Table 1.

Platinum derived drugs.

Electrolyte disorder	Drug	Incidence (%) Type of study	Mechanism(s)
Hyponatremia	Cisplatin Carboplatin	43-59 (B) (29, 30) 20 (C) (31)	SIADH; RSWS, DNA damage of the gene encoding the thiazide-sensitive chloride channel (29, 32–34)
Hypernatremia	Platinum-drugs	n.a.	Acquired NDI (32)
Hypokalemia	Cisplatin Carboplatin	27 (D,B) (31, 35)	Renal potassium wasting due to hypomagnesemia; Decreased intestinal absorption due to enterocyte cytoxicity (35, 36)
Hypomagnesemia	Cisplatin Carboplatin	56-90 (B, D) (22, 23, 37) 7-29 (D) (38–40)	Calcium-sensing receptor impairment; TRPM6/EGF pathway downregulation (18, 22, 41) Gitelman-like syndrome (42)
Hypocalcemia	Cisplatin Carboplatin	6-20 (B, D) (43) 16-31 (B, D) (43)	Impaired PTH release due to hypomagnesemia (24, 44, 45) Altered bone metabolism due to hypomagnesemia; Low vitamin D due to decreased 1-alpha-OHase activity (24, 43, 46)
Hypophosphatemia	Cisplatin alone (combined with Cyclophosphamide)	10-77 (D) (47, 48)	Partial proximal tubular damage; Acquired FS (47, 49)

Incidence and type of study column: the letter after the percentage indicates the type of evidence available: A isolated case; B case series; C pharmacovigilance notifications or registry; D observational study, clinical trial, metanalysis of clinical trials. n.a. not available. References in bracket square. FS = Fanconi Syndrome; NDI, Nephrogenic Diabetes Insipidus; PTH, Parathyroid hormone; RSWS = Renal Salt Wasting Syndrome; SIADH, Syndrome of inappropriate antidiuretic hormone secretion; TRPM6, Transient Receptor Potential Cation Channel, subfamily M, member 6/EGF = Epidermal Growth Factor.