Hyperuricemia causes several renal conditions due to kidney deposition of uric acid. These conditions can be divided into three types:
Chronic urate nephropathy: a rare form of renal insufficiency caused by deposition of urate crystals in the kidney’s medullary interstitium, resulting in chronic inflammatory response.
Acute uric acid nephropathy: a reversible cause of renal insufficiency that results from deposition of large amounts of uric acid crystals in the renal tubules and characterized by severe oliguria or anuria.
Uric acid nephrolithiasis: may develop as a consequence of persistently low urine pH and sometimes hyperuricemia. Kidney stones caused by uric acid crystals occur in approximately 15% of patients with gout (compared to 8% in people without gout) and may cause kidney damage. Large stones can block one of the ureters, thus preventing the kidney from removing wastes and causing genitourinary tract infections.
Who Should Be Suspected?
Chronic urate nephropathy can be considered in patients with chronic renal insufficiency and severe hyperuricemia that is out of proportion to the degree of renal insufficiency.
Acute uric acid nephropathy is suspected in patients with acute onset of oliguria or anuria, especially following chemotherapy or radiation therapy for a hematologic malignancy or, less commonly, a nonhematologic tumor (tumor lysis syndrome). It can be also suspected in patients with Lesch-Nyhan disease, which results in overproduction of uric acid, and in those with decreased uric acid reabsorption in the proximal tubules (Fanconi-like syndrome).
Uric acid nephrolithiasis is mainly suspected in patients with gout and those on uricosuric drugs, in subjects exposed to dehydration or chronic diarrhea, and in those with diabetes, metabolic syndrome, or myeloproliferative neoplasms.
Laboratory Findings
Urinalysis: twenty-four–hour urine collection may reveal hyperuricemia. Uric acid crystals may be visualized in the urine sediment. Calcium oxalate and amorphous urate crystals can also be seen.
Serum uric acid may be increased and is greatly elevated in the tumor lysis syndrome.
Early renal damage is indicated by decreased renal concentrating ability, mild proteinuria, and decreased phenolsulfonphthalein (PSP) excretion. Later renal damage is indicated by slowly progressive azotemia with slight albuminuria.
In uric acid nephrolithiasis, urinary pH is low (5.5 or lower).
