Heart failure therapies inducing an early decline in eGFR are associated with improved patient outcomes and a more gradual long-term decline in renal function.
Does an early decline in eGFR during the initiation of heart failure therapies indicate true worsening kidney function or a favorable hemodynamic adjustment?
Early declines in eGFR following the initiation of heart failure therapies reflect favorable intraglomerular hemodynamic changes rather than true renal injury, and are associated with improved long-term outcomes.
Background: Recent advancements in heart failure (HF) therapy have significantly enhanced the management of patients across all phenotypes of left ventricular ejection fraction. However, these multidrug regimens frequently induce alterations in renal function by influencing intrarenal hemodynamics, thereby modifying glomerular capillary pressure. This phenomenon could result in a mild to moderate decline in estimated glomerular filtration rate (eGFR), often classified as “worsening kidney function.” This nomenclature stems from consistent observations of eGFR reductions recorded during HF treatment in clinical trials. This narrative review aims to elucidate why the observed eGFR declines in clinical practice may represent either loss of functioning glomeruli or pharmacologically mediated reductions in intraglomerular pressure that ultimately safeguards long-term renal and cardiovascular outcomes. Methods: By a comprehensive re-examination of data from HF clinical trials conducted with various classes of medications, all affecting eGFR, we sought to provide evidence that the decline in eGFR is associated with the activation of specific mechanisms that collectively contribute to a reduction in glomerular filtration pressure, a prominent factor in maladaptive neurohormonal responses. Results: From the investigation of angiotensin-converting enzyme inhibitors to the more recent non-steroidal mineralocorticoid receptor antagonist, the renal effects of these therapeutic regimens correlate with improvements in patient outcomes. The data consistently indicate that an early decline in eGFR, when coupled with an enhancement in HF outcomes, is associated with a more gradual decline in eGFR during long-term follow-up. Conclusions: Clinicians should recognize early declines in eGFR as indicators of favorable intraglomerular hemodynamic adjustments that mitigate maladaptive neurohormonal responses and contribute to improved long-term outcomes in patients with HF.
Gronda et al. (Wed,) conducted a review in Heart failure. Heart failure therapies was evaluated. Heart failure therapies inducing an early decline in eGFR are associated with improved patient outcomes and a more gradual long-term decline in renal function.