Chronic renal magnesium loss, hypocalciuria and mild hypokalaemic metabolic alkalosis after cisplatin

Pediatr Nephrol. 1990 May;4(3):219-22. doi: 10.1007/BF00857658.


Renotubular handling of sodium, potassium (K) calcium (Ca), phosphate, hydrogen ions and glucose, and urinary concentrating ability were studied in three children (aged 8, 8.5, 11 years) with renal magnesium (Mg) loss, persisting for more than 2 years after discontinuation of cisplatin treatment for neuroblastoma. A group of healthy children served as controls. Besides renal Mg wasting, a clear-cut tendency towards reduced calciuria associated with normal or slightly elevated plasma Ca was observed. Plasma K tended to be low (3.4-3.7 mmol/l), and plasma chloride was normal. Plasma bicarbonate (HCO3) ranged from 24.9 to 27.8 mmol/l, and urinary pH was always less than 6.0, indicating a renal HCO3 threshold exceeding 24 mmol/l. Plasma creatinine levels, glucosuria and phosphaturia, and urinary concentrating capacity were adequate. Comparable features were found in three children (aged 4.5, 9, 13 years) with primary renotubular hypomagnesaemia-hypokalaemia and hypocalciuria. This study complements the picture of chronic cisplatin tubulopathy in childhood demonstrating that, apart from Mg wasting, a reduced Ca excretion, and a tendency to hypokalaemia and metabolic alkalosis exist. Thus cisplatin may induce renal functional damage identical to that found in primary renotubular hypomagnesaemia--hypokalaemia with hypocalciuria.

MeSH terms

  • Alkalosis / chemically induced*
  • Bicarbonates / blood
  • Calcium / blood
  • Calcium / metabolism*
  • Calcium / urine
  • Child
  • Cisplatin / adverse effects*
  • Female
  • Glycosuria / chemically induced
  • Humans
  • Hypokalemia / chemically induced*
  • Kidney Concentrating Ability
  • Kidney Tubules / metabolism
  • Magnesium Deficiency / chemically induced*
  • Male
  • Serum Albumin / metabolism


  • Bicarbonates
  • Serum Albumin
  • Cisplatin
  • Calcium