Hypomagnesemia and Renal Magnesium Wasting in Patients Treated With Cisplatin

Lam, Mildred; Adelstein, David J.

doi:10.1016/s0272-6386(86)80020-8

Cited by 85 publications

(40 citation statements)

References 12 publications

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“…Prior studies have found inconsistent relationships between CD of cisplatin and long-term declines in GFR (1,12,19,(22)(23)(24). Dose intensity and frequency have been previously shown to correlate with cisplatin nephrotoxicity (24).…”

Section: Discussionmentioning

confidence: 99%

Long–Term Renal Outcomes after Cisplatin Treatment

Latcha

Jaimes

Patil

et al. 2016

CJASN

177

125

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Background and objectives Nephrotoxicity remains the dose-limiting side effect of cisplatin, an effective chemotherapeutic agent with applications across diverse tumor types. This study presents data on renal outcomes across multiple tumor types in 821 adults. We report on incidence of AKI, initial and long-term changes in eGFR after cisplatin, and relationships between cumulative dose, initial eGFR, age, sex, and long-term renal function.Design, setting, participants, & measurements This was a retrospective study of adult patients treated with cisplatin from January 1, 2000 to September 21, 2011 who had survived $5 years after initial dose. The Modification of Diet in Renal Disease equation was used to calculate eGFR. AKI was defined as an increase from the baseline creatinine of .25% within 30 days after the first cycle of cisplatin. Chi-squared tests were done to evaluate the relationships between categorical or ordinal variables; ANOVAs or t tests were used to evaluate continuous or categorical variables. Changes in eGFR over time were evaluated in a growth curve model.Results Mean follow-up was 6 years (25th and 75th percentiles, 4 and 9 years). AKI occurred in 31.5% of patients, with a median initial decline in eGFR of 10 ml/min per 1.73 m 2 (25th and 75th percentiles, 241.5 and 223.3 ml/min per 1.73 m 2 ). At any time point after the first cycle of cisplatin, ,3% of patients progressed to eGFR,29 ml/min per 1.73 m 2 , and none were known to be on dialysis. Age was associated with a higher risk for AKI after cisplatin. Compared with age ,25 years old, the odds ratios for AKI versus no AKI are 1.22 for .26-44 years old (95% confidence interval [95% CI], 0.60 to 2.4), 1.54 for .45-65 years old (95% CI, 0.78 to 3), and 2.96 for .66 years old (95% CI, 1.4 to 6.1). The lowest dose categories of cisplatin (#100 and 101-250 mg/m 2 ) are associated with increases in eGFR (P=0.06 and P=0.02, respectively) compared with the highest dose category (.701 mg/m 2 ).Conclusions This is the largest study of adult patients with cancer who received cisplatin for treatment across multiple tumor types. Most patients experience small but permanent declines in eGFR, but none progressed to ESRD requiring hemodialysis.

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Section: Discussionmentioning

confidence: 99%

Long–Term Renal Outcomes after Cisplatin Treatment

Latcha

Jaimes

Patil

et al. 2016

CJASN

177

125

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“…The efficacy of administering high-dose cisplatin has been confirmed; however, severe adverse events, including hematotoxicity, anorexia, nausea and nephrotoxicity have been also reported (3,6,7). Large amounts of hydration with saline, mannitol and furosemide are accepted as the standard of care for patients treated with regimens containing high-dose (≥60 mg/m 2 ) cisplatin (3,10,11).…”

Section: Discussionmentioning

confidence: 99%

“…5 is a schema for the rationale of the present study. Cisplatin induces renal Mg wasting and hypomagnesemia through its renal toxicity by directly injuring the mechanisms of Mg reabsorption (6,7,28). Hypomagnesemia reduces the expression of certain transporters in renal tubules in order to maintain serum Mg concentrations.…”

Section: Discussionmentioning

confidence: 99%

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Influence of magnesium and parathyroid hormone on cisplatin-induced nephrotoxicity in esophageal squamous cell carcinoma

et al. 2017

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Abstract. Magnesium (Mg) supplementation has previously been demonstrated to confer protective effects against nephrotoxicity induced by cisplatin. Parathyroid hormone (PTH) regulates Mg homeostasis. The aim of present study was to determine the protective effects of Mg supplementation against cisplatin-induced nephrotoxicity and its association with PTH levels in patients with esophageal squamous cell carcinoma (ESCC). A total of 55 patients with primary ESCC who received chemotherapy with high-dose cisplatin were examined. Mg was administered intravenously, and serum concentrations of PTH, parathyroid hormone-related protein (PTH-rP), creatinine and Mg were prospectively measured. Of the 55 patients, 37 received Mg supplementation. Post-chemotherapeutic creatinine concentrations were significantly increased in patients without Mg supplementation (P=0.01), with grade 1 and 2 increases of 22.2 and 5.6%, respectively, whereas these increases were suppressed by Mg supplementation (change in creatinine, P=0.21), with grade 1 and 2 increases of 8.1 and 0%, respectively. In addition, PTH and PTH-rP concentrations were high in 8 (14.5%) and 6 (10.9%) of all 55 patients, respectively. Alterations in creatinine concentrations (post-/pre-chemotherapy) due to chemotherapy were higher in patients with high levels of PTH regardless of Mg supplementation (P<0.01). Pre-therapeutic creatinine concentrations did not correlate with the alterations in creatinine concentrations due to chemotherapy. Intravenous Mg supplementation therefore conferred protective effects against cisplatin-induced nephrotoxicity in patients with ESCC. Furthermore, increases in PTH or PTH-rP may have influenced the extent of nephrotoxicity.

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“…Chiefly, among those is hypomagnesaemia as first described by Schilsky and Anderson in 1979 and repeatedly confirmed (Schilsky et al, 1982;Buckley et al, 1984;Lam & Adelstein, 1986;Stewart et al, 1985), which is thought to occur as a result of renal tubular magnesium wasting (Safirstein et al, 1986). The majority of patients affected by hypomagnesaemia show no signs or symptoms, but its manifestations can include neuromuscular irritability, weakness, confusion, seizures and ventricular arrhythmias (Vallee et al, 1960;Winkler et al, 1979;Willox et al, 1986).…”

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confidence: 99%