Background: There is a broad spectrum of glomerular histological findings in postinfectious glomerulonephritis (PIGN). We conducted this retrospective study to compare the clinicopathological features between two distinct morphology of PIGN.
Methods: Thirteen patients with typical endocapillary proliferation and eight patients with atypical mesangial proliferation were enrolled in this study. The patients' records were reviewed with respect to clinical presentation, microbiology, serology, morphology of renal biopsy, and clinical course.
Results: In comparison of histological parameters, glomerular neutrophil infiltration was more commonly present in typical endocapillary proliferation group (p = 0.018). Glomerular IgA dominant or co-dominant deposition was more frequently seen in atypical mesangial proliferation group (p = 0.032). In a comparison of clinical parameters, atypical mesangial proliferation group had lesser degrees of proteinuria, higher serum levels of complement, and higher rates of staphylococcal infection, although none of the differences was statistically significant. Glomerular morphology did not seem to affect the renal outcome. Moreover, our data suggested that the percentage of patients with atypical mesangial proliferation significantly increased over time (p < 0.001).
Conclusions: Atypical mesangial proliferation may represent a resolution stage of PIGN. The nature of subclinical infection with a more protracted course may contribute to the increasing recognition of this resolving PIGN at the time of renal biopsy. Another possible explanation is that the atypical morphology may be a peculiar pattern of post-staphylococcal glomerulonephritis, which was increasingly identified in PIGN over the past 10 years.
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http://dx.doi.org/10.3109/08860220903367494 | DOI Listing |
Neurochem Int
December 2024
Master and PhD Programs in Pharmacology and Toxicology, School of Medicine, Tzu Chi University, Hualien, 970, Taiwan; Department of Pharmacology, School of Medicine, Tzu Chi University, Hualien, 970, Taiwan. Electronic address:
Previous studies have shown that celecoxib or NSAID may paradoxically induce cyclooxygenase-2 (COX-2) expression and trigger inflammation-like responses in airway smooth muscle cells and renal mesangial cells. Despite the extensive research on celecoxib, its atypical biological effect on the induction of COX-2 in astroglial cells within the central nervous system (CNS) remains unexplored. In the present study, we investigated the impact of celecoxib on COX-2 and Glial Fibrillary Acidic Protein (GFAP) expression and explored the mechanisms underlying celecoxib-regulated COX-2 expression in cortical astrocytes of rats.
View Article and Find Full Text PDFBackground: COQ8B nephropathy is a hereditary mitochondrial kidney disease. Most cases present with steroidresistant nephrotic syndrome and focal segmental glomerulosclerosis, whereas this patient exhibited asymptomatic isolated proteinuria and mild renal histopathology.
Methods: Appropriate laboratory tests, abdominal ultrasonography, renal biopsy, and whole exome sequencing were performed to explore the cause of the disease.
J Mol Histol
December 2024
Department of Histology and Embryology, Faculty of Medicine, Aksaray University, Aksaray, Türkiye.
Cytopathology
January 2025
Department of Pathology, Health Research Institute 'San Carlos' (IdISCC), Hospital Universitario Clínico San Carlos, Universidad Complutense de Madrid, Madrid, Spain.
An incidental finding in urine smears from a patient with a presumptive diagnosis of an IgA mesangial nephropathy is presented. A possible example of the potential value of urine cytology in functional renal disorders. We report a case of an incidental finding in urine cytology from a patient with a presumptive diagnosis of an IgA mesangial glomerulonephritis, previously diagnosed as atypical urothelial cells.
View Article and Find Full Text PDFMed Clin (Barc)
October 2024
The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, China.
Objective: Copper metabolism disorder disease is thought to contribute to renal symptoms in Wilson's disease (WD). Nonetheless, there remains limited knowledge regarding the precise characteristics of renal damage in individuals with Wilson's disease, encompassing clinical presentations, biochemical indicators, imaging findings, and renal histopathological alterations.
Methods: In this study, 20 patients diagnosed with Wilson's disease and renal involvement were enrolled in our hospital.
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