Late effects on renal glomerular and tubular function in childhood cancer survivors

Pediatr Blood Cancer. 2004 Nov;43(6):668-73. doi: 10.1002/pbc.20143.


Background: Late nephrotoxicity among childhood cancer survivors is poorly documented.

Methods: We investigated 115 patients and 86 controls assessing serum cystatin C concentration (CysC), urinary N-acetyl-beta-D-glucosaminidase activity (NAG), and microalbuminuria. Proteinuria was quantified and electrophoresis performed. Polymorphism of the angiotensin convertase enzyme (ACE) gene was determined by genomic PCR.

Results: CysC was elevated in Wilms tumor (WT) patients. Gross proteinuria was observed in 30 patients including three patients with progressive proteinuria who improved on ACE-inhibitor treatment. Neither patients with proteinuria nor the entire study population differed from controls with respect to ACE polymorphism. Pathologically elevated urinary NAG was noted in 38% of leukemia/lymphoma, 54% of solid tumor, 20% of WT survivors. A similar distribution of pathological microalbuminuria was found.

Conclusions: Mild-to-moderate subclinical glomerular and tubular damage can be identified in many childhood cancer survivors. However, most patients experience some spontaneous recovery from acute nephrotoxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Albuminuria / urine
  • Case-Control Studies
  • Child
  • Child, Preschool
  • Creatinine / blood
  • Cystatin C
  • Cystatins / blood
  • Female
  • Follow-Up Studies
  • Humans
  • Infant
  • Kidney Function Tests
  • Kidney Glomerulus / drug effects*
  • Kidney Glomerulus / pathology
  • Kidney Glomerulus / physiology
  • Kidney Glomerulus / physiopathology*
  • Kidney Tubules / drug effects*
  • Kidney Tubules / pathology
  • Kidney Tubules / physiology
  • Kidney Tubules / physiopathology*
  • Male
  • Neoplasms / drug therapy*
  • Peptidyl-Dipeptidase A / genetics
  • Polymorphism, Genetic / genetics
  • Survivors*
  • Time Factors


  • CST3 protein, human
  • Cystatin C
  • Cystatins
  • Creatinine
  • ACE protein, human
  • Peptidyl-Dipeptidase A