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URAT1 をコードする遺伝子 SLC22A12 の変異が,家族性腎性低尿酸血症(OMIM220150)を引き起こすことから,URAT1 が腎臓において尿酸再吸収を担う中心的な輸送体であると考えられている.腎臓の尿酸輸送は種々の薬物によって制御されることが知られている.例えば薬物誘発性の高尿酸血症は,腎臓での尿酸再吸収の亢進ないし尿酸排出の抑制により生じると考えられ,また逆に低尿酸血症は尿酸再吸収の抑制および尿酸排出の亢進により生じると考えられてきた.その中でピラジナミド,プロベネシド,そしてサリチル酸は,腎臓の尿酸排泄に対する paradoxical な効果を持つことが報告されていた.すなわち低濃度のこれらの薬物は,腎臓での尿酸排泄を低下させ,高濃度では腎臓での尿酸排泄を増加させる.

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 loss-of-function mutation mutations ofin the SLC22A12 gene (OMIM220150) encoding the transporter URAT1  causes familial renal hypouricemia (OMIM220150);, therefore, URAT1 is considered to be a transporter playing an important major role in renal urate reabsorption.  Renal urate transport is known to be controlled affected 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 hand, hypouricemia has been considered to be caused by reduced renal urate reabsorption and enhanced renal 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 at high concentrations  increase it at high concentrations..

Because A loss-of-function mutation mutations ofin SLC22A12 gene (OMIM220150) encoding the urate transporter URAT1  causes familial renal hypouricemia (OMIM220150);, therefore, URAT1 is considered to be a transporter playing an important major role in renal urate reabsorption.  Renal urate transport is known to be controlled affected 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 hand, hypouricemia has been considered to be caused by reduced renal urate reabsorption and enhanced renal 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 at high concentrations  increase it at high concentrations..

URAT1 をコードする遺伝子 SLC22A12 の変異が,家族性腎性低尿酸血症(OMIM220150)を引き起こすことから,URAT1 が腎臓において尿酸再吸収を担う中心的な輸送体であると考えられている.腎臓の尿酸輸送は種々の薬物によって制御されることが知られている.例えば薬物誘発性の高尿酸血症は,腎臓での尿酸再吸収の亢進ないし尿酸排出の抑制により生じると考えられ,また逆に低尿酸血症は尿酸再吸収の抑制および尿酸排出の亢進により生じると考えられてきた.その中でピラジナミド,プロベネシド,そしてサリチル酸は,腎臓の尿酸排泄に対する paradoxical な効果を持つことが報告されていた.すなわち低濃度のこれらの薬物は,腎臓での尿酸排泄を低下させ,高濃度では腎臓での尿酸排泄を増加させる.

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.

URAT1 をコードする遺伝子 SLC22A12 の変異が,家族性腎性低尿酸血症(OMIM220150)を引き起こすことから,URAT1 が腎臓において尿酸再吸収を担う中心的な輸送体であると考えられている.腎臓の尿酸輸送は種々の薬物によって制御されることが知られている.例えば薬物誘発性の高尿酸血症は,腎臓での尿酸再吸収の亢進ないし尿酸排出の抑制により生じると考えられ,また逆に低尿酸血症は尿酸再吸収の抑制および尿酸排出の亢進により生じると考えられてきた.その中でピラジナミド,プロベネシド,そしてサリチル酸は,腎臓の尿酸排泄に対する paradoxical な効果を持つことが報告されていた.すなわち低濃度のこれらの薬物は,腎臓での尿酸排泄を低下させ,高濃度では腎臓での尿酸排泄を増加させる.

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.

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