How to Handle the Creatinine “Bump”—Analysis of ACCORD-BP Data

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For patients with type 2 diabetes, increases in serum creatinine after starting blood pressure–lowering treatment—even greater than 30%—do not necessarily mean that antihypertensive therapy should be decreased, reports a study in Hypertension.

The researchers performed a post hoc analysis of data from the ACCORD-BP (Action to Control Cardiovascular Risk in Diabetes Blood Pressure) trial, which compared intensive versus standard BP-lowering therapy (systolic BP cutoffs of 120 and 140 mm Hg, respectively). The analysis included 4733 patients with type 2 diabetes. Mean age was 62.2 years, with a mean estimated glomerular filtration rate of 81.5 mL/min/1.73 m2.

Patients were classified into three groups, based on the extent of increase in serum creatinine from baseline to 4 months: less than 10%, 10% to 30%, and more than 30%. The effects of creatinine increase during antihypertensive therapy on a primary outcome of all-cause mortality, major cardiovascular events, and renal failure were analyzed. Mean follow-up was 4.9 years.

Follow-up data were available for 4446 patients: 2231 assigned to intensive BP control and 2215 to standard treatment. Neither group showed an association between serum creatinine increase and the risk of adverse outcomes.

Patients with a serum creatinine increase greater than 30% had a higher rate of adverse outcomes, with no difference between the intensive and standard therapy groups: hazard ratios were 1.32 and 1.47, respectively. There was no significant association for patients with a 10% to 30% increase.

Previous studies have linked an initial serum creatinine increase during antihypertensive therapy to an increased risk of adverse outcomes. These reports led to recommendations to reduce antihypertensive therapy for patients with serum creatinine increases of greater than 30%.

The new analysis finds that serum creatinine increase of greater than 30% is associated with higher risks, with similar increases for patients receiving intensive versus standard antihypertensive therapy. “These data suggest that a serum creatinine increase that coincides with a lower BP should not be interpreted as harmful and lead to a reduction in BP-lowering medication,” the researchers write. They call for further studies to assess the optimal cutoff point for serum creatinine increase after antihypertensive therapy.

In an accompanying editorial [Hypertension 2018; 72:1274–1276], Drs. George L. Bakris and Rajiv Agarwal discuss the implications for managing the creatinine “bump” after antihypertensive therapy. They conclude: “What we learn from the ACCORD analysis is that a rise in serum creatinine of >30% is a marker of future nonrenal morbidity and mortality. What we do about it is a matter of clinical judgment” [Collard D, et al. Creatinine rise during blood pressure therapy and the risk of adverse clinical outcomes in patients with type 2 diabetes mellitus: a post hoc analysis of the ACCORD-BP randomized controlled trial. Hypertension 2018; 72:1337–1344].