Uric Acid Nephropathy Clinical Presentation

  • Author: Mark T Fahlen, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Sep 21, 2011
 

History

  • Acute uric acid nephropathy is usually observed in patients shortly after presentation for acute neoplastic disorders or within 1-2 days of initiation of chemotherapy.
  • The most frequently observed symptoms are nausea, vomiting, lethargy, and seizures.
  • A history consistent with chronic urate nephropathy is progressive renal failure in a patient with coexisting gout or uric acid nephrolithiasis and no other identifiable cause for renal failure.
  • Hypertension is common, and pyelonephritis may complicate the presence of obstructing calculi.
  • Uric acid nephrolithiasis should be considered in a patient with a history of gout who presents with flank pain, urinary frequency, and dysuria.
  • Hematuria is also common. However, note that uric acid nephrolithiasis often precedes the onset of gouty arthritis in patients with both conditions.
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Physical

  • Occasionally, ureteral obstruction from uric acid sludge can cause severe flank pain, abdominal pain, and dysuria.
  • Oliguria is the primary sign of the onset of urate nephropathy, with edema and congestive heart failure occurring subsequently.
  • The well-recognized clinical entity of various combinations of hyperuricemia, azotemia, hyperkalemia, hyperphosphatemia, lactic acidosis, and hypocalcemia is known as tumor lysis syndrome.
  • The physical examination may reveal subcutaneous tophi or the typical arthritic changes of gout.
  • Much debate exists regarding the incidence of chronic urate nephropathy; the presence of another comorbidity, such as diabetes or hypertension, often provides a better explanation for the renal insufficiency.
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Causes

  • Most cases of acute uric acid nephropathy occur during treatment for leukemia or lymphoma. Uric acid nephropathy is observed more commonly in persons with an acute leukemia than in persons with a chronic form of the disease. It also has been described in association with other malignancies, such as metastatic breast carcinoma, bronchogenic carcinoma, and disseminated adenocarcinoma.
  • Seizures or ischemic states can lead to extensive release of cell metabolites and consequent hyperuricemia.
  • Hyperuricemic acute renal failure has also been reported during pregnancy-related preeclampsia[12] or eclampsia, as well as in the setting of cyclosporine use and renal transplantation.
  • Chronic hyperuricemia and gout are the only causes of chronic urate nephropathy, if it exists as a clinical entity.
  • The hereditary enzyme disorder HGRPT deficiency, which leads to overproduction of urate, is an indisputable cause of a chronic urate nephropathy leading to renal insufficiency. Several other rare diseases are in this category, including the following:
    • Uric acid nephrolithiasis can be caused by any underlying disorder that causes hyperuricosuria. This includes all of the previously mentioned causes of acute uric acid nephropathy, such as malignancy, hypercatabolic states, and the hereditary enzyme deficiencies.
    • Uric acid stones develop in 20% of people with gout.
    • Acute diarrheal states may increase urinary uric acid concentration through excessive water loss and dehydration, leading to stone formation.
    • Urinary pH also tends to decrease with extracellular volume contraction, and gastrointestinal bicarbonate loss may contribute to the acidic urine, thus promoting stone formation.
    • Aspirin and probenecid augment uric acid secretion and may lead to stone formation, especially in people with a purine-rich diet.
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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 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

Specialty Editor Board

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.

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

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

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 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: Renal Ventures Ownership interest Other

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.

References

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  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].

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  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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