acute renal failure Flashcards
definition of ARF
significant decrease in GFR over hours to days
oliguria
<400 cc urine/day
anuria
<100cc urine/day
clinical aspects of AKI
confusion, confluent speech, extremity weakness. dry furrowed tongue, dry mucous membranes, dry axilla, sunken eyes. typically history of vomiting or diarrhea
common nephrotoxic agents that cause AKI
aminoglycosides, radiocontrast dye and chemo.
allergens that can cause AKI
antibiotics, NSAIDs, PPI and many others.
what impairs the auto regulation of GFR? how do they do this?
NSAIDs, ACEi, ARBs. NSAIDs inhibit COX and thus prostaglandins. the prostaglandins cause autovasodilation of the afferent arteriole (also a source of hyper filtration injury)
what is the difference between prerenal azotemia and ARF
prerenal azotemia has intact tubular function. ARF does not.
what is the classic urinary sediment in ARF?
renal tubular cells, granular muddy brown casts.
what other classic signs indicate renal failure
decreased concentration of urine, increased urine sodium, decreased urine/plasma creatinine ratio, fractional excretion of sodium > 2% fractional excretion of urea >35.
what causes the manifestations of prerenal azotemia
hypovolemia leads to RAAS with intact tubules this leads to sodium retention and a urine sodium concentration decrease. there is also subsequent ADH secretion and water retention which causes a decrease in urine osmolarity
what are the causes of decreased GFR in ATN?
tubular cell sloughing causes obstruction and fluid dynamic push back. there is backleak and tubuloglomerular feedback to the afferent arteriole.
where are the prominent areas of necrosis in ischemic ATN
sparse proximal tube and thick ascending limb
where are the areas of necrosis in toxic ATN
the entire proximal tube and thick ascending limb.
causes of thrombotic microangiopathy
hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, malignant HTN and scleroderma kidney
causes of HUS
shiga toxin HUS, atypical HUS with unregulated complement activation, drugs, or antiphospholipid syndrome. neuramidase-associated pneumococci.
causes of TTP
ADAMSTS13
what is the differential of acellular mesangial expansion?
diabetes, amyloidosis, kappa light chain nephropathy, sclerotic phase MPGN.
what is natural progression of Diabetic nephropathy
preclinical hyper filtration with episodic microalbuinemia, clinical overt proteinuria, progresssive ESRD.
effective treatment for DN
metabolic control and ACEi
histology of DN
mesangial expansion, afferent and efferent hyaline arteriolosclerosis. capsular drops. formation of fibrin caps.
what is the cause of diabetic nephropathy?
ultimately glucosuria. this causes a dilution of the urine sodium because glucose osmotically increases the volume of urine. this causes the MD to think that the GFR is low due to low salt hitting the sensor. afferent dilation causes hyperfiltration injury
what causes the mesangial expansion in DN
there is non enzymatic glycosylation of the membrane which decreases its porosity (Kf). this ultimately leads to nephrosclerosis.
does the non enzymatic glycosylation cause proteinuria?
yes. any disturbance of the glomerular basement membrane will most likely give you proteinuria
