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Renal Flashcards

1
Q

Definition of AKI

A

Cr increase .3
or by 50%
or .5ml/kg/h over 6 hours decrease in urine

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2
Q

Labs to be ordered in AKI

A

BMP, CBC wdif, urinalysis (osmolality, sediment, output, electrolytes), ABG (expect metabolic acidosis),

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3
Q

In AKI when do we order serologies? ultrasound? biopsy?

A

suspecting glomerular disease
PKD, hydronephrosis, post renal cause
suspecting glomerular disease

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4
Q

What are the dialysis indications.

A

When refractory to treatment
A- Acidemia
E- electrolyte disturbances (hyperK, phos, tumor lysis)
I- Intoxication (methanol, glycols, lithium, salicylates)
O- Overload
U- uremia (encephalopathy, pericarditis, bleeding from platelet dysfunction)

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5
Q

All forms of acute renal failure cause an increase in what?

A

BUN and Cr

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6
Q

How do we diagnose post-renal azotemia?

A

catheterization, renal ultrasound (pre and post urination)

>100 mmL remaining in bladder = voiding obstruction

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7
Q

AKI testing algorithm?

A

Rule out post renal
rule out pre-renal
determine intrarenal

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8
Q

What is the post renal urine osmol? FeNA? BUN:Cr?

A

urine osmol 2%, BUN:Cr>15.

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9
Q

Besides volume depletion and low Cardiac output, what are causes of pre renal azotemia?

A

cirrhosis, sepsis, NSAIDS, cyclosporine, ACEI, ARBs

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10
Q

What is orthostatic hypotension?

A

S-BP decrease >20 HR increase >20

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11
Q

In pre-renal azotemia what is the FENa?

A
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12
Q

What is the BUN:Cr? FENa? FEurea? Urine osmol? Ua dipstick SG in pre-renal?

A

> 20, 500, >1.020

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13
Q

What is the BUN:Cr? FENa? FEurea? Urine osmol? Ua dipstick SG in intra-renal?

A

2%, >55%,

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14
Q

What toxin is pre-renal by vasoconstriction and ATN?

A

contrast

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15
Q

what drugs cause ATN? 4

A 
aminoglycosides
vanco
amphotericin
cisplatin
and contrast!
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16
Q

What endogenous substances cause ATN?

A

hemoglobin, myoglobin

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17
Q

Why does myeloma cause ATN?

A

light chains

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18
Q

What crystals cause ATN>

A

uric acid, acyclovir, MTX, indinavir

19
Q

What are the allergic causes of AIN? 5 drugs

A
  • B-lactams (penicillins, cephalosporins, monobactams and carbapenems)
  • sulfa drugs
  • NSAIDS
  • PPIs
  • allopurinol
20
Q

What infections cause AIN?

A

pyelonephritis, legionella, TB, Leptospira

21
Q

What infiltrative malignancies cause AIN?

A

sarcoid, lymphoma, leukemia

22
Q

What autoimmune diseases cause AIN?

A

Sjogren’s, SLE, cryoglobulins

23
Q

nephrotoxic ATN causes necrosis where? what about ischemic ATN?

A

PCT

PCT and TAL

24
Q

what is the pathogenesis of ATN?

A

necrosis–> necrotic debries plugs tubules–> decrease GFR–> tubular dilation and flattening of cells with cast formation

25
Q

In ATN, Heme 4+ with no RBC would signify what?

A

hemoglobin or myoglobin

26
Q

What is the clinical triad of AIN?

A

oliguria, fever, rash

27
Q

What are the diagnostic hallmarks of AIN?

A

eosinophilia, inflammatory infiltrate in interstitium, WBC casts, rare eosinophils in urine

28
Q

How do we prevent contrast- induced AKI? Cr inc by .5 or 25% in 48 hrs

A
  1. isotonic IV fluids
  2. Hold ACEI, ARB, diuretics, NSAIDS
  3. N-acetylcysteine
29
Q

What are the pauci immune diseases?

A

wegeners, churg strauss, microscopic polyangiitis

30
Q

What are the 3 causes of cresentric GN?

A

goodpasteurs
pauci immune
Immune complex GN (sle, PSGN, membranoprolipherative GN)

31
Q

If the serum complement is low in nephritic syndrome, what labs do we need to differentiate the diseases?

A

ASO tite, ANA/dsDNA, HepB/C serology, blood cultures

32
Q

If the serum complement is normal in nephritic syndrome, what labs do we need to differentiate the diseases?

A

Anca, anti-GBM

33
Q

What disease has subepithelial humps? subendothelial humps?

34
Q

Membranoproliferative GN is associated highly with what?

35
Q

What is the treatment for good pasteurs

A

steroids, cytotoxic agents, plasmapheresis

36
Q

Is wegener’s c-anca? what differentiates it from goodpasteurs?

A

yes, involvement of the naso pharynx

37
Q

p anca microscopic polyangiitis has what clinical uniqueness?

A

mononeuritis multiplex (wrist drop, foot drop)

38
Q

what are the 3 major features of the p-anca churg strauss syndrome?

A

granulomatous inflammation + eosinophilia + asthma

39
Q

What are 2 key differences of IgA nephropathy from PSGN?

A

follows mucosal infection 2-4 days and serum complement is normal.
(also IgA deposits in mesangium are different, but this is with biopsy)

40
Q

What is minimal change associated with? drug + cancer

A

NSAIDS, Hodgkins

selective hypoalbuminemia

41
Q

What is focal segmental glomerulosclerosis associated with?

A

HIV, heroin, sickle cell disease, obesity

42
Q

What is the EM appearance of membranous nephropathy?

A

spike + dome appearance

43
Q

What is the treatment for diabetic nephropathy?

A

ACEIs and ARBs

IM (11 decks)

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