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Renal > Acute RF + nephrotic syndrome > Flashcards

Acute RF + nephrotic syndrome Flashcards

1
Q

Increased BUN and creatinine

A

azotemia

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2
Q

Acute severe decrease in renal function (w/i days) marked by azotemia and oliguria (low production of urine)

A

Acute renal failure

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3
Q

ARF due to decreased blood flow to kidneys (e.g. cardiac failure)

A

Prerenal azotemia

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4
Q

ARF due to obstruction of urinary tract downstream from the kidney

A

Postrenal azotemia

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5
Q

serum BUN:CR>15;
FENa < 1%
urine osm > 500

A

Prerenal azotemia

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6
Q

Normal BUN:Cr

A

15

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7
Q

Serum BUN:CR< 15
FENa > 2%
urine osm < 500

A

postrenal azotemia (long-standing) or intrarenal (ATN)

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8
Q

Injury and necrosis of tubular epithelial cells –> necrotic cells plug tubules –> obstruction decreases GFR –> brown granular casts in urine

A

acute tubular necrosis

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9
Q

Causes of intrarenal azotemia

A

acute tubular necrosis
acute interstitial nephritis
renal papillary necrosis

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10
Q

Etiology of acute tubular necrosis (ATN)

A

ischemic or nephrotoxic

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11
Q

Decreased blood supply results in necrosis of tubules (often preceded by prerenal azotemia)

A

Ischemia ATN

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12
Q

Parts of the kidney that are most susceptible to ischemic ATN

A

proximal tubule and medullary segment of thick ascending limb

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13
Q

part of the kidney that is most susceptible to nephrotoxic ATN

A

proximal tubule

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14
Q
  1. Aminoglycosides
  2. Heavy metals (lead)
  3. Myoglobinuria (crush injury)
  4. Ethylene glycol (antifreeze –> oxylate crystals)
  5. radiocontrast dye
  6. urate (tumor lysis syndrome, prevent with allopurinol and hydration)
A

Causes of nephrotoxic ATN

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15
Q

Oliguria with brown granular cases,
elevated BUN and creatinine,
hyperkalemia w/ metabolic acidosis (inc anion gap),

A

clinical features of ATN

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16
Q

Treatment of ATN

A

supportive dialysis bc electrolyte imbalances can be fatal (NB: ATN is reversible)

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17
Q

Why does oliguria persist for 2-3 weeks after ATN?

A

Tubular cells (stable cells) take time to reenter the cell cycle and regenerate

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18
Q

Drug-induced HSR of interstitium and tubules –> intrarenal ARF

A

acute interstitial nephritis

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19
Q

eos in the urine

A

acute interstitial nephritis

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20
Q

3 causes of acute interstitial nephritis

A

NSAIDs, PCN, diuretics

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21
Q

oliguria + fever + rash + eos in urine days to weeks after starting a drug

A

acute interstitial nephritis

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22
Q

Treatment of acute interstitial nephritis

A

stop the drug!

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23
Q

possible complication of acute interstitial nephritis

A

renal papillary necrosis

24
Q

Gross hematuria + flank pain

A

renal papillary necrosis

25
Q
  1. chronic analgesic abuse (e.g long-term phenacetin or aspirin use)
  2. diabetes mellitus
  3. sickle cell trait or disease
    4 severe acute pyelonephritis
A

renal papillary necrosis

26
Q

glomerular disorders characterized by proteinuria > 3.5 g/day

A

nephrotic sydnrome

27
Q

Nephrotic syndrome –> hypoalbuminemia presents as:

A

pitting edema

28
Q

nephrotic syndrome –> hypogammaglobulinema presents as:

A

increased risk of infection

29
Q

why does nephrotic syndrome –> hypercoagulable state?

A

loss of antithrombin III

30
Q

nephrotic syndrome –> hyperlipidemia + hypercholesterolemia (liver trying to beef up urine)–> ?

A

fatty cases in urine

31
Q

5 Hs of nephrotic syndrome

A

hypoalbuminemia
hypogammaglobunemia
hypercoagulable state
hyperlipidemia & hypercholesterolemia

32
Q

nephrotic syndromes

A 
Minimal change disease (MCD)
focal segmental glomerulosclerosis
membranous nephropathy
membranoproliferative GN
diabetes mellitus
systemic amyloidosis
33
Q

most common cause of nephrotic syndrome in children; usually idiopathic; may be associated w/ Hodgkin lymphoma

A

Minimal change disease

34
Q

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)

A

MCD

35
Q

Treatment of MCD

A

steroids! (excellent response bc damage is mediated by cytokines from T cells)

36
Q

most common cause of nephrotic syndrome in Hispanics & African Americans; usually idiopathic but may be associated with HIV, heroin use, or sickle cell anemia

A

FSGS

37
Q

focal and segmental sclerosis on H&E
Effacement of foot processes on EM
no immune complex deposits; negative IF

A

FSGS

38
Q

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)

A

Membranous nephropathy

39
Q

Thick glomerular basement membrane on H&E;

Due to immune complex deposition (granular IF); subepithelial deposits with “spike and dome” appearance on EM

A

membranous nephropathy

40
Q

thick capillary membranes (“tram-track” appearance) on H&E; due to immune complex deposition (granular IF)

A

membranoproliferative glomerulonephritis

41
Q

Type I membranoproliferative glomerulonephritis

A

subendothelial; associated with HBV & HCV; most associated with tram tracks

42
Q

Type II membranoproliferative glomerulonephritis

A

dense deposit disease - intramembranous; associated with C3 nephritic factor

43
Q

autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulating C3

A

C3 nephritic factor (type II glomerulonephritis)

44
Q

two systemic diseases that can cause nephrotic syndrome

A

diabetes mellitus & systemic amyloidosis

45
Q

NEG

A

nonenzymatic glycosylation (DM)

46
Q

high blood sugar –> NEG of vascular membrane –> hyaline arteriolosclerosis of efferent > afferent arteriole –> high GFR –> hyperfiltration injury –> microalbuminuria –> nephrotic syndrome

A

how DM –> nephrotic syndrome

47
Q

What slows progression of hyperfiltration-induced damage (–> nephrotic syndrome) in DM?

A

ACE inhibitors

48
Q

Characterized by sclerosis of the mesangium with formation of Kimmelstiel-Wilson nodules

A

DM –> nephrotic syndrome

49
Q

most commonly involved organ in systemic amyloidosis

A

kdney

50
Q

amyloid deposits in mesangium –>

A

nephrotic syndrome

51
Q

apple-green birefringence under polarized light

A

systemic amyloidosis

52
Q

BUN:Cr < 15
FENa > 2%
urine osm < 500

A

postrenal or intrarenal (ATN)

53
Q

What does FENa represent?

A

tubular function (fractional excretion of sodium, lower is better)

54
Q

What does urine osmolality represent?

A

ability to concentrate urine (low is bad)

55
Q

what nephrotic syndrome is associated with lupus?

A

membranous nephropathy! (but they more often get diffuse proliferative glomerulonephritis - a nephritic syndrome)

Renal (22 decks)

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