EXPERIMENTAL-MODEL OF FOCAL SCLEROSIS .1. RELATIONSHIP TO PROTEIN EXCRETION IN AMINONUCLEOSIDE NEPHROSIS

  • 1 January 1977
    • journal article
    • research article
    • Vol. 36  (5) , 519-526
Abstract
An experimental model of focal sclerosis (FS) following chronic administration of aminonucleoside (AMNS) is described in rats with pathologic features similar to those observed in human steroid-resistant idiopathic nephrotic syndrome. Six groups of rats were given I.P. injections of either 0.9% normal saline or aminonucleoside (13 ng/100 g of body weight); 4 groups underwent a right nephrectomy on day 22; a 2 series of injections of saline or aminonucleoside were then administered to all 6 groups: group I (5 animals), saline-saline; group II (10 animals), AMNS-AMNS; group III (10 animals), AMNS-nephrectomy-AMNS; group IV (5 animals), AMNS-nephrectomy-saline; group V (5 animals), saline-nephrectomy-AMNS; group VI (5 animals), saline-nephrectomy-saline. A relationship between the percentage of glomeruli with focal sclerosis and the total amount of protein excreted during the course of the experiment was observed (r [correlation coefficient] = 0.80). An apparent threshold level of protein excretion essential for the development of FS was also noted in that all rats excreting greater than 2.2 integral units developed FS whereas those excreting less than this amount did not. The highest incidence of FS was seen in rats that had received AMNS after unilateral nephrectomy: 62% of glomeruli with FS in group III and 26% in group V; whereas no FS was seen in groups I and VI or in rats evaluated 7-23 days after a single injection of AMNS. A quantitative relationship between the breakdown in the permeability barrier to protein and the ultimate development of FS was found. The prior demonstration of epithelial cell alteration in acute AMNS disease and the morphologic changes presented in this and the subsequent paper support the concept that irreversible epithelial cell injury may be the primary event in the development of FS.

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