title: Cardiorenal protection in diabetes.
abstract: Diabetes is twice as common in hypertensive patients than in the general population, and is a major cause of cardiovascular morbidity. Diabetes is the most common cause of end-stage renal disease in the United States, and is primarily responsible for the 9% increase in prevalence of end-stage renal disease during the past 10 years. However, there is evidence that tight blood-pressure control can reduce the vascular complications of diabetes. This reduction was demonstrated in the United Kingdom Prospective Diabetes Study, in which patients who were randomized to a tight blood-pressure control group had 24% fewer vascular complications (including strokes and diabetic retinopathy) than patients in usual-care groups. Thus, the target goal for blood pressure in patients with diabetes is 130/85 mmHg. Microalbuminuria is an early marker of diabetic nephropathy, and is most pronounced in patients whose 24-hour blood pressure shows a nondipping pattern (failure of the blood pressure to fall at night). The prevalence of nondipping blood pressure is increased in patients with diabetes and in patients with renal disease due to other causes. Further, there is evidence that patients with nondipping blood pressure show more rapid deterioration of renal function than patients with dipping blood pressure. High nocturnal pressure in patients with nondipping blood pressure may accelerate glomerular damage. For example, studies of animals with diabetes have shown that the afferent glomerular arteriole is dilated when compared with the efferent arteriole, thereby exposing the glomerulus to the systemic arterial pressure. Numerous studies have shown that angiotensin-converting enzyme (ACE) inhibitors are superior to some antihypertensive agents (particularly beta blockers and diuretics) in the prevention of renal damage. This observation is based on results of a metaanalysis that demonstrated a 9%/year glomerular filtration rate decrease in patients taking beta blockers or diuretics, but only a 1%/year decrease in patients taking ACE inhibitors. The role of calcium channel blockers is more controversial, but there is evidence to suggest that nondihydropyridine calcium channel blockers may confer the same benefit as ACE inhibitors. Alpha blockers and angiotensin-receptor blockers show promise, but have been less widely studied.
authors.affiliation: Hypertension Center, New York Presbyterian Hospital-Cornell University Medical Center, 520 East 70th Street, New York, NY 10021, USA.
authors.forename: T G
authors.initials: TG
authors.lastname: Pickering
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D048909:Diabetes Complications; D003928:Diabetic Nephropathies / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D006978:Hypertension, Renovascular / Q000209:etiology / Q000517:prevention & control
chemical_list: D000959:Antihypertensive Agents