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135 Cards in this Set

  • Front
  • Back
JG cells located where, action
afferent arteriole, if sense decrease in BP secrete renin
Macula densa cells located where, senses what, 2 actions
on DCT on top of glomerulus
if sense decrease in NaCl, it causes dilation of afferent arterioles to increase GFR back to normal and causes renin secretion
Ureter passage relative to uterine artery and ductus deferens
"water passes under the bridge"- ureter passes under uterine artery and ductus deferens
60-40-20 rule of body weight
60% of body weight water
40% is intracellular, 20% extracellular
extracellular body fluid is intersitial compartment?
3/4 (only 1/4 is plasma volume)
Glomerular filtration barrier:
what composes size barrier?
what is responsible for electric barrier?
what layer are podocyte foot proccesses?
fenestrated endothelium is size barrier

heparan sulfate bound to BM provides negative charge

podocytes compose epithelial layer
what happens if negative charge on glomerular BM lost?
nephrotic syndrome
Clearance equation and units
C = (urinary conc. * urinary volume)/ plasma concentration

ml/min
what is starling equation for GFR
C = Kf (Pressure glomerular capillary - bowmans space) - (oncotic pressure glomerular capillary - oncotic pressure bowmans space)
what substance best to determine GFR? what is calculation? what is normal GFR?
GFRinulin = C*V/P

(just clearance of inulin)

normal is about 100 ml/min
does creatinine over or underestimate GFR?
overestimates because moderate secreted into tubule
what is effective renal plasma flow and what substance is used to estimate it?

is it the same as renal perfusion rate?
flow of blood through the renal arteriole

Cpah= U*V/P

PAH because all PAH is excreted

renal perfusion rate is about 10% higher
Filtration fraction equation?
use what to estimate it?
normal value?
filtration fraction = GFR/RPF
GFR = clearance of inulin or creatinine
RPF = clearance of SAH

normal = 20%
Filtered load equation
GFR * plasma concentration
change in GFR, RPF, FF if dilate afferent arteriole?

1 substance that dilates?
1 substance that constricts?
GFR increases
RPF increases
FF stays the same

prostaglandins dilate afferent arteriole
NSAIDs constrict afferent arteriole
what is pathway of blood from efferent arteriole to renal vein?
efferent arteriole, vasa recta, interlobular vein, interlobar vein, renal vein
Constriction of efferent arteriole changes:
GFR
RPF
FF
1 substance that preferentially constricts efferent arteriole
GFR increases
RPF decreases
FF increase

Angiotensin II (so ACE inhibitor causes efferent dilation)
if decrease plasma protein concentraion, what changes:
GFR
RPF
FF
GFR increases (less oncotic pressure in glomerular capillary)
RPF doesn't change
FF increases
if ureter constricts, what changes:
GFR
RPF
FF
GFR decreases
RPF doesn't change
FF decreases
how do you calculate resorption and secretion rates
secretion = excretion - filtration

reabsorption = filtration- excretion

filtered load = GFR*Plasma conc.
excretion rate = U*V
glucose reabsorbed where by what

at what level does glucosuria start? at what point is transporter saturated?
in PCT by Na/glucose cotransporter

160-200 mg/dL
350 mg/dL saturated
where are AAs reabsorbed in kidney, by what type of transporter
PCT by Na+ cotransporter (at least 3 distinct carrier systems)
what deficiency of kidney tubule reabsorption can cause pellagra (dermatitis, dementia, diarrhea)?
Hartnup disease - deficiency of neutral amino acid transport (including tryptophan, which is needed to make niacin)
PCT absorbs all what (2)?
absorbs most of what (5)
what type of absorption (isotonic/hypertonic/hypotonic)?
actively secreted what?
absorbs all glucose and AAs
Na, HC03, Cl-, H20, K+
isotonic
actively secrete NH3
PTH inhibits what to increase phosphate excretion?
what to stimulate Ca reabsorption?
inhibits phosphate/ reabsorption in PCT
stimulates Ca++ reabsorption in DCT
Angiotensin II stimulates what transporter in PCT?
Na/H+ antiporter so Na and H20 reabsorption increase (but can cause contraction alkalosis)
Thick ascending loop:
directly reabsorbs?
indirectly reabsorbs (2)
directly reabsorbs Na, K, 2 Cl

indirectly absorbs Mg and Ca

concentrates urine as it ascends
thin ascendig loop absorbs what, how
passively reabsorbs water by medullary hypertonicity (concentrates urine)
DCT makes urine more dilute or hypertonic?
more dilute by absorbing more NaCl (inhibited by thiazide diuretics)
2 actions of principal cell, location
in Collecting duct

1. stimulated by aldosterone to insert Na+ channels on luminal side and reabsorb Na+ while excreting H+ and K+

2. stimulated by ADH (via V2 receptor) to insert aquaporin channel on luminal surface
Intercalated cell, secretes what, reabsorbs what, located where
in collecting duct

secretes H+, reabsorbs HC03
3 stimulators of renin secretion, what cells secrete it?
decreased BP sensed by juxtaglomerular cells

decreased Na delivery to DCT sensed by macula densa cells--> stimulat JG cells

increased sympathetic tone
ATII effects on:
hypothalamus
pituitary
adrenals
kidney
glomerulus
vasculature
hypothalamus- stimulates thirst
Pituitary - stimulates ADH secretion
Adrenals - stimulates aldosterone release
Kidney - stimulates Na+ reabsorption in PCT
glomerulus - stimulates efferent arteriole contraction
vasculature - stimulates vascular smooth muscle contraction
ADH respond to osmolarity or BP?
both, primarily osmolarity but can be overriden by low BP
ANP
messenger system?
effect on GFR? renin?
cGMP (increases, vasodilates smooth muscle)

increase GFR, decrease renin

acts to inhibit RAAS system
Is there reflex bradycardia when angiotensin II causes peripheral vasoconstriction?
No, because ang II prevents reflex bradycardia by affecting barorecptor function
PTH stimulates what enzyme in kidney
1 alpha-hydroxylase (converts 25OH vitamin D to 1,25-OH vitamin D)
how can NSIADs cause acute renal failure
inhibit prostaglandins which dilate afferent arteriole, so GFR decreases
Net effect of Atrial Naturetic Peptide? secreted from where
secreted from atria in response to increased blood volume

dilates vascular smooth muscle (inc. cGMP), inc. GFR, increase Na+ filtration, DOES NOT REABSORB Na+ so more Na and H20 excreted
2 stimulatory conditions for aldosterone secretion
decrease blood volume, increased [K+]
6 situations K+ shifted out of cell (hyperkalemia) and 2 transporters involved
Acidosis (inc. K/H+ exchanger)
Beta adrenergic antagonists (dec. Na/K ATPase)
Digoxin (dec. Na/K ATPase)
Hypoinsulinemia (dec. Na/K ATPase)
cell lysis
hyperosmolarity
what is presentation in low Na serum osmolality
disorientation, stupor, coma
presentation for Na high Na serum osmolality
agitation, delirium, coma
Cl- high in what states:
metabolic state
kalemia
volemia
aldosterone level
Cl- high in

metabolic alkalosis
hypokalemia
hypovolemia
increased aldosterone

(think of overactive loop diuretics)
when is Cl- low?
2ndary metabolic acidosis
U waves in ECG indicate
hypokalemia
wide QRS indicates what lab abnormality
hyperkalemia
Peaked T waves indicate what lab abnormality
hyperkalemia
arrhythmias in hypokalemia or hyperkalemia
both
neuromuscular irritability and tetany seen in what lab abnormality
hypocalcemia
delirium, kidney stones, abdominal pain seen in what lab abnormality
hypercalcemia
neuromuscular irritability and arrhythmias seen in what lab abnormality
low Mg2+
decreased tendon reflexes, pulmonary edema, can become cardiovaascular collapse (eletcrolyte imbalance)
high Mg2+
renal stones and metastatic calcifications seen in what lab abnormality
high P04
In metabolic and respiratory disorders, does compensation increase in same direction or opposite direction as primary change?
same direction (HCO3 increase.decrease in respiratory abnormalities slow so may initially not be same direction
for every -1 HCO3 change, change in pC02?

for every +1 HC03 change, change in pC02?
-1 HCO3 = -1.2 pCO2

+1 HCO3 = + 0.7 pCO2
Anion Gap Acidosis causes (and anion gap equation)
AG (9-12 normal) = Na - (HCO3 + Cl)

MUDPILES
Methanol
Uremia
DKA
Phenformin, paraldehyde
INH, Iron, Ibuprofen
Lactic Acid
Ethylene Glycol
Salicylates
2 causes of respiratory alkalosis
hyperventilation (early high altitude exposure)

early aspirin overdose
4 causes of metabolic alkalosis
vomiting
diuretic use
antacid use
hyperaldosteronism
4 causes non-ionic gap metabolic acidosis
diarrhea
glue sniffing
renal tubular acidosis
hyperchloremia
Renal Tubular Acidosis Type 1
cause? affects where? 2 complications?
decreased H+ excretion in CCT

hypokalemia
calcium kidney stones
Renal Tubular Acidosis Type 2
cause? affects where? 2 complications?
decreased reabsorption of HC03 in PCT

hypokalemia
hypophosphatemic rickets
Renal Tubular Acidosis Type 4
cause? affects where? 2 complications
due to hypoaldosteronism or lack of nephron response (in principal cell of CCT)

HYPERkalemia (with decreased urine pH)
decreased NH4+ excretion in PCT
5 types of renal casts
RBCs
WBCs
Granular
hyaline
waxy
2 causes of RBC casts
glomerulonephritis
ischemia
malignant HTN
3 causes of WBC casts
tubulointersitial nephritis
pyelonephritis
transplant rejection
cause of granular cast
renal tubular necrosis
waxy casts indicate
chronic renal failure
what presents with pyruia but no casts
acute cystitis
what presents with hematuria but no casts (2)
bladder cancer, kidney stone
5 characteristics of nephritic syndrome
azotemia
rbcs/casts in urine
proteinuria (>3.5 g/day)
HTN
oliguria
2 nephritic syndromes with granular appearance on immunoflorescence
poststreptococcal glomerulonephritis, diffuse proliferative glomerulonephritis (SLE or MPGN caused)
nephritis with peripheral and periorbital edema
Acute post-streptococcal glomerulonephritis
what changes occur in poststreptococcal glomerulonephritis
immune complexes deposit subepithelially, PMNs infiltrate to clear, causes a
"lumpy-bumpy" appearance on light microscope
List 2 disease classes that present with rapidly progressive (crescentic) glomerulonephritis
Anti-GBM diseases

ANCA diseases
Anti-GBM diseases
have linear immunoflurescent stain

Anti-GBM crescentic glomerulonephritis

Goodpasture's disease (lung hemorrhage)
ANCA diseases (4)
all have non-linear immunoflurescence

1. pauci-immune glomerulonephritis
2. microscopic polyangiitis (p-ANCA)
3. Wegner's Granulomatosis (granulomatous lung involvement)
4. Churg-Strauss (granulomas plus eosinophilia)
p-ANCA association
microscopic polyangiitis
c-ANCA association
Wegner's granulomatosis
crescent shapes in glomeruli indicate what class of nephritis and are composed of what
rapidly progressive (crescentic) glomerulonephrits

fibrin, C3b, plasma proteins

poor prognosis (renal failure in days-weeks)
2 causes of diffuse proliferative glomerulonephritis
SLE and MPGN
kindey disease with "wire-looping" capillaries granular immunofluorescent staining?
what is causing problem?
Diffuse Proliferative Glomerulonephritis

DNA-antiDNA immune complexes (type III hypersenstivity) cause subendothelial deposits

SLE and MPGN are causes
nephritis after URI or gastroenteritis?

what is being deposited, where, to cause damage?
IgA nephropathy (Berger's Disease)

IgA complexes deposit in mesangium
nephritis and deafness?

inheritance?
Alport's syndrome
can also present with ocular and nerve disorders

problem with type 4 collagen, will split basement membrane

X-LINKED DOMINANT inheritance
Nephrotic syndrome:
4 characteristics
2 associated complications
characteristics: dyslipidemia, proteinuria (>3.5g/day), edema, fatty casts

associations - increased risk of thromboembolism, infection (decreased immunoglobulins)
most common adult nephrotic syndrome is what and looks like what
Membranous glomerolnephropathy,

thickening of BM and capillary

"spike and dome" appearance of subepithelial deposits
neprhotic syndrome with subepithelial deposits, 4 causes
membranous glomerulnephropathy

most common adult nephropathy

"spike and dome" deposits

SLE (nephrotic presentation), drugs, tumors, infections
Most common nephropathy in kids

can be triggered by what

selective loss of what (not foot processes, though this too)

treatment?
Minimal change disease
can be triggered by recent infection

selective loss of albumin because of loss of heparan sulfate maintaining anionic BM charge. no loss of Ig

tx- corticosteroids
Diabetic Glomerulonephropathy:
change in GFR?
what part of glomeruli changes

what is damage pattern
nonenzymatic glcosylation of BM causes expansion of mesangium

more leaky, GFR increases

nodular glomerulosclerosis (with Kimmelsteil-Wilson lesions)
nephropathy with segmental sclerosis and hyalinosis?

most common nephropathy in what patient population?
Focal segmental glomerulosclerosis

HIV patients
nephropathy: subendothelial IC deposits and granular immunofluorescence? Association with types?
Membranoproliferative Glomerulonephropathy

Type 1- with "tram-track" lines - associated with HBV, HCV

type 2- with "dense deposits" - associated with C3 nephritic factor
which type of membranoproliferative glomerulonephropathy/nephritis has "dense deposits?" association?
"tram lines?" association?
type 1 - tram lines (split BM from mesangial expansion), associated with HBV and HCV

type 2 - dense deposits, associated with C3 nephritic factor (will have very low serum C3 levels)
4 types of kidney stones
-calcium (most common)
-ammonium magnesium phosphate
-uric acid (radioluscent)
-cystine
hexagonal, radiopaque kidney stone is? tx?
Cysteine (usually associated with cysteinuria)

tx- alkalinization of urine
what is radioluscent kidney stone made of?
uric acid (gout, leukemia and other high cell turnover states)
2 causes of calcium oxalate kidney stones
ethylene glycol poisoning, vitamin C abuse
what are calcium kidney stone components
either calcium phosphate or calcium oxalate

seen in PTH, cancer
Staghorn canaliculi seen with what type of stone?
complication of staghorn canaliculi?
ammonium magnesium phosphate crystals

can be nidus for UTI
3 causes of Ammonium magnesium phosphate crystals?

worsened by what condition
bacteria = staph, klebsiella, proteus

alkaline urine
cancer composed of polygonal clear cells arising from renal tubular cells
Renal Cell Carcinoma
2 risk factors for RCC

2 places it likes to spread (and likes to spread through what)
smoking, obesity

likes bone and lung, spreads through IVC
4 paraneoplastic substances produced by RCC
Prolactin
Epo
ACTH
PTHrp
huge palpable flank mass with hematuria in kid 2-4 is?

association?
Nephroblastoma (Wilm's tumor)

WAGR complex (Wt1 gene, chromsome 11)
Wilm's tumor
aniridia
genitourinary abnormalities
retardation
painless hematuria suggests?

3 causes
transitional cell bladder cancer (occurs anywhere from renal calyces to bladder)

associated with problems in your Pee SAC

pheniacetin
Aniline dyes
cyclophosphamide
Acute pyelonephritis usually affects what, spares what, has what in urine
affects cortex
spares glomeruli
white casts in urine
eosinophilic casts in tubules can indicate what
chronic pyelonephritis
what disease can present with blunted calyx and corticomedullary scarring
chronic pyelonephritis
5 drugs that can cause drug-induced interstitial nephritis
aspirin, sulfonamides, penicillin derviatives, rifampin
drug-induced nephritis, symptoms occur how long after administration, presentation
1-2 weeks

eosinophilic pyuria and azotemia (can also have rash, fever, CVA tenderness, hematuria)
with things such as septic shock and obstetric catastrophies (like abruptio placenta), there can be acute cortical necrosis of kidneys. This is probably caused by both
vasospasm and DIC
what is most common cause of acute renal failure in hospitals?
reversible?
characteristic finding?
Acute Tubular Necrosis
reversible if treated, but fatal if not
characteristic finding= granular brown casts in urine
3 stages of acute tubular necrosis, and how long is usual timecourse
inciting event
maintenance (oliguria)
recovery (usually takes about 2-3 weeks)
3 causes of acute tubular necrosis
ischemia (septic shock, etc)
myoglobinuria (from crush injury)
toxins
most common cause of microscopic hematuria in adult males
BPH
urine dipstick measures
albumin
2 conditions with increased Creatinine clearance
pregnancy
early diabetic nephropathy
what is gold standard to evaluate renal disease
urinalysis
Diffuse segmental glomerulonephropathy has association with what disease
HBsAg
renal papillary necrosis may present after what?

4 associations
presents with gross heamturia and proteinuria

may be after recent infection/immunologic stimulus

DM
acute pyelonephritis
phenacetin use
sickle cell anemia
Prerenal Azotemia (acute renal failure) cause
changes in:
osmolarity
FEna
Serum BUN/Cr
hypotension

osmolarity >500
FEna <1%
Serum BUN/Cr >20 (normal 15)
Renal Azotemia (acute renal failure) cause
changes in:
osmolarity
FEna
Serum BUN/Cr
kidney disease (ATN, ischemia, crescentic glomerulonephritis, toxins)

osmolarity <350
FEna >2%
Serum BUN/Cr <15
Postrenal Azotemia (acute renal failure) cause
changes in:
osmolarity
FEna
Serum BUN/Cr
bilateral obstruction (BPH, stones, congenital anomalies)
osmolarity <350
FEna >4%
Serum BUN/Cr >15
platelet dysfunction, encephalopathy, pericarditis can all be caused by
uremia
Renal osteodystrophy caused by:
and changes seen
renal failure

decreased reabsorption of Ca2+ and excretion of PO4- causes secondary hyperparathyroidism

(calcium levels low until end stage when GFR too low to excrete calcium)
can dyslipidemia result from renal failure?
yes, especially increased TGs
what changes seen in renal failure? (8)
Na/H20 retention
hyperkalemia
acidosis
uremia
anemia (decreased Epo)
dyslipidemia (especially increased TGs)
Renal Osteodystrophy
growth retardation
what is most common genetic cause of renal failure in adults, and genes involved?
AD polycystic kidney disease

APKD1 or APKD2
Multiple large bilateral kidney cysts in adult with progressive kidney disease is what? death usually due to what (2)
ADPCKD (progressive destruction of parenchyma)

due to complications from chronic kidney disease, or HTN (may secrete renin)
AD polycystic Kidney Disease associations (3)
Berry aneurysms
Polycystic liver disease
Mitral valve prolapse
AR polycystic kidney disease:

association in utero
congenital association
3 adult associations
utero- Potter's

congenital - hepatic fibrosis

adult- portal HTN, HTN, renal insufficiency
can long-standing dialysis result in renal cysts?
yes, both medullary and cortical
thin, non-enhancing, cortical, fluid filled simple cyst in adult is
simple cyst, benign and common
Medullary sponge kidney get cysts where, complication
in medullary collecting tubules

can get kidney stones
Medullary cystic disease
get cysts where, complication
corticomedullary cysts that cause fibrosis and progressive renal insufficiency, US shows small kidney

poor prognosis
2 places in nephron mannitol works as diuretic
thin loop of henle
CCT