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Effect of furosemide on left ventricular mass in non-dialysis chronic kidney disease patients: a randomized
Pasquale Zamboli1, Luca De Nicola, Roberto Minutolo
1Division of Nephrology, Second University of Naples, Naples, Italy. roberto.minutolo@unina2.it
Insights
Loop diuretics like furosemide effectively reduce left ventricular mass index (LVMI) in patients with chronic kidney disease (CKD). This reduction in LVMI is linked to better volume management, not just blood pressure changes.
Area of Science:
- Nephrology
- Cardiology
- Pharmacology
Background:
- Chronic kidney disease (CKD) patients often have volume-dependent hypertension.
- Loop diuretics are used to manage hypertension in CKD, but their impact on left ventricular mass index (LVMI) is not well understood.
Purpose of the Study:
- To investigate the effect of furosemide on LVMI in hypertensive CKD patients.
- To assess the safety and efficacy of furosemide in this patient population.
Main Methods:
- A randomized controlled trial involving 40 hypertensive CKD patients on renin-angiotensin system (RAS) inhibitors.
- Patients were assigned to receive either furosemide or a non-diuretic antihypertensive treatment (control).
- The primary endpoint was the change in LVMI after 52 weeks, with blood pressure targets of <130/80 mmHg.
Main Results:
- Both groups achieved similar reductions in office blood pressure.
- Furosemide treatment led to a significantly greater reduction in LVMI compared to the control group.
- Extracellular water (ECW) decreased with furosemide, and this change correlated with LVMI reduction; no significant side effects were reported.
Conclusions:
- Add-on furosemide effectively reduces LVMI in hypertensive CKD patients on RAS inhibitors, independent of blood pressure changes.
- The beneficial effect of furosemide on LVMI may be mediated by improved control of volume expansion.
Background:
In chronic kidney disease (CKD), loop diuretics correct volume-dependent hypertension, but their effect on left ventricular mass index (LVMI) is unknown.
Methods:
Forty hypertensive CKD patients (estimated creatinine clearance 60-15 mL/min/1.73 m²), treated with renin-angiotensin system (RAS) inhibitors, were randomized to receive furosemide or non-diuretic antihypertensive treatment (control group). Office blood pressure (BP) < 130/80 mmHg was pursued in both groups. Primary end point was the reduction of LVMI after 52 weeks. Secondary aims were to verify safety related to furosemide treatment and its effects on ambulatory and clinic BP and body fluid volumes.
Results:
Office BP similarly declined in the furosemide group (from 161 ± 14/80 ± 10 to 139 ± 14/74 ± 8 mmHg) and in controls (from 159 ± 16/81 ± 10 to 137 ± 16/75 ± 10 mmHg). We detected a greater reduction (P = 0.013) of LVMI in patients receiving furosemide (-7.9, IQR from -15.8 to -1.4 g/h(2.7)) than in controls (0.0, IQR from -6.2 to + 9.5 g/h(2.7), P = 0.013). Bio-impedance analysis-derived extracellular water (ECW) significantly decreased in furosemide-treated patients (from 18.7 ± 3.9 to 17.7 ± 3.3 L) while remained unchanged in the control group (from 19.5 ± 2.2 to 19.6 ± 1.9 L). Absolute change of LVMI correlated with changes of ECW in furosemide-treated patients (r = 0.458, P = 0.042) but not in controls. In the furosemide group, no patient experienced side effects requiring drug withdrawal.
Conclusions:
In hypertensive CKD patients treated with RAS inhibitors, add-on furosemide efficaciously reduces LVMI independently from BP changes. The effect is possibly mediated by better control of volume expansion.
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