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Bjørneklett R, Vikse BE, Smerud HK, Bostad L, Leivestad T, Hartmann A, Iversen BM. Pre-transplant course and risk of kidney transplant failure in IgA nephropathy patients. Clin Transplant 2011: 25: E356-E365. © 2011 John Wiley & Sons A/S. There is lack of knowledge to what degree clinical/morphological presentation and course of IgA nephropathy (IgAN) prior to end-stage renal disease are risk factors for graft loss after kidney transplantation. Patients with IgAN between 1988 and 2006 (registered in the Norwegian Kidney Biopsy Registry) who later received a kidney transplant (registered in the Norwegian Renal Registry) were included. The cohort was followed up regarding death-censored graft loss throughout 2008. Graft survival with a rapid progressive (RP) vs. a slow progressive (SP) course of pre-Tx IgAN (annual GFR > or <30 mL/min/1.73 m) was studied. Among 106 included patients, there were 14 graft losses giving a graft loss rate of 1.9/100 patient years. Follow-up until the first kidney transplant was 6.9 ± 4.4 (range 0.1-19) yr. Patients with pre-Tx RP had a higher graft loss rate compared with SP patients (6.3 vs.1.3/100 patient years, p < 0.001). Graft loss rate with living-related donor (LRD) was similar to unrelated donor (UD) grafts. Most RP patients had received LRD grafts, and in SP patients, graft survival with LRD grafts was better than UD grafts (0.3 vs.2.1/100 patient years, p = 0.055). A rapid pre-transplant course is a strong risk factor for transplant failure in patients with IgAN. [ABSTRACT FROM AUTHOR]

Background. Coeliac disease is more frequent in IgA nephropathy (IgAN) patients compared to the healthy population. Several hypotheses postulate that food antigens like gluten may be involved in the onset of IgAN. Methods. In this study, we used a recently developed mucosal patch technique to evaluate the rectal mucosal inflammatory reaction to gluten in patients with IgAN (n = 27) compared to healthy subjects (n = 18). The rectal mucosal production of nitric oxide (NO) and release of myeloperoxidase (MPO) and eosinophil cationic protein (ECP) were measured. Serum samples were analysed for IgA and IgG antigliadin antibodies (AGA), IgA antibodies against tissue transglutaminase and IgA endomysium antibodies. Results. Gluten reactivity, defined as increase in MPO and/or NO after gluten exposure, was observed in 8 of 27 IgAN patients. The prevalence of HLA-DQ2 and DQ8 was not increased among gluten-sensitive patients, and the total prevalence among IgAN patients was the same as for the normal population. An elevated serum IgA AGA response was seen in 9 of 27 IgAN patients. The increase in IgA AGA did not correlate with the gluten sensitivity as measured by NO and/or MPO. A specific serum IgG AGA response was seen in one patient only. Antibodies against tissue transglutaminase and endomysium were not observed. Conclusion. It is concluded that approximately one-third of our IgAN patients have a rectal mucosal sensitivity to gluten, but without signs of coeliac disease, and we hypothesize that such sub-clinical inflammation to gluten might be involved in the pathogenesis of IgAN in a subgroup of patients. [ABSTRACT FROM AUTHOR]