Molecular biochemical advances in renal disease.
Srivastava, L.M. (2002) Molecular biochemical advances in renal disease. 33rd Annual Conference of Indian Society of Nephrology, Jaipur. pp. 221-222.
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This paper pertaining to Biochemical advances in renal disease on molecular basis deals with (i) hyperhomocyteinemia (ii) oxidative stress as measures by total antioxidant status and (iii) proteins of the complement system and therapeutic role of complement receptors in preventing glomerulonephritis and hyper-acute graft rejection (Xenotransplantation). (i) Hyperhomocyteinemia: This refers to an elevated circulating levels of the sulfur-containing amino acid homocysteine and has been shown to be a risk factor for vascular disease in the general population. In patients with renal failure, hyperhomocysteinemia is a common feature. The underlying pathophysiological mechanism for this phenomenon is unknown. Proposed mechanisms include reduced renal elimination of homocysteine and impaired non-renal disposal because of inhibition of crucial enzymes in the methionine-homocysteine metabolism. Absolute or relative deficiencies of folate, vitamin B6 or B12 may also play a role. Moreover, the impact of the C677T polymorphism of the MTHFERgene in haemodialysis patients has recently been studied in several global populations. A significant influence of genotype on total homocysteine (tHcy) has been observed. (ii) Oxidative stress/total antioxidant status: Total antioxidant status in acute renal failure patients is significantly lower than normal controls. Parameters of oxidative stress seem to be very important in the inter-organ relationship between kidneys and heart/blood vessels in chronic renal failure. The elevated levels of oxidants in renal failure would represent a cardiovascular risk for the patients. Myocardial infarction is also connected with Mitochondrial DNA damage and dysfunction due to oxidative stress.
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