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Currently available experimental observations in renal and non-renal tissues appear to suggest the possibility that these other mechanisms may operate through glomerular growth promoters, which have the capacity to induce both glomerular hypertrophy and mesangial matrix accumulation, leading to the typical glomerular sc1erotic lesion. It should be emphasized, however, that there are potentially numerous biological substanees as yet undiseovered which are eapable of promoting glomerular growth and mesangial matrix aeeumulation.
36. 37. 38. 39. 40. 41. 42. 43. 44. 45. Seyer-Hansen K, Hansen J, Gundersen HJG: Renal hypertrophy in experimental diabetes. Diabetologia, 18: 501-505, 1980. Mauer SM, Steffes MW, Azar S, Sandberg SK, Brown D: The effect of Goldblatt hypertension on development of the glomerular lesions of diabetes mellitus in the rat. Diabetes, 27: 738-744, 1978. Neugarten J, Feiner HD, Schacht RG, Gallo GR, Baldwin DS: Aggravation of experimental giomerulonephritis by superimposed clip hypertension. Kidney Int, 22: 257-263, 1982.
Initial disease-specifie pathogenie processes lead to a loss of funetioning nephrons, resulting in alterations of funetion and metabolism in intact glomeruli, whieh promote growth of intaet glomeruli and aeeumulation of extraeellular matrix in the mesangium area, whieh ultimately produees selerosis and further loss of nephrons. The ultimate outeome of this vieious eycle is the end-stage kidney. In both focal glomerular sclerosis and diabetes, the initial disease specifie pathophysiologie meehanisms, per se, are linked to glomerular hypertrophy.