Can long-term ivermectin use lead to liver or kidney damage?

1. Why routine monitoring is still recommended despite reassuring population data

Large-scale public-health experience and recent randomized trials describe ivermectin as generally safe when used at recommended doses: mass drug-administration cohort monitoring in Tanzania found a 4.8% adverse event rate, mostly mild and resolving within days, and a 2025 phase 3 cluster-randomised trial reported good tolerability and no signal of increased hepatic or renal harm over repeated community dosing ^{[1] [2]}. These programmatic data cover thousands of participants and emphasize that common side effects are non-severe, but they do not fully rule out rare idiosyncratic reactions. Mass administration studies typically monitor short-term events and lack the power to reliably detect very rare organ-specific toxicities that might emerge only in susceptible individuals or after prolonged, unsupervised use. Public-health safety therefore rests on continued pharmacovigilance and targeted monitoring in high-risk subgroups rather than on assumptions of absolute absence of risk.

2. Case reports that change the narrative: single-patient severe liver injury

Several case reports document clinically apparent liver injury temporally linked to ivermectin exposure, including reports of liver failure and biopsy-proven drug-induced liver injury that resolved after stopping the drug and, in one case, treating with corticosteroids ^{[4] [5]}. Case reports cannot establish incidence or causality for the general population, but they identify plausible, serious outcomes that randomized trials and mass-administration surveillance might miss. These reports often lack complete dosing histories or information about concomitant medicines and comorbidities, limiting interpretability; nevertheless, they demonstrate that idiosyncratic hepatotoxicity is possible and that clinicians should consider recent ivermectin exposure when evaluating unexplained liver injury.

3. Animal and mechanistic signals: nephrotoxicity in experimental models

Experimental work in juvenile and adult rats showed kidney structural and functional changes after repeated ivermectin dosing, including altered antioxidant enzyme activity and glomerular changes, with partial protection from co-administered vitamin C ^[6]. Animal models identify biologically plausible mechanisms for nephrotoxicity but do not directly predict human risk at therapeutic doses. Translational gaps include differences in dosing, metabolism, and developmental stage; juvenile rat findings emphasize caution in young or otherwise vulnerable patients. Animal evidence therefore serves as a signal that deserves targeted human research and cautious clinical practice rather than proof that routine therapeutic use causes widespread renal damage.

4. Weighing the total evidence: population safety versus rare serious events

Authoritative safety reviews list ivermectin as unlikely to cause frequent severe liver injury, noting only rare cases and mostly transient aminotransferase elevations; no pattern of acute liver failure or chronic liver disease has emerged from systematic surveillance ^[3]. This contrasts with isolated human case reports and localized studies suggesting kidney parameter changes in treated populations ^{[7] [5]}. The balanced interpretation is that ivermectin’s population-level safety profile is strong, but the literature contains credible, if rare, signals of organ-specific toxicity. Differences in study designs — randomized trials, cohort monitoring, case reports, and animal experiments — explain much of the apparent conflict: large studies show low overall risk, while small or individual studies highlight exceptions.

5. Practical guidance drawn from the evidence and unresolved gaps

Clinicians and public-health programs should continue routine use of ivermectin for approved indications while maintaining active pharmacovigilance, counseling against unsupervised long-term or high-dose self-medication, and evaluating liver and kidney function when clinically indicated or when treating patients with pre-existing organ disease ^{[1] [5] [3]}. Research gaps include robust longitudinal human studies on chronic or repeated high-dose exposure and mechanistic work linking animal findings to human outcomes; until those gaps are filled, rare idiosyncratic hepatotoxicity and potential renal effects remain plausible though uncommon. Public messaging must therefore balance the well-documented community-level safety with transparent acknowledgment of rare but serious individual harms and the importance of medical supervision.