A significant rise in the intracellular calcium content has been shown to play a key role in the pafhophysiolog-ical mechanism of several types of ARF [135, 136]. This observation prompted the use of calcium channel block-ers in ARF. Calcium antagonists can reverse renal afferent arteriolar vasoconstriction, thus improving GFR. The
systemic infusion of verapamil to anesthetized rabbits prevented, or partly reversed, the hypoxemia-induced renal vasoconstnction and its accompanying fall in GFR  Intrarenal administration of the inorganic calcium channel blocker manganese resulted in a selective protection from renal hypoxemic changes  In hypo-xemic human neonates, the use of calcium antagonists such as verapamil and nifedipme is still under investigation  Unfortunately the presently available calcium antagonists produce severe systemic effects that overshadow their beneficial renal actions
The beneficial effects of thyroxine treatment on renal cellular injury are probably also mediated by restoration of the cellular ATP pool  Stabilization of cell membranes and activation of Na+-K+-ATP-ase achieve this. When thyroxine was given to rats immediately after the induction of renal ischemia, the recovery from lsch-emic ARF was accelerated  This protection was sustained and accompanied not only by renal functional improvement but also by enhanced repair of damaged tubular epithelium. Eight children with ARF have been successfully treated with thyroxine (5-6 pg/kg per day) . Thyroxine (50 ug) was recently also effective in neonatal, hypoxemic ARF .
A variety of growth factors are implicated in renal parenchymal damage The exogenous administration of several of these cytokines offers theoretical possibilities to prevent, reverse, or ameliorate ARF [112, 143] Future treatment with disintegnns to counteract the mtratu-bular obstruction with cell debris may also be beneficial.
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