Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis

Wilhelm Kriz; Thorsten Wiech; Hermann-Josef Gröne

doi:10.1016/j.ajpath.2022.08.007

Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis

Standard

Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis. / Kriz, Wilhelm; Wiech, Thorsten; Gröne, Hermann-Josef.

In: AM J PATHOL, Vol. 192, No. 12, 12.2022, p. 1670-1682.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Kriz, W, Wiech, T & Gröne, H-J 2022, 'Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis', AM J PATHOL, vol. 192, no. 12, pp. 1670-1682. https://doi.org/10.1016/j.ajpath.2022.08.007

APA

Kriz, W., Wiech, T., & Gröne, H-J. (2022). Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis. AM J PATHOL, 192(12), 1670-1682. https://doi.org/10.1016/j.ajpath.2022.08.007

Vancouver

Kriz W, Wiech T, Gröne H-J. Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis. AM J PATHOL. 2022 Dec;192(12):1670-1682. https://doi.org/10.1016/j.ajpath.2022.08.007

Bibtex

@article{62d06e6c5add47768e489cef99e52dcd,

title = "Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis",

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.",

keywords = "Rats, Humans, Animals, Podocytes/pathology, Glomerulosclerosis, Focal Segmental/pathology, Nephrosclerosis/complications, Capillaries/pathology, Glomerular Basement Membrane/pathology, Hypertension, Renal/complications",

author = "Wilhelm Kriz and Thorsten Wiech and Hermann-Josef Gr{\"o}ne",

year = "2022",

month = dec,

doi = "10.1016/j.ajpath.2022.08.007",

language = "English",

volume = "192",

pages = "1670--1682",

journal = "AM J PATHOL",

issn = "0002-9440",

publisher = "Elsevier Inc.",

number = "12",

}

RIS

TY - JOUR

T1 - Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis

AU - Kriz, Wilhelm

AU - Wiech, Thorsten

AU - Gröne, Hermann-Josef

PY - 2022/12

Y1 - 2022/12

N2 - 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.

AB - 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.

KW - Rats

KW - Humans

KW - Animals

KW - Podocytes/pathology

KW - Glomerulosclerosis, Focal Segmental/pathology

KW - Nephrosclerosis/complications

KW - Capillaries/pathology

KW - Glomerular Basement Membrane/pathology

KW - Hypertension, Renal/complications

U2 - 10.1016/j.ajpath.2022.08.007

DO - 10.1016/j.ajpath.2022.08.007

M3 - SCORING: Journal article

C2 - 36150506

VL - 192

SP - 1670

EP - 1682

JO - AM J PATHOL

JF - AM J PATHOL

SN - 0002-9440

IS - 12

ER -