Blood Pressure Levels and the Progression of Chronic Kidney Disease: A Systematic Review

Introduction: Elevated blood pressure is both a cause and a modifiable risk factor for chronic kidney disease (CKD) progression, but the optimal target levels remain debated. Rising evidence suggests that more intensive BP lowering may slow decline in glomerular filtration rate (GFR) but also carries risks. These uncertainties necessitate an updated synthesis of data. Objective: The main objective is to systematically review human studies evaluating the association between achieved blood pressure levels (or BP targets) and the progression of CKD. Secondary objectives include assessing the impact of BP variability, the differential effects by CKD stage, and adverse events associated with intensive BP control. Methods: We searched PubMed, Scopus, Web of Science, Cochrane Library, LILACS, ClinicalTrials.gov, and ICTRP for studies published in the past five years (expanded to ten years if fewer than ten eligible). Eligible studies included randomized controlled trials, cohort studies, and controlled observational studies in human CKD patients that reported on BP levels and renal progression outcomes. Two independent reviewers performed study selection, data extraction, and risk-of-bias assessments (using RoB 2, ROBINS-I, QUADAS-2). Evidence certainty was evaluated with GRADE, and results were synthesized qualitatively and quantitatively where possible. Results and Discussion: Included trials and cohorts generally indicated that lower systolic BP (e.g. ≤ 120 mmHg) was associated with slower GFR decline and reduced incidence of end-stage renal disease (ESRD), though results varied by baseline risk and CKD stage. BP variability metrics such as visit-to-visit SD, coefficient of variation, and variation independent of mean were independently associated with faster progression in several cohorts. Some trials, however, showed minimal incremental benefit of intensive BP lowering regarding renal endpoints, with increased risks of acute kidney injury and hypotension. Heterogeneity in BP measurement methods, CKD definitions, and follow-up durations limits pooled inference. Overall certainty ranged from low to moderate. Conclusion: Lower achieved blood pressure levels, particularly in systolic BP ≤ 120 mmHg, may slow CKD progression in selected patients, but benefits must be balanced against risks of overaggressive lowering. Clinicians should individualize BP targets based on patient comorbidities, baseline kidney function, and tolerance. Further large randomized trials with standardized BP assessment, stratified CKD populations, and long-term renal endpoints are needed to refine optimal targets. Descriptors (MeSH terms): Blood Pressure, Chronic Kidney Disease, Renal Insufficiency, Treatment Outcome