Search PubMed⌕ Search

PubMed · 9102922

[Pathologic changes in the interstitium in IgA nephropathy].

Abstract

Some of tubulointerstitial changes are frequently found in glomerular disorders. A wide range of interstitial lesions have also been observed in patients with IgA nephropathy. Percutaneous biopsy specimens taken from 74 kidneys of IgA nephropathy patients have been analysed. Obtained tissues were examined by LM, If and EM. Light microscopy, immunofluorescence and electron microscopy Morphologic changes have been classified into 5 groups according to WHO classification. Interstitial changes, cellular infiltrations, fibrosis and other lesions from all renal tissues have been analysed and according to their intensity semiquantitatively graded into 4 groups. Histopathologic analysis has most frequently revealed interstitial fibrosis and less frequently mononuclear cellular infiltration particularly in patients with more prominent glomerular changes. Therefore, we have as well as other authors, confirmed that interstitial changes represent an important prognostic factor in the IgA nephropathy development. However, analysis of repeated biopsy specimens to confirm this hypothesis is necessary.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Dimitrijević, Dj Maksić, P Spasić, R Hrvacević. 1996. [Pathologic changes in the interstitium in IgA nephropathy].. https://pubmed.ncbi.nlm.nih.gov/9102922/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Binding capacity of in vitro deglycosylated IgA1 to human mesangial cells.

IgA nephropathy (IgAN) is the most common glomerular disease and it is characterized by deposition of IgA1 molecules in mesangium. Recent studies had demonstrated that serum and mesangial IgA1 in IgAN were deglycosylated and IgA1 could bind to human mesangial cells (HMC) through a novel receptor. The aim of the current study is to investigate and compare the binding capacities of different in vitro deglycosylated IgA1 on human mesangial cells. Serum IgA1 was purified by jacalin affinity chromatography and then was desialylated (DesIgA1) and/or degalactosylated (Des/DeGalIgA1) with neuraminidase and/or beta-galactosidase. The efficacy of deglycosylations was assessed by Peanut agglutinin (PNA) and Vicia villosa (VV) lectin. The sizes of normal IgA1 and deglycosylated IgA1 were determined by Sephacryl S-300 chromatography and binding capacities to primary HMC were evaluated by radioligand binding assays. Normal IgA1 and deglycosylated IgA1 could bind to HMC in a dose-dependent, saturable manner. The maximal binding capacities and binding sites/cell of DesIgA1 and Des/DeGalIgA were significantly higher than that of normal IgA1. However, more aggregated IgA1 was found in DesIgA1 and Des/DeGalIgA1. Scatchard analysis revealed a similar Kd of normal IgA1 and deglycosylated IgA1. The current study suggested that the binding capacities of DesIgA1 and Des/DeGalIgA1 to HMC were significantly higher than that of normal IgA1, which at least in part was due to more macromolecular IgA1 in deglycoslated IgA1. However, there were no significant differences in the affinities of normal IgA1, DesIgA1 and Des/DeGalIgA1 with HMC. Deglycosylated IgA1 might play an important role in pathogenesis of IgAN.

Glomerulonephritis, IGA↗

The IgA nephropathy treatment dilemma.

Although IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide, our understanding of the pathogenesis of this complex disease remains limited. IgA nephropathy may appear with a variety of clinical presentations, a number of different clinical and histopathologic risk factors for progressive renal disease, and a very variable course over time. Thus, it is not surprising that a single therapeutic treatment plan has not been established. Many of the studies dealing with IgAN are retrospective, lack statistical significance, or have confounding designs, which hinder their general acceptance. Nevertheless, a number of well-designed studies have been performed. This paper reviews currently available therapeutic options for IgAN. It attempts to address several important questions: Why do we treat patients with IgAN? How do we decide which patients should be treated? What are the general treatment guidelines for all IgAN patients? What is the role of specific therapy such as fish oils, tonsillectomy, and immunosuppression in the treatment of patient with IgAN? It also addresses several on-going trials and goals for future therapeutic studies for IgAN patients.

Glomerulonephritis, IGA↗