Renal resistive index reflects Fontan pathophysiology and predicts mortality

The renal resistive index (RRI) reflects non-renal pathophysiology, such as great artery stiffness, haemodynamics and even end-organ damage in patients with hypertension. This study was conducted to clarify the clinical significance of the RRI in Fontan pathophysiology.

We measured the RRI in 280 consecutive Fontan patients and 36 healthy controls.

The patients exhibited a higher RRI than the controls (0.71±0.07 vs 0.60±0.04, p<0.0001). A high central venous pressure, low arterial pressure, greater pulse pressure and low arterial oxygen saturation (SaO₂) independently predicted a high RRI (p<0.05-0.0001). The RRI was inversely correlated with the peak oxygen uptake (PVO₂) and 24-hour creatine clearance, and was positively correlated with the plasma levels of brain natriuretic peptide (BNP) (p<0.0001 for all). The high RRI was also associated with liver dysfunction and postprandial hyperglycaemia during the oral glucose tolerance test (p<0.001). During the follow-up period, 18 patients died. Age, RRI, SaO₂, BNP, use of diuretics and antiarrhythmic drugs, and PVO₂ predicted mortality. When PVO₂ was excluded, RRI (HR: 1.13; 95% CI: 1.04 to 1.23; p<0.01) or RRI ≥0.81 (HR: 12.0; 95% CI: 3.4 to 50; p<0.0001) independently predicted mortality.

The RRI reflected heart failure severity, hepatorenal function and glucose intolerance, and predicted all-cause mortality in Fontan patients. Therefore, the RRI may be a useful marker of Fontan-associated multiorgan pathophysiology.