Uric Acid Nephropathy Clinical Presentation

Updated: Nov 20, 2015
  • Author: Mark T Fahlen, MD; Chief Editor: Vecihi Batuman, MD, FASN  more...
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  • 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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  • 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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  • 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 [18] 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.