Recurrent glomerulonephritis after kidney transplantation: a practical approach

Souza, Laura De; Prunster, Janelle; Chan, Doris; Chakera, Aron; Lim, Wai H.

doi:10.1097/mot.0000000000000887

Cited by 7 publications

(13 citation statements)

References 144 publications

(160 reference statements)

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“… 13 Some biomarkers for the prediction of post-transplant IgAN recurrence have been studied, such as IgA and IgA-complexes (IgA-IgG and IgA-soluble CD89), galactose-deficient IgA1 (Gd-IgA1), and anti-Gd-IgA1 autoantibodies, although its clinical application is not entirely known. 14 Graft dysfunction related to recurrence is rare before three years of follow-up. 15 After that, the recurrence becomes clinically relevant, reaching 10–15% of recurrence-related graft dysfunction at five years.…”

Section: Iga Nephropathymentioning

confidence: 99%

“… 26 The post-transplant rise of anti-PLA2R may also help identify the possibility of MN recurrence and may be associated with disease progression and resistance to treatment. 14 , 27 The diagnostic and prognostic application of measuring other autoantibodies, such as THSD7A or glomerular staining of PLA2R, is still undetermined. 14 The post-transplant surveillance measurement of proteinuria or albuminuria is recommended to identify the recurrence early, especially among patients with a high risk of recurrence.…”

Section: Membranous Nephropathymentioning

confidence: 99%

“… 14 , 27 The diagnostic and prognostic application of measuring other autoantibodies, such as THSD7A or glomerular staining of PLA2R, is still undetermined. 14 The post-transplant surveillance measurement of proteinuria or albuminuria is recommended to identify the recurrence early, especially among patients with a high risk of recurrence. 24 Proteinuria should be evaluated monthly for at least the first year post-transplant in cases of MN not associated with anti-PLA2R antibodies, and graft biopsy is indicated in cases of proteinuria higher than 1 g/d.…”

Section: Membranous Nephropathymentioning

confidence: 99%

“… 27 The treatment goals for recurrent idiopathic MN are to control symptoms and prevent the progression of podocyte injury. 14 The nonspecific treatment of MN includes dietary sodium restriction, dietary protein intake reduction, blood pressure control, and antiproteinuric therapy with ACEi and ARB. 22 Although SGLT-2 inhibitors have been shown to decrease the risk of CKD progression, their use on patients with nephrotic syndrome and/or immunosuppressed is lacking.…”

Section: Membranous Nephropathymentioning

confidence: 99%

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Post-Transplant Glomerulonephritis: Challenges and Solutions

de Sousa

2024

IJNRD

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Glomeruli can be damaged in several conditions after kidney transplantation, with a potential impact on the graft function and survival. Primary glomerulonephritis, a group of glomerular immunological damage that results in variable histological patterns and clinical phenotypes, can occur in kidney transplant recipients as a recurrent or de novo condition. Specific immunologic conditions associated with kidney transplantation, such as acute rejection episodes, can act as an additional trigger after transplantation, impacting the incidence of these glomerulopathies. The post-transplant GN recurrence ranges from 3% to 15%, varying according to the GN subtype and post-transplant time, mainly occurring after 3–5 years of kidney transplantation. Advances in the knowledge of glomerulonephritis pathophysiology have provided new approaches to pre-transplant risk evaluation and post-transplant monitoring. Glomeruli can be affected by several systemic viral infections, such as human immunodeficiency virus (HIV), hepatitis C virus (HCV), hepatitis B virus (HBV), severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), cytomegalovirus (CMV), and BK virus. The diagnosis of these infections, as well as the identification of possible complications associated with them, are important to minimize the negative impacts of these conditions on kidney transplant recipients’ outcomes.

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Section: Iga Nephropathymentioning

confidence: 99%

Section: Membranous Nephropathymentioning

confidence: 99%

Section: Membranous Nephropathymentioning

confidence: 99%

Section: Membranous Nephropathymentioning

confidence: 99%

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Post-Transplant Glomerulonephritis: Challenges and Solutions

de Sousa

2024

IJNRD

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“…The potential pitfalls in the timing of posttransplantation biopsy are also discussed. Recurrent, or de novo glomerulonephritis, one of the major causes of renal allograft dysfunction occurring in various posttransplant periods, is beyond the scope of this review, and readers are referred to the recent reviews [3, 4].…”

Section: Introductionmentioning

confidence: 99%

The Chronology of Renal Allograft Dysfunction: The Pathological Perspectives

Hara

2023

Nephron

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Background: Antibody-mediated rejection (ABMR), T-cell-mediated rejection (TCMR), BK polyomavirus nephropathy, and calcineurin inhibitor (CNI) toxicity are all common causes of kidney allograft dysfunction that can affect long-term allograft function. Summary: The prevalence of various pathological diagnoses changes over time for both indication and protocol biopsies. Active ABMR and CNI toxic tubulopathy are the leading causes of kidney allograft dysfunction in the early posttransplant period. Active ABMR can also manifest as thrombotic microangiopathy. Acute TCMR, borderline for acute TCMR, and BK polyomavirus nephropathy will occur, then comes a causal peak of renal allograft dysfunction, followed by chronic active ABMR. Active ABMR in the late posttransplant period would progress to chronic active ABMR, indicating sequential evolution from the incipient to advanced phase of chronic active ABMR. CNI toxicity also manifests as chronic lesions of arteriolar hyalinosis. Interstitial fibrosis and tubular atrophy are the result of multiple insults and are linked to underlying diseases, particularly in the late posttransplant period. Even with established pathological criteria of the Banff scheme, it can be still challenging to clearly delineate the causes of the allograft dysfunction, especially in the complicated cases. Understanding the chronological causes of renal allograft dysfunctions improves comprehension of renal allograft pathology. Key Messages: Identifying the time-dependent prevalence of renal allograft dysfunction can be a critical and effective approach to pathological diagnosis.

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