We analyzed clinical and pathologic data from 36 recipients of 38 renal allografts who developed nephrotic syndrome following transplantation. Three groups were identified on the basis of histologic changes in the graft, and each group had a distinct clinical course. Nine grafts (23.7%) had recurrent glomerulonephritis (GN) (5 membrano-proliferative, 4 focal glomerulosclerosis) and developed nephrotic syndrome at 5.1 months (mean) posttransplant. Renal function deteriorated rapidly, with a 2-year graft survival of 29.7%. Four grafts (10.5%) with de novo GN (3 epimembranous, 1 minimal change) developed nephrotic syndrome at 32 months posttransplant, and all functioned for more than 3 years. Twenty-five grafts (65.8%) had allograft glomerulopathy with the onset of nephrotic syndrome at 9.1 months posttransplant and a 2-year graft survival of 66.6%. The differences in duratin of graft function between grafts with allograft glomerulopathy and recurrent GN (P < 0.01) and in graft survival rates at 2 years among the three groups (P < 0.05) are statistically significant. This analysis indicates that allograft glomerulopathy is the most common cause of kidney transplant nephrotic syndrome. Membranoproliferative GN and focal glomerulosclerosis may recur soon after transplantation and rapidly progress to renal failure in marked contrast to grafts with either de novo epimembranous nephropathy or minimal glomerular change, lesions that are compatible with prolonged graft function.

Download full-text PDF

Source
http://dx.doi.org/10.1038/ki.1980.146DOI Listing

Publication Analysis

Top Keywords

nephrotic syndrome
24
developed nephrotic
12
syndrome months
12
months posttransplant
12
graft survival
12
allograft glomerulopathy
12
kidney transplant
8
transplant nephrotic
8
three groups
8
focal glomerulosclerosis
8

Similar Publications

Background: KEPs (kidney exchange programs) facilitate living donor kidney transplantations (LDKT) for patients with incompatible donors, who are typically higher risk than non-KEP patients because of higher sensitization and longer dialysis vintage. We conducted a comparative analysis of graft outcomes and risk factors for both KEP and non-KEP living donor kidney transplants.

Methods: All LDKTs performed in the Netherlands between 2004-2021 were included.

View Article and Find Full Text PDF

Potentially paraneoplastic glomerulopathies in a Brazilian cohort: a retrospective analysis.

J Bras Nefrol

January 2025

Universidade Federal de São Paulo (UNIFESP), Departamento de Medicina, Divisão de Nefrologia, São Paulo, SP, Brazil.

Introduction: Glomerular diseases can be associated with solid or hematopoietic malignancies. The prevalence of these associations varies according to the studied glomerular disease. This study aimed to evaluate the frequency and type of neoplasms in patients with glomerular diseases as well as their clinical, laboratory, and histopathological features and the relationship with immunosuppressive therapy.

View Article and Find Full Text PDF

Background: Primary coenzyme Q10 (CoQ10) deficiency is an autosomal recessive genetic disease caused by mitochondrial dysfunction. Variants in Coenzyme Q8B () can cause primary CoQ10 deficiency. -related glomerulopathy is a recently recognized glomerular disease that most often presents as steroid-resistant nephrotic syndrome (SRNS) in childhood.

View Article and Find Full Text PDF

Expanding the clinical spectrum of 19p13.3 microduplication syndrome: a case report highlighting nephrotic syndrome and literature review.

BMC Pediatr

January 2025

Pediatric Internal Medicine, Yantai Yuhuangding Hospital, No.20 Yuhuangding East Road, Zhifu District, Yantai City, Shandong, 264000, China.

Background: Common clinical findings in patients with 19p13.3 duplication include intrauterine growth restriction, intellectual disability, developmental delay, microcephaly, and distinctive facial features. In this study, we report the case of a patient with 19p13.

View Article and Find Full Text PDF

Wernicke's encephalopathy (WE) is a severe neurological condition caused by the deficiency of thiamine, which is a vitamin B1 molecule. Herein, we present the case of a 3-year-old girl with steroid-resistant nephrotic syndrome (SRNS) who did not achieve remission despite steroid pulse therapy (MPT) and rituximab. She had frequent vomiting and decreased oral intake on the 61st day.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!