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IM Nephrology > 334 Acute Kidney Injury > Flashcards

334 Acute Kidney Injury Flashcards

1
Q

Common diagnostic features of AKI

A

Increase in BUN and/or increase in serum crea, reduction in urine volume

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2
Q

ICU mortality rates in AKI

A

May exceed 50%

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3
Q

Causes of AKI

A

Prerenal Azotemia
Intrinsic renal Parenchymal disease
Post renal Obstruction

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4
Q

Most comon form of AKI

Inadequate renal plasma flow and intraglomerular hydrostatic pressure

A

Prerenal Azotemia

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5
Q

Common clinical conditions in Prerenal azotemia

A

Hypovolemia
Dec cardiac output
Medications: NSAIDs, ARBs, ACEi

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6
Q

Prolonged periods of prerenal azotemia may lead to ischemic injury termed as

A

Acute TUbular NEcrosis (ATN)

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7
Q

Renal blood flow accounts for _ % of cardiac output

A

20%

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8
Q

This maintains GFR despite decreased renal blood flow by renal efferent vasoconstriction

A

Angiotensin II

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9
Q

This leads to dilataion in the setting of low perfusion pressure therefor maintaining GFR

A

Myogenic Reflex, prostaglandins, kinins, NO

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10
Q

Renal autoregulation usually fails once SBP falls below __ mm Hg

A

80 mmHg

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11
Q

These limits renal afferent vasodilation:

A

Long standing hpn, hyalinosis, myointimal hyperplasia

NSAIDs

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12
Q

These limits renal efferent vasodilation

A

ACE inhibitors, ARBs

Bilateral renal artery stenosis, unilateral renal artery stenosis

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13
Q

This poses a particularly high risk for developing prerenal azotemia

A

NSAIDs + ACE inhibitors

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14
Q

Type of Hepatorenal syndrome in which AKI without an alternate cause PERSISTS despite volume administration and witholding of diuretics

A

Type 1 HRS

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15
Q

This type of Hepatorenal syndrome is less severe form - characterized by REFRACTORY ASCITES

A

Type 2 HRS

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16
Q

Most common causes of intrinsci AKI

A

Sepsis, ischemia, nephrotoxins

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17
Q

Pathophysiology of sepsis-induced AKI

A

Tubular injury, inflammation, mitochondrial dysfunction and interstitial edema

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18
Q

Hemodynamic effects of sepsis in AKI

A

Generalized arterial vasodilation, expression of NO synthase -> decreased GFR

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19
Q

Healthy kidneys recieve _% of cardiac output and account for _% of resting o2 consumption

A

20% of cardiac output

10% of o2 cosumption

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20
Q

One of the most hypxic regions in the body

A

Renal medulla - outer medulla

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21
Q

Most common procedures associated with AKI

A

Cardiac surgery with bypass, vascular procedures with aortic clamping, intraperitoneal procedures

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22
Q

Risk factors for post op AKI

A

CKD, old age, DM, CHF, Emergency procedures

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23
Q

AKI is a complication of burns affecting 25% of individuals with more than _% of Total body surface area

A

10%

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24
Q

Intraabdominal pressure of _mmHG lead to renal vein compression and reduced GFR

A

20 mmHg

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25
Q

Leading cause of AKI

A

Iodinated contrast agents for CV and CT imaging

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26
Q

Clinical course of contrast nephropathy

A

Rise in SCr 24-48 hrs following exposure, peak of 3-5 days, resolving within 1 week

27
Q

Antibiotics causing tubular necrosis

A

Aminoglycosides and amphotericin B, mainfests after 5-7 days of therapy

28
Q

Common finding in antibiotic induced AKI

A

Hypomagnesemia

29
Q

Amphotericin B causes AKI by

A

renal vasoconstriction from increased tubuloglomerular feedback AND direct tubular troxicity; dose and duration dependent

30
Q

Clinical features of Amphotericin B nephrotoxicity

A

Hypomagnesemia, hypocalcemia, nongap metabolic acidosis

31
Q

May cause hemorrhagic cystitis and tubular toxicity; type 2 RTA (Fanconi’s syndrome), polyuria, hypokalemia and decline in GFR

A

Ifosfamide

32
Q

Cause of chinese Herb Nephropathy and Balkan Nephropathy

A

Aristocholic acid

33
Q

Uromodulin, the most common protein in urine and produced in thick ascending loop of henle

A

Tamm- Horsfall protein

34
Q

Uric acid levels in Tumor lysis syndrome

A

> 15mg/dl

35
Q

Tumor lysis syndrome:electrolyte features

A

hyperkalemia and hyperphosphatemia and hypocalcemia

36
Q

Occurs when normally unidirectional flow of urine is blocked

A

Post renal AKI

37
Q

Diagnosis of AKI

A

Rise from baseline of at least 0.3mg/dl within 48 hours at least 50% higher than baseline wihtin 1 week or
Reduction in UO less than 0.5ml/Kg /hr for longer than 6 hours

38
Q

AKI with palpable purpura, pulmonary hemorrhage or sinusitis raises the possibility of

A

systemic vasculitis with glomerulonephritis

39
Q

AKI from ATN due to ischemic injury, sepsis or certain nephrotoxins has characteristic urine sediment findings of :

A

“Muddy Brown” Granular casts and tubular epithelial casts

40
Q

Oxalate crystals in AKI should prompt evaluation for

A

Ethylene glycol toxicity

41
Q

A measure of both the kidney’s ability to reabsorb sodium as well as endogenously and exogenously administired factors that affcet tubular reabsorption

A

Fractional excretion of Na (Fe Na)

42
Q

A type 1 transmembrane protein abundant in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin/ ichemic or nephrotoxic injury

A

Kidney injury molecule-1 (KIM-1)

43
Q

NGAL (lipocalin-2 or siderocalin)

Neutrophile gelatinase associated lipocalin

A

Biomarker of AKI, bind to iron siderophoere an dmay have tissue protective effects; detected in plasma and urine within 2h of Cardiopulmonary bypass- associated AKI

44
Q

Hallmark of AKI

A

Buildup of nitrogenous waste products, elevated BUN

45
Q

BUN level which causes metal status changes, bleeding complications

A

> 100mg/dl

46
Q

Most concerning complication of AKI

A

Hyperkalemia

47
Q

Definitive treatment of hepatorenal syndrome

A

orthotopic liver transplantation

48
Q

Scleroderma renal crisis should be treated with

A

ACE inhibitors

49
Q

Idiopathic TTP-HUS should be treated promptly with

A

Plasma exchange

50
Q

Patients with rhabdomyolysis may initially require _L of fluid per day

A

10L

51
Q

Diuretics may be used if fluid repletion is adequate but unsuccesful in achieving urinary flow rates of _

A

200-300mL/hr

52
Q

Metabolic acidosis is generally not treated unless severe at pH_ and bicarbonate of _mmol/L

A

pH <7.20 and bicarbonate at <15mmol/L

53
Q

According to KDIGO, AKI patients should achieve total energy intake of

A

20-30kcal/kg/day

54
Q

Protein intake in non severe AKI, no need for dialysis

A

0.8 to 1.0 g/kg/perday

55
Q

Protein intake in patients on dialysis

A

1.0-1.5 g/kg per day

56
Q

Protein intake if hypercatabolic and receiving CRRT

A

1.7 g/kg per day

57
Q

Many nephro initiate dialysis for AKI empirically when BUN exceeds:

A

100 mg/dl

58
Q

Most common form of renal replacement therapy for AKI

A

Hemodialysis

59
Q

_% may develop ESRD - among survivors of AKI requiring temporary dialysis

A

10%

60
Q

Case: 60 M with constitutional symptoms, bone pain
Lab: Monoclonal spike in urine, low anion gap, anemia

A

Multiple myeloma

61
Q

Case: Aminoglycosisde antibiotics, cisplatin, antivirals, ethylene glycol ingestion, melamin ingestion
Lab: urine sediment: granular casts, renal tubular epithelial cell casts, FeNa >1%

A

Tubular injury

62
Q

Case: Recent medication exposure with fever, rash , arthralgias
Lab: Urine has eosinophilia, sterile pyuria, nonoliguric

A

Interstitial nephritis

63
Q

Case: Neurologic abnormalities present, recent diarrhea, with AKI, use of calcineurin inhibitors, pregnancy or post partum
Lab: schistocytes on PBS, elevated LDH, anemia and decreased plt, ADAMTS13 activity

A

TTP/HUS
Typical HUS - AKI with diarrhea (Shiga toxin, E.coli)
Atypical HUS- inherited or acquired complement dysregulation
TTP HUS - sporadic cases

IM Nephrology (3 decks)

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