eMedicine Specialties > Nephrology > Acute Kidney Failure

Uric Acid Nephropathy: Differential Diagnoses & Workup

Author: Mark T Fahlen, MD, Inc
Coauthor(s): Mahendra Agraharkar, MD, MBBS, FACP, FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine, President & CEO, Space City Associates of Nephrology
Contributor Information and Disclosures

Updated: Feb 9, 2009

Differential Diagnoses

Other Problems to Be Considered

Establishing the diagnosis of acute uric acid nephropathy is sometimes complicated by the variety of nephrotoxic drugs, radiographic studies, and associated clinical problems often observed during the early presentation of malignancies. Dehydration, contrast nephropathy, and acute tubular necrosis caused by nephrotoxic drugs or sepsis-related renal failure must be considered in this high-risk population.

Renal complications associated with malignancies that may result in the sudden cessation of kidney function include hypercalcemia; tumor infiltration of the kidneys, ureter, or bladder; and the monoclonal gammopathies, which may cause a myeloma-type kidney disorder. In addition, chemotherapeutic agents may produce nephropathy with a secondary elevation of urate levels. Other causes of elevated urate levels are preexisting renal failure and drugs, including diuretics, salicylates (<2 g/d), ethambutol, pyrazinamide, vitamin A, cyclosporine, and tacrolimus.

The differential diagnosis for chronic urate nephropathy includes alternative etiologies of chronic renal insufficiency, including diabetes, hypertension, atherosclerotic disease, and primary glomerular diseases. Environmental lead poisoning is another consideration in a patient with hypertension, gout, hyperuricemia, and chronic kidney disease.11

Other metabolic stone diseases can mimic uric acid nephrolithiasis, and hyperuricosuria is a known risk factor for calcium stone formation.

Workup

Laboratory Studies

  • Hyperuricemia is an important finding; urate levels in the plasma often exceed 15 mg/dL and can peak as high as 50 mg/dL. However, tumor lysis syndrome in the context of normouricemia has been reported.13 Progressive azotemia and hyperphosphatemia are other important findings.
  • An increased serum lactate dehydrogenase level is suggestive of a large tumor burden and correlates with risk.
  • Urinalysis results are usually bland.
    • Uric acid and sodium monourate crystals may be observed.
    • Although variable, uric acid levels in the urine may be as high as 150-200 mg/dL.
  • A random ratio of urinary uric acid to creatinine higher than 1 is also suggestive of acute uric acid nephropathy.
  • A disproportionate elevation in serum uric acid levels also can be a diagnostic clue.
  • Elevated serum and urinary uric acid levels correlate with the frequency of nephrolithiasis, and 50% of patients with serum uric acid levels greater than 13 mg/dL or urinary uric acid secretion higher than 1100 mg/d will form stones. Uric acid stones are radiolucent, and the urinary uric acid crystals are reddish-orange. Urate crystals have several forms but tend to be needle-shaped or flat, square plates; both are strongly birefringent.

More on Uric Acid Nephropathy

Overview: Uric Acid Nephropathy
Differential Diagnoses & Workup: Uric Acid Nephropathy
Treatment & Medication: Uric Acid Nephropathy
Follow-up: Uric Acid Nephropathy
References
Further Reading
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References

  1. Conger JD. Acute uric acid nephropathy. Med Clin North Am. Jul 1990;74(4):859-71. [Medline].

  2. Guest SS. Uric acid and the kidney. In: Nephrology Rounds 4. Snell Medical Communications; 2001:1-5.

  3. Dykman D, Simon EE. Hyperuricemia and uric acid nephropathy. Arch Intern Med. Jul 1987;147(7):1341-5. [Medline].

  4. Nickeleit V, Mihatsch MJ. Uric acid nephropathy and end-stage renal disease--review of a non-disease. Nephrol Dial Transplant. Sep 1997;12(9):1832-8. [Medline]. [Full Text].

  5. Mene P, Punzo G. Uric acid: bystander or culprit in hypertension and progressive renal disease?. J Hypertens. Nov 2008;26(11):2085-92. [Medline].

  6. Avram Z, Krishnan E. Hyperuricaemia--where nephrology meets rheumatology. Rheumatology (Oxford). Jul 2008;47(7):960-4. [Medline].

  7. Iseki K, Ikemiya Y, Inoue T, et al. Significance of hyperuricemia as a risk factor for developing ESRD in a screened cohort. Am J Kidney Dis. Oct 2004;44(4):642-50. [Medline].

  8. Edwards NL. The role of hyperuricemia and gout in kidney and cardiovascular disease. Cleve Clin J Med. Jul 2008;75 Suppl 5:S13-6. [Medline]. [Full Text].

  9. Johnson RJ, Segal MS, Srinivas T, et al. Essential hypertension, progressive renal disease, and uric acid: a pathogenetic link?. J Am Soc Nephrol. Jul 2005;16(7):1909-19. [Medline]. [Full Text].

  10. Pea F. Pharmacology of drugs for hyperuricemia. Mechanisms, kinetics and interactions. Contrib Nephrol. 2005;147:35-46. [Medline].

  11. Lin JL, Yu CC, Lin-Tan DT, et al. Lead chelation therapy and urate excretion in patients with chronic renal diseases and gout. Kidney Int. Jul 2001;60(1):266-71. [Medline]. [Full Text].

  12. Bainbridge SA, Deng JS, Roberts JM. Increased xanthine oxidase in the skin of preeclamptic women. Reprod Sci. Feb 5 2009;[Medline].

  13. Mukherjee E, Mukherji D, Jayawardene SA, et al. Tumor lysis syndrome and acute renal failure--an increasing spectrum of presentations. Clin Nephrol. Sep 2007;68(3):186-9. [Medline].

  14. Fagugli RM, Gentile G, Ferrara G, et al. Acute renal and hepatic failure associated with allopurinol treatment. Clin Nephrol. Dec 2008;70(6):523-6. [Medline].

  15. Ueng S. Rasburicase (Elitek): a novel agent for tumor lysis syndrome. Proc (Bayl Univ Med Cent). Jul 2005;18(3):275-9. [Medline]. [Full Text].

  16. Hochberg J, Cairo MS. Rasburicase: future directions in tumor lysis management. Expert Opin Biol Ther. Oct 2008;8(10):1595-604. [Medline].

  17. Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med. Oct 23 2008;359(17):1811-21. [Medline].

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Keywords

uric acid nephropathy, kidney, renal, gout, kidney disease, kidney and, renal failure, kidney failure, uric acid, kidney problems, acute renal failure, allopurinol, nephropathy, purine, purines, high uric acid, end stage renal disease, kidney diseases, chronic renal failure, kidney problem, hyperuricemia, nephrolithiasis, acute kidney failure, leukemia, lymphoma, chemotherapy, end stage renal failure, end-stage renal failure, kidney disorder, urate nephropathy, tumor lysis syndrome, gouty nephropathy, uric acid nephrolithiasis, gout nephropathy, renal disease, renal disorder, kidney disorder, renal calculi, renal calculus, kidney stone, uric acid stone, chemotherapy reaction, chemotherapy complication, urate nephrolithiasis, cancer treatment reaction, leukemia treatment reaction, lymphoma treatment reaction, dialysis, chemotherapeutic reaction, HGPRT syndrome, HGPRT deficiency, Lesch-Nyhan syndrome

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Contributor Information and Disclosures

Author

Mark T Fahlen, MD, Inc
Mark T Fahlen, MD is a member of the following medical societies: American College of Physicians and Renal Physicians Association
Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP, FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine, President & 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

Medical Editor

Frank C Brosius III, MD, Nephrology Program Director, Professor of Internal Medicine and Physiology, Department of Internal Medicine, Division of Nephrology, University of Michigan School of Medicine
Frank C Brosius III, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Society of Nephrology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
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: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

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.

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