medwireNews: Research shows that intensive blood pressure (BP) control increases the risk for new-onset chronic kidney disease (CKD), particularly in patients with type 2 diabetes, creating a potential treatment dilemma.
The findings, based on an analysis of patients in the ACCORD and SPRINT trials who had a baseline estimated glomerular filtration rate (eGFR) of at least 60 mL/min per 1.73 m2 (ie, no CKD), are published in The Lancet Diabetes & Endocrinology.
In a linked commentary, Giuseppe Mancia (Policlinico di Monza, Italy) writes that the results “should discourage treatment strategies that pursue renal protection via aggressive reduction in blood pressure.”
The 4311 patients with type 2 diabetes (all from ACCORD) had a higher overall risk for CKD than the 6715 without (all from SPRINT), with the 3-year cumulative rates among patients who were treated to standard BP targets being 4.1% versus 1.0%.
Intensive treatment, to a systolic BP of less than 120 mmHg, resulted in CKD rates of 10.0% and 3.5% in patients with versus without diabetes, equating to absolute risk increases of 5.9% and 2.5%, respectively.
The risk increase associated with intensive BP treatment in diabetes patients was significantly greater than that in patients without diabetes, report Srinivasan Beddhu (University of Utah School of Medicine, Salt Lake City, USA) and study co-authors. This was despite intensive treatment achieving a significantly larger systolic BP reduction in SPRINT than ACCORD, at 15.2 versus 13.9 mmHg.
Underlining the high CKD risk in diabetes patients was the change in eGFR function during the first year of treatment; it declined by 11.6 mL/min per 1.73 m2 in those treated intensively and by 5.5 mL/min per 1.73 m2 in the standard treatment group.
The researchers say that their findings “suggest caution is warranted in extrapolating SPRINT findings to people with type 2 diabetes.”
In his commentary, Mancia says the study “raises a question that might be difficult to answer,” highlighting that the findings potentially create a conflict between treating BP intensively to reduce cardiovascular risk and less so to preserve renal function.
“Might we have to partly sacrifice renal protection to pursue the most achievable cardiovascular protection, a goal that has greater impact for the general population?” he asks.
However, he suggests that an intermediate target may exist, “at which both cardiovascular and renal protection are maximised.”
He writes: “This target might lie in the upper portion of the 120–130 mm Hg systolic range (ie, closer to 130 mm Hg), a value unexplored by SPRINT and the ACCORD trial.”
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