Ch 334: Acute Kidney Injury Flashcards
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 __________.
structural
parenchyma
What is the most common form of AKI?
prerenal azotemia
Prolonged periods of prerenal azotemia may lead to ischemic injury, often termed…
…acute tubular necrosis (ATN).
The causes of AKI have traditionally been divided into three broad categories:
prerenal azotemia
intrinsic renal parenchymal disease
postrenal obstruction
(p. 1799)
What is prerenal azotemia?
(from azo-, meaning nitrogen)
A rise in serum creatinine or BUN due to inadequate renal plasma flow and intraglomerular hydrostatic pressure.
(p. 1799)
What are the most common clinical conditions associated with prerenal azotemia? (Name 4)
- Hypovolemia
- Decreased cardiac output
- Decreased effective circulating volume (as seen in CHF or liver failure)
- Impaired renal autoregulation (due to drugs like NSAIDs, ACEI/ARBs, cyclosporine)
(p. 1800)
What will prolonged periods of prerenal azotemia lead to?
Ischemic injury, often termed acute tubular necrosis
p. 1800
Normal GFR is maintained in part by the ________ ___________ of the ________ and ________ renal arterioles.
relative resistances
afferent and efferent
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.
compensatory
decreased effective circulating volume
cerebral
coronary
(p. 1800)
Renal blood flow accounts for __% of the cardiac output.
20%
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.
angiotensin II
norepinephrine
vasopressin
renal efferent
(p. 1800)
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.
dilation
biosynthesis
kallikrein
nitric oxide
(p. 1800)
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.
tubuloglomerular
solute
(p. 1800)
Despite all these counterregulatory mechanisms, even in healthy adults, renal autoregulation usually fails once the….
….systolic blood pressure falls below 80 mm Hg.
p. 1800
What are the most common causes of intrinsic AKI?
sepsis
ischemia
nephrotoxins (both endogenous and exogenous)
(p. 1800)
What is nephrotoxin-associated AKI?
kidney injury that occurs as a result of exposure to circulating toxins
Describe the clinical course associated with contrast nephropathy?
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)
What antibiotics are commonly associated with AKI?
aminoglycosides
amphotericin B
vancomycin
penicillins cephalosporins quinolones sulfonamides rifampin
(p. 1804)
What are some other toxins associated with AKI?
ethylene glycol
endogenous compounds can cause AKI, including myoglobin, hemoglobin, uric acid, and myeloma light chains
What is seen with allergic acute tubulointerstitial disease?
Inflammatory infiltrate and often peripheral and urinary eosinophilia.
(p. 1804)
Define AKI.
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.
Which two imaging studies should be done in AKI to rule out obstruction (unless an alternate diagnosis is apparent)?
Ultrasound or CT of the kidneys
p. 1808
Enlarged kidneys in a patient with AKI suggests the possibility of….
….acute interstitial nephritis.
p. 1808
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.
nephrogenic system fibrosis
p. 1808
Healthy kidneys account for __% of resting oxygen consumption, despite constituting only __% of the human body mass.
10%
0.5%
(p. 1801)
The renal medulla is one of the most _______ regions in the body.
hypoxic
p. 1801
Can you stage kidney disease with rapidly changing lab values?
No, the GFR is only valid if serum creatinine is steady.
What are the leading causes of CKD? (Table 335-2)
- Diabetic nephropathy
- Glomerulonephritis
- Hypertension-associated CKD (includes vascular and ischemic kidney disease and primary glomerular disease with associated hypertension)
- Autosomal dominant polycystic kidney disease
- Other cystic and tubulointerstitial nephropathy
What are hypercalcemia and hyperphosphatemia associated with?
Increased vascular calcification
