Key result
Renal denervation reduced fasting plasma glucose by 17.1 mg/dl at 6 months in hypertensive patients with chronic kidney disease (P=0.015), a significantly greater reduction than in non-CKD patients.
Why the study?
Renal denervation has shown conflicting results regarding insulin secretion and glucose homeostasis, prompting an evaluation of its impact on glycaemic control in hypertensive patients with chronic kidney disease.
Does renal denervation improve fasting plasma glucose and HbA1c in hypertensive patients with and without chronic kidney disease?
Observational (n=155)
Does renal denervation improve fasting plasma glucose and HbA1c in hypertensive patients with and without chronic kidney disease?
Mean Difference: -17.1
p-value: p=0.015
Renal denervation may provide metabolic benefits beyond blood pressure reduction by improving fasting plasma glucose, particularly in hypertensive patients with chronic kidney disease.
RDN-associated FPG reduction in hypertensive CKD is hypothesis-generating; prospective RCTs needed before considering metabolic effects beyond BP lowering.
Backgroun Sympathetic overactivation is associated with numerous pathologies, including arterial hypertension, diabetes, metabolic syndrome and chronic kidney disease (CKD). Renal denervation (RDN) has emerged as an adjacent therapy for the management of hypertension. By modulating sympathetic activity in the whole body, RDN has shown conflicting results regarding insulin secretion and glucose homeostasis. The aim of this study is to analyse the impact of RDN on glycaemic control in patients with CKD. Methods A total of 155 hypertensive patients with (n = 45) or without CKD (n = 110) were included in this post hoc analysis. All patients underwent radiofrequency-, ultrasound- or alcohol injection–based RDN. Fasting plasma glucose (FPG) and haemoglobin A1c levels were measured at baseline, 3 months and 6 months after RDN in parallel with the office and 24-h ambulatory blood pressure. CKD was defined either by clinical diagnosis, an estimated glomerular filtration rate (eGFR) of 15–59 ml/min/1.73 m2 and/or A2/A3 albuminuria in hypertensive patients, repeatedly confirmed, or several of these criteria. Results In the total study cohort, FPG decreased by 5.1 ± 29.1 mg/dl (P = .032) and by 7.9 ± 32.7 mg/dl (P = .003) at 3 and 6 months after RDN, respectively. The change in FPG levels was related to the change in 24-h systolic BP (r = 0.286, P = .008) 3 months after RDN. Among patients with CKD, FPG levels decreased by 13.5 ± 43.5 mg/dl at 3 months (P = .043) and by 17.1 ± 45.2 mg/dl at 6 months (P = .015) following RDN. These reductions were greater compared with the non-CKD group (P = .021 and P = .024, respectively). After excluding patients on oral antidiabetic or insulin therapy, patients with CKD (but not those without CKD) exhibited a reduction in FPG levels of 6.7 ± 15.3 mg/dl (P = .043) at 6 months post-RDN. No significant changes were observed in eGFR in either group. Conclusion We observed that FPG levels improved to a greater extent in hypertensive patients with CKD after RDN. Thus RDN may have a broader therapeutic impact beyond blood pressure reduction in CKD patients.
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Bytyqi et al. (2025) conducted an observational in Hypertension with and without chronic kidney disease (n=155). Renal denervation vs. Non-CKD patients / Baseline was evaluated on Change in fasting plasma glucose at 6 months (MD -17.1 mg/dl, p=0.015). Renal denervation reduced fasting plasma glucose by 17.1 mg/dl at 6 months in hypertensive patients with chronic kidney disease (P=0.015), a significantly greater reduction than in non-CKD patients.
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