Skip to main content
NCBI home page
British Medical Journal (Clinical Research Ed.) logoLink to British Medical Journal (Clinical Research Ed.)
. 1986 Mar 22;292(6523):789–792. doi: 10.1136/bmj.292.6523.789

Remission of idiopathic nephrotic syndrome after treatment with cyclosporin A.

A Meyrier, P Simon, G Perret, M C Condamin-Meyrier
PMCID: PMC1339719  PMID: 3082443

Abstract

Nephrotic syndrome in minimal change lipoid nephrosis and focal segmental glomerulosclerosis may be due to alteration of glomerular anionic sites by a lymphokine. Six adults with nephrotic syndrome who were resistant to treatment with corticosteroids and immunosuppressants were treated with cyclosporin A. In three patients with minimal change lipoid nephrosis who had been nephrotic for 3.5 to 23 years proteinuria resolved within 12 to 42 days. Subsequently, these patients became dependent on cyclosporin A. In three patients with focal segmental glomerulosclerosis who had been nephrotic for four to six years mean (SD) 24 hour urinary protein decreased from 14.7 (8.4) g to 3.6 (0.6) g within 20 to 25 days, serum albumin concentration rose, and oedema subsided. One patient died of myocardial infarction when still in partial remission after 11 weeks' treatment. Two patients remained proteinuric despite continuing treatment with cyclosporin A, but control of sodium balance was easy and serum albumin concentrations remained higher than without cyclosporin A. In all patients renal function improved during treatment. These preliminary results show that cyclosporin A may be effective in the treatment of patients with nephrotic syndrome that resists every other form of treatment and especially in the treatment of those with minimal change lipoid nephrosis. The results are in keeping with a T lymphocyte mediated mechanism of minimal change lipoid nephrosis and focal segmental glomerulosclerosis, but they also suggest that minimal change lipoid nephrosis and focal segmental glomerulosclerosis are separate entities.

Full text

PDF
789

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Beale M. G., Nash G. S., Bertovich M. J., MacDermott R. P. Immunoglobulin synthesis by peripheral blood mononuclear cells in minimal change nephrotic syndrome. Kidney Int. 1983 Feb;23(2):380–386. doi: 10.1038/ki.1983.30. [DOI] [PubMed] [Google Scholar]
  2. Brown C. B., Cameron J. S., Turner D. R., Chantler C., Ogg C. S., Williams D. G., Bewick M. Focal segmental glomerulosclerosis with rapid decline in renal function ("malignant FSGS"). Clin Nephrol. 1978 Aug;10(2):51–61. [PubMed] [Google Scholar]
  3. Brown E. A., Markandu N., Sagnella G. A., Jones B. E., MacGregor G. A. Sodium retention in nephrotic syndrome is due to an intrarenal defect: evidence from steroid-induced remission. Nephron. 1985;39(4):290–295. doi: 10.1159/000183392. [DOI] [PubMed] [Google Scholar]
  4. Bunjes D., Hardt C., Röllinghoff M., Wagner H. Cyclosporin A mediates immunosuppression of primary cytotoxic T cell responses by impairing the release of interleukin 1 and interleukin 2. Eur J Immunol. 1981 Aug;11(8):657–661. doi: 10.1002/eji.1830110812. [DOI] [PubMed] [Google Scholar]
  5. Dall'Aglio P., Meroni P. L., Barcellini W., Brigati C., Chizzolini C., De Bartolo G., Migone L., Zanussi C. Altered expression of B lymphocyte surface immunoglobulins in minimal change nephrotic syndrome and focal glomerulosclerosis. Nephron. 1984;37(4):224–228. doi: 10.1159/000183253. [DOI] [PubMed] [Google Scholar]
  6. Fillit H. M., Zabriskie J. B. Cellular immunity in glomerulonephritis. Am J Pathol. 1982 Nov;109(2):227–243. [PMC free article] [PubMed] [Google Scholar]
  7. Geers A. B., Koomans H. A., Roos J. C., Boer P., Dorhout Mees E. J. Functional relationships in the nephrotic syndrome. Kidney Int. 1984 Sep;26(3):324–330. doi: 10.1038/ki.1984.176. [DOI] [PubMed] [Google Scholar]
  8. Giangiacomo J., Cleary T. G., Cole B. R., Hoffsten P., Robson A. M. Serum immunoglobulins in the nephrotic syndrome. A possible cause of minimal-change nephrotic syndrome. N Engl J Med. 1975 Jul 3;293(1):8–12. doi: 10.1056/NEJM197507032930103. [DOI] [PubMed] [Google Scholar]
  9. Hess A. D., Tutschka P. J., Santos G. W. Effect of cyclosporin A on human lymphocyte responses in vitro. III. CsA inhibits the production of T lymphocyte growth factors in secondary mixed lymphocyte responses but does not inhibit the response of primed lymphocytes to TCGF. J Immunol. 1982 Jan;128(1):355–359. [PubMed] [Google Scholar]
  10. Hoyer J. R., Vernier R. L., Najarian J. S., Raij L., Simmons R. L., Michael A. F. Recurrence of idiopathic nephrotic syndrome after renal transplantation. Lancet. 1972 Aug 19;2(7773):343–348. doi: 10.1016/s0140-6736(72)91734-5. [DOI] [PubMed] [Google Scholar]
  11. Ichikawa I., Rennke H. G., Hoyer J. R., Badr K. F., Schor N., Troy J. L., Lechene C. P., Brenner B. M. Role for intrarenal mechanisms in the impaired salt excretion of experimental nephrotic syndrome. J Clin Invest. 1983 Jan;71(1):91–103. doi: 10.1172/JCI110756. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Kalman V. K., Klimpel G. R. Cyclosporin A inhibits the production of gamma interferon (IFN gamma), but does not inhibit production of virus-induced IFN alpha/beta. Cell Immunol. 1983 May;78(1):122–129. doi: 10.1016/0008-8749(83)90265-4. [DOI] [PubMed] [Google Scholar]
  13. Kerpen H. O., Bhat J. G., Kantor R., Gauthier B., Rai K. R., Schacht R. G., Baldwin D. S. Lymphocyte subpopulations in minimal change nephrotic syndrome. Clin Immunol Immunopathol. 1979 Sep;14(1):130–136. doi: 10.1016/0090-1229(79)90133-8. [DOI] [PubMed] [Google Scholar]
  14. Lagrue G., Xheneumont S., Branellec A., Hirbec G., Weil B. A vascular permeability factor elaborated from lymphocytes. I. Demonstration in patients with nephrotic syndrome. Biomedicine. 1975 Feb 10;23(1):37–40. [PubMed] [Google Scholar]
  15. Levin M., Smith C., Walters M. D., Gascoine P., Barratt T. M. Steroid-responsive nephrotic syndrome: a generalised disorder of membrane negative charge. Lancet. 1985 Aug 3;2(8449):239–242. doi: 10.1016/s0140-6736(85)90290-9. [DOI] [PubMed] [Google Scholar]
  16. Mallick N. P. The pathogenesis of minimal change nephropathy. Clin Nephrol. 1977 Mar;7(3):87–95. [PubMed] [Google Scholar]
  17. Shalhoub R. J. Pathogenesis of lipoid nephrosis: a disorder of T-cell function. Lancet. 1974 Sep 7;2(7880):556–560. doi: 10.1016/s0140-6736(74)91880-7. [DOI] [PubMed] [Google Scholar]
  18. Vanrenterghem Y., Roels L., Lerut T., Gruwez J., Michielsen P., Gresele P., Deckmyn H., Colucci M., Arnout J., Vermylen J. Thromboembolic complications and haemostatic changes in cyclosporin-treated cadaveric kidney allograft recipients. Lancet. 1985 May 4;1(8436):999–1002. doi: 10.1016/s0140-6736(85)91610-1. [DOI] [PubMed] [Google Scholar]
  19. Zimmerman S. W. Increased urinary protein excretion in the rat produced by serum from a patient with recurrent focal glomerular sclerosis after renal transplantation. Clin Nephrol. 1984 Jul;22(1):32–38. [PubMed] [Google Scholar]

Articles from British Medical Journal (Clinical research ed.) are provided here courtesy of BMJ Publishing Group

RESOURCES