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Abstract
The possible relationship between mesangial dysfunction and development of glomerular
sclerosis was studied in the puromycin aminonucleoside (PAN) model. Five male Wistar
rats received repeated subcutaneous PAN injections; five controls received saline
only. After 4 weeks the PAN rats were severely proteinuric (190 +/- 80 mg/24 hr),
and all rats were given colloidal carbon (CC) intravenously. At 5 months glomerular
sclerosis was found in 7.6 +/- 3.4% of the glomeruli of PAN rats; glomeruli of the
controls were normal. Glomeruli of PAN rats contained significantly more CC than glomeruli
of controls. Glomeruli with sclerosis contained significantly more CC than non-sclerotic
glomeruli in the same kidneys. CC was preferentially localized within the sclerotic
areas of the affected glomeruli. Since mesangial CC clearance from the mesangium did
not change during chronic PAN treatment, we conclude that this preferential CC localization
within the lesions is caused by an increased CC uptake shortly after injection in
apparent vulnerable areas where sclerosis will develop subsequently. Cluster analysis
showed a random distribution of lesions in the PAN glomeruli in concordance with the
random localization of mesangial areas with dysfunction in this model. Similar to
the remnant kidney model in PAN nephrosis the development of glomerular sclerosis
may be related to "mesangial overloading."