Kidney Toxicity of Drugs for the Heart: An Updated Perspective
Abstract
:1. Introduction
2. Mechanisms of Drug-Induced Nephrotoxicity
2.1. Changes in Glomerular Hemodynamics
2.2. Tubular Cell Toxicity
2.3. Inflammation
2.4. Crystal Nephropathy
2.5. Rhabdomyolysis
2.6. Thrombotic Microangiopathy
3. Renal Toxicity of Cardiovascular Drugs
3.1. Diuretics
3.2. Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers
3.3. Calcium Channel Blockers
3.4. Beta-Blockers
3.5. Antiplatelet Agents
3.6. Anticoagulants
3.7. Statins
3.8. Proton-Pump Inhibitors
3.9. Contrast Media
4. Role of Oxidative Stress in Drug-Induced Nephrotoxicity
- developing novel and specific biomarkers of oxidative stress and drug-induced nephrotoxicity that can reflect the degree and location of renal injury, predict the risk and outcome of drug-induced nephrotoxicity, monitor the response to treatment, and guide personalized therapy [10];
- identifying novel and effective antioxidants that can target specific sources or pathways of oxidative stress and drug-induced nephrotoxicity, modulate redox signaling, protect renal cells and tissues from oxidative damage, and preserve or restore renal function [192];
- designing personalized and precise antioxidant therapy based on individual characteristics and needs, such as genetic background, epigenetic modifications, comorbidities, co-administered drugs, environmental factors, and oxidative stress status;
- exploring the potential synergistic or additive effects of combining antioxidant therapy with other therapeutic modalities, such beta-blockers [193];
- assessing the long-term benefits and risks of antioxidant therapy for drug-induced nephrotoxicity on various clinical outcomes, such as renal function preservation, cardiovascular protection, quality of life improvement, and survival extension.
5. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Glomerulus | Tubules | Other Renal Toxic Effects | Factors That Enhance Toxicity | |
---|---|---|---|---|
Diuretics (loop) | Reduction of RBF and GF | Obstruction (Tamm–Horsfall protein formation) | Paradoxical stimulation of RAAS | ACEIs/NSAIDs |
ACEIs and ARBs | Reduced IG-P (dilation Eart) | - | - | NSAIDs and diuretics (triple whammy) |
CCBs | Increase IG-P (dilation Aart) (more proteinuria) | - | - | CYP3A4 inhibitors (Clarithromycin) |
BBs | Decrease in GFR (mild) | - | - | - |
APAs | Decrease in GFR for intense vasoconstriction (PGEi) | AIN | - | Dehydration, HF, LC, sepsis, diuretics, and ACEIs; statins |
ACs | Occlusive casts Bowman space | Occlusive cast | - | Dehydration |
Statins | - | TIN | Suppression Q10 | Rhabdomyolysis |
PPIs | - | TIN | Hypomagnesemia | Enteric infection |
CM | Vasospasm | Direct tubular cell damage | - | Hypotension, microembolism, and bleeding; metformin |
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Caiati, C.; Arrigoni, R.; Stanca, A.; Lepera, M.E. Kidney Toxicity of Drugs for the Heart: An Updated Perspective. Metabolites 2025, 15, 191. https://doi.org/10.3390/metabo15030191
Caiati C, Arrigoni R, Stanca A, Lepera ME. Kidney Toxicity of Drugs for the Heart: An Updated Perspective. Metabolites. 2025; 15(3):191. https://doi.org/10.3390/metabo15030191
Chicago/Turabian StyleCaiati, Carlo, Roberto Arrigoni, Alessandro Stanca, and Mario Erminio Lepera. 2025. "Kidney Toxicity of Drugs for the Heart: An Updated Perspective" Metabolites 15, no. 3: 191. https://doi.org/10.3390/metabo15030191
APA StyleCaiati, C., Arrigoni, R., Stanca, A., & Lepera, M. E. (2025). Kidney Toxicity of Drugs for the Heart: An Updated Perspective. Metabolites, 15(3), 191. https://doi.org/10.3390/metabo15030191