acute renal failure

Question 1

definition of ARF

Answer 1

significant decrease in GFR over hours to days

Question 2

oliguria

Answer 2

<400 cc urine/day

Question 3

anuria

Answer 3

<100cc urine/day

Question 4

clinical aspects of AKI

Answer 4

confusion, confluent speech, extremity weakness. dry furrowed tongue, dry mucous membranes, dry axilla, sunken eyes. typically history of vomiting or diarrhea

Question 5

common nephrotoxic agents that cause AKI

Answer 5

aminoglycosides, radiocontrast dye and chemo.

Question 6

allergens that can cause AKI

Answer 6

antibiotics, NSAIDs, PPI and many others.

Question 7

what impairs the auto regulation of GFR? how do they do this?

Answer 7

NSAIDs, ACEi, ARBs. NSAIDs inhibit COX and thus prostaglandins. the prostaglandins cause autovasodilation of the afferent arteriole (also a source of hyper filtration injury)

Question 8

what is the difference between prerenal azotemia and ARF

Answer 8

prerenal azotemia has intact tubular function. ARF does not.

Question 9

what is the classic urinary sediment in ARF?

Answer 9

renal tubular cells, granular muddy brown casts.

Question 10

what other classic signs indicate renal failure

Answer 10

decreased concentration of urine, increased urine sodium, decreased urine/plasma creatinine ratio, fractional excretion of sodium > 2% fractional excretion of urea >35.

Question 11

what causes the manifestations of prerenal azotemia

Answer 11

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

Question 12

what are the causes of decreased GFR in ATN?

Answer 12

tubular cell sloughing causes obstruction and fluid dynamic push back. there is backleak and tubuloglomerular feedback to the afferent arteriole.

Question 13

where are the prominent areas of necrosis in ischemic ATN

Answer 13

sparse proximal tube and thick ascending limb

Question 14

where are the areas of necrosis in toxic ATN

Answer 14

the entire proximal tube and thick ascending limb.

Question 15

causes of thrombotic microangiopathy

Answer 15

hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, malignant HTN and scleroderma kidney

Question 16

causes of HUS

Answer 16

shiga toxin HUS, atypical HUS with unregulated complement activation, drugs, or antiphospholipid syndrome. neuramidase-associated pneumococci.

Question 17

causes of TTP

Answer 17

ADAMSTS13

Question 18

what is the differential of acellular mesangial expansion?

Answer 18

diabetes, amyloidosis, kappa light chain nephropathy, sclerotic phase MPGN.

Question 19

what is natural progression of Diabetic nephropathy

Answer 19

preclinical hyper filtration with episodic microalbuinemia, clinical overt proteinuria, progresssive ESRD.

Question 20

effective treatment for DN

Answer 20

metabolic control and ACEi

Question 21

histology of DN

Answer 21

mesangial expansion, afferent and efferent hyaline arteriolosclerosis. capsular drops. formation of fibrin caps.

Question 22

what is the cause of diabetic nephropathy?

Answer 22

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

Question 23

what causes the mesangial expansion in DN

Answer 23

there is non enzymatic glycosylation of the membrane which decreases its porosity (Kf). this ultimately leads to nephrosclerosis.

Question 24

does the non enzymatic glycosylation cause proteinuria?

Answer 24

yes. any disturbance of the glomerular basement membrane will most likely give you proteinuria