Kriteria RIFLE pada Acute Kidney Injury

Abstract

Abstrak Acute kidney injury (AKI) merupakan masalah yang menyulitkan dalam dunia kedokteran. Acute kidney injury diartikan sebagai peningkatan kreatinin serum ataupun produk metabolisme nitrogen yang bersifat reversibel dan ketidakmampuan ginjal untuk meregulasi cairan dan elektrolit kekeadaan homeostasis tubuh. Kriteria risk, injury, failure, loss, and end stage renal disease (RIFLE) telah ditetapkan sebagai kriteria standar AKI pada orang dewasa. Pada anak telah digunakan klasifikasi RIFLE yang dimodifikasi yang disebut dengan pediatric RIFLE (pRIFLE). Perbedaan antara RIFLE pada dewasa dan pRIFLE pada anak adalah nilai cut-off kreatinin serum yang lebih rendah untuk mencapai kategori F (failure), dan waktu pengeluaran urin yang diperlukan untuk menentukan risk dan injury. Penyebab AKI dibedakan menjadi penyebab pre renal, renal, dan uropati obstruktif. Beberapa biomarker seperti neutrophil gelatinase-associated lipocalin (NGAL) plasma, kadar sistatin C dan perubahan kadar urin NGAL, interleukin 18, kidney injury molecule-1 (KIM-1) dan KIM-3 sedang dalam tahap penelitian. Mortalitas pada pasien dengan AKI (31,2%) lebih tinggi dibandingkan dengan pasien tanpa AKI (6,9%). Angka mortalitas meningkat seiring peningkatan stadium yaitu R sebesar 18,9%, I sebesar 36,1% serta F sebesar 46,5%.
Kata kunci: gagal ginjal akut, RIFLE, oliguria, laju filtrasi glomerulus, kreatinin

Abstract Acute kidney injury (AKI) is a complicated problem in medicine. Acute kidney injury is defined as a reversible increase in serum creatinine or nitrogen metabolism products and inability of kidney to regulate fluid and electrolyte to homeostatic state. Risk, injury, failure, loss, and end stage renal disease (RIFLE) has been established as a standard criteria of AKI in adults. In children, there is a modified RIFLE classification called pediatric RIFLE (pRIFLE). The differences between adult RIFLE and child pRIFLE are lower cut-off point of serum creatinine to reach F (failure) category and diuresis time to establish risk and injury. Causes of AKI can be divided into prerenal, renal and obstructive uropathy. Several biomarkers for AKI such as plasma neutrophil gelatinase-associated lipocalin (NGAL), cystatin C level and changes in urinary level of NGAL, interleukin 18, kidney injurymolecule-1 (KIM-1) and KIM-3 are still on research. The mortality of patients with AKI (31,2%) is higherthan those without AKI (6,9%). The mortality rate increases along with the increase of AKI stages, stage R:18,9%, stage I:36,1% and stage F:46,5%.
Key words: acute kidney injury, RIFLE, oliguria, glomerular filtration rate, creatinin