Central pulse pressure links microalbuminuria with plasma B-type natriuretic peptide elevation: causal implication for cardiorenal syndrome in hypertension.

OBJECTIVE: A pathological connection between the heart and kidney is well recognized as a cardiorenal syndrome, but the underlying mechanism remains undetermined. We hypothesized that this connection is attributable to central haemodynamic alterations.

METHODS: In 386 patients with hypertension, the radial, carotid and femoral pressure waveforms were recorded with applanation tonometry to estimate the aortic pressure and pulse wave velocity (PWV). The plasma B-type natriuretic peptide (BNP) concentration and urinary albumin/creatinine ratio (UACR), cardiac and renal damage biomarkers, respectively, were also measured for each patient.

RESULTS: The BNP was correlated positively with UACR, aortic pulse pressure and PWV, but inversely with the estimated glomerular filtration rate (eGFR, P < 0.001). The aortic pulse pressure tended to more closely correlate with BNP than the brachial pulse pressure. The presence of (micro)albuminuria (UACR ≥30 mg/g) was associated with BNP elevation (≥50 pg/ml) independently of age, BMI, mean arterial pressure, eGFR and β-blocker treatment (odds ratio: 2.41; P = 0.04). However, further adjustment for the aortic pulse pressure or PWV rendered this albuminuria-BNP relationship insignificant (P = 0.25) and, instead, the aortic pulse pressure emerged as the strongest determinant of BNP elevation (odds ratio: 1.51 per 10mmHg; P = 0.001). Differently from albuminuria, lower eGFR was consistently related to higher plasma BNP, even after controlling for the aortic pressure and PWV.

CONCLUSION: Concomitant plasma BNP elevation with (micro)albuminuria can be explained by increases in aortic pulse pressure and PWV. This finding suggests that the altered central haemodynamics causes simultaneous damage/dysfunction in the heart and kidney, which could then contribute to cardiorenal syndrome in hypertension.