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Interstitial myofibroblasts in IgA glomerulonephritis

T D Hewitson¹, G J Becker

¹Department of Nephrology, Royal Melbourne Hospital, Australia.

American Journal of Nephrology

|January 1, 1995

Summary

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Myofibroblast cells expressing alpha-smooth muscle actin (alpha-SMA) are significantly increased in IgA glomerulonephritis, contributing to progressive renal fibrosis and tubulointerstitial injury.

Area of Science:

Nephrology
Pathology
Cell Biology

Background:

Mesangial IgA glomerulonephritis is a common cause of progressive kidney disease.
The role of myofibroblasts in renal interstitial fibrosis is not fully understood.

Purpose of the Study:

To investigate the presence and role of myofibroblasts in progressive renal interstitial fibrosis in patients with mesangial IgA glomerulonephritis.

Main Methods:

Examination of renal biopsy specimens from 25 patients with IgA glomerulonephritis and 6 controls.
Identification of myofibroblasts using morphology and alpha-smooth muscle actin (alpha-SMA) immunostaining.
Correlation of alpha-SMA staining with interstitial leukocytes, collagen III, tubular atrophy, and renal function.

Main Results:

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Fractional volume of interstitial alpha-SMA staining was significantly higher in IgA glomerulonephritis patients (17.2%) compared to controls (1.3%).
Alpha-SMA staining correlated positively with tubular atrophy/dilation, interstitial connective tissue, leukocytes, and collagen III.
Alpha-SMA expression correlated with impaired renal function at biopsy and after 2 years of follow-up.

Conclusions:

Cells with a myofibroblast-like phenotype play a significant role in the progression of tubulointerstitial injury in IgA glomerulonephritis.
Alpha-SMA staining serves as a marker for myofibroblast activity and correlates with disease severity and progression.