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Abstract
Chronic renal faliure (CRF) is the progressive loss of kidney function. Damaged by disease or another insult, the kidneys gradually lose their ability to perform their main functions: removing fluid and wastes from the body, maintaining kidney-regulated chemicals in the blood stream and converse electrolytes. In many cases , CRF leads to incurable end-stage renal disease (ESRD) (Levey,et al., 2003).
Serum leptin levels are incerased in CRF patients, primarly due to decreased clearence by Kidneys. As leptin is 16 Kda protein it is also not cleared by dialysis using conventional dialysers. However elevated serum leptin is not universally present in sever renal faliure. Elevated leptin levels are corrected after successful renal transplanation. Leptin, insulin and body mass index are interrelated and a direct correlation has been noted between insulin and leptin (Enyioma, et al., 2002).
Since pure insulin level in ESRD represents the result of both secretion and elimination, reduced elimination by dialyzers, reduced hepatic insulin clearence as in other subjects with insulin resistance, and over secretion of insulin, with decreased sensitivity to insulin in peripheral tissues, may contribute to hyperinsulinemia (Liberman and Eldar, 2005).
Albumin is synthesized exclusively in the liver. Three independent processes have been implicated in suppressing the albumin synthetic rate in patients with chronic renal faliure; metabolic acidosis, impaired protein intake and inflammation. Metabolic acidosis has been reported to decrease albumin synthesis and increase protein breakdown in chronic dialysis patients.