Pediatric Nephrology

, Volume 4, Issue 5, pp 451–454

Testicular function following cyclophosphamide treatment for childhood nephrotic syndrome: long-term follow-up study

  • Radovan Bogdanović
  • Miloš Banićević
  • Angelina Čvorić
Original Article


Testicular function of 17 males treated in childhood or adolescence for nephrotic syndrome (NS) with cyclophosphamide (CY) for a mean time of 240 days (mean total dosage of 16.4 g or 641 mg/kg body weight) was evaluated at a mean time of 11.8 years after treatment. Five were azoopsermic, 1 oligospermic, and 11 normospermic. There was a significant inverse correlation of sperm density with CY dosage and duration of treatment. All patients had undergone normal pubertal development and had normal sexual characteristics. Both basal and gonadotropin-releasing hormone-stimulated follicle-stimulating hormone (FSH) and luteinizing hormone (LH) concentrations were significantly raised in oligo- and azoospermic patients. Raised basal and peak FSH and LH concentrations in normospermic patients with a sperm count of less than 40×106/ml were in keeping with impairment of two testicular components. However, mean basal plasma testosterone levels and mean peak plasma testosterone responses to human chrionic gonadotropin (HCG) did not differ significantly between patients and controls. Although LH responses to gonadotropin-releasing hormone suggested compensated Leydig cell failure in patients with testicular tubular damage, secretory reserve capacity of these cells, estimated by a HCG stimulation test, was preserved. Further follow-up is required to ascertain whether in these patients Leydig cell failure will develop with time.

Key words

Testicular function Cyclophosphamide Childhood nephrotic syndrome 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Coldbeck JH (1963) Experience with alkylating agents in the treatment of childhood nephrotic syndrome. Med J Aust 1: 987–989Google Scholar
  2. 2.
    Barratt TM, Soothill JF (1970) Controlled trial of cyclophosphamide in steroid-sensitive relapsing nephrotic syndrome of childhood. Lancet II: 479–482Google Scholar
  3. 3.
    Chiu J, McLaine PN, Drummond KN (1973) A controlled prospective study of cyclophosphamide in relapsing, corticosteroid-responsive, minimal-lesion nephrotic syndrome in childhood. J Pediatr 82: 607–613PubMedGoogle Scholar
  4. 4.
    Fairley KF, Barrie JU, Johnson W (1972) Sterility and testicular atrophy related to cyclophosphamide therapy. Lancet I: 568–569Google Scholar
  5. 5.
    Rapola J, Koskimies O, Huttunen NP, Floman P, Vilska J, Hallman N (1973) Cyclophosphamide and the pubertal testis. Lancet I: 98–99Google Scholar
  6. 6.
    Penso J, Lippe B, Ehrlich R, Smith FG (1974) Testicular function in prepubertal and pubertal male patients treated with cyclophosphamide for nephrotic syndrome. J Pediatr 84: 831–836PubMedGoogle Scholar
  7. 7.
    Etteldorf JN, West CD, Pitcock JA, Williams DL (1976) Gonadal function, testicular histology, and meiosis following cyclophosphamide therapy in patients with nephrotic syndrome. J Pediatr 88: 206–212PubMedGoogle Scholar
  8. 8.
    Lentz RD, Bergstein J, Steffes MW, Brown DR, Prem K, Michael AF, Vernier RL (1977) Postpubertal evaluation of gonadal function following cyclophosphamide therapy before and during puberty. J Pediatr 91: 385–394PubMedGoogle Scholar
  9. 9.
    Hsu AC, Folami AO, Bain J, Rance CP (1979) Gonadal function in males treated with cyclophosphamide for nephrotic syndrome. Fertil Steril 31: 173–177PubMedGoogle Scholar
  10. 10.
    Parra A, Santos D, Cervantes C, Sojo I, Carranco A, Cortes-Gallegos V (1978) Plasma gonadotropins and gonadal steroids in children treated with cyclophosphamide. J Pediatr 92: 117–124PubMedGoogle Scholar
  11. 11.
    Greifer I, Barnett HL (1972) International workshop on risk/benefit assessment of cyclophosphamide in renal disease. Kidney Int 2: 352–353Google Scholar
  12. 12.
    Trompeter RS, Evans PR, Barratt TM (1981) Gonadal function in boys with steroid-responsive nephrotic syndrome treated with cyclophosphamide for short periods. Lancet I: 1177–1179Google Scholar
  13. 13.
    Watson AR, Rance CP, Bain J (1985) Long-term effects of cyclophosphamide on testicular function. Br Med J 291: 1457–1460Google Scholar
  14. 14.
    WHO laboratory manual for the examination of human semen and semen-cervical mucus interactions (1980) WHO Press Concern, SingaporeGoogle Scholar
  15. 15.
    Arbeitsgemeinschaft für Pädiatrische Nephrologie (1982) Effects of cytotoxic drugs in frequently relapsing nephrotic syndrome with and without steroid dependence. N Engl J Med 306: 451–454Google Scholar
  16. 16.
    Buchanan JD, Fairley KF, Barrie JU (1975) Return of spermatogenesis after stopping cyclophosphamide therapy. Lancet II: 156–157Google Scholar
  17. 17.
    Rosen SW, Weintraub BD (1971) Monotropic increase of serum FSH correlated with low sperm count in young men with idiopathic oligospermia and aspermia. J Clin Endocrinol 32: 410–415Google Scholar
  18. 18.
    Mecklenburg RS, Sherins RJ (1974) Gonadotropin response to luteinizing hormone-releasing hormone in men with germinal aplasia. J Clin Endocrinol Metab 38: 1005–1008PubMedGoogle Scholar
  19. 19.
    Lipsett MB (1980) Physiology and pathology of the Leydig. N Engl J Med 303: 682–688PubMedGoogle Scholar
  20. 20.
    Kirkland RT, Bongiovanni AM, Cornfeld D, McCormick JB, Parks JS, Tenore A (1976) Gonadotropin responses to luteinizing releasing factor in boys treated with cycloposphamide for nephrotic syndrome. J Pediatr 89: 941–944PubMedGoogle Scholar

Copyright information

© IPNA 1990

Authors and Affiliations

  • Radovan Bogdanović
    • 1
  • Miloš Banićević
    • 1
  • Angelina Čvorić
    • 1
  1. 1.Institute for Mother and Child Health Care of SerbiaBelgradeYugoslavia

Personalised recommendations