Three patterns of renal disease have been described III patients with hyperuricaemia or hyperuricosuria:
1 Gouty or chronic hyperuricaemic nephropathy
2 Acute hyperuricaemic nephropathy
3 Uric acid stone formation
Considerable controversy surrounds the possible role of chronic hyperuricaemia as a cause of tubulo-interstitial disease and progressive renal damage. While uric acid ‘tophi’ may be found in the kidneys of patients with gout, there is no convincing evidence that chronic hyperuricaemia per se causes progressive renal failure, nor that allopurinol treatment improves renal function. There is one important exception: a rare form of familial hyperuricaemia and gout occurring in adolescence is associated with renal impairment and allopurinol therapy both improves and protects kidney function.
Acute hyperuricaemic nephropathy
This is a well-recognized cause of acute renal failure in patients with marked hyperuricaemia due to lymphoproliferative or myeloproliferative disorders. This may occur prior to treatment but most often occurs on commencement of treatment, when there is rapid lysis of malignant cells, release of large amounts of nucleoprotein and increased uric acid production. Renal failure is due to intrarenal and extrarenal obstruction caused by deposition of uric acid crystals in the collecting ducts, pelvis and ureters. The condition is manifest in oliguria or anuria with increasing uraemia. There may be flank pain or colic. Plasma urate levels are above 0.75 mmol Iitre “! and may be as high as 4.5 mrnol litre ” ‘. Diagnosis is based on the hyperuricaemia and the clinical setting. Ultrasound demonstrates extrarenal obstruction due to stones but a negative scan does not exclude this where there is coexistent intrarenal obstruction.
It is now regular practice to prescribe allopurinol 100- 200 mg three times daily for 5 days prior to and continuing throughout treatment with radiotherapy or cytotoxic drugs. A high rate of urine flow must be maintained by oral or parenteral fluid and the urine kept alkaline by the administration of sodium bicarbonate 600 mg four times daily and acetazolamide 250 mg three times daily.
Allopurinol treatment should be commenced immediately and a forced alkaline diuresis attempted with intravenous 1.26% sodium bicarbonate plus acetazolamide (500 mg dose, then 250 mg three times daily). In severely oliguric or anuric patients, dialysis is required to lower the plasma urate, which allows urate to diffuse out of the obstructed collecting ducts into the peritubular capillaries. Percutaneous nephrostomy may be required to relieve extrarenal obstruction due to stones in the pelvis or ureters. Such stones may subsequently be passed spontaneously or may require surgical removal.