Diabetic nephropathy occurs in approximately 35% of all diabetic patients, both insulin and non-insulin dependent. It accounts for the largest proportion increase of all diseases as a cause for endstage renal disease in the United States. Certian populations, i.e., Pima Indians and Mexican and black Americans, have a higher propensity for developing diabetic nephropathy. The reasons for this increased incidence, however, are unclear.

Pathophysiologically, numerous changes in vascular reactivity and renal physiology occur in early diabetes. These include increased sodium avidity, lower threshold for vasoconstriction secondary to angiotensin II and norepinephrine, a greater than 50% of normal increase in renal vasodilation following a protein meal, and loss of renal autoregulation. These differences are not seen in nondiabetic hypertensive subjects. The therapeutic approach to lower elevated arterial pressure in these patients should take these changes in physiology into account. Specifically, antihypertensive agents are preferred that have natriuretic properties and also blunt the effects of vasoconstrictors on both the vasculature and the cellular level, i.e., inhibit mesangial hypertrophy and matrix expansion, the hallmark of diabetes. Ideal agents, therefore, are angiotensin converting enzyme (ACE) inhibitors in the early stages of the disease, and certain calcium antagonists once renal insufficiency occurs. These choices are largely due to the hemodynamic, natriuretic, and anti-proteinuric effects of these agents.

Good blood pressure control is essential for preservation of renal function, regardless of agents used. The ACE inhibitors and calcium antagonists of the verapamil and diltiazem groups have demonstrated superior efficacy for preservation of renal function over conventional therapy.