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What are the proposed biological mechanisms by which ivermectin could cause kidney injury?
Executive summary
Available studies and surveillance give mixed signals: clinical reviews and drug information generally state ivermectin is not known to cause kidney injury in humans [1] [2], but animal experiments and some small clinical observations report renal effects potentially linked to oxidative stress, mitochondrial dysfunction, altered antioxidant enzymes, and transient proteinuria after dosing [3] [4] [5]. Mechanistic work in renal cells and multiple rat studies point to mitochondria-targeted toxicity and oxidant/antioxidant imbalance as the most commonly proposed pathways [4] [6] [3].
1. Mitochondrial dysfunction: a direct cellular energy hit
Laboratory studies on renal cell models and renal cell carcinoma report that ivermectin can reduce mitochondrial membrane potential, impair mitochondrial respiration and lower ATP production; these changes produce an “energy crisis” that can trigger apoptosis and organelle dysfunction in kidney cells [4] [6]. In the cancer-cell work, antioxidants or mitochondrial fuels reversed ivermectin’s effects, which underscores mitochondria as a plausible mechanistic target [6]. These are in vitro and animal-focused findings; available clinical guidelines and major drug-safety summaries do not present mitochondria-mediated kidney injury as a common human effect [1] [2].
2. Oxidative stress and depleted antioxidant defenses
Multiple animal studies observed that ivermectin administration lowered activities of renal antioxidant enzymes and increased markers of oxidative damage; co‑treatment with antioxidants such as vitamin C attenuated histological and biochemical kidney damage in rats, suggesting reactive oxygen species (ROS) are involved [3] [7]. The mitochondrial dysfunction described above is mechanistically linked to excess ROS production — mitochondria both generate and are damaged by oxidative stress — making the two pathways complementary rather than exclusive [4] [3].
3. Matrix metalloproteinase activity and structural damage
Experimental rat work found increased matrix metalloproteinase‑9 (MMP‑9) activity after ivermectin, together with histopathological changes and impaired renal function tests; MMP‑9 elevation is a candidate mechanism because metalloproteinases remodel extracellular matrix and can worsen tissue injury and inflammation in kidney disease [3] [7]. These findings are from animal models and have not been established as a routine clinical pathway in human pharmacovigilance reports [2].
4. Transient glomerular/tubular changes seen after mass treatment campaigns
A clinical study of onchocerciasis patients reported a small but statistically significant rise in urinary albumin and alpha1‑microglobulin five days after ivermectin treatment, and higher short‑term proteinuria in patients with heavy microfilarial loads — suggesting transient glomerular and tubular perturbation after therapy [5]. Public-health mass‑treatment monitoring also documents mild liver and kidney parameter changes in populations under repeated ivermectin distribution, though authors described these as generally minor [8]. These clinical observations do not equate to established causal long‑term nephrotoxicity, but they show short‑term renal effects can occur in some contexts [5] [8].
5. Hemodynamic and indirect mechanisms — limited and inconsistent evidence
Some animal pharmacology reports and reviews note transient changes in renal blood flow and serum urea after antiparasitic dosing, which could impair renal secretory function and contribute to lab abnormalities; however, evidence for sustained hemodynamic kidney injury in humans is not found in the reviewed clinical summaries [9]. In clinical practice resources and drug side‑effect pages ivermectin is generally described as not known to cause kidney side effects in standard dosing [1] [2].
6. Conflicting results and context-dependence: dose, species, disease and co‑factors matter
Preclinical toxicity often appears at specific doses, regimens, or in younger animals (greater effect in juvenile rats was reported) and in cell systems that differ from normal human renal tissue; conversely, some animal studies show neutral or even protective effects depending on co‑exposures [10] [3]. Human safety literature emphasizes that ivermectin is largely eliminated in feces and typically does not need renal dose adjustment, which is consistent with a low intrinsic nephrotoxicity signal in routine clinical use [11] [12] [2].
7. What the sources do not say / remaining uncertainties
Available sources do not present large-scale human causality studies definitively linking ivermectin at approved doses to clinically meaningful acute kidney injury (AKI) or chronic kidney disease (not found in current reporting). They do not settle whether observed short‑term proteinuria or lab changes translate to long‑term harm or only reflect transient effects from parasite die‑off or dosing context [5] [8].
Bottom line for clinicians and the public: mechanistic and animal data point to mitochondrial toxicity, oxidative stress, MMP activation and transient hemodynamic or tubular changes as plausible ways ivermectin might harm kidneys under some conditions [4] [3] [6], but authoritative clinical summaries and large human trial reports generally do not list kidney injury as a common or established adverse effect at standard doses [1] [2]. Where concern exists — high doses, off‑label use, pediatric/juvenile exposure, co‑toxic drugs or preexisting CKD — closer monitoring and attention to emerging clinical data are reasonable given the preclinical signals [3] [9].