Uric acid renal diseases

INTRODUCTION

There are three different types of renal disease induced by uric acid or urate crystal deposition: acute uric acid nephropathy, chronic urate nephropathy, and uric acid nephrolithiasis [1]. The first two disorders will be reviewed here, while uric acid nephrolithiasis is discussed separately. (See "Uric acid nephrolithiasis".)

Uric acid is a weak organic acid and exists in one of two forms in biological systems, depending upon the prevailing pH (see "Uric acid nephrolithiasis"): the sparingly soluble undissociated uric acid form (the most highly represented form when the pH is less than 5.5), and the substantially more soluble urate anion form (the most highly represented form [98 percent] at the physiologic pH of 7.4). For the purposes of this discussion, we use the term "uric acid" to denote the poorly soluble undissociated form and the term "urate" to denote the soluble dissociated urate anion.

ACUTE URIC ACID NEPHROPATHY

Acute uric acid nephropathy (UAN) is characterized by acute oliguric or anuric renal failure due to uric acid precipitation within the tubules [1,2]. This is most often due to overproduction and overexcretion of uric acid in patients with lymphoma, leukemia, or a myeloproliferative disease (such as polycythemia vera), particularly after chemotherapy or radiation has induced rapid cell lysis. (See "Tumor lysis syndrome: Definition, pathogenesis, clinical manifestations, etiology and risk factors" and "Overview of the complications of acute myeloid leukemia".)

Less frequent causes of UAN include tissue catabolism due to seizures or treatment of solid tumors, primary overproduction of uric acid due to the rare syndrome of severe hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome), or hyperuricosuria due to decreased urate reabsorption in the proximal tubule, as can occur with a Fanconi-like syndrome [1-4] or with exercise in patients with familial renal hypouricemia due to an inherited deficiency in the activity of the urate-anion transporter URAT1. (See "Hyperkinetic movement disorders in children", section on 'Lesch-Nyhan syndrome' and "Hypouricemia: Causes and clinical significance", section on 'Familial renal hypouricemia' and "Hypouricemia: Causes and clinical significance", section on 'Acute kidney injury'.)

Clinical manifestations — UAN is typically associated with no symptoms referable to the urinary tract, although flank pain can occur if there is renal pelvic or ureteral obstruction. The diagnosis should be suspected when acute kidney injury develops in any of the above settings in association with marked hyperuricemia (plasma urate concentration generally above 15 mg/dL or 893 µmol/L). This is in contrast to most other forms of acute kidney injury in which the plasma urate concentration usually is less than 12 mg/dL (714 µmol/L), except for prerenal disease in which there is an increase in proximal sodium and urate reabsorption.

    

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Literature review current through: Mar 2014. | This topic last updated: Oct 28, 2013.
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References
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  1. Rose, BD. Pathophysiology of Renal Disease, 2d ed, McGraw-Hill, New York, 1987, pp. 418-425.
  2. Kjellstrand CM, Cambell DC 2nd, von Hartitzsch B, Buselmeier TJ. Hyperuricemic acute renal failure. Arch Intern Med 1974; 133:349.
  3. Crittenden DR, Ackerman GL. Hyperuricemic acute renal failure in disseminated carcinoma. Arch Intern Med 1977; 137:97.
  4. Hricik DE, Goldsmith GH. Uric acid nephrolithiasis and acute renal failure secondary to streptozotocin nephrotoxicity. Am J Med 1988; 84:153.
  5. Kelton J, Kelley WN, Holmes EW. A rapid method for the diagnosis of acute uric acid nephropathy. Arch Intern Med 1978; 138:612.
  6. Monballyu J, Zachee P, Verberckmoes R, Boogaerts MA. Transient acute renal failure due to tumor-lysis-induced severe phosphate load in a patient with Burkitt's lymphoma. Clin Nephrol 1984; 22:47.
  7. Razis E, Arlin ZA, Ahmed T, et al. Incidence and treatment of tumor lysis syndrome in patients with acute leukemia. Acta Haematol 1994; 91:171.
  8. Coiffier B, Altman A, Pui CH, et al. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008; 26:2767.
  9. Johnson RJ, Kivlighn SD, Kim YG, et al. Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease. Am J Kidney Dis 1999; 33:225.
  10. Batuman V, Maesaka JK, Haddad B, et al. The role of lead in gout nephropathy. N Engl J Med 1981; 304:520.
  11. Craswell PW, Price J, Boyle PD, et al. Chronic renal failure with gout: a marker of chronic lead poisoning. Kidney Int 1984; 26:319.
  12. TALBOTT JH, TERPLAN KL. The kidney in gout. Medicine (Baltimore) 1960; 39:405.
  13. Beck LH. Requiem for gouty nephropathy. Kidney Int 1986; 30:280.
  14. Moe OW. Posing the question again: does chronic uric acid nephropathy exist? J Am Soc Nephrol 2010; 21:395.
  15. Murray T, Goldberg M. Chronic interstitial nephritis: etiologic factors. Ann Intern Med 1975; 82:453.
  16. Sorensen LB. Role of the intestinal tract in the elimination of uric acid. Arthritis Rheum 1965; 8:694.
  17. Sorensen LF. Gout secondary to chronic renal disease: studies on urate metabolism. Ann Rheum Dis 1980; 39:424.
  18. So A, Thorens B. Uric acid transport and disease. J Clin Invest 2010; 120:1791.