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Updated: Sep 28, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
Published on: August 19, 2020
[A case of mesangial proliferative glomerulonephritis with endothelial damage]
Yusuke Miki1, Hideaki Shimizu, Atsushi Danbara
1Department of Internal Medicine, Division of Nephrology, Chubu Rousai Hospital, Japan.
Insights
This study details a case of severe glomerular endothelial damage in a patient with hypertension and aortic aneurysm, leading to mesangial proliferative glomerulonephritis without immune response.
Area of Science:
- Nephrology
- Cardiovascular Pathology
Background:
- The patient had a history of hypertension, myocardial infarction, and abdominal aortic aneurysm.
- Presented with significant proteinuria and extremity edema.
Observation:
- Kidney biopsy revealed mesangial proliferative glomerulonephritis and glomerular paralysis.
- Electron microscopy showed endothelial damage and subendothelial widening.
Findings:
- Immunofluorescence studies did not detect immunoglobulin or complement deposition.
- Pathological findings mimicked thrombotic microangiopathy, but lacked HUS/TTP clinical signs.
Implications:
- Hypertension, atherosclerosis, and aortic aneurysm-induced turbulence may cause severe glomerular endothelial damage.
- This damage can lead to immune-negative mesangial proliferative glomerulonephritis.
Abstract:
We describe a 71-year-old man, who had been treated for hypertension, myocardial infarction and abdominal aortic aneurysm, and was admitted to our hospital because of proteinuria(3.9 g/day at the outpatient clinic and 1.5 g/day at the time of admission) and edema in the extremities. Light microscopic study of the kidney biopsy specimen revealed mesangial proliferative glomerulonephritis and glomerular paralysis. Electron microscopic findings showed endothelial damage, including widening of the subendothelial space and detachment of endothelial cells from the glomerular basement membrane. Deposition of immunoglobulins and complement was not detected by immunofluorescence studies. These pathological findings resemble the findings of thrombotic microangiopathy, but there were no clinical pictures of HUS/TTP. These findings suggest that hypertension, atherosclerosis and circulating turbulence caused by an aortic aneurysm induced severe glomerular endothelial damage leading to mesangial proliferative glomerulonephritis without an immune response.
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