PERAN HIPOKSIA PADA PATOGENESIS PENYAKIT GINJAL

Abstract

Chronic kidney disease is a current major worldwide health problem with an increasing prevalency.
Kidney is a sensitive organ with hypoxic condition relate to its high tubular epithelial cells and vascular oxygen
consumption. Chronic peritubular ischemia may occur through several interrelating mechanisms. The activation
of local renin-angiotensin system, angiotensin II, could induce hypoxia by means of hemodinamic and nonhemodinamic
mechanisms.
Anemia in renal disease could accelerate the decline of renal function through the induction of
tubulointerstitial hypoxia. Non Steroidal Anti Inflamatory Drugs (NSAID) could evoke renal medullar hypoxia
by its regional hypoperfusion mechanism and the escalation of tubular transport. The Outer region of renal
medulla and tubulus are main target of hypoxic renal damage. The mechanism of hypoxia induced Acute
Kidney Disease involves renal vascular and tubulus through the reduction of blood flow and the increasing of
tubular oxygen demands. The Patofisiology of hypoxia induced chronic kidney disease occurs by
tubulointerstitial damage which induce fibrogenesis, causing interference of peritubular blood flow and oxygen
consumption.