Objective: In chronic kidney disease (CKD), hypertension is often accompanied by sodium sensitivity. Uromodulin promotes sodium sensitivity by activating tubular sodium transporters (NKCC2, NCC). In the general population, individuals with higher urine uromodulin have a positive association between 24-h urine sodium and 24-h blood pressure (BP), whereas those with lower uromodulin show a negative association between these parameters. Whether similar patterns occur in CKD remains unclear. This study evaluated the effect of urine uromodulin on the relationship between 24-h urine sodium excretion and 24-h BP in CKD patients. Design and method: 130 patients with CKD stages 1–5 on stable antihypertensive treatment were included. All participants underwent 24-h ambulatory BP monitoring with ABPMpro device and 24-h urine collections. Patients were divided into two groups using the median 24-h urine uromodulin. Associations between 24-h urine sodium excretion and 24-h BP were examined applying multivariable linear regression models. Results: Mean age was 62.6±14.9 years and mean eGFR 49.0±25.1 mL/min/1.73m2. 24-h systolic (SBP), diastolic BP (DBP) and 24-h urine sodium levels did not differ across CKD stages, whereas urine uromodulin decreased significantly with advancing CKD (p<0.001). In the multivariable linear regression models of the overall population, neither 24-h urine sodium nor urine uromodulin alone predicted 24-h SBP/DBP. However, in stratified models, higher 24-h urine sodium was associated with higher 24-h SBP (β=0.051, 95%CI:0.018–0.087, p=0.005) and DBP (β=0.041, 95%CI:0.018–0.068, p=0.002) only in the high-uromodulin group. In contrast, in the low-uromodulin group, no significant associations were observed. The β-coefficients for urine sodium differed significantly between uromodulin groups for both 24-h SBP and DBP models (p=0.025 and p=0.004 respectively). Conclusions: In CKD, urine uromodulin modifies the association between dietary sodium intake and ambulatory BP. Patients with higher urine uromodulin show a positive association between 24-h sodium excretion and BP, whereas this finding is absent in those with lower uromodulin. These findings support urine uromodulin as a useful biomarker of sodium sensitivity in CKD.
Karagiannidis et al. (Fri,) studied this question.