The development and progression of diabetic nephropathy is dependent on glucose homeostasis and many other contributing factors. Diabetic nephropathy is a leading cause of end-stage renal failure, accounting for 35 to 40% of all new cases that require dialysis therapy worldwide. Recent clinical studies clearly demonstrated that hyperglycemia and oxidative stress is an important causal factor in mediating the development and progression of diabetic kidney disease.
To evaluate the therapeutic effect of levamesole in diabetic nephropathy .
The study included 10 rabbits Weight (1kg ±20 gm); they were followed up for 7months. Blood was aspirated from marginal ear vein after agitation with xylol for estimation of fasting blood glucose and malondialdehyde (MDA) which is used as marker of oxidative stress. Rabbits were given 110 mg / kg alloxan to induce diabetes. In the second month rabbits became diabetic without development of nephropathy. After 1 month from being diabetic a bosture dose of alloxan was given (125 mgkg). After 1 month of the bosture dose blood glucose level further increased and rabbits developed albumin urea. Once rabbits developed albumin urea they received levamesole 2 mgkg EOD for 6 weeks.
The study results showed that diabetic nephropathy is associated with high blood glucose level (300-400mgdl) and oxidative stress (significant increase in MDA level). The nephropathy (albumin urea) and oxidative stress can be reversed by levamesole.
The antioxidant effect and immune modulating properties of levamesole provided a protective therapy against the development of diabetic nephropathy.
KEY WORDS: diabetic nephropathy, levamesole, MDA.