Background: Previous studies have recognized risk factors for recurrent IgA nephropathy (r-IgAN) in renal transplantation. However the clinical significance of latent IgA deposition from the donor kidney remains to be determined.
Patients And Methods: Between 1992 and 1999, 0-hour allograft biopsies were performed in 510 renal transplantation recipients at the Kidney Center of Tokyo Women's Medical University. Among these 510 patients, there were 49 whose primary disease was identified as IgAN. Among these 49 patients, 13 patients (26.5%) were diagnosed as having r-IgAN based on renal biopsy. We compared risk factors of r-IgAN, including IgA deposition, between the r-IgAN and non-r-IgAN groups.
Results: We assessed factors previously reported to be risk factors for r-IgAN, such as follow-up period after transplantation, sex, ages of donors and recipients, donor type, ABO compatible or incompatible transplantation, number of HLA-A, B, and DR mismatches, number of donors with HLA-A2, B35, B46, and/or DR4, duration to end stage renal disease, duration of dialysis, and latent IgA deposition from donor kidneys. Latent IgA deposition was the only risk factor that differed significantly in frequency between patients with and without recurrence (38.5% in r-IgAN group vs. 9.1% in non-r-IgAN group, p = 0.037). Other factors did not differ significantly between the two groups. Clinical factors, such as urinary protein excretion, urinary red blood cell sediment and serum creatinine, were significantly worse and the number of patients who required hemodialysis 5 yr after transplantation was significantly higher in the r-IgAN group than in the non-r-IgAN group (38.5 vs. 5.6%, p = 0.001). Four of the five patients who required hemodialysis in the r-IgAN group had latent IgA deposition from the donor kidney.
Conclusion: Our data suggest that 26.5% out of patients with primary IgAN will develop recurrence within 5 yr after transplantation. Latent IgA deposition from the donor kidney was one of the risk factors of r-IgAN and it would lead to the development of r-IgAN. Moreover, r-IgAN will compromise graft survival, especially in cases with latent IgA deposition from the donor kidney.
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http://dx.doi.org/10.1111/j.1399-0012.2005.00403.x | DOI Listing |
CEN Case Rep
December 2024
Division of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Minato-Ku, Tokyo, 105-8461, Japan.
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide with heterogeneous histopathological phenotypes. Although IgAN with membranoproliferative glomerulonephritis (MPGN)-like features has been reported in children and adults, treatment strategies for this rare IgAN subtype have not been established. Here, we present the case of a 56-year-old man with no history of kidney disease who initially presented with nephrotic syndrome.
View Article and Find Full Text PDFSci Rep
December 2024
Laboratory of Molecular and Cellular Immunology, Institute of Molecular Biology NAS RA, 7 Hasratyan Str., Yerevan, 0014, Armenia.
Antiphospholipid syndrome (APS) is associated with recurrent pregnancy morbidity, yet the underlying mechanisms remain elusive. We performed multifaceted characterization of the biological and transcriptomic signatures of mouse placenta and uterine natural killer (uNK) cells in APS. Histological analysis of APS placentas unveiled placental abnormalities, including disturbed angiogenesis, occasional necrotic areas, fibrin deposition, and nucleated red blood cell enrichment.
View Article and Find Full Text PDFIran J Kidney Dis
December 2024
Department of Nephrology, The First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology.
Introduction: To evaluate the impact of TACI fusion protein (TACI-Ig) on IgA nephropathy (IgAN) in rats, and to explore its mechanism and relationship with TLR4/MyD88/NF-κB pathway.
Method: Sprague Dawley(SD)rats were divided into six groups: control, model, TACI-Ig low dose (TACI-Ig-L), medium dose (TACI-Ig-M), high dose (TACI-Ig-H), and prednisone acetate (PAT) group. The control group and model group received physiological saline injections, while the TACI-Ig groups were administered doses of 7.
The combination of nephrotic syndrome with mild histopathological lesions of IgA nephropathy is considered by some as a special form of IgA nephropathy with superimposed minimal change disease (MCD) while by others as coincidental deposition of IgA in patients with MCD (MCD-IgAN). We present the first case of complete remission of nephrotic syndrome in a 55-year-old man with MCD-IgAN after the administration of targeted-release formulation of budesonide (TRF-budesonide). The patient's treatment with TRF-budesonide, even though methylprednisolone, mycophenolate mofetil, and cyclophosphamide had been previously tried, is of particular importance because it not only suggests that TRF-budesonide appears to be a promising treatment for MCD-IgAN but may also provide a new therapeutic option for patients with podocytopathies.
View Article and Find Full Text PDFTissue Cell
December 2024
School of Pharmacy & Technology Management, SVKM's Narsee Monjee Institute of Management Studies (NMIMS), Polepally SEZ, TSIIC, Jadcherla, Mahbubnagar, Hyderabad 509301, India.
In this study, we investigated the efficacy of oxymatrine, a phytochemical alkaloid, in reducing inflammation and fibrosis in a rat model of IgA nephropathy (IgAN) through modulation of the TGF-β/SMAD signaling pathway. Thirty Sprague Dawley rats were randomized into control, IgAN, and treatment groups, the latter receiving oxymatrine postinduction of IgAN. Induced by bovine serum albumin, carbon tetrachloride, and lipopolysaccharides, the disease model was validated by immunofluorescence and histopathological analyses, confirming significant renal deposition of IgA and increased fibrosis markers (IL-6, TGF-β, SMAD 3, and α-SMA).
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