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These studies suggest that lisinopril has renoprotective effects by reducing albuminuria, controlling blood pressure, and slowing kidney disease progression, with potential benefits when combined with other treatments, although combination therapy with an ARB may increase adverse events.
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Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is widely used for managing hypertension and heart failure. Recent studies have also highlighted its potential benefits in protecting kidney function, particularly in patients with diabetic nephropathy and other chronic kidney diseases (CKD).
Several studies have compared the effects of lisinopril with other antihypertensive agents in patients with diabetic nephropathy. One study compared lisinopril with atenolol in hypertensive non-insulin-dependent diabetes mellitus (NIDDM) patients. Both drugs effectively reduced blood pressure, but lisinopril significantly reduced albuminuria by 45% compared to 12% with atenolol, indicating better kidney protection . Another study compared lisinopril with nisoldipine, a calcium antagonist, in type 1 diabetic patients. Lisinopril reduced albuminuria by 52%, whereas nisoldipine showed no significant change, suggesting superior renoprotective effects of lisinopril.
Long-term studies have also demonstrated the benefits of lisinopril in slowing the progression of kidney disease. A 42-month study showed that lisinopril and atenolol both effectively reduced the decline in glomerular filtration rate (GFR), but lisinopril had a more pronounced effect on reducing urinary albumin excretion. Another study highlighted that lisinopril, when combined with avosentan, an endothelin receptor antagonist, provided complete protection from tubulointerstitial damage and induced regression of glomerular lesions in diabetic nephropathy.
Lisinopril has also shown promise in non-diabetic nephropathies. A study involving patients with mild proteinuria (<1.0 g/day) and chronic renal insufficiency demonstrated that lisinopril was more effective than other antihypertensive agents in slowing the progression of kidney disease. The study found a significant difference in the decline of renal function between the lisinopril group and the control group, supporting the specific renoprotective effect of ACE inhibitors.
In experimental models of adriamycin nephropathy, lisinopril reduced proteinuria and prevented glomerulosclerosis. The study suggested that the antiproteinuric effect of lisinopril could predict its long-term renoprotective benefits. Another study indicated that lisinopril might attenuate adriamycin-induced kidney injury by controlling blood pressure and modulating renalase expression and secretion.
Combining lisinopril with other agents has shown enhanced renoprotective effects. For instance, combining lisinopril with L-arginine, a precursor of nitric oxide, significantly reduced proteinuria and improved renal function in a rat model of membranous nephropathy. This combination therapy also normalized exaggerated urinary endothelin-1 levels, suggesting a synergistic effect in halting disease progression.
Moderate swimming exercise combined with lisinopril also showed beneficial effects in a rat model of adenine-induced CKD. The combination improved histopathological kidney parameters more effectively than exercise alone, indicating that physical activity might enhance the nephroprotective effects of lisinopril.
Lisinopril has demonstrated significant potential in protecting kidney function across various types of nephropathies, particularly in diabetic nephropathy. Its ability to reduce proteinuria and slow the progression of kidney disease makes it a valuable therapeutic option. Additionally, combination therapies involving lisinopril and other agents or lifestyle modifications may offer enhanced renoprotective benefits. Further long-term studies are needed to fully understand the implications of these findings and optimize treatment strategies for kidney protection.
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