Renal Protection

Renal protection, achieved with BP and glucose control, is a primary objective in diabetic care. The urine should be checked for microalbuminuria yearly. Finding marginal elevations indicates that control should be tightened and an ACE inhibitor or angiotensin receptor blocker (ARB) prescribed or increased. However, if BP is normal, pharmacotherapy can be difficult because of potential orthostasis. Another measure that could affect microalbuminuria is weight, which relates to the total-body water and the nitrogenous load the kidney must excrete. An appropriate weight reduction will decrease renal perfusion and microalbuminuria. If micro-albuminuria increases, more aggressive BP drugs should be used. The onset of edema indicates advanced albumin losses or underlying renal or cardiac dysfunction. Diuretic management can significantly reduce micro- or macroalbuminuria, even though its effect on renal perfusion may cause a rise in serum creatinine (usually reversible when diuretic discontinued). Thus, diuretic therapy may need to be cyclic, depending on edema accumulation and renal function.

Screening for microalbuminuria is controversial because it fails traditional tests of acceptability, including agreement on diagnostic criteria (e.g., measurement of albumin/creatinine ratio in spot collection; 24-hour creatinine collection, with simultaneous measurement of creatinine clearance; time collection of 4-8 hours) and confusing rationale for ongoing testing when the patient is already taking an ACE inhibitor.

The development of significant macroalbuminuria above 300 mg/day despite treatment indicates significant glomeru-lar changes with risk of progression to nephritic syndrome or renal failure. Evidence of the nephrotic syndrome may become apparent with hyperlipidemia and more hypertension. The objective of therapy at this point is to attenuate the slope of renal decline and prevent congestive symptoms associated with coincident cardiac dysfunction. Treatment is based on BP and volume control. Dietary limitation of salt, potassium, protein, and fluid intake will be helpful. We believe exposure to nephrotoxic agents can cause a quantum leap in the decline of the diabetic kidney at any stage of the pathophysiologic process. Unfortunately, nephrotoxicity is frequently the result of radiocontrast agents used repeatedly to detect and treat coronary artery disease or overexposure to antibiotics.

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