The long-term outcome of renal transplantation of IgA nephropathy and the impact of recurrence on graft survival

Moroni, Gabriella; Longhi, Selena; Quaglini, Silvana; Gallelli, Beniamina; Banfi, Giovanni; Montagnino, Giuseppe; Messa, Piergiorgio

doi:10.1093/ndt/gfs472

Cited by 101 publications

(118 citation statements)

References 32 publications

(85 reference statements)

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“…14,15 The frequency of recurrence in the present study was 36.7%, similar to recurrence rates reported in the literature. [1][2][3] To search for biomarkers of recurrent IgAN, we compared values obtained in the pre-transplantation serum of the R group of patients with those of the NR group.…”

Section: Discussionsupporting

confidence: 90%

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

Berthelot

Robert

Vuiblet

et al. 2015

Kidney International

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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.

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Section: Discussionsupporting

confidence: 90%

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

Berthelot

Robert

Vuiblet

et al. 2015

Kidney International

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“…This correlates with findings in transplant patients showing high levels of recurrence, with about 50% demonstrating evidence of IgA deposition on renal biopsy up to 10 years post transplantation [30]. Graft failure due to IgA nephropathy appears to be time-dependent: only 1-2% of allografts are lost to IgA nephropathy in the first decade after transplantation, with graft loss reaching a clinically significant level of 8-10% only between 10 and 15 years post transplant [31,32].…”

Section: Diagnosis and Prognosissupporting

confidence: 78%

Immunoglobulin A Nephropathy: Advances in Understanding of Pathogenesis and Treatment

Lafayette

Kelepouris

2018

Am J Nephrol

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Background: Immunoglobulin A (IgA) nephropathy is the most common form of primary glomerulonephritis and has clinical associations with a wide range of inflammatory and infectious diseases. There is a substantial variation in clinical course and outcomes, with many patients not diagnosed until they present with sequelae, which may include gross hematuria, hypertension, renal insufficiency, and/or significant proteinuria. Treatment options are currently limited and directed mainly toward control of these sequelae and have limited ability to reduce the incidence of end-stage renal disease or treat the primary IgA defect. Summary: Growing knowledge about the pathogenesis of IgA nephropathy and research into its genetic basis are helping to elucidate the course of this widely variable disease. IgA accumulation in the kidneys is thought to be the result of a number of different pathways in a “multi-hit” process that includes an initial traumatic trigger (often infection related) and subsequent memory responses that are amplified in those with a genetic predisposition to the disease and lead to an inflammatory response in susceptible individuals. Genome-wide association studies are providing new insights into the genetic variance of this autoimmune disease and are yielding information that may address both its causes and consequences. Key Messages: New treatment approaches are urgently required for the management of patients with IgA nephropathy. Novel interventions based around its inflammatory nature and “multi-hit” pathogenesis are being investigated to potentially limit disease progression.

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“…The clinical significance of IgA deposition is frequently unclear as it may be detected in protocol biopsies without clinical signs of nephritis. Contrary to what has been previously purported, a more recent study has associated recurrent IgAN with decreased graft survival at 15 years [56]. Patient and graft survival after kidney transplantation for IgAN without recurrent disease is similar to that of controls.…”

Section: Kidney Transplantationcontrasting

confidence: 71%

Management of Vasculitic Glomerulonephritis

Pendergraft

Nachman

2016

Curr Treat Options in Rheum

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The long-term outcome of renal transplantation of IgA nephropathy and the impact of recurrence on graft survival

Abstract: IgAN emerged as an independent predictor of worse graft outcome in the long-term. Recurrence of IgAN seems to progressively reduce in transplants performed from 1981 to 2010.

Cited by 101 publications

References 32 publications

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

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

Immunoglobulin A Nephropathy: Advances in Understanding of Pathogenesis and Treatment

Management of Vasculitic Glomerulonephritis

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