Should We Sweat the Small (Micro) Things?

Abstract

Thirty years ago, a physician whose patient had diabetes and was urine protein dipstick–positive could only say, “You will most likely progress to end-stage renal disease in 10 years and need dialysis or a kidney transplant, and there is not much we can do about it.” Following the landmark microalbuminuria study of Mogensen and Christensen in 1984 (1), clinicians could say to patients with diabetes and microalbuminuria, “The good news is, we can now tell you 20 years ahead of time that you will likely progress to end-stage renal disease, but the bad news is that we still cannot do anything about it.” However, by the early 1990s, it was shown that treatment of microalbuminuric diabetic patients with ACE inhibitors to control blood pressure, diet modification, and intensive glucose control could slow or prevent progression to end-stage renal disease (ESRD)3 (2). Microalbumin quickly became a textbook example of a new laboratory test with profound impact on treatment and long-term outcomes of patients with a chronic disease. Since then, the term microalbumin has been abandoned in favor of urine albumin because there is nothing “small” or “low molecular weight” about the albumin measured in urine. Urine albumin assays are simply immunoassays capable of measuring albumin concentrations that are more than 3 orders of magnitude lower than those encountered in serum, which are measured by dye-binding methods. Since its first use in patients with diabetes, urine albumin concentration has shown to predict progression to all-cause chronic kidney disease (CKD) and be an independent risk factor for cardiovascular disease (3). Today, numerous clinical practice guidelines exist for the use of urine albumin to predict progression to CKD and cardiovascular risk (4). Two of the most cited are the Kidney Disease Improving Global Outcomes (KDIGO) and the American Diabetes Association (ADA) Standards of …