Searched over 200M research papers
10 papers analyzed
Some studies suggest lisinopril can improve kidney function and prevent damage in various conditions, while other studies indicate it may worsen renal azotaemia in certain patients.
11 papers analyzed
20 papers analyzed
Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is widely used to manage hypertension, heart failure, and chronic kidney disease. Given its extensive use, understanding its impact on kidney function is crucial, especially concerning potential kidney damage.
Several studies have investigated the effects of lisinopril on kidney function in patients with diabetic nephropathy. Research comparing lisinopril to atenolol in hypertensive non-insulin-dependent diabetes mellitus (NIDDM) patients with diabetic nephropathy found that both drugs effectively reduced the decline in kidney function. However, lisinopril was more effective in reducing urinary albumin excretion, a marker of kidney damage, suggesting a protective effect rather than causing harm .
In hypertensive rat models induced by Nω-nitro-L-arginine methyl ester (L-NAME), lisinopril demonstrated significant renoprotective effects. It reduced oxidative stress markers and improved renal function parameters, indicating that lisinopril can mitigate renal damage caused by hypertension-related oxidative stress.
In a rat model of unilateral ureteral obstruction, lisinopril was shown to prevent early renal damage. The treated group exhibited fewer signs of renal injury and apoptosis compared to the untreated group, suggesting that lisinopril may protect against certain types of kidney damage.
A long-term study comparing lisinopril to nisoldipine in hypertensive type 1 diabetic patients with diabetic nephropathy found that both drugs had similar beneficial effects on kidney function over four years. Lisinopril significantly reduced albuminuria, a key indicator of kidney damage, further supporting its protective role.
The EURODIAB Controlled Trial of Lisinopril in IDDM patients highlighted that the ACE gene polymorphism might influence the progression of renal disease and the efficacy of lisinopril. Patients with the II genotype showed a significant reduction in albumin excretion rate when treated with lisinopril, indicating a potential genetic predisposition to benefit from ACE inhibitors.
In children with sickle cell anemia and microalbuminuria, lisinopril significantly reduced microalbuminuria, suggesting it can delay the progression of kidney damage in this population. This finding underscores lisinopril's potential protective effects on the kidneys.
Despite the generally protective effects observed in various studies, there are isolated reports of adverse renal outcomes associated with lisinopril. For instance, a case report described worsening renal azotemia in a patient with secondary hypertension, which was attributed to lisinopril therapy. This highlights the need for careful monitoring of kidney function in certain patients.
Overall, the majority of research indicates that lisinopril does not cause kidney damage; rather, it often provides a protective effect against renal decline, particularly in patients with diabetic nephropathy, hypertension-induced oxidative stress, and sickle cell nephropathy. However, individual responses can vary, and adverse effects, though rare, necessitate vigilant monitoring.
Most relevant research papers on this topic