Acute RF + nephrotic syndrome Flashcards
Increased BUN and creatinine
azotemia
Acute severe decrease in renal function (w/i days) marked by azotemia and oliguria (low production of urine)
Acute renal failure
ARF due to decreased blood flow to kidneys (e.g. cardiac failure)
Prerenal azotemia
ARF due to obstruction of urinary tract downstream from the kidney
Postrenal azotemia
serum BUN:CR>15;
FENa < 1%
urine osm > 500
Prerenal azotemia
Normal BUN:Cr
15
Serum BUN:CR< 15
FENa > 2%
urine osm < 500
postrenal azotemia (long-standing) or intrarenal (ATN)
Injury and necrosis of tubular epithelial cells –> necrotic cells plug tubules –> obstruction decreases GFR –> brown granular casts in urine
acute tubular necrosis
Causes of intrarenal azotemia
acute tubular necrosis
acute interstitial nephritis
renal papillary necrosis
Etiology of acute tubular necrosis (ATN)
ischemic or nephrotoxic
Decreased blood supply results in necrosis of tubules (often preceded by prerenal azotemia)
Ischemia ATN
Parts of the kidney that are most susceptible to ischemic ATN
proximal tubule and medullary segment of thick ascending limb
part of the kidney that is most susceptible to nephrotoxic ATN
proximal tubule
- Aminoglycosides
- Heavy metals (lead)
- Myoglobinuria (crush injury)
- Ethylene glycol (antifreeze –> oxylate crystals)
- radiocontrast dye
- urate (tumor lysis syndrome, prevent with allopurinol and hydration)
Causes of nephrotoxic ATN
Oliguria with brown granular cases,
elevated BUN and creatinine,
hyperkalemia w/ metabolic acidosis (inc anion gap),
clinical features of ATN
Treatment of ATN
supportive dialysis bc electrolyte imbalances can be fatal (NB: ATN is reversible)
Why does oliguria persist for 2-3 weeks after ATN?
Tubular cells (stable cells) take time to reenter the cell cycle and regenerate
Drug-induced HSR of interstitium and tubules –> intrarenal ARF
acute interstitial nephritis
eos in the urine
acute interstitial nephritis
3 causes of acute interstitial nephritis
NSAIDs, PCN, diuretics
oliguria + fever + rash + eos in urine days to weeks after starting a drug
acute interstitial nephritis
Treatment of acute interstitial nephritis
stop the drug!
possible complication of acute interstitial nephritis
renal papillary necrosis
Gross hematuria + flank pain
renal papillary necrosis
- chronic analgesic abuse (e.g long-term phenacetin or aspirin use)
- diabetes mellitus
- sickle cell trait or disease
4 severe acute pyelonephritis
renal papillary necrosis
glomerular disorders characterized by proteinuria > 3.5 g/day
nephrotic sydnrome
Nephrotic syndrome –> hypoalbuminemia presents as:
pitting edema
nephrotic syndrome –> hypogammaglobulinema presents as:
increased risk of infection
why does nephrotic syndrome –> hypercoagulable state?
loss of antithrombin III
nephrotic syndrome –> hyperlipidemia + hypercholesterolemia (liver trying to beef up urine)–> ?
fatty cases in urine
5 Hs of nephrotic syndrome
hypoalbuminemia
hypogammaglobunemia
hypercoagulable state
hyperlipidemia & hypercholesterolemia
nephrotic syndromes
Minimal change disease (MCD) focal segmental glomerulosclerosis membranous nephropathy membranoproliferative GN diabetes mellitus systemic amyloidosis
most common cause of nephrotic syndrome in children; usually idiopathic; may be associated w/ Hodgkin lymphoma
Minimal change disease
normal glomeruli on H&E;
lipid may be seen in proximal tubule cells
effacement of foot processes (podocytes) on EM
No immune complex deposits (negative IF)
selective proteinuria (loss of albumin, not immunoglobulin)
MCD
Treatment of MCD
steroids! (excellent response bc damage is mediated by cytokines from T cells)
most common cause of nephrotic syndrome in Hispanics & African Americans; usually idiopathic but may be associated with HIV, heroin use, or sickle cell anemia
FSGS
focal and segmental sclerosis on H&E
Effacement of foot processes on EM
no immune complex deposits; negative IF
FSGS
Most common cause of nephrotic syndrome in Caucasian adults; usually idiopathic but may be associated with hepatitis B or C, solid tumors, SLE, or drugs (NSAIDs or penicillamine)
Membranous nephropathy
Thick glomerular basement membrane on H&E;
Due to immune complex deposition (granular IF); subepithelial deposits with “spike and dome” appearance on EM
membranous nephropathy
thick capillary membranes (“tram-track” appearance) on H&E; due to immune complex deposition (granular IF)
membranoproliferative glomerulonephritis
Type I membranoproliferative glomerulonephritis
subendothelial; associated with HBV & HCV; most associated with tram tracks
Type II membranoproliferative glomerulonephritis
dense deposit disease - intramembranous; associated with C3 nephritic factor
autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulating C3
C3 nephritic factor (type II glomerulonephritis)
two systemic diseases that can cause nephrotic syndrome
diabetes mellitus & systemic amyloidosis
NEG
nonenzymatic glycosylation (DM)
high blood sugar –> NEG of vascular membrane –> hyaline arteriolosclerosis of efferent > afferent arteriole –> high GFR –> hyperfiltration injury –> microalbuminuria –> nephrotic syndrome
how DM –> nephrotic syndrome
What slows progression of hyperfiltration-induced damage (–> nephrotic syndrome) in DM?
ACE inhibitors
Characterized by sclerosis of the mesangium with formation of Kimmelstiel-Wilson nodules
DM –> nephrotic syndrome
most commonly involved organ in systemic amyloidosis
kdney
amyloid deposits in mesangium –>
nephrotic syndrome
apple-green birefringence under polarized light
systemic amyloidosis
BUN:Cr < 15
FENa > 2%
urine osm < 500
postrenal or intrarenal (ATN)
What does FENa represent?
tubular function (fractional excretion of sodium, lower is better)
What does urine osmolality represent?
ability to concentrate urine (low is bad)
what nephrotic syndrome is associated with lupus?
membranous nephropathy! (but they more often get diffuse proliferative glomerulonephritis - a nephritic syndrome)
