Penatalaksanaan hiperurisemia simtomatik pada pasien dengan penyakit ginjal kronis meliputi pendekatan nonfarmakologi dan farmakologi. Berbeda dari pasien tanpa insufisiensi ginjal, pendekatan farmakologi pada pasien penyakit ginjal kronis membutuhkan penyesuaian dosis obat.
Manusia, tidak seperti mamalia lainnya, tidak memiliki enzim urikase yang mampu mengoksidasi asam urat menjadi produk yang mudah larut dalam air ( 5-hydroxyisourate, allantoin) sehingga mudah dikeluarkan lewat urin. Oleh karena itu, produk metabolisme purin pada manusia hanya berakhir dalam bentuk asam urat yang sukar larut. Kondisi ini menyebabkan manusia rentan mengalami hiperurisemia.[1-3]
Secara fisiokimia, hiperurisemia didefinisikan sebagai konsentrasi asam urat yang melampaui solubilitasnya dalam darah. Hiperurisemia dapat diakibatkan oleh peningkatan produksi atau menurunnya ekskresi asam urat. Skenario klinis hiperurisemia simtomatik dapat berupa gout arthritis, batu ginjal, atau nefropati asam urat.[2,4]
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Referensi
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13. Sanchez-Niño MD, Zheng-Lin B, Valiño-Rivas L, et al. Lesinurad: what the nephrologist should know. Clin Kidney J. 2017;10(5):679–687. doi:10.1093/ckj/sfx036
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