GENETIC ANALYSIS AND PHARMACOGENOMIC STUDY OF HUMAN POLYCYSTIC KIDNEY DISEASE POPULATION

We are in an era of the mass-analysis of genetic information, which will signal the beginning of the study of living organisms on the basis of their most detailed plan: the DNA base-sequence. Throughout the 20th century, the chief epidemiologic impression of polycystic kidney disease (PKD) has been what an early observer described as its outstandingly hereditary character. An Autosomal dominant form of the disease is indeed among the most common genetic disorders affecting about one third of people with diabetes and is caused by a combination of factors including blood sugar control, high blood pressure and inherited factors. The first sign of kidney disease often is protein spilled into the urine called microalbuminuria. Kidney disease may progress to end stage renal disease, a serious condition in which the kidneys fail to remove the wastes from the body and hence must be treated by dialysis or kidney transplant. According to the National Institute of Health, each year more than 50,000 Americans are diagnosed with end stage renal failure [ESRD] disease, and diabetes, which affects an estimated 16 million Americans, is the most common cause. In 1994, the federal government spends $9.3 billion on care for patients with ESRD. According to NIH, African Americans and Native Americans develop diabetes, kidney disease and end stage renal disease at rates higher than average. This is a first attempt study in Indian scenario initiated to clinically analyse the Genetic and Pharmacogenomic study of Human Polycystic Kidney.