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Kidneys play a critical role in the excretion of uric acid. Improved knowledge of the renal tubular uric acid transport mechanisms helps to better understand, why hyper- or hypouricemia can develop without the external influence of purine intake. Besides the genetic mutations, several drugs and specific medical conditions can significantly influence the tubular excretion of uric acid and thus the serum uric acid level. It seems evident that the renal function per se has a relevant impact on the uric acid excretion. It is however not clear, whether uric acid has a causal role in the development of chronic kidney disease and if so, to what extent. In order to better understand the impact of hyper- and hypouricemia and especially their clinical relevance, further researches on the renal tubular physio- and pathophysiology and also high quality intervention studies are required.

Different types of kidney disease are known to be associated with hyperuricemia. The underlying pathophysiologic mechanisms strongly vary, and different ways of therapeutic approach are therefore required. In tumor lysis syndrome, a rapid, excessive increase of serum uric acid level can cause an acute renal failure. For chronic urate nephropathy, on the other hand, constantly elevated serum uric acid level for a longer period seems to be important. Being still controversial as a disease entity however, the aetiology for putative chronic urate nephropathy might be in fact chronic lead intoxication, as suggested by quite an amount of association data. In terms of uric acid nephrolithiasis, the major risk factor is a urinary acidification defect with persistently acidic urine pH, and not necessarily hyperuricemia or hyperuricosuria. Evidence suggests that metabolic diseases with increased insulin resistance are strongly associated with urinary acidification defect. Patients with uric acid kidney stones should therefore be thoroughly evaluated for such metabolic diseases and in a positive case adequately treated.

Nephrolithiasis is a common disease with a high recurrence rate. It is associated with a significant morbidity for an individual patient, but also an immense socioeconomic burden. A better understanding and recognition of underlying risk factors and prevention strategies are therefore of great importance. The evaluation for metaphylaxsis consists of a thorough patient history, metabolic examination of blood and urine, imaging of the kidney and urinary tract, and whenever possible a stone analysis. On the basis of the results, preventative measures can be performed. Therapeutic goals in stone prevention are to reduce the urine saturation of stone forming salts, to increase the urine concentration of stone formation inhibitors, and if necessary, the modification of urine pH. A dietary modification is the cornerstone of a successful metaphylaxis.