title: Normal renal function 8 to 13 years after cyclosporin A therapy in 285 diabetic patients.
abstract: BACKGROUND
  Cyclosporin A (CyA) may induce acute nephrotoxicity. The question has been raised of the possible long-term unfavorable course of CyA-induced lesions. Advantage was taken of a large cohort of diabetic patients treated for several months using moderate CyA dosage to evaluate the long-term evolution of renal function in such patients.
  
  
  METHODS
  Two hundred and eighty five recently diagnosed type 1 diabetic patients having received CyA for a mean of 19.9 months were monitored for 13 years, in parallel with 100 similar patients treated with insulin alone.
  
  
  RESULTS
  In the CyA-treated group, a transient increase in creatininemia levels occurred during the first 18 months of treatment associated with a transient increase in renal vascular resistance. Both effects disappeared later on: creatininemia levels then remained normal. Inulin and p-aminohippurate (PAH) clearances remained normal throughout follow-up. Neither permanent renal failure nor progressive deterioration of renal function occurred in either group or in individual patients. A 10 to 12% increase in inulin and PAH clearance was elicited by IV amino acid infusion at 7 to 10 years, a finding consistent with a normal renal functional reserve. Patients with moderate kidney lesions on biopsy at 1 year had normal and stable clearance values at 7 to 13 years. The prevalence of arterial hypertension and retinopathy was lower in the CyA-treated group than in the control group, possibly because of the tighter metabolic control obtained in the CyA group.
  
  
  CONCLUSIONS
  These results suggest that low-dose CyA treatment combined with thorough monitoring does not result in long-term renal dysfunction.
authors.affiliation: Service de Diabétologie, Hôpital Bichat, Paris, France.
authors.forename: Roger
authors.initials: R
authors.lastname: Assan
authors.forename: Françoise
authors.initials: F
authors.lastname: Blanchet
authors.forename: Gilles
authors.initials: G
authors.lastname: Feutren
authors.forename: José
authors.initials: J
authors.lastname: Timsit
authors.forename: Etienne
authors.initials: E
authors.lastname: Larger
authors.forename: Christian
authors.initials: C
authors.lastname: Boitard
authors.forename: Claude
authors.initials: C
authors.lastname: Amiel
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Bach
mesh_terms: D000328:Adult; D001327:Autoimmune Diseases / Q000188:drug therapy*; D003404:Creatinine / Q000097:blood; D016572:Cyclosporine / Q000008:administration & dosage / Q000633:toxicity*; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000139:chemically induced; D007166:Immunosuppressive Agents / Q000627:therapeutic use / Q000633:toxicity*; D007444:Inulin / Q000493:pharmacokinetics; D007668:Kidney / Q000187:drug effects* / Q000503:physiopathology; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology; D007677:Kidney Function Tests; D008297:Male; D011247:Pregnancy; D011507:Proteinuria / Q000139:chemically induced; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D007166:Immunosuppressive Agents; D016572:Cyclosporine; D007444:Inulin; D003404:Creatinine