Recent observations of urate excretion by the kidney in genetic overproducers of urate have contributed to our understanding of the mechanisms of renal damage in gout. Some of these overproducers showed normal serum urate concentrations when their urine urate excretions were high, putting them at risk from uric acid crystalluria and calculi. Others developed acute renal failure which was completely reversed by an intense alkaline diuresis. Some overproducers developed varying degrees of renal insufficiency while others members of the same family with the same genetic mutation retained normal renal function. How can these observations be reconciled with existing knowledge of the gouty kidney?
