Flashcards - Renal
fetal hydronephrosis
failure to canalize uteropelvic junction
fetal renal embryology
pronephros (week 4) –> mesonephros (1st trimester) –> metanephros (5th week on)
mulitcystic dysplastic kidney
defect when ureteric bud (caudal) meets with metanephric mesenchyme to induce differentiation, usually unilateral cystic kidney
Fanconi syndrome
PCT defect - loss of AA, glu, HCO3, PO4 = metabolic acidosis
Bartter syndrome
thick ascending loop defect - Na/K/2Cl (lasix)
Gitelman syndrome
DCT - NaCl reabsorption defect (thiazide)
Liddle syndrome
collecting tubule - increased epithelial Na channel activity (increased Na absorption)
Genetic causes of Horseshoe kidney
Edwards, Down, Patau, Turner
Hartnup disease
AR - neutral AA transporter defect (tryptophan –> decreased niacin, pellagra)
RTA Type I
DCT - inability to excrete H+ - urine pH >5.5 - hypokalemia
RTA Type II
PCT - unable to reabsorb HCO3 - urine pH <5.5 - hypokalemia
RTA Type IV
no aldosterone - adrenal/collecting tubule - hyperK –> decreased NH4 excretion - urine pH
heparan sulfate
provides negative charge barrier in basement membrane - lost in nephrotic syndrome
Loop diuretic
TALH - blocks Na/K/2Cl ATPase - can cause hypokalemia, gout, ototoxocity
Thiazide
DCT - blocks Na/Cl co transporter - can cause hyperGLUC, hypoK
Angiotensin II - tubule effect
PCT - stimulates Na+/H+ exchanger (increased Na+ absorption)
ANP/BNP
relaxes smooth muscle via cGMP –> increased GFR, decreased renin
Macula densa
senses decreased NaCl delivery to DCT –> adenosine release –> vasocontriction
Digitalis
blocks Na+/K+ - hyperkalemia
RBC casts
Glomerulonephritis, malignant hypertension.
WBC casts
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection. Nephrotic syndrome.
Fatty casts (“oval fat bodies”)
Acute tubular necrosis.
Granular (“muddy brown”) casts
End-stage renal disease/chronic renal failure and ATN
Waxy casts Hyaline casts
Nonspecific, can be a normal finding, often seen in concentrated urine samples.
IF: starry-sky, lumpy bumpy (IgM, IgG, C3 deposition in GBM and mesangium) EM: subepithelial immune complex humps
acute post-strep glumerulonephritis - group A b-hemolytic strep (pyo) - decreased complement levels, type III hypersensitivity
LM and IF—crescent moon shape of fibrin and plasma proteins
Rapidly progressive (crescentic) glomerulonephritis (RPGN) –>
Goodpasture syndrome - Anti-GBM (type II hypersensitivity), linear IF;
GPA - negative IF;
MPA - negative IF
Diffuse proliferative - SLE - granular IF
LM - “wire looping” of capillaries. EM—subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition, IF—granular
Diffuse proliferative glomerulonephritis (DPGN)
LM—mesangial proliferation, EM—mesangial IC deposits, IF—IgA-based IC deposits in mesangium –> HSP
IgA nephropathy (Berger disease)
Alport syndrome
XL - Mutation in type IV collagen - hematuria, hearing loss, ocular disturbances
Membrano proliferative glomerulonephritis (MPGN)
Type I - HBV, HCV (tram-tracks); Type II - C3 nephritic factor deposits (autoantibody stabilizes C3 convertase, increased complement activation)
LM: thick glomerular basement membrane, EM: “spike and dome” sub epithelial deposits
membranous nephropathy - HCV, HBV, SLE
Bence Jones proteins
light chains from MM - nephrotoxic
Tamm Horsfall protein
eosinophilic casts from light chains - MM
acute interstitial nephritis
drug induced (NSAIDs, PCN, diuretics) - eosinophils in tubules and interstitium
renal papillary necrosis
analgesic abuse (phenacetin, aspirin), DM, sickle cell, pyelo
acute tubular necrosis
reversible, may require dialysis –> tubule cells can regenerate from stable state (2-3 weeks)
ovoid hyaline masses in the glomerular mesangium
Kimmelstiel-Wilson lesions - eosinophilic and PAS+ - diabetic nepropathy
Amphotericin B renal side effects
tubular necrosis - hypoK and hypoMg
renal cell carcinoma
epithelial malignancy of PCT tubules - “clear cell” of carbs/lipids - paraneoplastic (EPO, renin, PTHrP, ACTH) - loss of VHL on Ch3 = increased IGF1
angiomyolipma
hamartoma associated with tuberous sclerosis
calcium phosphate/oxalate
envelope/dumbbell shaped - treat w/ Ca-sparing HCTZ
ammonium magnesium phosphate
coffin lid shaped - staghorn calculi (infection w/ urease+ bacteria)
uric acid
rhomboid - only radiolucent stone - alkalinalize urine
cysteine
hexogonal - staghorn calculi - sodium nitroprusside + - alkanalize urine
calcineurin
dephosphorylates NFAT –> NFAT enters nucleus –> binds to IL-2 receptor –> growth/differentiation of T cell
HUS
shiga-toxin - microangiopathic hemolytic anemia - acute kidney injury
urothelial (transitional) carcinoma risks
cigarette smoke (polycystic hydrocarbons), nathylamine, azo dyes, cyclophosphamide, phenacetin - early p53 mutation = flat, high grade
wilms tumor genetic association
associated with turner syndrome,
WAGR syndrome
WT1 deletion - Wilms, anidria, genital abnormalities, mental/motor retardation
Denys-Drash syndrome
WT1 mutation - Wilms, progressive glomeruli disease, male pseudohermaphroditism
Beckwith-Wiedemann
WT2 mutation - Wilm’s, hypoglycemia, acromegaly (glossitis)
eosinophlic cells with abundant mitochondria without perinuclear clearing
benign - Renal oncocytoma - usually resected
K+ sparing diuretics
amiloride, triamterene, spironolactone
Normal filtration fraction
20% (GFR/RPF)
principal cell
NA+/K+ ATPase (K into lumen, Na out into blood) and aquaporins (ADH on V2 receptor)
alpha intercalated
H+/K+ ATPase and H+ pump (H+ out into lumen)
juxtaglomerular cells
modified smooth muscle in afferent arterial
Vitamin D 25OH to 1,25-OH2 conversion location
PCT cells
drugs causing HyperK
digitalis, beta-blockers
LM—segmental sclerosis and hyalinosis A.
IF—nonspecific for focal deposits of IgM, C3, C1.
EM—effacement of foot process similar to minimal change disease.
Focal segmental glomerulosclerosis - idiopathic, or HIV, sickle cell, heroin, obesity, IFN
squamous cell carcinoma of bladder
chronic irritation - schistosoma haematobium infection (middle east)
prerenal azotemia
BUN:Cr >15 - decreased blood flow, tubules intact FeNa <1%
postrenal azotemia
late BUN:Cr 2% - outflow obstruction, tubular damage
EPO production location
peritubular interstitial cells