Renal function in patients with significant tricuspid regurgitation: pathophysiological mechanisms and prognostic implications

Abstract

Background: The pathophysiological mechanisms linking tricuspid regurgitation (TR) and chronic kidney disease (CKD) remain unknown. This study aimed to determine which pathophysiological mechanisms related to TR are independently associated with renal dysfunction and to evaluate the impact of renal impairment on long-term prognosis in patients with significant (≥ moderate) secondary TR.

Methods: A total of 1234 individuals (72 [IQR 63-78] years, 50% male) with significant secondary TR were followed up for the occurrence of all-cause mortality and the presence of significant renal impairment (eGFR of <60 mL min^-1 1.73 m^-2 ) at the time of baseline echocardiography.

Results: Multivariable analysis demonstrated that severe right ventricular (RV) dysfunction (TAPSE < 14 mm) was independently associated with the presence of significant renal impairment (OR 1.49, 95% CI 1.11 to 1.99, P = 0.008). Worse renal function was associated with a significant reduction in survival at 1 and 5 years (85% vs. 87% vs. 68% vs. 58% at 1 year, and 72% vs. 64% vs. 39% vs. 19% at 5 years, for stage 1, 2, 3 and 4-5 CKD groups, respectively, P < 0.001). The presence of severe RV dysfunction was associated with reduced overall survival in stage 1-3 CKD groups, but not in stage 4-5 CKD groups.

Conclusions: Of the pathophysiological mechanisms identified by echocardiography that are associated with significant secondary TR, only severe RV dysfunction was independently associated with the presence of significant renal impairment. In addition, worse renal function according to CKD group was associated with a significant reduction in survival.

Keywords: chronic kidney disease; renal dysfunction; right ventricular dysfunction; tricuspid regurgitation.

Fig. 1

Spline curves demonstrating the probability of significant renal impairment (eGFR <60 mL min⁻¹ 1.73 m⁻²) according to TAPSE in unadjusted (a) and adjusted models (b). The curve in panel a demonstrates the probability of significant renal impairment according to TAPSE measured at the time of index echocardiogram, with overlaid 95% confidence intervals displayed (shaded blue areas). The curve in panel b demonstrates the probability of significant renal impairment according to values of TAPSE, adjusted for age, diabetes mellitus, hypertension, ACEi/ARB use, diuretic use, aldosterone antagonist use, LV end‐diastolic volume, LV ejection fraction, the presence of significant MR, RV end‐diastolic area, tricuspid annulus diameter, TR regurgitant volume, estimated RAP and PASP. ACEi, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; eGFR, estimated glomerular filtration rate; LV, left ventricle; MR, mitral regurgitation; PASP, pulmonary artery systolic pressure; RAP, right atrial pressure; RV, right ventricle; TAPSE, tricuspid annular plane systolic excursion; TR, tricuspid regurgitation.

Fig. 2

Kaplan–Meier estimates for all‐cause mortality stratified by renal function group and according to the presence of severe RV dysfunction (TAPSE < 14 mm). The Kaplan–Meier curves demonstrate reduced survival with worsening renal function (panel A) and the improved survival rates of patients with TAPSE ≥ 14 mm (blue line) compared to those with TAPSE <14 mm (red line) in renal function stage 1 (panel b), 2 (panel c) and 3 (panel d) CKD. For patients with severe renal impairment (stage 4 and 5 CKD, eGFR <30 mL min⁻¹ 1.73 m⁻²), the presence of severe RV dysfunction did not portend a worse prognosis (panel e). CKD, chronic kidney disease; GFR, glomerular filtration rate; TAPSE, tricuspid annular plane systolic excursion.

Fig. 3

Pathophysiological interactions between the right ventricle and kidney in significant tricuspid regurgitation. CVP, central venous pressure; EDV, end‐diastolic volume; LV, left ventricle; MAP, mean arterial pressure; RV, right ventricle; SV, stroke volume; TR, tricuspid regurgitation.