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Updated: Dec 19, 2025

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
High Blood Pressure Is Associated with Tubulointerstitial Damage along with Glomerular Damage in Glomerulonephritis.
Claudio Bazzi1, Teresa M Seccia2, Pietro Napodano3
1D'Amico Foundation for Renal Disease Research, 20145 Milan, Italy.
Insights
Hypertension worsens kidney damage in glomerulonephritis (GN). This study found that high blood pressure is linked to more severe tubulointerstitial damage (TID) in GN patients, independent of proteinuria.
Area of Science:
- Nephrology
- Pathology
Background:
- Arterial hypertension is a known driver of chronic kidney disease (CKD) progression.
- The specific impact of hypertension on tubulointerstitial damage (TID) within glomerulonephritis (GN) requires further clarification.
Purpose of the Study:
- To determine if TID is associated with glomerular damage in GN.
- To investigate if hypertensive GN patients exhibit more severe tubulointerstitial damage.
Main Methods:
- Retrospective analysis of 448 patients with biopsy-diagnosed primary GN, lupus nephritis (LN), or nephroangiosclerosis (NAS).
- Microscopic examination of at least six glomeruli per biopsy using light and immunofluorescence microscopy.
- Assessment of global glomerulosclerosis (GGS%), TID, and arteriolar hyalinosis (AH) as CKD severity markers.
Main Results:
- Hypertension was present in 52% of patients; 88.9% of NAS patients were hypertensive.
- Hypertensive GN patients showed greater glomerular and tubular damage than normotensive patients, irrespective of proteinuria levels.
- Both hypertension and global glomerulosclerosis (GGS%) were significantly associated with increased TID in GN.
Conclusions:
- In glomerulonephritis patients, high blood pressure contributes to both glomerular and tubulointerstitial damage.
- The severity of tubulointerstitial damage in GN is associated with hypertension.
Abstract:
The key role of arterial hypertension in chonic kidney disease (CKD) progression is widely recognized, but its contribution to tubulointerstitial damage (TID) in glomerulonephritis (GN) remains uncertain. Hence, the objective of this study is to clarify whether TID is associated with glomerular damage, and whether the damage at the tubulointerstitial compartment is more severe in hypertensive patients. The study included retrospectively consecutive patients referred to the Nephrology Unit with diagnoses of primary glomerulonephritis, lupus nephritis (LN), and nephroangiosclerosis (NAS) at biopsy. At least six glomeruli per biopsy were analysed through light and immunofluorescence microscopy. Global glomerulosclerosis (GGS%), TID, and arteriolar hyalinosis (AH) were used as markers of CKD severity. Of the 448 patients of the cohort, 403 received a diagnosis of GN, with the remaining being diagnosed with NAS. Hypertension was found in 52% of the overall patients, with no significant differences among those with GN, and reaching 88.9% prevalence rate in NAS. The hypertensive patients with GN had more marked damage in glomerular and tubular compartments than normotensives independently of the amount of proteinuria. Moreover, hypertension and GGS% were found to be strongly associated with TID in GN. In GN patients, not only the severity of glomerular damage but also the extent of TID was associated with high blood pressure.
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