Abstract
Albuminuria has a strong, continuous, direct, linear relationship with adverse cardiovascular (CV) outcomes and chronic kidney disease progression. Even at levels below the accepted upper limit of what is considered “normal” daily albumin excretion (< 30 mg/24 h), a relationship between albumin excretion level and adverse CV events is evident. Primary care clinicians (eg, physicians, nurse practitioners, physicians' assistants) are usually the first point of contact for patients at risk for CV and kidney disease. Hence, identifying and treating problematic albuminuria levels are important in primary care. Both the American Diabetes Association (ADA) and the National Kidney Foundation (NKF) endorse routine annual screening for microalbuminuria (small amounts of albumin in the urine). Once excess albumin excretion is detected, clinicians must employ aggressive CV risk reduction. To optimize outcomes, treatment of microalbuminuria often requires the combined skills of experts in primary care, cardiology, metabolic disease, and nephrology. Although blood pressure reduction usually improves microalbuminuria, agents that block the renin-angiotensin-aldosterone system (RAAS) are most efficacious. Renin-angiotensin-aldosterone system blockers (ie, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, direct renin inhibitors) may confer CV and kidney advantages in high-risk patients. Their effects on microalbuminuria reduction are greater than those associated with attaining guideline-recommended blood pressure goals. Effective RAAS blockade sometimes induces transient changes in creatinine and potassium, which merit consistent monitoring for the first 2 to 3 months of their use, but rarely necessitate discontinuation. This article also presents an approach to managing increases in creatinine and potassium that should fit comfortably in the hands of primary care clinicians.