Uric acid renal diseases
- Gary C Curhan, MD, ScD
Gary C Curhan, MD, ScD
- Section Editor — Chronic Kidney Disease
- Editor-in-Chief Emeritus
- Clinical Journal of the American Society of Nephrology
- Professor of Medicine
- Harvard Medical School
- Michael A Becker, MD
Michael A Becker, MD
- Section Editor — Crystal Diseases
- Professor Emeritus of Medicine
- University of Chicago Pritzker School of Medicine
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 . 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 .To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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