It was shown that loss of sulfated proteoglycans and anionic regions in the basal membrane of the glomerulus and the
mesangial mat rix caused excess accumulation of proteoglycans such as chondroitin sulphate and dermatan sulphate in these areas.3 This causes a decrease in charge-dependent renal selectivity and an increase in the thickness of the basal membrane.
Light microscopy indicated a proliferation of
mesangial cells and
mesangial matrix, with only a minority of tissue samples showing segmental sclerosis.
Histopathology showed presence of fetal glomeruli & mild
mesangial matrix accentuation in one glomerulus.
In the glomeruli, this receptor seems to be present in all major renal cells, including
mesangial cells, endothelial cells, and podocytes.
But in our case due to the absence of hematuria and the classical features such as
mesangial segmental hypercellularity, increased
mesangial matrix and granular IgA deposits in the mesangium, the possibility of IgA nephropathy was ruled out.
Glomerular global sclerosis was observed in one glomerulus and increased
mesangial cells and matrix, and glomerular hypertrophy in other glomerulus.
The light microscopic examination of a kidney biopsy revealed two out of 15 glomeruli with global sclerosis, a diffuse endocapillary and
mesangial proliferative pattern without crescents, and 30% interstitial fibrosis and tubular atrophy.
Renal biopsy showed mild focal glomerular
mesangial expansion.
Several glomeruli showed focal and segmental increase in
mesangial cellularity and sclerosis.
CKD is defined clinically by prolonged and progressive loss of kidney function measured by a declined glomerular filtration rate (GFR) and the presence of albuminuria with pathological findings of
mesangial expansion, inflammation, and renal fibrosis [1].