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Review
. 2019 Mar 1;116(9):149-158.
doi: 10.3238/arztebl.2019.0149.

Acute Renal Failure of Nosocomial Origin

Mark Dominik Alscher, Christiane Erley, Martin K Kuhlmann
Review

Acute Renal Failure of Nosocomial Origin

Mark Dominik Alscher et al. Dtsch Arztebl Int. .

Abstract

Background: 10-20% of hospitalized patients develop acute kidney injury (AKI)/acute renal failure during their hospital stay. The mortality of nosocomial AKI is approximately 30%.

Methods: This review is based on relevant publications retrieved by a search in multiple databases (PubMed and Uptodate), archives, and pertinent medical journals.

Results: The most common causes of nosocomial AKI are volume depletion, sepsis, heart diseases, polytrauma, liver diseases, and drug toxicity. AKI can also be of postrenal (obstructive) origin, or a result of renal diseases including glomeruloneph- ritis, vasculitis, tubulointerstitial nephritis, and cholesterol embolism. In about 13% of cases, nosocomial AKI develops on the basis of pre-existing chronic renal disease. Patients with AKI are at elevated risk of developing chronic renal disease and must be followed up appropriately after they are discharged from the hospital. Indispens- able elements of the evaluation of nosocomial AKI include renal ultrasonography, the exclusion of postrenal obstruction, urine chemistry, and microbiological urinaly- sis. Potentially nephrotoxic drugs and those that impair renal hemodynamics must be avoided to the greatest possible extent in patients with acute renal damage. Hypotension must be avoided as well.

Conclusion: Early, specific nephrological diagnosis and treatment are important components of the management of nosocomial AKI, particularly because causally directed treatment is available for some of the conditions that underlie it.

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Figures

Figure 1
Figure 1
How to proceed in acute kidney injury (AKI)
Figure 2
Figure 2
Differential diagnoses for acute kidney injury of non-prerenal origin ACE, angiotensin-converting enzyme; GN, glomerulonephritis; HUS, hemolytic–uremic syndrome; RAS, renal artery stenosis; RPGN, rapidly progressive glomerulonephritis; SLE, systemic lupus erythematosus; TTP, thrombotic–thrombopenic purpura
Figure 3
Figure 3
Prerenal azotemia and acute tubular necrosis; AKI, acute kidney injury
Figure 4
Figure 4
Urinalysis findings in acute kidney injury (AKI) a) and b) In the event of diffuse pathology of the tubules (e.g., acute tubular necrosis), tubular epithelial and urothelial cells are often found in the urine; c) granular cylinders (e.g., pyelonephritis); d) leukocyte cylinders (e.g., interstitial nephritis); e) pigment cylinders (rhabdomyolysis, hemolysis); f) hyaline cylinders (e.g., nephrotic syndrome); g) dysmorphic erythrocytes (suspicion of glomerulonephritis)
eFigure
eFigure
How to proceed after diagnosis of acute kidney failure (AKI) by a nephrologist; BW, body weight
See this image and copyright information in PMC

Comment in

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