Key result
In patients with chronic left-heart failure, the presence of pulmonary hypertension did not significantly affect the last estimated GFR compared to those without pulmonary hypertension (52 vs 49 mL/min/1.73 m2, p=0.62).
Why the study?
The clinical and hemodynamic factors associated with changes in renal function in patients with pulmonary hypertension secondary to chronic heart failure were not well understood.
Does pulmonary hypertension affect renal function dynamics in patients with chronic left-heart failure?
Cohort (n=108)
No
Does pulmonary hypertension affect renal function dynamics in patients with chronic left-heart failure?
Absolute Event Rate: 52% vs 49%
p-value: p=0.62
Renal function decline in left heart failure is driven by baseline creatinine, age, diabetes, low LVEF, and MRA use, with a distinct non-linear GFR decline pattern in those with concurrent pulmonary hypertension.
Renal monitoring in left-heart failure need not prioritize pulmonary hypertension; leaves open independent roles of baseline creatinine, diabetes, and low LVEF for prospective study.
Objectives: Cardiorenal syndrome (CRS) is a complex disorder characterized by concurrent dysfunction of the heart and kidneys, with their detrimental effects perpetuating a bidirectional cycle. This study aimed to examine the clinical and hemodynamic factors associated with changes in renal function in patients with pulmonary hypertension (PH) secondary to chronic heart failure (HF). Methods: A total of 108 patients with HF were evaluated using right-heart catheterization. Results: 75 patients (69.4%) were diagnosed with PH. The mean baseline estimated GFR (beGFR) was similar in noPH (64 ± 21 mL/min/1.73 m2) and PH group (63 ± 23 mL/min/1.73 m2) (p = 0.71). After a median follow-up of 7 months, the last eGFR (leGFR) in the noPH and PH groups was comparable (49 ± 24 vs. 52 ± 25 mL/min/1.73 m2 respectively; p = 0.62). However, in the PH group, for patients with baseline Cr (bCr) < 1.5 mg/dL, the reduction in eGFR showed a graded inverse relationship to serum creatinine, as compared with bCr ≥ 1.5 mg/dL, for whom beGFR and leGFR demonstrated large overlap. In a multivariable regression analysis, the primary independent predictors of leGFR were baseline creatinine, age, diabetes mellitus, left ventricular ejection fraction below 45%, and use of mineralocorticoids antagonists. The model explained 66% of the variance in leGFR. Conclusions: In a cohort of left HF and PH, an inverse non-linear and graded association between the baseline serum creatinine levels and the variation in estimated GFR was demonstrated, contrary to those without PH, for whom this relationship was linear and constant. The distinct patterns of GFR decline influenced by age, low ejection fraction, diabetes, and mineralocorticoid underscore the need for individualized treatment strategies.
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Dragu et al. (2025) conducted a cohort in Chronic left-heart failure (n=108). Pulmonary hypertension vs. No pulmonary hypertension was evaluated on Last estimated GFR (leGFR) (p=0.62). In patients with chronic left-heart failure, the presence of pulmonary hypertension did not significantly affect the last estimated GFR compared to those without pulmonary hypertension (52 vs 49 mL/min/1.73 m2, p=0.62).
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