmental glomerulosclerosis?

Back 14

reductions in renal mass (injury) -->
adaptive chgs in glomeruli (hypertrophy and glomerular capillary HTN) and systemic HTN --> epi-/endothelial injury -->
mesangial hyperplasia/ECM deposition, intraglomerular coag -->
glomerulosclerosis --> more renal cell injury

Front 15

what is the common link behind all diseases presenting with a nephritic syndrome?

Back 15

inflammation in the glomeruli

Front 16

In what diseases is nephritic syndrome a common complication?

Back 16

multisystem dzs (SLE, microscopic polyangiitis)

acute proliferative GN and crescentic GN

Front 17

most common pathogens in Poststrep GN?

Back 17

Group A β-hemolytic streptococci (S. pyogenes)

Front 18

Elevated titer in poststrep GN?

Back 18

Anti-streptolysin O (ASO)

Front 19

microscopic appearance of poststrep GN?

Back 19

diffuse GN w/ globally hypercellular glomeruli;
granular deposits of IgG, IgM, and C3 in mesangium and along GBM; "humps and bumps" on EM

Front 20

young child abruptly develops malaise, fever, nausea, oliguria, hematuria; has RBC casts, mild proteinuria, periorbital edema, mild HTN; onset 1-2 wks after sore throat. Dx?

Back 20

Post strep GN

Front 21

Most common cause of acute renal failure?

Back 21

Acute tubular necrosis

Front 22

what are causes of acute tubular necrosis?

Back 22

ischemia
nephrotoxins
acute tubulointerstitial nephritis (drug hypersensitivity rxn)
urinary obstruction

Front 23

cause of acute tubular necrosis that presents with hemoglobinuria/myoglobinuria?

Back 23

mismatched blood transfusions

Front 24

what factors modulate the pathogenic vasoconstriction and reduction in GFR in acute tubular necrosis?

Back 24

Activation of renin-angiotensin system

Increased endothelin

Decreased NO and PGI2

Front 25

What morphological changes characterize ischemic acute tubular necrosis?

Back 25

patchy tubular necrosis, esp in thick descending tubule and thick ascending limb; cellular and protein casts in distal tubule and collecting duct; usually is relatively lesser degrees of tubular cell injury

Front 26

what morphological changes are seen in toxic acute tubular necrosis?

Back 26

variable degrees of tubular injury/necrosis, affects proximal tubules most often; cellular and protein casts in distal tubules and collecting ducts

Front 27

If calcium oxalate crystals are found in tubular lumens of a pt w/ ATN, what is dx?

Back 27

ingestion of ethylene glycol

Front 28

If large acidophilic inclusions are seen in tubules of a pt w/ ATN, what is dx?

Back 28

Mercuric chloride poisoning

Front 29

what are the phases (and characteristics) of the clinical course of ATN?

Back 29

Initiating stage (kidney dysfxn caused by inciting event, slight oliguria w/ rise in BUN)

Maintenance stage (persistent renal flr, increased oliguria, hyperkalemia, acidosis)

Recovery phase (steady increase in urine w/ loss of water and electrolytes, possible hypokalemia)

Front 30

In what situations is the mortality associated with ATN significant?

Back 30

shock related to sepsis, burns or other causes of multi-organ failure

Front 31

What morphologic features help distinguish acute from chronic tubulointerstitial nephritis?

Back 31

Acute has edema, neutrophils and eosinophils

Chronic has fibrosis and tubular atrophy

Front 32

What are the typical sxs of UTI?

What are the sxs in pyelonephritis?

Back 32

Dysuria and frequency

flank pain and fever

Front 33

most common etiologic agent in UTI/pyelonephritis?

Back 33

E. coli

(Proteus, Klebsiella, Enterobacter are next most common)

Front 34

What diseases can predispose to hematogenous seeding of UTI?

Back 34

septicemia
infective endocarditis

Front 35

what anatomical abnormality predisposes to ascending infections of ureters/kidneys?

Back 35

incompetence of vesicoureteral valve

Front 36

What diseases is characterized by patchy, suppurative inflammation of the renal interstitium, tubular necrosis, and intratubular neutrophil casts?

Back 36

Acute pyelonephritis

Front 37

what complication of pyelonephritis is seen in diabetics and those with UT obstruction?

Back 37

papillary necrosis

Front 38

what complication of pyelonephritis is seen in pts with total obstruction high in the urinary tract?

Back 38

pyonephrosis (suppurative exudate fills renal pelvis, calyces and ureter)

Front 39

what one finding distinguishes upper from lower UTI?

Back 39

neutrophil casts indicates renal involvement

Front 40

what are the two main causes of chronic pyelonephritis?

Back 40

Reflux (d/t congenital vesicoureteral reflux and intrarenal reflux)

Chronic obstruction

Front 41

Morphological changes in chronic pyelonephritis?

Back 41

broad scars, deformed calyces, significant tubulointerstitial inflammation and fibrosis.

can lead to secondary FGS and HTN

Front 42

what does a BUN:Cr > 15 indicate?

Back 42

Pre-renal azotemia

Post-renal azotemia
(initially >15, but will drop <15 if obstruction isn't cleared and tubular damage occurs)

Front 43

why does BUN:Cr rise above normal in pre-renal azotemia?

Back 43

Reduced GFR = reduced creatinine clearance and reduced BUN Clearance, but BUN is also reabs in proximal tubule --> disproportionately increased BUN compared to Cr

Front 44

what is the most common cause of ischemic ATN?

Back 44

prerenal azotemia

Front 45

morphological difference between ischemic and nephrotoxic ATN?

Back 45

Ischemic affects multiple parts of nephron, and BM disrupted;
Nephrotoxic affects proximal tubule and BM is intact

Front 46

How is reflux nephropathy often discovered?

Back 46

When investigating HTN in children

Front 47

Pt presents with abrupt onset oliguria, fever, eosinophilia, rash, hematuria, mild proteinuria, and leukocyturia 15 days after taking methicillin for an infection of S. aureus. What is dx?

Back 47

Acute drug-induced interstitial nephritis

Front 48

Drugs involved in acute drug-induced interstitial nephritis?

Back 48

synthetic penicillins (methicillin, ampicillin), other synthetic abx (rifampin), NSAIDs, thiazide diuretics, allopurinol, cimetidine

Front 49

What type of reaction is acute drug-induced interstitial nephritis?

Back 49

T cell-mediated delayed hypersensitivity (type IV)

Front 50

mechanism of injury in analgesic abuse nephropathy?

Back 50

Aspirin inhibits renal PG's and thus inhibiting vasodilation (Ang II vasoconstricts)
Acetaminophen FRs damage medullary tubules
Cumulative damage can lead to papillary necrosis

Front 51

what disorders can cause papillary necrosis?

Back 51

analgesic nephropathy, diabetes, urinary obstruction, sickle cell dz, renal tuberculosis (focal)

Front 52

what pts are at higher risk for urate nephropathy?

Back 52

Acutely in pts with leukemias/lymphomas undergoing chemotherapy (increased cell apoptosis --> increased uric acid)

Chronically in pts with gout and lead exposure

Front 53

What conditions predispose to nephrocalcinosis?

Back 53

hyperparathyroidism, multiple myleoma, vit D intox, metastatic cancer, excess Ca intake

Front 54

What pathology does excess phosphate load lead to?

Back 54

acute phosphate nephropathy (phosphate causes precipitation of calcium phosphate and possible renal insufficiency several weeks after exposure)

Front 55

what are the mechanisms of myeloma kidney?

Back 55

Bence Jones (light chain) proteins are toxic to epithelial cells; also, precipitate in tubule lumen --> inflammatory reaction around casts

Hypercalcemia and hyperuricemia --> nephrocalcinosis --> tubular dysfxn

Front 56

What groups of patients are at increased risk of renal failure as a consequence of benign nephrosclerosis?

Back 56

Blacks, ppl w/ severe HTN, and pts w/ underlying diseases, esp. diabetics

Front 57

Benign nephrosclerosis?

Back 57

renal changes associated with sclerosis of renal arterioles and small arteries; narrowing of arteriolar lumens d/t wall thickening and hyalinization

Front 58

Pathogenesis of malignant HTN and accelerated nephrosclerosis?

Back 58

vascular injury w/ fibrinoid necrosis caused by severe HTN, intravascular thrombosis and arteritis --> renal ischemia --> stimulation of renin/ang and other vasoconstrictive systems --> more ischemia --> more renin --> etc.

Front 59

Clinical features of malignant HTN?

Back 59

Systolic > 200, Diastolic > 120
Proteinuria, hematuria
Papilledema, encephalopathy
CV abnormalities
Renal failure

Front 60

Most common cause of typical HUS?

Back 60

follows infection with E. coli (O157:H7)

Front 61

Clinical presentation of typical HUS?

Back 61

follows influenza-like or diarrheal prodrome --> sudden onset hematemesis and melena, severe oliguria, hematuria

Front 62

Pathogenesis of typical HUS?

Back 62

Shigella-like toxin causes increased leukocyte adhesion, increased endothelin and decreased NO production (vasoconstriction), and endothelial lysis

Front 63

What is the inciting factor in HUS vs. TTP?

Back 63

HUS = endothelial injury

TTP = platelet activation and aggregation

Front 64

Causes of atypical HUS?

Back 64

1. inherited deficiency of complement-regulatory proteins (factor H usually breaks down C3 convertase)
2. Antiphospholipid syndrome (1° or 2° SLE)
3. Postpartum renal failure
4. Chemotherapy and immunosuppressive drugs
5. kidney irradiation

Front 65

Manifestations of TTP?

Back 65

fever, neurologic sxs, microangiopathic hemolytic anemia, thrombocytopenia, renal failure

Front 66

What is the inherent cause of idiopathic TTP?

Back 66

antibodies to, or genetic defects in ADAMTS13 (which normally cleaves vonWillebrand factor - uncleaved vWF leads to enhanced plt aggregation)

Front 67

How can one differentiate between atypical HUS and TTP?

Back 67

atypical HUS will have normal plasma ADAMTS13

Front 68

complication of aortic surgery on elderly pt with compromised renal function?

Back 68

atheroembolic renal disease

Front 69

What factors predispose pts with SCA to nephropathy?

Back 69

Hypertonic, hypoxic milieu of renal medulla causes accelerated sickling; hyperosmolarity dehydrates RBCs and increases intracellular HbS concentrations

Front 70

what is the most common cause of renal infarcts?

Back 70

emboli from mural thrombosis in LA and LV from prior MI

Front 71

What is the most common site of fusion in horseshoe kidney?

Back 71

lower pole

Front 72

To what structures does a horseshoe kidney lie anterior?

Back 72

Aorta and IVC

Front 73

What disease is characterized by multicystic, enlarged kidneys with extremely irregular tissue organization?

Back 73

Multicystic renal dysplasia
(abnormality in metanephric differentiation)

Front 74

What disease is associated with mutations of one or both alleles of the PKD gene?

Back 74

autosomal dominant polycystic kidney disease

Front 75

characteristics of ADPKD?

what other abnormalities is it associated with?

Back 75

B/L, kidneys enlarged and composed of large cysts; sxs: flank pain from hemorrhage into cysts, hematuria, HTN, proteinuria, progressive renal flr

Liver cysts, cerebral berry aneurysms, MV prolapse

Front 76

Difference btwn adult and childhood PKD?

Back 76

Childhood PKD: smooth external surface, cysts are dilated collecting ducts, liver cysts in almost all cases

Adult PKD: cysts apparent externally, only 40% have liver cysts

Front 77

What are pts with medullary sponge kidney predisposed to?

Back 77

calcifications in dilated ducts, hematuria, infection, and renal calculi

Front 78

what is the cause of renal insufficiency in nephronophthisis disease complex?

Back 78

cortical tubulointerstitial damage (corticomedullary junction is predominant locus of cysts, cause cortical tubular atrophy)

Front 79

what is a pathogenic complication of prolonged dialysis?

Back 79

Acquired cortical and medullary cysts;
May be lined by hyperplastic that can develop into renal cell carcinoma

Front 80

What are the main differentiating factors for diagnosis of a renal cyst vs. renal tumor?

Back 80

Cysts:
Have smooth contours
Are almost always avascular
Give fluid rather than solid signal on ultrasound

Front 81

what causes dilation of the renal pelvis and calyces, and eventually renal atrophy, in hydronephrosis?

Back 81

Continued glomerular filtration after obstruction of urinary flow, compression of medullary vasculature

Front 82

what signs help differentiate pyelonephritis from cystitis?

Back 82

fever, WBC casts, and CVA tenderness

Front 83

What s&s associated with B/L partial urinary tract obstruction?

Back 83

Inability to concentrate (polyuria, nocturia)
Distal tubular acidosis
Salt wasting
Renal calculi
Scarring and atrophy of papilla and medulla (chronic tubulointerstitial nephritis)

Front 84

most common type of kidney stone?

Back 84

calcium oxalate

Front 85

what causes calcium stones?

Back 85

hypercalciuria (incr gut abs of Ca or decreased tubular reabs of Ca) w/ or w/o hypercalcemia

increased uric acid secretion

hyperoxaluria (intestinal overabsorption of oxalates)

Front 86

What commonly causes magnesium ammonium phosphate (struvite) stones?

Back 86

bacteria (Proteus) that convert urea to ammonia create alkaline urine that causes precipitation of struvite stones

Front 87

What are staghorn calculi made of?

Back 87

Magnesium ammonium phosphate (struvite)

Front 88

When are uric acid stones seen?

How do they appear on radiography?

Back 88

gout, leukemia, pts w/ acidic urine

radiolucent (not visible)

Front 89

characteristics of renal papillary adenoma?

Back 89

benign papillary tissue found invariably in cortex; encapsulated; small

Front 90

characteristics of angiomyolipoma?

Back 90

benign, consists of vessels, sm muscle, and fat, common in pts with tuberous sclerosis

Front 91

characteristics of oncocytoma?

Back 91

benign epithelial tumor of large eosinophilic cells; arises ffrom intercalated cells of collecting ducts

Front 92

risk factors for renal cell carcinoma?

Back 92

tobacco, asbestos, petroleum products, heavy metals, and von Hippel-Lindau syndrome;
increased incidence in chronic renal failure, acq cystic dz, and tuberous sclerosis

Front 93

classifications of renal cell carcinomas?

Back 93

clear cell carcinoma
papillary "
chromophobe "
collecting duct "

Front 94

most common type of renal cell carcinoma?

Back 94

clear cell carcinoma

Front 95

gross appearance of renal cell carcinoma?

Back 95

large, solitary yellow mass
Most commonly in upper pole
Areas of necrosis and hemorrhage
May invade renal vein, extend into IVC and heart

Front 96

what genetic abnormalities are associated with sporadic papillary carcinoma?

Back 96

Trisomy 7, 16, 17
Loss of Y in male pts
Mutated, activated MET proto-oncogene

Front 97

what genetic abnormalities are associated with familial papillary carcinoma?

Back 97

Trisomy 7
Mutated, activated MET proto-oncogene

Front 98

what genetic abnormalities are associated with sporadic and hereditary clear cell carcinoma?

Back 98

Loss of or inactivation/mutation of VHL gene

Front 99

what is the clinical triad of renal cell carcinoma?

what are other manifestations?

Back 99

hematuria, palpable mass, and flank pain (10%)

paraneoplastic syndromes (ectopic hormones)

may cause amyloidosis, leukemoid reaction or eosinophilia

Front 100

in what population of pts are Wilms tumors found?

Back 100

children

Front 101

small, benign-appearing neoplasm that produces noticeable hematuria, may block urinary outflow, and are assoc'd with tumors of pelvis, ureters, and bladder

Back 101

Urothelial carcinomas of the renal pelvis