Roughly 40% of all diabetic patients, whether insulin dependent or not, develop persistent albuminuria (over 300 mg/24 hr), a decrease in the glomerular filtration rate, and elevated blood pressure, ie, diabetic nephropathy. Diabetic nephropathy is the single most important cause of end stage renal disease in the Western world, and accounts for over a quarter of all end stage renal disease. It also is a major cause of the increased morbidity and mortality seen in diabetic patients; for example, the cost of end stage renal care in the United States currently exceeds +1.8 billion per year for diabetic nephropathy alone and is rapidly rising. Increased arterial blood pressure is an early and common finding in incipient and overt diabetic nephropathy. Fluid and sodium retention with normal concentrations of active renin, angiotensin I and II, and aldosterone has been demonstrated in diabetic renal disease. An impaired nocturnal decline in blood pressure is more prevalent in patients with diabetic nephropathy and autonomic neuropathy, and may contribute to the enhanced cardiovascular morbidity found in such patients. Moreover, raised blood pressure accelerates both the development and progression of diabetic nephropathy in insulin-dependent and non-insulin-dependent diabetes. The relationship between arterial blood pressure and diabetic nephropathy thus seems to be a complex one: nephropathy increasing blood pressure and blood pressure accelerating the course of nephropathy. Effective blood pressure reduction reduces albuminuria, delays the progression of nephropathy, and postpones renal insufficiency in diabetic nephropathy. Calcium antagonists and angiotensin converting enzyme inhibitors induce an acute increase in the glomerular filtration rate, renal plasma flow, and renal sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)