Renal Tubular Basement Membrane Changes in Tubulointerstitial Damage in Patients with Glomerular Diseases

• Published in: Ultrastructural pathology Vol. 23; no. 6; pp. 359 - 368
• Main Author: Raja Sinniah, Tahir N. Khan
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 1999; Taylor & Francis
• Subjects: Basement Membrane - metabolism; Basement Membrane - ultrastructure; Collagen - ultrastructure; Complement C1q - metabolism; Complement C3 - metabolism; Diabetic Nephropathies - metabolism; Diabetic Nephropathies - pathology; Fluorescent Antibody Technique, Indirect; Glomerulonephritis - metabolism; Glomerulonephritis - pathology; Humans; Kidney Glomerulus - metabolism; Kidney Glomerulus - pathology; Kidney Tubules - metabolism; Kidney Tubules - ultrastructure; Lupus Nephritis - metabolism; Lupus Nephritis - pathology; Microscopy, Electron; Nephritis, Interstitial - metabolism; Nephritis, Interstitial - pathology; Nephrosis, Lipoid - metabolism; Nephrosis, Lipoid - pathology; Tubular Basement Membrane
• ISSN: 0191-3123; 1521-0758
• DOI: 10.1080/019131299281329

Injury to renal tubules and interstitium occur in various glomerular diseases, leading to functional impairment. Tubular basement membrane (TBM) is an important component in maintaining tubular epithelial cell integrity. Because ultrastructural changes in these structures had not been studied in detail, the authors analyzed 30 patients with various types of glomerular diseases, including minimal change disease (MCD), focal segmental glomerular sclerosis, IgA nephropathy, diffuse proliferative glomerulonephritis, membranous nephropathy, and lupus nephritis, by light, electron, and immunofluorescence microscopy. Ultrastructural changes in the TBM were studied and morphometric measurements were performed. The tubular basement membranes showed membranous structures, lucent or lytic areas, and tubular epithelial detachment. There was significant linear correlation between these tubular basement membrane changes and terminal complement complex neoantigens. The interstitial widening was due to banded collagen fibers, with anchoring fibers in the TBM. The various glomerular diseases lead to tubulointerstitial damage via changes in the TBM, leading to renal dysfunction.