Intensive blood pressure lowering favored to not induce kidney disease, contrary to prior research
1. Patients managed with intensive blood pressure reduction were found to have significantly greater decreases in kidney damage biomarkers compared to standard blood pressure management.
2. Higher levels of kidney damage biomarkers at baseline were associated with greater odds of developing chronic kidney disease.
Study Rundown: Systolic blood pressure (SBP) management is a well-established method of improving cardiovascular health. The Systolic Blood Pressure Intervention Trial (SPRINT) clinical trial demonstrated that intensive SBP lowering (target <120mmHg) reduced rates of major cardiovascular events and mortality. This study measured serum creatinine levels and demonstrated that intensive BP lowering was associated with a 3-fold increase in incidence of CKD. Considering this association has important implications for treatment of cardiovascular disease, the authors of this study aimed to determine whether there is truly an increased incidence of chronic kidney disease (CKD) following intensive SBP reduction. Specifically, they compared changes in kidney damage biomarkers of patients with and without CKD, as well as those with intensive versus standard SBP management. Generally, they observed that intensive SBP lowering might not actually induce true kidney disease. Limitations of the study included follow up, where kidney damage biomarkers were only measured at baseline and 1 year. Study results may also not be generalizable to all patients with hypertension, such as those that were not included in the SPRINT trial.
Relevant Reading: Management of hypertension in CKD: beyond the guidelines
In-Depth [case-control study]: The authors of this study conducted a nested case-control study within the previous SPRINT trial, which assessed impacts of SBP interventions on cardiovascular health and other outcomes. The study participants included patients who developed incident CKD during trial follow up (n = 162) and matched control participants. Study outcomes then included 9 urinary biomarkers of kidney damage, which were measured in patients at baseline and at 1 year after the SBP intervention. Results were analyzed via linear mixed-effects models. Generally, the odds ratio of developing CKD was found to be higher in patients with elevated baseline concentrations of urinary albumin (adjusted odds ratio per doubling: 1.50 [95% CI, 1.14 to 1.98]), as well as two other kidney damage biomarkers, kidney injury molecule-1 and monocyte chemoattractant protein-1. Furthermore, incident CKD with intensive SBP lowering was associated with decreases in kidney damage biomarkers.
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