Renal Flashcards
nephrotic synd
massive proteinuria (>3.5g/day, frothy urine), hyperlipidemia, fatty casts, edema; ass. w/ thromboembolism (bc of ATIII loss in urine; present w/ flank pain + hematuria), increase risk of infection NO RBC OR RBC CASETS IN URINE
FSGS membranous nephropathy minimal change dz (lipoid nephrosis) amyloidosis - ass w/ chronic conditions MPGN diabetic glomerulonephropathy
nephritic synd
inflammatory!! (hypercellular, inflamed glomeruli from immune-complex dep)
hematuria, RBC casts in urine, azotemia, oliguria, HTN, mild proteinuria
PSGN RPGN DPGN Berger's dz (IgA nephropathy) Alport synd
FSGS
- segmental sclerosis + hyalinosis (LM)
- effacement of foot processes (EM)
- adults (Hisp, Af Am)
- NO response to steroids
- ass w/ HIV, heroin abuse, obesity, sickle cell dz
membranous nephropathy
- diffuse capillary + GBM thickening (bc immune-complex dep) (LM)
- “spike-and-dome” appearance w/ SUBEPITHELIAL deposits [b/w epith cells + BM, under podocytes] (EM)
- granular IF (w/ IgG + C3 dep)
- SLE’s nephrotic presentation
- idiopathic (85%)!!
- also by use of NSAIDs/penicillamine, Hep C or B, DM
- Caucasian adults
minimal change dz
- NORMAL glomeruli (LM)
- foot process effacement - bc of cytokine damage (EM)
- selective loss of albumin, not Ig
- may be triggered by recent infection/immune stim
- children (usually idiopathic)
- responds to steroids (ONLY ONE)
MPGN
type I:
- granular IF (SUBENDOTHELIAL DEP)
- tram-track appearance bc GBM splitting (from mesangial ingrowth)
- thick capillary membranes
- ass w/ HBV, HCV + subacute bacterial endocarditis
type II:
- INTRAMEMBRANOUS DEP
- ass w/ C3 nephritic factor (auto-Ab stabilizes C3 convertase)
**both have granular IF and LARGE HYPERCELLULAR GLOMERULI
diabetic glomerulonephropathy
-hyaline arteriosclerosis
-NEG of GBM –> increased permeability, thickening
NEG of efferent arterioles –> increases GFR
GBM thickening, Kimmelsteil-Wilson nodules (ovoid hyaline mass; eosinophilic nodular glomerulosclerosis)
ACE inhibitors slow injury process!!
acute post-strep GN
- type III HST
- “lumpy-bumpy” appearance (glomeruli enlarged and hypercellular, neutrophils) (LM)
- SUBEPITHELIAL immune complex humps (EM)
- granular IF (IgG, IgM, C3 deposition) - decreased C3, normal C4
- children
- periph + periorbital edema
- dark urine
- after group A-beta strep infection of SKIN (impetigo) or PHARYNX - WEEKS after! + resolves spontaneously
- elevated ASO titers, or anti-DNase B!
RPGN
- crescent-moon shape (consist of fibrin, plasma proteins like C3b, macrophages, glomerular parietal cells, monocytes) w/in BOWMAN’S SPACE (LM and IF)
- poor prognosis
can result from:
- Goodpasture’s synd (type II HST) - linear IF
- Wegener’s granulomatosis (c-ANCA) - neg IF
- microscopic polyangiitis, Churg Strauss (p-ANCA) - neg IF
Goodpasture’s synd
type II HST
Ab to GBM and alveolar BM
linear IF (C3 and IgG deposited along GBM)
hematuria/hemoptysis
DPGN
- due to SLE (most common cause of death in SLE) or MPGN
- “wire looping” of capillaries (LM)
- SUBENDOTHELIAL OR INTRAMEMBRANOUS IgG based immune complexes often w/ C3 dep
- granular IF
Berger’s dz (IgA nephropathy)
- related to Henoch-Schonlein purpura
- mesangial prolif (LM); mesangial IC dep (EM)
- IgA-based immune complex dep in mesangium (IF)
- NORMAL complement levels
- presents/flares w/ URI or acute gastroenteritis
- follows mucosal infection (bc excess prod of IgA)
- most common nephropathy worldwide
Alport synd
- mut in type IV collagen –> split BM
- X-linked
- GN, deafness, eye problems (cataracts, etc.)
early prox tubule reabsorb/secrete?
all of glucose and AA
most of bicarb, Na, Cl, phosphate, water (ISOTONIC absorption)
65-80% Na reabsorbed
secretes ammonia (to buffer H)
PTH function in prox tubule
inhib Na/phosphate cotransport –> phosphate excretion
thin descending LOH function?
passive reabsorp of water (via medullary hypertonicity)
concentrating segment –> makes urine HYPERTONIC!
thin desc LOH impermeable/permeable to?
imperm to Na
perm to urea
thick ascending LOH reabsorb?
active reabsorption of Na, K, Cl
indirectly reabsorb Mg, Ca (by + lumen potential from K backleak) - paracellular
10-20% Na reabsorbed
thick ascending LOH impermeable to?
WATER
makes urine LESS concentrated as it ascends
early distal convoluted tubule (DCT) reabsorb?
ACTIVE reabsorb of Na, Cl (urine hypotonic)
5-10% Na reabsorbed
MOST DILUTE SEGMENT
PTH effect on DCT?
increase Ca/Na exchange –> Ca reabsorb
DCT impermeable to?
water (unless vasopressin levels adeq to promote reabsorp) and urea
collecting ducts reabsorb?
Na in exchange for K, H secretion (reg by aldosterone)
3-5% Na reabsorbed
HYPERTONIC
Potter synd?
clubfeet flat face w/ low-set ears, other facial deformities pulmonary hypoplasia (most common cause of death)
caused by bilat renal agenesis*** (mostly), ARPKD, posterior urethral valves
most bladder cancers are?
transitional cell carcinoma aka UROTHELIAL carcinoma
GFR calc measured by?
inulin
creatinine can estimate
PAH best measure of?
RPF; underestimated by ~10%
horseshoe kidney trapped under what artery?
IMA
RBF =
RPF/(1-hematocrit) = (PAH clearance)/(1-hematocrit)
or (renal artery pressure - renal vein pressure)/renal vascular resistance
no ureteric bud =
bilat kidney agenesis
horseshoe kidney ass w/ what?
Turner’s synd
what property of glomerular filtration barrier lost in nephrotic synd?
charge barrier
what keeps negative charge barrier?
BM + heparan sulfate
renal clearance =
(U x V)/P
FF =
GFR/RPF
normally 20%
filtered load =
GFR x plasma concentration
glucose reabsorpt?
prox tubule via Na/glucose co-transport
@160 mg/dL –> glucosuria (threshold)
@350 mg/dL –> all transporters fully saturated
Hartnup disease is?
deficiency of tryptophan –> decreased vit B3 –> pellagra
in PCT, ATII action is?
stim Na/H exchange –> increased Na, H2O, HCO3 reabsorption; secrete H
causes contraction alkalosis!
TF/P > 1 when
solute absorbed less quickly than water
ex. PAH, Creatinine, inulin, urea, Cl
TF/P = 1 when
solute + water reabsorbed @ same rate
ex. K, Na
TF/P < 1 when
solute reabsorbed faster than water
ex. HCO3, AA, glucose
functions of ATII
potent vasoconstrictor
constricts efferent arterioles –> maintains GFR by increasing FF
stim aldosterone prod, ADH release
increases PCT Na/H activity –> contraction alkalosis
stim hypothal –> thirst
ANP effect in kidney
increase GFR
decrease renin
JG cells are modified what?
modified SM of afferent arteriole
in renal artery stenosis what happens to JG cells
JG cells of affected kidney(s) –> hypertrophy + hyperplasia bc increased release of renin
what part of kidney converts to active vit D
PCT
afferent arteriole mediators
prostaglandins - vasodil
NSAIDS - oppose prostaglandins
efferent arteriole mediators
AT II - vasoconstriction
ACE inhib - oppose AT II
protein effects in glomerulus
if increased - increases glomerular capillary oncotic pressure –> decreased GFR, FF; no change RPF
if decreased - decreases glomerular capillary oncotic pressure –> increased GFR, FF; no change RPF
impt function of ATII to prevent further decrease in vol loss
compensatory Na reabsorp. @ PCT and DCT!!!
increased serum Mg levels –>
decreased DTRs, bradycardia, lethargy, etc.
winter’s formula
PCO2 = 1.5(HCO3) + 8 +/- 2
anion gap =
Na - (Cl + HCO3)
normal = 8-12 mEq/L
increased anion gap metab acidosis
MUDPILES! Methanol (formic acid) Uremia DKA Propylene glycol INH or Iron tablets Lactic acidosis (ex. in shock) Ethylene glycol (oxalic acid) Salicylates (LATE)
normal anion gap metab acidosis
HARDASS! Hyperalimentation (ex.overeating, parenteral nutrition) Addison's dz Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
RTA type 1
“distal”
defect in collecting tubule ability to EXCRETE H+ [intercalated cells]
urine pH > 5.5
hypokalemia
increased risk for Ca phosphate kidney stones bc of increased urine pH + bone resorption
RTA type 2
"proximal" urine pH < 5.5 defect in PCT reabsorption of HCO3 hypokalemia increased risk of hypophosphatemic rickets may be ass w/ Fanconi synd
RTA type 4
“hyperkalemic”
HYPOALDOSTERONISM or collecting tubule lack of response to aldost
hyperkalemia –> impairs ammoniagenesis in PCT –> decreased buffering capacity + urine pH decreased
what 2 synd can present as both nephritic/nephrotic
DPGN
MPGN
SLE
diff b/w IgA neph + PSGN
IgA neph - few DAYS after URI infection
PSGN - few WEEKS after infection
complications of kidney stones
hydronephrosis (expansion of renal pelvis)
pyelonephritis
all kidney stones are radiopaque EXCEPT
Uric acid stones = radiolUcent (not seen on x-ray)
view on CT or US
lowest pH in nephrons is @
DCT
collecting tubules
2 factors that prevent crystallization of stones
- citrate (binds free Ca –> facilitates its excretion)
- fluids!
calcium phosphate stones
alkaline pH
causes: hypercalcemia (cancer, increased PTH, sarcoidosis), Crohn’s
tx = citrate, thiazide diuretics
calcium oxalate stones
acidic pH
**can result from ethylene glycol (antifreeze) or vit C abuse
other causes: hypercalcemia (cancer, increased PTH, sarcoidosis), Crohn’s
tx = citrate, thiazide diuretics
common kidney stone presentation
calcium oxalate stones in pt w/ hypercalciuria + normal serum calcium (idiopathic hypercalciuria)
ammonium magesium phosphate stones (struvite)
alkaline pH
infection w/ urease-positive bugs (Proteus, Staph, Klebsiella)
staghorn calculi (nidus for UTIs)
uric acid stones
acidic pH
radioLUCENT
from hyperuricemia (gout); seen in dz w/ increased cell turnover like LEUKEMIA
tx = alkalinization of urine
cystine stones
acidic pH
HEXAGONAL crystals - of sulfur-containing compounds!
2ndary to cystinuria
tx = alkalinization
RCC originates from what cells
PCT cells - clear cells! (filled w/ lipids + carbs)
RCC spread =
hematogenously by invading renal vein –> IVC
RCC ass w/ what paraneoplastic synd
ectopic EPO
ACTH
PTHrP
prolactin
Wilm’s tumor (nephroblastoma) contains what cells
embryonic glomerular structures (blastema)
acute pyelonephritis histo + casts
neutrophilic infiltrate
WBC casts
chronic pyelonephritis histo + casts
lymphocytic infiltration + corticomedullary fibrosis (scarring) eosinophilic casts (thyroidization of kidney)
drugs implicated in drug-induced interstital nephritis
1-2 wks after: penicillin derivatives, diuretics, sulfonamides, rifampin
months after: NSAIDS
chronic interstitial nephritis: lithium, cyclosporine
diffuse cortical necrosis ass w/?
obstetric complic (ex. placenta abruptio)
septic shock
ARDS
acute tubular necrosis features?
- 3 stages (inciting, maintenance, recovery)
- inj + necrosis of tubular epith cells
- ass w/ aminoglycosides, cisplatin, amphotericin B, foscarnet, heavy metals, ethylene glycol, crush injury (myoglobiuria), toxins, renal ischemia (shock, sepsis)
- granular “muddy brown” casts seen**
- w/ drugs/toxins –> PCT suscept; w/ renal ischemia –> PCT + medullary segment of thick ascending limb suscept
in ATN, death occurs usually in what phase
inciting
maintenance phase of ATN =
oliguria
risk of hyperkalemia
1-3 wks
recovery phase of ATN =
polyuria
risk of hypokalemia (bc of high vol + hypotonic urine)
BUN + serum creatinine fall
renal papillary necrosis ass w/
DM
acute pyelonephritis + UT obstruction
chronic phenacetin use (ex. acetominophen)
sickle cell anemia/trait
prerenal azotemia =
- bc of decreased RBF (ex. hypotension, NSAIDs)
- Na/H2O and urea retained to conserve vol
- INCREASED BUN/creatinine ratio
intrinsic renal failure =
- cause = ATN or ischemia/toxins
- patchy necrosis
- epith/granular casts in urine
- DECREASED BUN/creatine ratio
postrenal azotemia =
- due to outflow obstuction (stones, BPH, neoplasia, etc.) - forces BUN back into blood
- ONLY w/ bilat obstruction
- INCREASED BUN/creatinine ratio
features of uremia
pericarditis N/V asterixis encephalopathy platelet dysfunt (qualitative dysfunct; NORMAL platelet count) INCREASED BUN/creatinine ratio
histo in renal osteodystrophy
subperiosteal thinning of bones
medullary cystic disease
- AD
- tubulointerstital fibrosis (cysts in medullary CD)
- inability to conc urine
- SHRUNKEN KIDNEYS on US
