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Abstract
First, what is the magnitude of the risk? As is outlined by Mann, an increase of the CV risk by a factor of 2 to 4 with elevated creatinine or microalbuminuria retrospectively has been recognized in multiple populations (6–16 ⇓ ⇓ ⇓ ⇓ ⇓ ⇓ ⇓ ⇓ ⇓ ⇓ ), including (1) in the general population, i.e., the Framingham study (14) and confirmed in the prospective Hoorn study (17); (2) in individuals with hypertension (18); and (3) in individuals at high CV risk (19) as well as (4) in patients with heart failure (20). Furthermore, recent studies in patients with acute myocardial infarction (7, 8 ⇓ ) documented a substantial increase of in-hospital and postdischarge mortality in individuals with acute myocardial infarction. This was explained only in part by iatrogenic factors, particularly withholding therapeutic options such as thrombolysis and interventional measures (coronary artery bypass graft and percutaneous transluminal coronary angioplasty) or cardioprotective medication (platelet inhibitors, β blockers, angiotensin-converting enzyme inhibitors). These results have been confirmed in a large international prospective observational study (21). These findings are further complemented by a recent analysis (22) indicating that the mortality after percutaneous transluminal coronary angioplasty increased progressively with increasing serum creatinine concentrations in the high-normal to slightly elevated range, so the evidence is overwhelming (1) that in the individual with even slightly reduced renal function, the risk of a CV event is dramatically increased, comparable in magnitude to that conferred by diabetes (19, 23 ⇓ ); and (2) that slight renal dysfunction exposes the patient with a cardiac event to an excessive cardiac mortality.