Mesangial injury and capillary ballooning precede podocyte damage in Nephrosclerosis

• Verfasst von: Kriz, Wilhelm [VerfasserIn]
• Verfasst von: Wiech, Thorsten [VerfasserIn]
• Verfasst von: Gröne, Hermann-Josef [VerfasserIn]
• Titel: Mesangial injury and capillary ballooning precede podocyte damage in Nephrosclerosis
• Verf.angabe: Wilhelm Kriz, Thorsten Wiech and Hermann-Josef Groene
• E-Jahr: 2022
• Jahr: December 2022
• Umfang: 13 S.
• Fussnoten: Gesehen am 29.03.2023
• Titel Quelle: Enthalten in: The American journal of pathology
• Ort Quelle: New York [u.a.] : Elsevier, 1925
• Jahr Quelle: 2022
• Band/Heft Quelle: 192(2022), 12, Seite 1670-1682
• ISSN Quelle: 1525-2191
• DOI: doi:10.1016/j.ajpath.2022.08.007
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: basement-membrane
• Sach-SW: blockade
• Sach-SW: cells
• Sach-SW: disease
• Sach-SW: glomerulosclerosis
• Sach-SW: pathogenesis
• Sach-SW: pathways
• Sach-SW: rats
• Sach-SW: stress
• K10plus-PPN: 184047839X

Abstract

The development of focal and segmental glomerulosclerosis (FSGS) as a consequence of glomerular hypertension resulting from arterial hypertension is widely considered a podocyte disease. However, the primary damage is encountered in the mesangium. In acute settings, mesangial cells disconnect from their insertions to the glomerular basement membrane, causing a ballooning of capillaries and severe changes of the folding pattern of the glomerular basement membrane, of the arrangement of the capillaries, and thereby of the architecture of the tuft. The displacement of capillaries led to contact of podocytes and parietal epithelial cells, initiating the formation of tuft adhesions to Bowman's capsule, the committed lesion to progress to FSGS. In addition, the displacement of capillaries also caused an abnormal stretching of podocytes, resulting in podocyte damage. Thus, the podocyte damage that starts the sequence to FSGS is predicted to develop secondary to the mesangial damage. This sequence was found in two hypertensive rat models of FSGS and in human hypertensive nephrosclerosis.