Because the mutation of gene SLC22A12 encoding URAT1 causes familial renal hypouricemia (OMIM220150), URAT1 is considered to be a transporter playing a major role in renal urate reabsorption.  Renal urate transport is known to be controlled by a variety of drugs. For example, drug-induced hyperuricemia has been considered to be caused by enhanced renal urate reabsorption or reduced renal excretion of uric acid. On the other hand, hypouricemia has been considered to be caused by reduced renal urate reabsorption or enhanced renal excretion of uric acid. Among these drugs, pyrazinamide, probenecid, and salicylic acid have been reported to have a paradoxical effect on renal excretion of uric acid. In other words, these drugs at low concentrations reduce renal excretion of uric acid, while at high concentrations increase it.

Because the mutationmutations of gene SLC22A12 gene encoding URAT1 causescause familial renal hypouricemia (OMIM220150), URAT1 is considered to be a transporter playing a major role in renal urate reabsorption. Renal urate transport is known to be controlled by a variety of drugs. For example, drug-induced hyperuricemia has been considered to be caused by enhanced renal urate reabsorption or reduced renal excretion of uric acid. On the other hand, hypouricemia has been considered to be caused by reduced renal urate reabsorption orand enhanced renal excretion of uric acid. Among thesethe drugs, pyrazinamide, probenecid, and salicylic acid have been reported to have a paradoxical effect on renal excretion of uric acid. In other words, these drugs at low concentrations reduce renal excretion of uric acid, while at high concentrations increase it.

Because a mutations ofin the SLC22A12 gene (OMIM220150) encoding URAT1  causes familial renal hypouricemia (OMIM220150), URAT1 is considered to be a transporter playing a major role in renal urate reabsorption.  Renal urate transport is known to be affected controlled by a variety ofvarious drugs. For example, drug-induced hyperuricemia has beenis considered to be caused by enhanced renal urate reabsorption or reduced renal urate excretion of uric acid. On the other handIn contrast, hypouricemia has beenis considered to be caused by reduced renal urate reabsorption and enhanced renal urate excretion of uric acid. Among the drugsIn particular, pyrazinamide, probenecid, and salicylic acid have been reported to have a paradoxical effect on renal urate excretion of uric acid. In other words, these drugs at low concentrations reduce renal urate excretion at low concentrations of uric acid, while and increase it at high concentrations increase it.

Because a mutations ofin the SLC22A12 gene (OMIM220150) encoding URAT1  causes familial renal hypouricemia (OMIM220150), the urate transporter URAT1 is considered to be a transporter playing a major role in renal urate reabsorption.  Renal urate transport is known to be affected controlled by a variety ofvarious drugs. For example, drug-induced hyperuricemia has beenis considered to be caused by enhanced renal urate reabsorption or reduced renal urate excretion of uric acid. On the other handIn contrast, hypouricemia has beenis considered to be caused by reduced renal urate reabsorption and enhanced renal urate excretion of uric acid. Among the drugsIn particular, pyrazinamide, probenecid, and salicylic acid have been reported to have a paradoxical effect on renal urate excretion of uric acid. In other words, : these drugs at low concentrations reduce renal urate excretion at low concentrations of uric acid, while and increase it at high concentrations increase it.

Because the mutation of gene SLC22A12 encoding URAT1 causes familial renal hypouricemia (OMIM220150), URAT1 is considered to be a transporter playing a major role in renal urate reabsorption.  Renal urate transport is known to be controlled by a variety of drugs. For example, drug-induced hyperuricemia has been considered to be caused by enhanced renal urate reabsorption or reduced renal excretion of uric acid. On the other hand, hypouricemia has been considered to be caused by reduced renal urate reabsorption or enhanced renal excretion of uric acid. Among these drugs, pyrazinamide, probenecid, and salicylic acid have been reported to have a paradoxical effect on renal excretion of uric acid. In other words, these drugs at low concentrations reduce renal excretion of uric acid, while at high concentrations increase it.

Because the mutationmutations of gene SLC22A12 gene encoding URAT1 causescause familial renal hypouricemia (OMIM220150), URAT1 is considered to be a transporter playing a major role in renal urate reabsorption. Renal urate transport is known to be controlled by a variety of drugs. For example, drug-induced hyperuricemia has been considered to be caused by enhanced renal urate reabsorption or reduced renal excretion of uric acid. On the other hand, hypouricemia has been considered to be caused by reduced renal urate reabsorption orand enhanced renal excretion of uric acid. Among thesethe drugs, pyrazinamide, probenecid, and salicylic acid have been reported to have a paradoxical effect on renal excretion of uric acid. In other words, these drugs at low concentrations reduce renal excretion of uric acid, while at high concentrations increase it.