title: Detection of apoptotic cells in glomeruli of patients with IgA nephropathy.
abstract: The purpose of the present study was to determine the relationship between the existence of apoptotic cells in glomeruli, clinical or histopathological findings and response to treatment in patients with IgA nephropathy. Renal biopsy specimens were obtained from 23 patients with IgA nephropathy. These patients were divided into two groups: mild glomerular damage (12 patients), and severe glomerular damage (11 patients). The nick end-labelling method (TUNEL) and fluorescent staining (Hoechst 33258) were used for the detection of apoptotic cells. Five of 6 patients with apoptotic cells in the glomeruli detected by TUNEL were in the severe glomerular damage group, and only 1 patient was in the mild glomerular damage group. Apoptotic cells in glomeruli were also detected by fluorescent staining in 3 of 5 patients in the severe glomerular damage group who showed apoptotic cells in TUNEL. However, no apoptotic cells were detected in patients in the mild glomerular damage group in fluorescent staining. Mean levels of urinary protein excretion at the time of renal biopsy in the patients with apoptotic cells were significantly higher than those in patients without apoptotic cells (p < 0.01). The mean levels of creatinine clearance (Ccr) in the patients with apoptotic cells were slightly lower than those in patients without such cells. There were no significant differences in the levels of serum creatinine (s-Cr) and BUN in patients with or without apoptotic cells. In the severe glomerular damage group, urinary protein excretion after treatment in the patients with apoptotic cells was significantly improved compared with that in the patients without such cells (p < 0.01). It appears that the levels of proteinuria and renal function tests might be influenced by apoptosis in patients with IgA nephropathy. It is postulated that apoptosis may induce reduction of excess proliferative mesangial cells and/or infiltrated cells, and tissue repair. Thereafter, these histological alterations may improve proteinuria and renal function.
authors.affiliation: Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Tashiro
authors.forename: S
authors.initials: S
authors.lastname: Kodera
authors.forename: Y
authors.initials: Y
authors.lastname: Takahashi
authors.forename: S
authors.initials: S
authors.lastname: Horikoshi
authors.forename: I
authors.initials: I
authors.lastname: Shirato
authors.forename: Y
authors.initials: Y
authors.lastname: Tomino
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000502:physiology*; D001706:Biopsy; D003404:Creatinine / Q000097:blood; D004253:DNA Nucleotidylexotransferase / Q000378:metabolism; D005260:Female; D005922:Glomerulonephritis, IGA / Q000503:physiopathology*; D006651:Histocytochemistry; D006801:Humans; D007677:Kidney Function Tests; D007678:Kidney Glomerulus / Q000473:pathology*; D008297:Male; D008856:Microscopy, Fluorescence; D011507:Proteinuria / Q000473:pathology
chemical_list: D003404:Creatinine; D004253:DNA Nucleotidylexotransferase