Acute Kidney Injury Flashcards

1
Q

Sudden impairment of kidney function –> retention of nitrogenous and other waste products normally cleared by the kidneys

A

Acute Kidney Injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Common Diagnostic Features of AKI

A

↑ in BUN concentration
↑ in plasma or serum creatinine concentration
↓ in urine volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

KDIGO 2012 Definition of AKI

A

↑ in SCr by >0.3 mg/dL (>26.5 mmol/L) w/n 48 hrs
↑ in SCr to >1.5 x the baseline - occured w/n the prior 7 days
urine volume <0.5 mL for 6 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MC form of AKI

A

prerenal azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration

A

prerenal azotemia

-NO parenchymal damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MC causes of intrinsic AKI

A

sepsis
ischemia
nephrotoxins (endogenous and exogenous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Very important cause of AKI in the developing world

A

sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The site of one of the most hypoxic regions in the body

A

renal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Intrinsic AKI

A

tubular damage
glomerular damage
interstitial damage
vascular damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Small Vessels Damage (Intrinsic AKI)

A
Glomerulonephritis
Vasculitis
TTP/HUS
DIC
Atheroemboli
Malignant HTN
Calcineurin inhibitors
Sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Tubules (Intrinsic AKI)

A
Toxic ATN
 Endogenous (rhabdomyolysis,hemolysis)
 Exogenous (contrast,  cisplatin, gentamicin)
Ischemic ATN
Sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Intratubular (Intrinsic AKI)

A
Endogenous
 • Myeloma proteins
 • Uric acid (tumor
 lysis syndrome)
 • Cellular debris

Exogenous
• Acyclovir, methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MC clinical conditions associated with prerenal azotemia

A

hypovolemia
↓ cardiac output
medications that interfere with renal autoregulatory responses (NSAID and inhibitors of Angiotensin II)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors for nephrotoxicity

A

age
CKD
prerenal azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical course of contrast AKI

A

↑ in SCr beginning 24–48 h following exposure
peaking within 3–5 days
resolving within 1 week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Common findings in contrast AKI

A

low fractional excretion of sodium (FeNa) < 1

benign urinary sediment without features of tubular necrosis

17
Q

MC protein in urine and produced in the THICK ascending limb of the loop of Henle

A

uromodulin

18
Q

Occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally

A

Postrenal Acute Kidney Injury

19
Q

Complete anuria early in the course of AKI is uncommon EXCEPT in the following situations:

A

complete urinary tract obstruction
renal artery occlusion
overwhelming septic shock
severe ischemia (often with cortical necrosis)
severe proliferative glomerulonephritis or vasculitis

20
Q

AKI leads to

A

hyperkalemia
hyperphosphatemia

hypocalcemia

21
Q

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

A

fractional excretion of sodium (FeNa)

22
Q

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)

23
Q

Highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 h of cardiopulmonary bypass–associated AKI

A

Neutrophil gelatinase associated lipocalin (NGAL aka lipocalin-2 or siderocalin)

24
Q

Hallmark of AKI

A

elevated BUN concentration

25
Q

Major complication of oliguric and anuric AKI due to impaired salt and water excretion

A

expansion of extracellular fluid volume

26
Q

An important complication of AKI particularly common in rhabdomyolysis, hemolysis, and tumor lysis syndrome due to release of intracellular potassium from damaged cells

A

Hyperkalemia

27
Q

Major cardiac complications of AKI

A

arrhythmias
pericarditis
pericardial effusion