Abstract
The use of antineoplastic drugs has a central role in treatment of patients affected by cancer but is often associated with numerous electrolyte derangements which, in many cases, could represent life-threatening conditions. In fact, while several anti-cancer agents can interfere with kidney function leading to acute kidney injury, proteinuria, and hypertension, in many cases alterations of electrolyte tubular handling and water balance occur. This review summarizes the mechanisms underlying the disturbances of sodium, potassium, magnesium, calcium, and phosphate metabolism during anti-cancer treatment. Platinum compounds are associated with sodium, potassium, and magnesium derangements while alkylating agents and Vinca alkaloids with hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH). Novel anti-neoplastic agents, such as targeted therapies (monoclonal antibodies, tyrosine kinase inhibitors, immunomodulators, mammalian target of rapamycin), can induce SIADH-related hyponatremia and, less frequently, urinary sodium loss. The blockade of epidermal growth factor receptor (EGFR) by anti-EGFR antibodies can result in clinically significant magnesium and potassium losses. Finally, the tumor lysis syndrome is associated with hyperphosphatemia, hypocalcemia and hyperkalemia, all of which represent serious complications of chemotherapy. Thus, clinicians should be aware of these side effects of antineoplastic drugs, in order to set out preventive measures and start appropriate treatments.
Highlights
A series of electrolyte derangements can develop during treatment with anti-cancer drugs
The aim of this review is to analyze in detail the mechanisms underlying the disorders of the metabolism of sodium, magnesium, potassium, calcium, and phosphate during anti-cancer drug treatment
Related search terms were used as follow: (“Hyponatremia”[Mesh]) OR “Diabetes Insipidus, Neurogenic”[Mesh]) OR “Diabetes Insipidus, Nephrogenic”[Mesh]) OR “Hypokalemia”[Mesh]) OR “Magnesium Deficiency”[Mesh]) OR “Hypercalcemia”[Mesh]) OR “Hypocalcemia”[Mesh]) OR “Hypophosphatemia”[Mesh]) AND “Antineoplastic Agents”[Mesh])
Summary
A series of electrolyte derangements can develop during treatment with anti-cancer drugs. While some of these alterations may be paraneoplastic [1], in many cases specific pharmacodynamic mechanisms can be identified impacting on fluid and electrolyte metabolism. Besides the possible occurrence of acute kidney injury, proteinuria, and hypertension [2], several antineoplastic agents can affect electrolytes tubular handling, as well as urinary water excretion by interfering with antidiuretic hormone (ADH). The aim of this review is to analyze in detail the mechanisms underlying the disorders of the metabolism of sodium, magnesium, potassium, calcium, and phosphate during anti-cancer drug treatment
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