DefinePK

Abstract

Chronic renal disease once established usually pro­gresses to end singe renal failure even when the primary cause of the renal insufficiency is removed. This progression occurs in various clinical settings, including chronic renal allograft injury1, vesicoureteral reflux2, after recovery from bilateral renal cortical necrosis3, after drug discontinuation in some patients with analgesic nephropathy4, after initial recovery from post streptococcal glomerulonephritis5 or acute renal failure6, or as a consequence of a congenital reduction in nephron number, as in the case of oligemeganephronia7 or a congenital solitary kidney8. A reduction in the number of functioning nephrons (where GFR is reduced to one fifth of the normal) causes eventual failure of the remaining nephron units. Much stress has been placed on immunological factors that can lead to progressive deterioration of renal functions. There are different mechanisms that can lead to progression of the disease9 and these have been studied by various workers to halt the in-exorable decline of renal function with time. The histological yardstick to measure progressive renal disease is glomerulosclerosis9 and chronic tubulo-interstitial damage10. The interstitial damage is characterized by mononuclear inflammatory cell infiltration and intratubular cast formation that eventually results in tubule atrophy accompanied by interstitial fibrosis. Clinical studies have demonstrated that progressive glomemlar injury in humans is haemodynamically mediated. Adaptive alterations in glomerular haemodynamics include hyper filtration, hypertension, hyper perfusion and hypertro­phy. Dietary protein. hyperlipidaemia or systemic hyperten­sion play an ancillary role. The tubular factors which have a significant contributary role, are hypermetabolism in the remnant nephron, interstitial calcium deposition and in­creased ammonia genesis.