title: Monoclonal gammopathy after intense induction immunosuppression in renal transplant patients.
abstract: OBJECTIVE
  Incidence and risk factors of post-transplant monoclonal gammopathy were studied in renal transplant patients who received their grafts between 1982 and 1992 (n = 390 grafts). Immunoelectrophoresis was performed at annual intervals after transplantation.
  
  
  RESULTS
  Forty-six cases of clonal gammopathy were detected: 35 monoclonal, 11 bi- or triclonal, with a predominance of IgG and kappa light-chain subtypes (IgG, 39; IgA, 3; IgM, 4; kappa, 35; lambda, 19). Gammopathy was incidence of gammopathy was 10.7%, much higher than expected for a group of similar age from the general population. Thirty of the 46 gammopathies appeared within the first 2 years of transplantation. Gammopathy never progressed to multiple myeloma during follow-up (median 1 year; (range 0-10)); one patient subsequently developed Kaposi sarcoma. The 2-year incidence of gammopathy was much higher in patients transplanted in 1989-1991 (23/142) than in 1982-1988 (7/248) (P < 0.0001). This coincided with the use of quadruple induction immunosuppression (cyclosporin A+azathioprine+prednisone plus either ATG-fresenius (ATG-F) or OKT3) since 1989. The risk for acquiring gammopathy within 2 years of transplantation was 14.7% (95% CI 9.2, 20.3%) in patients receiving quadruple induction therapy, but only 3.0% (CI 1.2, 6.1%) without such therapy (P < 0.0001). The risk for patients receiving quadruple immunosuppression with OKT3 was 24.5%, significantly greater than with ATG-F (11.8%, P < 0.05). Discriminant analysis revealed that the type of immunosuppression, but not age or year of transplantation, were independent risk factors for gammopathy.
  
  
  CONCLUSIONS
  Monoclonal gammopathy frequently occurs after renal transplantation. Risks are higher for patients receiving quadruple induction immunosuppression, particularly if it includes OKT3. Follow-up of these patients is warranted for the early detection of malignant transformation.
authors.affiliation: Department of Internal Medicine, Kantonsspital Basel, Switzerland.
authors.forename: J
authors.initials: J
authors.lastname: Passweg
authors.forename: G
authors.initials: G
authors.lastname: Thiel
authors.forename: H A
authors.initials: HA
authors.lastname: Bock
mesh_terms: D000961:Antilymphocyte Serum / Q000494:pharmacology; D001379:Azathioprine / Q000494:pharmacology; D016572:Cyclosporine / Q000494:pharmacology; D006801:Humans; D007122:Immunoelectrophoresis; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents / Q000494:pharmacology; D015994:Incidence; D016030:Kidney Transplantation / Q000009:adverse effects / Q000276:immunology; D016853:Muromonab-CD3 / Q000494:pharmacology; D010265:Paraproteinemias / Q000453:epidemiology* / Q000209:etiology; D011241:Prednisone / Q000494:pharmacology; D012307:Risk Factors; D013557:Switzerland / Q000453:epidemiology; D013997:Time Factors
chemical_list: D000961:Antilymphocyte Serum; D007166:Immunosuppressive Agents; D016853:Muromonab-CD3; D016572:Cyclosporine; D001379:Azathioprine; D011241:Prednisone