The Phenotype of Arterial Hypertension in Patients With Diabetic Kidney Disease

Objective: Diabetic kidney disease (DKD) is defined by the presence of diabetes accompanied by persistent albuminuria and/or a reduced estimated glomerular filtration rate for at least three months, in the absence of alternative causes of kidney damage. Hypertension represents not only a major risk factor for DKD progression but also a frequent consequence of ongoing renal injury. Multiple pathophysiological mechanisms contribute to the development of hypertension in DKD (Figure 1). The aim of this study was to characterise the phenotype of hypertension in a DKD patient cohort. Design and method: We enrolled 50 patients (mean age 67.0±7.6 years, range 43-79 years, 70% male) treated with finerenone in our outpatient clinic between June 1st 2023 and January 1st 2026. Basic demographic, anthropometric, and laboratory data were collected. Central blood pressure and arterial stiffness parameters were assessed by using applanation tonometry (SphygmoCor®, AtCor Medical, Sydney, Australia). Volume status was evaluated by bioimpedance spectroscopy (BIS; BCM®, Fresenius Medical Care, Germany). Statistical analyses was performed by using SPSS® version 26.0 (IBM Corp., Chicago, IL, USA). Results: All patients had hypertension, with a mean BMI of 30.1±5.0 kg/m2 and a mean diabetes duration of 14.2±8.4 years. The most commonly prescribed antihypertensives were RAAS inhibitors (94%), diuretics (62%), beta blockers (44%), and calcium channel blockers (36%). Laboratory, central blood pressure, arterial stiffness, and bioimpedance data are shown in Table 1. Central aortic systolic blood pressure (caSBP) correlated with carotid–femoral pulse wave velocity (cfPWV; r=0.43, p=0.005), augmentation index (AIx; r=0.49, p<0.001), and augmentation pressure (AP; r=0.68, p<0.001). The association between caSBP and cfPWV remained independent of age, albuminuria, and kidney function (beta=0.210, p=0.001). Diabetes duration was also independently associated with higher caSBP (beta=0.87, p=0.007), whereas no other associations were observed between caSBP and HbA1c or between blood pressure parameters and body composition measures. Conclusions: In patients with DKD, hypertension was universal and characterized by elevated caSBP driven primarily by arterial stiffness rather than volume status or metabolic control. Longer diabetes duration independently predicted higher caSBP, underscoring arterial stiffening as a key mechanism and therapeutic target in DKD-related hypertension.