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Cell & Tissue Transplantation & Therapy

De-Novo  IgA Nephropathy and Cyclosporine Toxicity After Heart Transplantation

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Cell & Tissue Transplantation & Therapy 2008:1 9-13

Published on 24 Nov 2008


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Terje Forslund1, Kai Nyman2, Reijo Sironen3 and Kaisa Salmenkivi4

1Division of Nephrology and 2Division of Cardiology Department of medicine and 3Department of Pathology Central Finland Health Care District Hospital Jyväskylä, Finland, 4Department of Pathology HUSLAB and Hartmann Institute University of Helsinki, Helsinki, Finland.

Abstract

IgA nephropathy (IgAN) is the most common type of glomerulonephritis (GN) accounting for about 15%–20% of all GNs in Europe and 30%–40% in Japan but is less often observed in North-America (1,2). The diagnostic hallmark of IgAN is mesangial deposition of immunoglobulin A (IgA) often together with complement-3 (C3) in the glomeruli and some patients with IgAN may have increased levels of circulating immuno-complexes containing IgA. IgAN, initially considered to be a disease with benign prognosis, may eventually progress to end-stage-renal disease (ESRD) in 15%–40% of the cases (2,3,4). In order to predict outcome in patients with IgAN a grading of glomerular changes from kidney biopsies has been used (5). The etiology of IgAN is still not known but several observations point to some involvement of ethnic and genetic factors (6,7). Acute myocarditis (AM) accompanied with acute heart failure may need intensive care treatment and with a progressive course an early heart transplantation (HTx) might be offered if a suitable heart- donor is present. Different kinds of viruses may often cause AM and Coxsackie B-virus, Cytomegalo- virus, Adenovirus, and Infl uenza A-virus, are accounting for most of the cases. End-stage renal failure (ESRF) is a well known late complication of HTx (8) with a poorer outcome than in other ESRF (9) subjects. ESRF may be related to hypertension regardless of their immunosup- pressive regimen (9,10), or related to different infections, including sepsis, and to their treatments (9,10). However, calcineurin inhibitor nephrotoxicity (CIN) is the most recognized late renal complication after HTx (10,11). Different forms of de-novo GNs like membranous, membranoproliferative GN, and IgAN have been reported after solid organ transplantation (12,13). Immune-complex deposit glomeru- lopathy (15), and focal segmental glomerulosclerosis have been observed after HTx (10,14). Our case had acute myocarditis with rapid progressive heart failure needing a heart transplantation. Subsequently chronic renal failure developed and a kidney biopsy performed seven years after HTx confi rmed global glomerular sclerosis and IgA nephropathy.



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