Mesangial injury and capillary ballooning precede podocyte damage in Nephrosclerosis

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 t...

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Hauptverfasser: Kriz, Wilhelm (VerfasserIn) , Wiech, Thorsten (VerfasserIn) , Gröne, Hermann-Josef (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: December 2022
In: The American journal of pathology
Year: 2022, Jahrgang: 192, Heft: 12, Pages: 1670-1682
ISSN:1525-2191
DOI:10.1016/j.ajpath.2022.08.007
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.ajpath.2022.08.007
Verlag, lizenzpflichtig, Volltext: https://linkinghub.elsevier.com/retrieve/pii/S0002944022002838
Volltext
Verfasserangaben:Wilhelm Kriz, Thorsten Wiech and Hermann-Josef Groene
Beschreibung
Zusammenfassung: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.
Beschreibung:Gesehen am 29.03.2023
Beschreibung:Online Resource
ISSN:1525-2191
DOI:10.1016/j.ajpath.2022.08.007