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. 2020 Dec 1;10(12):4151–4164.

Table 1.

List of chemotherapy agents which cause nephrotoxicity

Nephrotoxic mechanism Associated conditions Management References
Alkylating agents Damage to proximal and distal tubules by metabolites and increased cellular oxidative stress SIADH induced severe hyponatremia, Fanconi’s syndrome in children Hyponatremia management with continuous infusion or bolus hypertonic saline; adequate hydration; AVP (V2) receptor antagonist (tolvaptan); Mesna or N-acetylcysteine electrolyte monitoring; discontinuation [3,32,33,99-101]
    Cyclophosphamide
    Ifosfamide
Cytotoxic agents Drug accumulation in proximal tubules resulting in proximal tubular dysfunction AKI, TMA, Fanconi’s syndrome, salt-wasting hyponatremia, Hypomagnesemia Aggressive Short-duration, low-volume hydration; dose adjustment for preexisting renal impairments; magnesium supplementation; mannitol supplementation for preexisting renal impairment and high-dose cisplatin; Forced diuresis; Amifostine radical scavenger; discontinuation; eculizumab for TMA resolution [3,21,25]
    Cisplatin
    Carboplatin
Antimetabolites Vasoconstriction of afferent arteries, reducing GFR; crystal precipitation in renal tubules Tubular acidosis, AKI, SIADH induced hyponatremia, hemolytic uremic syndrome and TMA Urinary alkylation, hydration, high-flux hemodialysis, carboxypeptidase-G(2) (CPDG2), leucovorin rescue; oral corticosteroids; hyponatremia management with hypertonic saline infusion, fluid restriction, AVP (V2) receptor antagonist (tolvaptan); discontinuation [3,28,29]
    Methotrexate
    Pemetrexed
    Gemcitabine
Vinca Alkaloids Neurotoxic effect on hypothalamus-pituitary axis resulting in altered osmotic control of ADH SIADH induced hyponatremia Hyponatremia management with continuous infusion or bolus hypertonic saline, fluid restriction, AVP (V2) receptor antagonist (tolvaptan); discontinuation [3,101-103]
    Vincristine
    Vinblastine
Antitumor antibiotics Induced glomerular endothelial cell and podocyte apoptosis, mesangiolysis Focal segmental glomerular sclerosis, nephrotic syndrome, hemolytic uremic syndrome, TMA, AKI Eculizumab for TMA resolution; nephrotic syndrome management through fluid and sodium restriction, oral or IV diuretics, and ACE inhibitors or ARBs [3,104-107]
    Doxorubicin
    Mitomycin C
Proteasome inhibitors Decreased vascular endothelial growth factor (VEGF) synthesis resulting in TMA; increased ADH secretion and effect on kidneys Acute interstitial nephritis, TMA, AKI, Tumor lysis syndrome, SIADH induced hyponatremia Glucocorticoid therapy for management of interstitial nephritis (inconclusive); N-acetyl-l-cysteine upon chemotherapy re-challenge (inconclusive); Hyponatremia management with continuous infusion or bolus hypertonic saline, fluid restriction, AVP (V2) receptor antagonist (tolvaptan); discontinuation [3,39,40,51,108]
    Bortezomib
    Carfilzomib