Do Renal Benefits with Sacubitril/Valsartan in HF Depend on the Kidney Endpoint Used?

When is a creatinine rise after starting sacubitril/valsartan acceptable, and when should I refer?

Continue and recheck if the creatinine rise is small and the patient is clinically stable; refer or escalate if the rise is marked, progressive, or accompanied by hyperkalaemia, hypotension, volume depletion, or low eGFR. For most RAAS-blocking therapy principles used for sacubitril/valsartan, a creatinine rise up to a

Why can eGFR slope and albuminuria give different impressions of renal benefit?

eGFR slope and albuminuria reflect different biological dimensions of CKD, so they do not always move in parallel and may suggest different magnitudes—or even directions—of renal benefit. Albuminuria mainly tracks glomerular barrier injury/hemodynamic stress, whereas eGFR slope reflects the net change in filtration ove

Which renal endpoint should carry the most weight when judging ARNI benefit in HF with CKD?

When judging ARNI renal benefit in heart failure with CKD, the endpoint that should carry the most weight is a hard kidney outcome composite: sustained major loss of kidney function (preferably ≥50% eGFR decline), progression to kidney failure/ESRD, or renal death. If hard renal events are too infrequent for practical

How should sacubitril/valsartan be managed when eGFR falls below 30 but HF benefit remains evident?

If eGFR falls below 30 mL/min/1.73 m² but sacubitril/valsartan is clearly improving heart failure status, the default approach is usually not automatic discontinuation. Available trial analysis suggests that clinical benefit can persist even after renal function declines below this threshold, without a clear excess saf

How can haemodynamic eGFR decline be distinguished from true AKI during ARNI and diuretic titration?

During ARNI and loop diuretic titration, a small early fall in eGFR / rise in creatinine is often haemodynamic rather than structural kidney injury, especially if the patient is clinically decongesting, haemodynamically stable, non-oliguric, and without progressive hyperkalaemia. With RAAS-pathway drugs, a creatinine r