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Table 2 Glomerular, tubular, and interstitial damage to the kidney caused by medications

From: Moving toward a contemporary classification of drug-induced kidney disease

Type of damage

Examples

Glomerular/vascular

Minimal change disease

Interferon alpha & beta, Lithium

Focal segmental glomerulosclerosis

Bisphosphonates (especially pamidronate and zoledronic acid), Lithium

Membranous nephropathy

Penicillamine, Anti-tumor necrosis factor agents

Vasculitis

Hydralazine, Propylthiouracil, Allopurinol, Phenytoin, Penicillamine, Minocycline

Thrombotic microangiopathy

Gemcitabine, Bevacizumab, Interferon alpha, Ticlopidine, Clopidogrel, Oral contraceptives

Cholesterol emboli

Warfarin, Streptokinase, Alteplase

Tubular

Acute tubular injury/necrosis

Aminoglycosides, Vancomycin, Colistin, Foscarnet, Pentamidine, Tenofovir, Cisplatin, Carboplatin, Zoledronic acid

Fanconi syndrome

Tenofovir, Sodium valproate, Deferasirox

Obstructive nephropathy

Acyclovir, Sulfonamides, Methotrexate, Indinavir, Atazanavir, Triamterene, Sodium phosphate

Rhabdomyolysis

Lovastatin, Simvastatin

Tumor lysis syndrome

Cytotoxic agents, Glucocorticoids

Osmotic nephrosis

Intravenous immunoglobulin, Hydroxyethyl starch

Nephrogenic diabetes insipidus

Lithium

Nephrogenic syndrome of inappropriate antidiuresis

Carbamazepine, Haloperidol, Cyclophosphamide, Selective serotonin reuptake inhibitors

Interstitial

Acute tubulointerstitial nephritis

Beta-lactam antibiotics, Rifampin, Aminosalicylates, Proton pump inhibitors

Chronic tubulointerstitial nephritis

Lithium, Aristolochic Acid

  1. The prevailing etiology of nephrotoxicity of these medications or medication classes is direct/indirect toxic effects on the kidney. Therefore, they mostly belong to the “damage without dysfunction” category. Notably, these medications may have more than one aspect of kidney damage. For example, apart from glomerular changes, cholesterol emboli induced by warfarin, streptokinase, or alteplase can also affect the peritubular microcirculation, leading to tubular damage. Similarly, in the case of crystal nephropathy caused by medications, both direct and indirect mechanisms are usually involved. Therefore, this table lists only some examples of medications/medication classes and should not be considered conclusive. In addition, this table does not consider medications with both damage and dysfunction features such as nonsteroidal anti-inflammatory drugs, amphotericin B, and calcineurin inhibitors