renal pathology Flashcards
acute renal failure
acute, severe decline in renal function (develops within days). hallmark is azotemia (increase in the BUN and creatinine) and often displays oliguria. split into three main pathologies prerenal, intrarenal and post renal pathology
what are the hallmarks of prerenal azotemia
due to decreased blood flow to the kidneys. this results in decreased GFR, increased BUN and Creatinine, and oliguria. tubular function remains intact.
what are the BUN:CRE ratio and fractional excretion of sodium for pre-renal
BUN:CRE > 20
FeNA < 1%
urine osmolal > 500/kg.
what happens with long standing post-renal renal kidney injury
tubular damage ensues. resulting in decreased absorption of BUN and thus the BUN:CRE <20. the tubular damage results in decreased reabsorption of sodium FeNA > 2% and inability to concentrate urine urine osmolal < 500 mosm/kg
what happens in post-renal kidney injury
this is due to obstruction of renal outflow. the decreased outflow results in decreased GFR, azotemia and oliguria.
what happens during early stages of post renal Aki based on the BUN and CRE
the increased pressure forces the BUN back into the blood. The tubular function is somewhat preserved and thus the BUN:CRE>20 and the FeNA is <1%
what happens during long term post renal AKI
tubular damage ensues resulting in decreased reabsorption of BUN and thus the BUN:CRE <20 the decreased reabsorption of sodium results in FENa >2%
what is acute tubular necrosis
injury and necrosis of the tubular epithelial cells. this is the most common cause of acute renal failure or intrarenal azotemia. necrotic cells plug the tubules and decrease the GFR. muddy brown casts.
what is the BUN/CRE like in ATN
there is decreased reabosrption of the BUN and thus the BUN:CRE is <20 the sodium is not reabsorbed as well either resulting in FENa >2%
what are the two circumstances in which you can have an ATN
1) ischemia, typically preceded by prerenal AKI. the proximal tube and the medullary segment are particularly vulnerable to ischemia
2) nephrotoxic result in the necrosis of tubules. common toxins are amino glycoside antibiotics, heavy metals such as lead, myoglobinemia, ethylene glycol, radio contrast dye, and urate.
what are the clinical features of ATN
oliguria, with muddy brown casts. elevated BUN/CRE. hyperkalemia.
is ATN reversible
yes but often requires dialysis since the electrolyte imbalances can be fatal. the oliguria can persist for 2-3 weeks before recovery. tubular cells take time to reenter the cell cycle and regenerate.
what is acute interstitial nephritis
drug induced hypersensitivity involving the interstitium and tubules. results in AKI.
what are the causes of acute interstitial nephritis
NSAIDs, penicillin, diuretics.
how does acute interstitial nephritis present
oliguria, fever, rash, after starting drug. often with eosinophilia.
what is the cure for acute interstitial nephritis
resolves with cessation of the offending agent. however, may progress to renal papillary necrosis.
what is renal papillary necrosis
necrosis and cell death of the renal papillary. presents with gross hematuria and flank pain.
what are the causes of renal papillary necrosis
analgesics abuse. DM. sickle cell trait or disease, severe acute pyelonephritis.
what are the features of nephrotic syndrome
proteinuria greater than 3.5g/24hr. that results in hypoalbuminemia and pitting edema. hypogammaglobinemia and an increased risk for infections. hyper coagulable state due to the loss of antithrombin III. hyperlipidemia and hypercholesterolemia may result in fatty casts in the urine.
what is minimal change disease
most common cause of nephrotic syndrome in children. usually idiopathic but can be associated with Hodgkins lymphoma and NSAID usage.
SELECTIVE LOSS OF ALBUMIN.
what are the hisotologcal features of minimal change disease
the glomeruli look normal on HE stain, there may be lipids in the proximal tubule cells. effacement of the foot processes on electron microscopy. NO IMMUNE COMPLEX DEPOSITION. There will be no immunofluorescence.
what is the treatment for minimal change
excellent response to steroids.
what is focal segmental glomerulonephritis
most common cause of nephrotic syndrome in hispanics and African Americans. usually idiopathic but is associated with obesity, HIV, heroin use, sickle cell anemia.
what are the histological features of FSGS
focal (some of the glomeruli) and segmental (involving only part of the glomeruli) sclerosis on HE. effacement of foot processes. NO IMMUNE COMPLEXES.
what is the treatment for FSGS
poor response to steroids. usually progresses to renal failure.
what is membranous nephropathy
most common cause of nephrotic syndrome in caucasian adults. usually idiopathic. maybe associated with HEP B and C, solid tumors such as adenocarcinoma, SLE, or drugs (NSAIDs and penicillamine)
what is the histology for membranous
thick glomerular membranes on HE DUE TO IMMUNE COMPLEX DEPOSITION. subnendothelial deposits with spike and dome appearance on EM.
what is the treatment for membranous
poor response to steroids. usually progresses to chronic renal failure.
what is membranoproliferative glomerulonephritis
two types. thick basement membrane on HE often with tram track appearance. DUE TO IMMUNE COMPLEX DEPOSITION.
what is associated with type I membranoproliferative glomerulonephritis
sub endothelial disease. HBV, HCV.
what is associated with type II membranoproliferative glomerulonephritis
dense deposit disease. intramembranous…this is associated with C3 nephritic factor. this is an autoantibody that stabilizes C3 convertase leading to over activation of complement, inflammation and low levels of circulating C3.
what is the treatment for membranoproliferative glomerulonephritis
poor response to steroids. usually progresses to renal failure.
what is nephritic syndrome
this is a syndrome of glomerular damage resulting in hematuria. there is limited proteinuria. there is azotemia and oliguria. salt retention with periorbital edema and hypertension. There is RBC casts and dysmorphic RBCs in the urine. biopsy reveals hypercellular and inflamed glomeruli. immune complex deposition activates complement; C5 attracts neutrophils which mediate damage.
what is poststreptococcal glomerulonephritis.
nephritic syndrome that arises after group A, beta-hemolytic strep infection of the skin or pharynx. occurs with nephritogenic strains.
when does poststreptococcal glomerulonephritis occur
occurs about 2-3 weeks after infection and presents as hematuria or cola-colored urine, oliguria, hypertension, and periorbital edema. usually seen in children, but it can occur in adults.
what is the histology of PSGN
mediated by immune deposition sub endothelial humps on EM.
what is the treatment for PSGN
suspportive children rarely progress to renal failure. some adults will develop rapidly progressively glomerulonephritis.
what is rapidly progressive glomerulonephritis
nephritic syndrome that progresses to renal failure in weeks to months. characterized by crescents in Bowman space. these are formed by fibrin and macrophages.
what is IgA nephropathy
most common cause of nephropathy globally. IgA immune complex deposition in the mesangium of glomeruli.
how does IgA nephropathy present
in childhood a episodic gross hematuria with RBC casts usually following mucosal infections such as gastroenteritis and URI. As IgA production is increased during infection.
this may slowly progress to renal failure.
what is alport syndrome
inherited type IV collagen defect. most commonly X-linked. results in thinning and splitting of the glomerular membrane
what is the clinical presentation of alport syndrome
hematuria, sensory neural hearing loss, and ocular disturbances.
what is the best way to control diabetic nephropathy
strict BP control
What is the likely underlying etiology of kidney disease with GBM thickening, mesangial expansion, and glomerular sclerosis?
diabetic nephropathy
