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64 Cards in this Set

  • Front
  • Back
morphology of minimal change disease?
effacement of foot processes, otherwise kidney appears normal
lipid laden renal cortices
morphology of focal segmental glomerulosclerosis?
not all of the glomeruli are involved and the entire glomerular region is not necessarily involved
usually onlly the glomeruli in the medulla are involved
morphology of membranous glomerulonephritis?
spike and dome (BM and mesangial cells)
IgG and C3 deposition in the subepithelium
granular immunofluorescence
morphology of diabetic nephropathy?
2 types of morphologies possible: (BM markedly thickened in both)
diffuse glomerulosclerosis
kimmelsteil-wilson nodules (nodular glomerulosclerosis)
morphology of renal amyloidosis?
amyloid deposition in the subendothelium and mesangium
criss-cross fibrillary pattern
what are the morphological features of lupus nephropathy?
5 forms:
I: no clinical consequence
II: hematuria with proteinuria (increase in mesangium)
III: focal proliferative form (<50% of glomeruli)
IV: wire-loop abnormalities, endothelial cell proliferation, subendothelial immune complex deposits
V: same as diffuse membranous glomerulonephritis
morphology of post-streptococcal glomerulonephritis?
hemorrhages on the surface of each kidney
enlarged, hypercellular, swollen, bloodless glomeruli
lumpy-bumpy immunofluorescence (IgG and C3)
subepithelial localization
morphology of RPGN
50% of the time is post-streptococcal with immune complex deposition
crescents between Bowman's capsule (fibrin deposition)

can also be pauci-immune type with no immune deposition or anti-glomerular BM AB
causes of RPGN
post-streptococcal (50%)
Goodpastrue's (10% of time)
what is the association of RPGN with ANCA?
can be associated with ANCA (type III, pauci-immune) or not associated with ANCA
if not, types I (with anti-glomerular BM AB) and type II (immune complex type)
morphology of renal dz seen in Goodpasture's
linear IgG immunofluorescence
clinical manifestations of Goodpasture's dz
nephritic syndrome
pneumonitis with hemoptysis
RPGN crescentic dz with linear immunofluorescence
morphology of focal glomerulonephritis
focal and segmental involvement, with inflammatory and proliferative changes (as opposed to sclerotic changes seen in FSGS)
cliical features of Alport syndrome
nerve deafness
ocular d/o
lens dislocation
renal failure by 30yo
morphology of alport syndrome
splitting of the lamina densa (basketweave)
IRREGULAR basement membrane thickening
Berger dz
IgA deposition in mesangium
very common dz
clinical picture of Berger Dz
benign recurrent hematuria in children, following an infection
lasts 1-2 days, has little clinical significance
can be a component of Henoch-Schnolein
presenting feature of Berger Dz
focal glomerulonephritis
clinical presentation of membranoproliferative glomerulonephritis
slow progression to chronic renal failure
morphology of MPGN
BM thickening and cellular proliferation
tram-track appearance of BM b/c of reduplication of glomerular BM into 2 layers from expansion of mesangial matrix into glomerular capillary loops
what are the different types of MPGN
type I: tram track appearance
type II: dense deposits with C3 adjacent (NOT within); caused by IgG autoantibody to C3 convertase that stabilizes the enzyme and constitutively activates convertase
renal colic
excruciating pain from distending ureter d/t stone
progressive dilation fo renal pelvis and calyces
clinical manifestations of urinary tract infections
increased urinary frequency
pyuria (PMNLs in urine)
causes and manifestations of acute drug-induced interstitial nephritis
caused by penicillin and it's derivatives or NSAIDS
immune etiology
acute interstitial inflammation
causes of papillary necrosis
DM (#1 cause)
aspirin or other NSAIDS, phenacetin (no longer OTC)
morphology of renal papillary necrosis
loss and atrophy of tubules
interstitial fibrosis
what is the most common cause of acute renal shutdown?>
acute tubular necrosis
is ATN reversible?
yes, just takes time for the necrotic renal tubular cells to be replaced with new healthy cells (approx 2 weeks)
complete return of renal fxn is possible if pt is maintained on dialysis while symptomatic
clinical progression of ATN
iniating stage from inciting events
initial oliguric phase (--> hyperkalemia and cardiac complications), renal failure
recovery stage with increased urine volumes and hypokalemia
causes of ATN
renal ischemia from prolonged hypotension/shock, gram negative sepsis, or crush injury

mercuric chloride, gentamycin, ethylne glycol
clinical presentation of fanconi syndrome
impaired reabsorption at the proximal tubules
glucosuria, phosphaturia, aminoaciduria, systemic acidosis, and hypophospatemia
hartnup dz
impaired tubular reabsorption of tryptophan
--> pellagra manifrestations
morphology of chronic pyelonephritis
deformity of renal pelvis and calyces
interstitial inflammatory infiltrate (early stages) and later with interstitial fibrosis with tubular atrophy
atrophic tubules contain eosinophilic protein casts that look like thyroid follicles
when is thyroidization of the kidney seen?
chronic pyelonephritis
clinical presentation of chronic pyelonephritis
chronic UTI and repeated bouts of inflammation
--> renal HTN and ESRD
causes of diffuse cortical necrosis
obstetric catastrophe
septic shock
what is nephrocalcinosis
Ca deposition in kidney parenchyma --> renal failure, caused by hypercalcemia or can be caused by hyperphosphatemia

can be a cause or an effect of renal failure
what is the milk alkali syndrome?
nephrocalcinosis and renal stones from self-medicating for peptic ulcer with milk and absorbable antacids
morphology of chronic tubular interstitial nephritis
kidneys are small and atrophic
tubular lumens show marked dilation
infiltrate is mononuclear and there is prominent interstitial fibrosis with tubular atrophy
clinical presentation of chronic interstitial nephritIS
no edema
minimal proteinuria
normal or slightly elevated BP
what is the morphologic difference between adult and juvenile onset polycycstic kidney dz
in juvenile onset: outer surface of kidney is smooth, with no visible cysts (cysts are closed and not connected to collecting ducts)
general features of chronic interstitial nephritis
any dz where tubulointerstitial area is more affected than glomeruli
how does protein affect nitrogen balance
if high protein, then + n balance, b/c higher BUN, thus raising BUN/Cr
what effect does rhabdo have on BUN:Cr?
it decreases the ratio by increasing the cr
what is nephronophthisis
cysts in medulla that result in renal failure
what causes acquired cystic dz of the kidney
long-term dialysis
morphology of acquired cystic dz of kidney
cysts, glomerular and tubular atrophy
what is associated with acquired cystic dz of kidney
renal cell carcinoma risk
characteristics of uremia
acidosis (from accumulation of phosphates, sulfates, adn organic acids)
abnormal control of fluid volume (early inability to [] urine, then inability to dilute urine)
neuro d/o
bleeding from d/o platelet fxn
accumulation in skin of urochrome and other pigments
fibrinous pericarditis
causes of prerenal azotemia
blood loss
peripheral pooling from gram negative sepsis
systemic hypovolemia
bilateral RAS
BUN:Cr in prerenal azotemia
what are the different types of RTA
type 1: distal tubular dfect (can't establish H+ gradient --> metabolic acidosis with urine pH >5.5)
type 2: proximal tubule failure to reabsorb HCO3-, urine pH >5.5 initially then <5.5 later
type 4: low aldosterone --> hyperkalemia and hyperchloremia; urine pH <5.5
what are the benign tumors of the kidney
what is angiomyolipoma
hamartoma consisting of fat, smooth muscle, BV
associated with tuberous sclerosis syndrome
what are the malignant tumors of the kidney
renal cell carcinoma
wilms tumor
transitional cell carcinoma
squamous cell carcinoma
demographics of renal cell carcinoma
men 50-70yo
what is the most common type of renal cell carcinoma
clear cell carcinoma (chrom 3 gene deletion)
where does renal cell carcinoma originate
renal tubules, usually at the upper pole
mets of renal cell carcinoma
usually hematogenous
travels through renal veins and IVC
histology of renal cell carcinoma
polygonal clear cells
clinical features of renal cell carcinoma
flank pain
palpable mass
flank pain
secondary polycythemia
ectopic production of various hormones
what drugs/toxic exposures has been associatd with transitional cell carcinoma
aniline dyes
etiology of squamous cell carcinoma
chronic inflammation
schistosoma haematobium infection
renal calculi