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PSBIM 2023 Nephro > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Definition of AKi

A

the impairment of kidney filtration and excretory function over days to weeks, resulting in the retention of nitrogenous waste products normally cleared by the kidneys

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2
Q

Common causes of community-acquired AKI

A

Volume depletion
Heart failure
Adverse effects of medications
Obstruction of Urinary Tract
Malignancy

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3
Q

Common causes of hospital-acquired AKI

A

Sepsis
Major surgical procedures
Critical Illness involving heart or liver failure
Nephrotoxic medical administration

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4
Q

Classification of major causes of AKI

A
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5
Q

Most common form of AKI

A

Pre-renal azotemia

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6
Q

Decreased perfusion pressure in the presence of NSAIDS

A

loss of vasodilatory prostaglandins increases afferent resistance

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7
Q

Decreased perfusion pressure in the presence of ACE-i or ARB

A

loss of angiotensin II action reduces efferent resistance

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8
Q

Threshold of systolic blood pressure when renal autoregulation falls

A

80 mmHG

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9
Q

Type 1 Hepatorenal Syndrome

A

defined as >two-fold increase in SCr to >2.5 mg/dL within 2 weeks without alternate cause, persists despite volume administration and withholding of diuretics

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10
Q

Type 2 Hepatorenal Syndrome

A

less severe from characterized mainly by refractory ascites

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11
Q

Most common causes of intrinsic AKI

A

Sepsis
ischemia
Nephrotoxins

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12
Q

At risk to develop ischemia-associated AKI

A

limited renal reserve (older age),
Coexisting insults:
-Sepsis
-Vasoactive or nephrotoxic drugs
-Rhabdomyolysis
-Systemic inflammatory states associated with burns and pancreatitis

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13
Q

Procedures most commonly associated with AKI

A

Cardiac surgery with cardiopulmonary bypass,
Vascular procedures with aortic cross clamping,
Intraperitoneal procedures

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14
Q

Common risk factors for postoperative AKI

A

Underlying CKD
Older age
Diabetes Mellitus
Congestive heart failure
Emergency procedures

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15
Q

Risk factors for Nephrotoxin associated AKI

A

Older age
CKD
Pre renal azotemia
Hypoalbuminemia (in some)

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16
Q

Most common clinical course of contrast nephropathy

A

rise in SCr beginning 24-48h following exposure, peaking within 3-5 days, and resolving within 1 week

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17
Q

Most common findings in CI -AKI

A

low fractional excretion of sodium (FeNa) and relatively benign urinary sediment without features of tubular necrosis

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18
Q

Clinical features of amphotericin B nephrotoxicity

A

Polyuria
Hypomagnesemia
Hypocalcemia
Nongap metabolic acidosis

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19
Q

Chemotherapeutic drugs that accumulates in the proximal tubular cells and cause necrosis and apoptosis

A

Cisplatin and carboplatin

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20
Q

Ifosfamide nephrotoxicity

A

Cause hemorrhagic cystitis and tubular toxicity manifested as type II renal tubular acidosis (Fanconi’ syndrome), polyuria, hypokalemia, and a modest decline in GFR

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21
Q

Chemotherapeutic drugs that cause thrombotic microangiopathy

A

Bevacizumab
Mitomycin C
Gemcitabine

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22
Q

Tumor lysis syndrome

A

Hyperuricemia
Hyperkalemia
Hyperphosphatemia
Hypocalemia

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23
Q

Occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally, leading to increased retrograde hydrostatic pressure and interference with glomerular filtration

A

Post-renal AKI

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24
Q

Common cause of postrenal AKI which impacts both kidneys

A

Bladder neck obstruction

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25
Q

Definition of AKI

A

-elevation in the SCr concentration or reduction in urine output

-a rise from baseline of at least 0.3 mg/dL within 48h or at least 50% higher than baseline within 1 week or a reduction in urine output to <0.5 ml/kg per h for longer than 6h

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26
Q

Key differences from CKD

A

Clues suggestive of CKD:
1. Radiologic studies
-small shrunken kidneys with cortical thinning on renal ultrasound
-evidence of renal osteodystrophy

  1. Laboratory findings
    -normocytic anemia in the absence of blood loss
    -secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
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27
Q

Clinical and laboratory features of prerenal azotemia

A
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28
Q

Clinical and laboratory features of sepsis-associated AKI

A
29
Q

Clinical and laboratory features of ischemia-associated AKI

A
30
Q

Clinical and laboratory features of endogenous nephrotoxin-associated AKI

A
31
Q

Clinical features of exogenous nephrotoxin associated AKI

A
32
Q

Clinical features of other causes of intrinsic AKI

A
33
Q

Urinary sediments in AKI

A
34
Q

Definition of Oliguria

A

defined as <400 ml/24h

35
Q

AKI conditions that may present with complete anuria

A

Complete urinary tract obstruction,
Renal artery occlusion,
Overwhelming septic shock,
Severe ischemia,
Severe GN or vasculitis

36
Q

AKI conditions that may present with preserved urine output

A

Nephrogenic DI (longstanding urinary tract obstruction),
Tubulointerstitial disease,
Nephrotoxicity from cisplatin or aminoglycosides, etc/

37
Q

Characteristic urine sediment of AKI from ATN (sepsis, ischemic injury, or certain nephrotoxins)

A

pigmented “muddy brown” granular casts and tubular epithelial cells

38
Q

Causes of disproportionate BUN elevation compared to creatinine

A

Prerenal azotemia
UGIB
Increased tissue catabolism
Glucocorticoid use

39
Q

the fraction of filtered sodium load that is reabsorbed by the tubules, and is a measure of both the kidney’s ability to reabsorb sodium as well as endogenously and exogenously administered factors that affect tubular reabsorption

A

FeNa

40
Q

Diagnostic and therapeutic in prerenal azotemia

A

Response of urine output to crystalloid or colloid fluid administration

41
Q

Conditions with urinary tract obstruction that can present without radiologic abnormalities

A

Volume depletion,
Retroperitoneal fibrosis,
Encasement with tumor,
Early in the course of obstruction

42
Q

CKD conditions with normal kidney size on radiologic evaluation

A

Diabetic nephropathy,
HIV-associated nephropathy,
Infiltrative disease

43
Q

AKI conditions with enlarged kidneys

A

Acute interstitial nephritis
Infiltrative diseases

44
Q

A rare but serious complication seen most commonly in patients with ESRD and severe AKI undergoing MRI with gadolinium based-contrast agents

A

Nephrogenic system fibrosis

45
Q

Provide definitive and prognostic information about AKI and CKD

A

Kidney biopsy

46
Q

Renal failure indices

A

BUN
Crea
FeNa
Urine osmolality

47
Q

Can be used as a prognostic test for Oliguric AKI

A

urinary flow rate in response to bolus IV furosemide 1.0-1.5 mg/kg

UO <200 ml over 2h post furosemide ->higher risk for progression to more severe AKI and the need for RRT

48
Q

a type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin

A

Kidney injury molecule-1 (KIM-1)

49
Q

a novel bioimarker that is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2h or cardiopulmonary bypass-associated AKI

A

Neutrophil gelatinase associated lipocalin (NGAL)

aka Lipocalin-2 or siderocalin

50
Q

Predictive biomarkers for higher risk of the development of moderate to severe AKI in critically ill patients

A

Insulin-like growth factor binding protein 7 (IGFBP7),
Tissue inhibitor of metalloproteinase 2 (TIMP-2)

51
Q

Hallmark of AKI

A

Build of nitrogenous waste products , manifested as an elevated BUN concentration

52
Q

Polyuric phase of recovery from AKI

A

may be due to an osmotic diuresis from retained urea and other waste products as well as delayed recovery of tubular reabsorptive functions

53
Q

Fluid contraindicated in AKI

A

Hydroxyethyl starch solutions

54
Q

Management of AKI - general principles

A
55
Q

Definitive treatment of hepatorenal syndrome

A

Orthotopic liver transplantation

56
Q

Bridge therapies that have shown promise in HRS

A

Terlipressin (a vasopressin analog),
Combination tx with octreotide (A somatostatin analog),
Midodrine (an a1 adrenergic agonist), and
norepinephrine in combination with IV albumin (25-50 g, max 100 g/d)

57
Q

Treatment for scleroderma renal criis

A

ACE inhibitors

58
Q

Treatment for idiopathic TTP-HUS

A

plasma exchange

59
Q

Treatment for rhabdomyolysis

A

Early and aggressive volume repletion , may initially require 10L of fluid per day

  • alkaline fluids may be beneficial
60
Q

Management in severe cases of volume overload

A

Furosemide may be given as a bolus (200 mg) followed by an intravenous drip(10-40 mg/h), with or without a thiazide diuretic

61
Q

General threshold of treatment of metabolic acidosis

A

Severe metabolic acidosis:
pH< 7.20
serum hco3 <15 mmol/L

62
Q

Total energy intake of patients with AKI

A

20-30 kcal/kg per day

63
Q

Protein intake of noncatabolic AKI without the need for dialysis

A

0.8-1.0 g/kg/day

64
Q

Protein intake of patients with AKI on dialysis

A

1.0-1.5 g/kg/day

65
Q

Protein intake of patients with AKI with hypercatabolic state receiving continuous renal replacement therapy

A

1.7 g/kg/day

66
Q

Indications for dialysis in AKI

A

When medical management fail to control volume overload, hyperkalemia, or acidosis; in some toxic ingestions; and when there are severe complications of uremia (asterixis, pericardial rub or effusion, encephalopathy, uremic bleeding)

67
Q

Small solutes are removed across a semipermeable membrane down thier concentration gradien

A

“Diffusive clearance”

68
Q

Solutes are removed along with the movement of plasma water

A

“Convective clearance”

69
Q

Conditions when CRRT is preferred in patients with AKI

A

Severe hemodynamic instability
Cerebral edema
Significant volume overload

PSBIM 2023 Nephro (8 decks)

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