IgA nephropathy recurs early in the graft when assessed by protocol biopsy

Ortiz, Fernanda; Gelpi, Rosana; Koskinen, Petri; Manonelles, Anna; Räisänen-Sokolowski, Anne; Carrera, Marta; Honkanen, Eero; Grinyó, Josep M.; Cruzado, Josep M.

doi:10.1093/ndt/gfr664

Cited by 88 publications

(66 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The reported frequency of histological or clinically significant recurrence of IgAN varies from 13% to 60% . This large variation showed in the reported literature is attributed to the differences in the duration of follow‐up and in the biopsy policy.…”

Section: Discussionmentioning

confidence: 99%

“…Longer follow‐ups have higher probabilities to find recurrent IgAN than shorter ones, and the frequency of histological recurrence of IgAN increases when protocol biopsy is performed because histological recurrence without evidence of clinical manifestation is common. Ortiz et al . reported that 52% of the IgAN recurrences diagnosed by protocol biopsies were not accompanied by proteinuria or haematuria.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Early recurrence of active IgA nephropathy after kidney transplantation

et al. 2014

View full text Add to dashboard Cite

ABSTRACT:IgA nephropathy (IgAN) is recurrent after transplantation; however, its time of recurrence is unpredictable. To date, factors influencing IgAN recurrence have not been elucidated. We present a case of a 23-year-old man with end-stage renal disease (ESRD) who underwent living-related ABOidentical pre-emptive kidney transplantation (PEKT) using his 57-year-old mother as a donor. IgAN started when the patient was 19 years old, and renal biopsy revealed the usual pathological findings of IgAN. In spite of steroid therapy including steroid pulse and tonsillectomy, the patient developed nephrotic syndrome and progressed to ESRD in 4 years. Protocol biopsy on day 19 following PEKT revealed active recurrent IgAN. Nephroticrange proteinuria and mild deterioration of kidney function developed regardless of strong immunosuppressive therapy such as steroid pulse, double filtration plasmapheresis and rituximab. We report a case of refractory IgAN that recurred 19 days after transplantation. This case is considered of value to elucidate factors leading to active IgAN recurrence.IgA nephropathy (IgAN) is the most common primary glomerulonephritis that causes end-stage renal disease (ESRD) in 20-40% of patients.1 The success rate of kidney transplantation for patients with IgAN-induced ESRD was believed to be good. However, few data are available on the long-term outcome of IgAN patients with renal transplantation. Moroni et al.2 reported that death-censored graft survival at 15 years was approximately 10% lower in IgAN patients than in controls, suggesting that the culprit is IgAN recurrence. In fact, IgAN is one of the most common recurrent glomerulonephritis. The majority of recurrent IgAN is not clinical but pathological. Factors deciding the activity of recurrent IgAN remain unclear. It is unpredictable when IgAN recurs and why these recurrences occur immediately after transplantation. We report a case of active IgAN that recurred 19 days after transplantation. A CASE OF REFRACTORY IgAN THAT RECURRED 19 DAYS AFTER TRANSPLANTATIONA 23-year-old man with ESRD underwent living-related ABO-identical pre-emptive kidney transplantation (PEKT) from his 57-year-old mother. At the age of 18, his urinalysis was normal. However, at the age of 19, 3+ proteinuria and 2+ occult blood were detected by annual physical examination. The abnormality on his urinalysis was diagnosed as IgAN by renal biopsy, which showed mild to moderate mesangial hypercellularity, with fibrocellular crescent in 1 of 10 glomeruli (Fig. 1a).Subsequently, tonsillectomy was performed and steroid pulse therapy was initiated. However, unfortunately, nephrotic-range proteinuria still developed. The patient then progressed to ESRD regardless of the treatment with steroid pulse therapy, cyclosporine (CyA), prednisolone, a reninangiotensin system inhibitor, an antiplatelet agent, and anticoagulation therapy. He was referred to our hospital to undergo PEKT from his mother. Laboratory data revealed ESRD with a serum creatinine concentration of 8.53 mg/dL, haemoglo...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Early recurrence of active IgA nephropathy after kidney transplantation

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Kidney transplantation is one of the therapeutic options offered to these patients; however, recurrence of IgAN on the graft can occur with a frequency ranging from 20 to 60%. [1][2][3][4] The immunosuppressive regimen seems to affect the recurrence rate, with antithymocyte globulin reportedly associated with a decrease in recurrence frequency, 5 whereas withdrawal of steroids is associated with an increased risk. 6 However, there is no specific treatment for recurrent IgAN.…”

mentioning

confidence: 99%

Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes

Berthelot

Robert

Vuiblet

et al. 2015

Kidney International

View full text Add to dashboard Cite

IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, frequently leads to end-stage renal disease and kidney transplantation. However, disease recurrence often occurs after transplantation. Here we evaluated the predictive value of three markers for IgAN recurrence: the presence of galactose-deficient IgA1, IgG anti-IgA autoantibodies, and IgA-soluble (s) CD89 complexes. This was analyzed in 38 kidney transplant recipients with IgAN recurrence and compared with 22 patients transplanted for IgAN but without recurrence and with 17 healthy controls. Pre-transplantation galactose-deficient IgA1 serum levels were significantly higher in the recurrence compared with the no recurrence or control groups. IgA-IgG complexes were significantly elevated in the recurrence group. Both the recurrence and no recurrence groups had increased values of IgA-sCD89 complexes compared with healthy controls, but values were significantly lower in patients with recurrence compared with no recurrence. Areas under the receiver operating curve of the markers in pre-transplantation sera were 0.86 for galactose-deficient-IgA, 0.82 for IgA-IgG, and 0.78 for sCD89-IgA; all significant. Disease recurrence was associated with decreased serum galactose-deficient IgA1 and appearance of mesangial-galactose-deficient IgA1 deposits, whereas increased serum IgA-sCD89 complexes were associated with mesangial sCD89 deposits. Thus, galactose-deficient-IgA1, IgG autoantibodies, and IgA-sCD89 complexes are valuable biomarkers to predict disease recurrence, highlighting major pathogenic mechanisms in IgAN.

show abstract

“…[6] Importantly, it was found that 52% of the IgAN recurrences diagnosed by protocol biopsies were not accompanied by proteinuria or hematuria. Thus, protocol biopsies with immunofluorescence analysis constitute an essential tool for the diagnosis of recurrence, even if it is clinically silent [7]. In our study, we were not able to rule out the possibility that IgA deposits were already present in the donors.…”

Section: Discussionmentioning

confidence: 65%