Abstract

Introduction and aim: EGF acts through EGF receptor and facilitates regeneration of tubular epithelial cells after injury. We investigated the role of urinary EGF excretion as biomarker for pathology and renal function outcome in glomerulonephritis.

Methods: EGF urinary levels were estimated in 3 forms of glomerular diseases: A. IgA nephropathy (IgAN), as chronic glomerulonephritis, [n=50, 21 female, age 39.8yrs (18- 65)]

B. Pauci immune rapidly progressive glomerulonephritis (RPGN), as acute glomerulonephritis, [n=38, 17 female, age 59.5yrs (25-80)]

C. Nephrotic syndrome (NS) due to focal segmental glomerulosclerosis (FSGS) [n=23, 9 female, age 47.5yrs(19-79)] and minimal change disease (MCD) [n=12, 7female, age 45.5yrs (37-62)]. Ten healthy volunteers were used as controls. First morning urine samples were collected on the day of renal biopsy. Patients were followed up for 7.5±2.1yrs.

Result: EGF urinary levels were: IgAN 0.13±0.2, FSGS 0.19±0.2, MCD 0.7±0.4, RPGN 0.15±0.3, controls 0.14±0.07pg/mgUcr. EGF urinary levels had significant negative correlation with severity of interstitial fibrosis, r=-0.6, p=0.02, in IgAN, with the percentage of fibrous crescents, r=-0.6, p=0.01 in RPGN, and finally, with the percentage of global sclerosed glomeruli, r=-0,5, p=0,04, degree of fibrosis, r=- 0.6, p=0.005 and interstitial infiltration, r=-0.6, p=0.01 in patients with NS. Declining renal function was associated with reduced urinary EGF levels in IgAN (0.04±0.04 vs. 0.2±0.2pg/mgUcr, p=0.01), and FSGS (0.007±0.004 vs. 0.6±0.04pg/mgUcr, p=0.009), but not in RPGN (0.05±0.1 vs. 0.2±0.4pg/mg cr, p=NS).

Conclusion: Reduction of EGF urinary levels in patients with glomerulonephritis is associated with “chronic” histological changes, and can predict renal function outcome mainly in patients with chronic forms of glomerulonephritis.