Acute Renal Failure Differential Diagnoses

  • Author: Biruh T Workeneh, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Feb 9, 2012
 
 

Diagnostic Considerations

Although acute kidney injury (AKI) potentially is a reversible condition, it can occur in patients with chronic renal failure. Every effort should be made to identify reversibility, even if improvement in renal function is marginal. The best way to identify reversibility is by tracking the rate of deterioration of renal function. If the rate of worsening renal function accelerates, the cause should be sought and treated.

Differentials to consider in AKI include the following:

  • Alcoholic Ketoacidosis
  • Anemia, Sickle Cell
  • Aneurysm, Abdominal
  • CHF and Pulmonary Edema
  • Diabetic Ketoacidosis
  • Obstructive Uropathy
  • GI Bleeding
  • Protein Overloading
  • Steroid Use
  • Pediatrics, Dehydration
  • Pediatrics, Diabetic Ketoacidosis
  • Pediatrics, Inborn Errors of Metabolism
  • Pediatrics, Sickle Cell Disease
  • Pediatrics, Urinary Tract Infections and Pyelonephritis
  • Renal Calculi
  • Renal Failure, Chronic and Dialysis Complications
  • Toxicity, Alcohols
  • Urinary Obstruction
  • Urinary Tract Infection, Female
  • Urinary Tract Infection, Male
  • Metabolic Acidosis

Urine output in differential diagnosis

Changes in urine output generally are poorly correlated with changes in GFR. Approximately 50-60% of all causes of AKI are nonoliguric. However, the identification of anuria, oliguria, and nonoliguria may be useful in the differential diagnosis of AKI, as follows:

  • Anuria (< 100 mL/d) - Urinary tract obstruction, renal artery obstruction, rapidly progressive glomerulonephritis, bilateral diffuse renal cortical necrosis
  • Oliguria (100-400 mL/d) - Prerenal failure, hepatorenal syndrome
  • Nonoliguria (>400 mL/d) - Acute interstitial nephritis, acute glomerulonephritis, partial obstructive nephropathy, nephrotoxic and ischemic ATN, radiocontrast-induced AKI, and rhabdomyolysis

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
Author

Biruh T Workeneh, MD  Assistant Professor of Nephrology, Baylor College of Medicine

Biruh T Workeneh, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, and Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP, FASN  Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and National Kidney Foundation

Disclosure: South Shore DaVita Dialysis Center Ownership interest Other

Rajiv Gupta, MD  Assistant Professor, Department of Medicine, Texas A&M Health Science Center College of Medicine; Consulting Staff, Veterans Affairs Medical Center

Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Aruna Agraharkar, MD, FACP Consulting Staff, Department of Gerontology, Space Center Clinic

Aruna Agraharkar, MD, FACP is a member of the following medical societies: American Medical Assocation

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Laura Lyngby Mulloy, DO, FACP Professor of Medicine, Chief, Section of Nephrology, Hypertension, and Transplantation Medicine, Glover/Mealing Eminent Scholar Chair in Immunology, Medical College of Georgia

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References

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  2. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. Aug 2004;8(4):R204-12. [Medline]. [Full Text].

  3. [Best Evidence] Kheterpal S, Tremper KK, Heung M, Rosenberg AL, Englesbe M, Shanks AM, et al. Development and validation of an acute kidney injury risk index for patients undergoing general surgery: results from a national data set. Anesthesiology. Mar 2009;110(3):505-15. [Medline].

  4. Goldberg R, Dennen P. Long-term outcomes of acute kidney injury. Adv Chronic Kidney Dis. Jul 2008;15(3):297-307. [Medline].

  5. Feest TG, Mistry CD, Grimes DS, Mallick NP. Incidence of advanced chronic renal failure and the need for end stage renal replacement treatment. BMJ. Oct 20 1990;301(6757):897-900. [Medline]. [Full Text].

  6. Pannu N, James M, Hemmelgarn BR, Dong J, Tonelli M, Klarenbach S. Modification of Outcomes After Acute Kidney Injury by the Presence of CKD. Am J Kidney Dis. Aug 2011;58(2):206-13. [Medline].

  7. Grams ME, Estrella MM, Coresh J, Brower RG, Liu KD. Fluid Balance, Diuretic Use, and Mortality in Acute Kidney Injury. Clin J Am Soc Nephrol. May 2011;6(5):966-973. [Medline]. [Full Text].

  8. James MT, Hemmelgarn BR, Wiebe N, Pannu N, Manns BJ, Klarenbach SW, et al. Glomerular filtration rate, proteinuria, and the incidence and consequences of acute kidney injury: a cohort study. Lancet. Dec 18 2010;376(9758):2096-103. [Medline].

  9. Molnar AO, Coca SG, Devereaux PJ, Jain AK, Kitchlu A, Luo J, et al. Statin use associates with a lower incidence of acute kidney injury after major elective surgery. J Am Soc Nephrol. May 2011;22(5):939-46. [Medline]. [Full Text].

  10. American College of Radiology. ACR Appropriateness Criteria® renal failure. National Guideline Clearinghouse. Available at http://guideline.gov/content.aspx?id=13685. Accessed March 24, 2011.

  11. Breidthardt T, Christ-Crain M, Stolz D, et al. A combined cardiorenal assessment for the prediction of acute kidney injury in lower respiratory tract infections. Am J Med. Feb 2012;125(2):168-75. [Medline].

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  13. Mancini E, Caramelli F, Ranucci M, et al. Is time on cardiopulmonary bypass during cardiac surgery associated with acute kidney injury requiring dialysis?. Hemodial Int. Nov 8 2011;[Medline].

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  15. [Best Evidence] Marenzi G, Assanelli E, Marana I, Lauri G, Campodonico J, Grazi M, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med. Jun 29 2006;354(26):2773-82. [Medline].

  16. [Best Evidence] Ho KM, Morgan DJ. Meta-analysis of N-acetylcysteine to prevent acute renal failure after major surgery. Am J Kidney Dis. Jan 2009;53(1):33-40. [Medline].

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Photomicrograph of a renal biopsy specimen shows renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells with loss of brush border is observed, suggesting acute tubular necrosis as the cause of acute renal failure.
Flattening of the renal tubular cells due to tubular dilation.
Intratubular cast formation.
Intratubular obstruction due to the denuded epithelium and cellular debris. Note that the denuded tubular epithelial cells clump together because of rearrangement of intercellular adhesion molecules.
Sloughing of cells, which is responsible for the formation of granular casts, is a feature of acute tubular necrosis.
Table 1. RIFLE Classification System for Acute Kidney Injury
Stage GFR** Criteria Urine Output Criteria Probability
RiskSCreat† increased × 1.5



or



GFR decreased >25%



UO‡ < 0.5 mL/kg/h × 6 hHigh sensitivity (Risk >Injury >Failure)
InjurySCreat increased × 2



or



GFR decreased >50%



UO < 0.5 mL/kg/h × 12 h
FailureSCreat increased × 3



or



GFR decreased 75%



or



SCreat ≥4 mg/dL; acute rise ≥0.5 mg/dL



UO < 0.3 mL/kg/h × 24 h



(oliguria)



or



anuria × 12 h



LossPersistent acute renal failure: complete loss of kidney function >4 wkHigh specificity
ESKD*Complete loss of kidney function >3 mo
*ESKD—end-stage kidney disease; **GFR—glomerular filtration rate; †SCreat—serum creatinine; ‡UO—urine output



Note: Patients can be classified by GFR criteria and/or UO criteria. The criteria that support the most severe classification should be used. The superimposition of acute on chronic failure is indicated with the designation RIFLE-FC; failure is present in such cases even if the increase in SCreat is less than 3-fold, provided that the new SCreat is greater than 4.0 mg/dL (350 μmol/L) and results from an acute increase of at least 0.5 mg/dL (44 μmol/L).



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