Ch 334: Acute Kidney Injury

Question 1

It is important to recognize that acute kidney injury is a clinical diagnosis, and not a __________ one. A patient may have AKI without injury to the kidney __________.

Answer 1

structural

parenchyma

Question 2

What is the most common form of AKI?

Answer 2

prerenal azotemia

Question 3

Prolonged periods of prerenal azotemia may lead to ischemic injury, often termed…

Answer 3

…acute tubular necrosis (ATN).

Question 4

The causes of AKI have traditionally been divided into three broad categories:

Answer 4

prerenal azotemia
intrinsic renal parenchymal disease
postrenal obstruction

(p. 1799)

Question 5

What is prerenal azotemia?

Answer 5

(from azo-, meaning nitrogen)
A rise in serum creatinine or BUN due to inadequate renal plasma flow and intraglomerular hydrostatic pressure.

(p. 1799)

Question 6

What are the most common clinical conditions associated with prerenal azotemia? (Name 4)

Answer 6

1. Hypovolemia
2. Decreased cardiac output
3. Decreased effective circulating volume (as seen in CHF or liver failure)
4. Impaired renal autoregulation (due to drugs like NSAIDs, ACEI/ARBs, cyclosporine)

(p. 1800)

Question 7

What will prolonged periods of prerenal azotemia lead to?

Answer 7

Ischemic injury, often termed acute tubular necrosis

p. 1800

Question 8

Normal GFR is maintained in part by the ________ ___________ of the ________ and ________ renal arterioles.

Answer 8

relative resistances

afferent and efferent

Question 9

Mild degrees of hypovolemia and reductions in cardiac output elicit ____________ renal physiologic changes. In response to _________ _________ ___________ ______ or cardiac output, renal vasoconstriction occurs, and salt and water are reabsorbed in order to maintain blood pressure and increase intravascular volume to sustain perfusion to the ________ and ________ vessels.

Answer 9

compensatory
decreased effective circulating volume
cerebral
coronary

(p. 1800)

Question 10

Renal blood flow accounts for __% of the cardiac output.

Answer 10

20%

Question 11

Mediators of the compensatory renal mechanisms include ___________ __, ______________, and ___________. Glomerular filtration can be maintained despite reducted renal blood flow by angiotensin II-mediated _____ ________ vasoconstriction, which maintains glomerular capillary hydrostatic pressure closer to normal and thereby prevents marked reductions in GFR if renal blood flow reduction is not excessive.

Answer 11

angiotensin II
norepinephrine
vasopressin

renal efferent

(p. 1800)

Question 12

In addition, a myogenic reflex (meaning originating in the muscle) within the afferent arteriole leads to ________ in the setting of low perfusion, thereby maintaining glomerular perfusion. Intrarenal ____________ of vasodilator prostaglandins (prostacyclin, prostaglandin E2), __________ and kinins, and possibly ______ _____ also increase in response to low renal perfusion pressure.

Answer 12

dilation
biosynthesis
kallikrein
nitric oxide

(p. 1800)

Question 13

Autoregulation is also accomplished by ________________ feedback, in which decreases in ______ delivery to the macula densa (specialized cells within the distal tubule) elicit dilation of the juxtaposed afferent arteriole in order to maintain glomerular perfusion, a mechanism mediated, in part, by nitric oxide.

Answer 13

tubuloglomerular
solute

(p. 1800)

Question 14

Despite all these counterregulatory mechanisms, even in healthy adults, renal autoregulation usually fails once the….

Answer 14

….systolic blood pressure falls below 80 mm Hg.

p. 1800

Question 15

What are the most common causes of intrinsic AKI?

Answer 15

sepsis
ischemia
nephrotoxins (both endogenous and exogenous)

(p. 1800)

Question 16

What is nephrotoxin-associated AKI?

Answer 16

kidney injury that occurs as a result of exposure to circulating toxins

Question 17

Describe the clinical course associated with contrast nephropathy?

Answer 17

The most common clinical course of contrast nephropathy is characterized by a rise in serum creatinine beginning 24 - 48 hours following exposure, peaking within 3 - 5 days, and resolving within one week.

(p. 1803)

Question 18

What antibiotics are commonly associated with AKI?

Answer 18

aminoglycosides
amphotericin B
vancomycin

penicillins
cephalosporins
quinolones
sulfonamides
rifampin

(p. 1804)

Question 19

What are some other toxins associated with AKI?

Answer 19

ethylene glycol

endogenous compounds can cause AKI, including myoglobin, hemoglobin, uric acid, and myeloma light chains

Question 20

What is seen with allergic acute tubulointerstitial disease?

Answer 20

Inflammatory infiltrate and often peripheral and urinary eosinophilia.

(p. 1804)

Question 21

Define AKI.

Answer 21

A rise from the baseline creatinine of at least 0.3 mg/dL within 48 hr or at least 50% higher than baseline within one week, or a reduction in urine output to less than 0.5 mL/kg per hour for longer than 6 hrs.

Question 22

Which two imaging studies should be done in AKI to rule out obstruction (unless an alternate diagnosis is apparent)?

Answer 22

Ultrasound or CT of the kidneys

p. 1808

Question 23

Enlarged kidneys in a patient with AKI suggests the possibility of….

Answer 23

….acute interstitial nephritis.

p. 1808

Question 24

MRI with gadolinium-based contrast agents should be avoided if possible in severe AKI due to the possibility of inducing ___________ ______ ________, a rare but serious complication seen most commonly in patients with ESRD.

Answer 24

nephrogenic system fibrosis

p. 1808

Question 25

Healthy kidneys account for __% of resting oxygen consumption, despite constituting only __% of the human body mass.

Answer 25

10%
0.5%

(p. 1801)

Question 26

The renal medulla is one of the most _______ regions in the body.

Answer 26

hypoxic

p. 1801

Question 27

Can you stage kidney disease with rapidly changing lab values?

Answer 27

No, the GFR is only valid if serum creatinine is steady.

Question 28

What are the leading causes of CKD? (Table 335-2)

Answer 28

1. Diabetic nephropathy
2. Glomerulonephritis
3. Hypertension-associated CKD (includes vascular and ischemic kidney disease and primary glomerular disease with associated hypertension)
4. Autosomal dominant polycystic kidney disease
5. Other cystic and tubulointerstitial nephropathy

Question 29

What are hypercalcemia and hyperphosphatemia associated with?

Answer 29

Increased vascular calcification