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Flashcards in Renal Deck (115)
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1

Differentiate cyst location in dysplastic kidney dz, PKD, Medullary cystic kidney dz

dysplastic => renal parenchyma & abnormal tissue

PKD=> bilateral enlarged kidneys w/ cysts in cortex & medulla

medullary => medullary collecting ducts w/ parenchymal fibrosis leading to shrunken kidneys

2

How does the ARPKD present?

baby w/ portal HTN due to congenital hepatic fibrosis

3

How does ADPKD present?

young adult w/ HTN, hematuria, progressive renal failure w/ FHx of death due to berry aneurysm rupture or chronic renal failure

4

What is the timeline & hallmark of acute renal failure?

azotemia (high BUN & Cr) w/in days often w/ oliguria

5

What is the cause of pre renal ARF? what are the assoc labs?

decreased Q to kidneys so decreased GFR;
BUN:Cr > 15
tubular fxn intact so FENa < 1% & urine osm > 500 mOsm/kg

6

What is cause of post renal azotemia?

obstruction of urinary tract downstream decreasing GFR (backup), azotemia & oliguria

7

Differentiate the timeline of early & long-standing post renal obstruction

early increase in pressure leads to BUN:Cr > 15
FENa < 1% & urine osm > 500mOsm

long term causes tubular damage causing BUN:Cr < 15
FENa > 2% & urine osm < 500mOsm

8

what is the MCC of acute renal failure?

intrarenal azotemia => injury & necrosis of tubular epithelial cells

9

What will be seen on urinalysis during ATN?

brown, granular casts in urine
serum BUN:Cr < 15
FENa > 2%
urine osm < 500 mOsm

10

What are the clinical features of ATN?

oliguria w/ brown granular casts
BUN:Cr < 15
Hyperkalemia (decresed renal fxn) w/ metabolic acidosis

11

Describe ATN if ischemia is the cause. What is the most susceptible part of kidney?

decreased Q so often preceded by pre renal azotemia =>
proximal tubule & medullary segment of thick ascending limb are most susceptible

12

What are nephrotoxic agents to the kidney that may lead to ATN?

MC is aminoglycosides;
heavy metals (lead);
myoglobinuria (crush injury to muscle);
ethylene glycol;
radiocontrast dye (CT scan);
urate (tumor lysis syndrome or high gout)

13

How will you know if someone ingested ethylene glycol?

oxalate crystals in urine

14

What are ways to avoid tumor lysis syndrome causing ATN?

hydration & allopurinol prior to CTX

15

If ATN occurs, how is it treated and can the pt recover? what is the timeframe?

Reversible => supportive dialysis due to severe electrolyte imbalances

oliguria can present for 2-3wks before recovery due to tubular cells regenerating

16

Why does it take 2-3wks for oliguria to remit?

tubular cells are stable cells so takes time to re-enter the cell cycle & regenerate

17

What causes acute interstitial nephritis? How is it treated? What happens if it is not?

Drug induced HSR causing infrarenal azotemia typically from NSAIDs, penicillin & diuretics
Resolves w/ drug stoppage;
if Rx is not pulled then renal papillary necrosis may occur

18

How does acute interstitial nephritis present?

oliguria, fever & rash varying from days to weeks (any time) after using a Rx => eosinophils MAY be in urine

19

How does renal papillary necrosis present? What are the common causes?

gross hematuria w/ flank pain
causes=>
Chronic analgesic pain (phenacetin or aspirin use);
DM;
Sickle cell disease OR trait;
Severe acute pyelonephritis

20

Define nephrotic syndrome & the 4 possible results

proteinuria > 3.5g/day

hypoalbuminemia - pitting edema;
hypogammaglobulinemia - increased infection risk;
hyper coagulable state - due to loss of AT-3;
hyperlipidemia & hypercholesterolemia - fatty casts in urine

21

How does the MCC of nephrotic syndrome in children present on H&E? EM? IF? urinalysis?

H&E: normal glomeruli;
EM: effacement of foot processes
IF: no IC deposits so negative IF

Urinalysis has selective proteinuria w/ loss of albumin but not Ig loss

22

What cancer is minimal change disease associated with? why?

Hodgkin lymphoma due to massive increase of cytokines from RS cells

23

What is the response to treatment of minimal change disease?

excellent response to steroids due to damage caused by cytokines from T cells

24

What is the MCC of nephrotic syndrome in Hispanics & AA?

Focal segmental glomerulosclerosis (FSGS)

25

What is FSGS associated with?

HIV; heroin use; sickle cell disease

26

How does FSGS appear on H&E? EM? IF?

HE: focal & segmental pink sclerosis
EM: effacement of foot processes
IF: no IC deposits = neg IF

27

What is the response to Tx in FSGS?

poor response to steroids leading to chronic renal failure

28

What is the MCC of nephrotic syndrome in caucasian adults?

membranous nephropathy

29

What is membranous nephropathy assoc w/?

HBV, HCV;
solid tumors;
SLE (usually diffuse proliferative GN);
Rx (NSAIDs & penicillamine)

30

How does membranous nephropathy appear on H&E? EM? IF?

HE: thick glomerular BM
EM: subepithelial deposits w/ 'Spike & dome" appearance
IF: IC deposits so granular IF