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"Glomerular obsolescence is a common histologic feature in various renal diseases, of which histogenesis remains unclarified especially in renal tuberculosis, and little has been attributed for the postulation of low prevalence of hypertension in such occasion. One hundred and fifty consecutive nephrectomy specimens with renal tuberculosis under the age of 50 were histopathologically analyzed along with comparison of 18 cases of chronic pyelonephritis, 15 hydronephrosis and 10 acute traumatic kidneys. Glomerular sclerosis following tuberculous glomerulitis seemed little significant in its histogenesis except in one case, which presented epitheliold cell reaction and crescent formation. Wrinkling and thickening of glomerular basement membrane and subsequent simplification of tufts with mesangiolysis(Stage I and II) represented the major alternative glomerulopathy in nodular renal tuberculosis, whereas in confluent ulcero - cavitary lesion the development of hyalin-knot within the Bowman`s space and collapse of the tufts (Stage III and IV) comprised the bulk, aside from frequent intraglomerular shunt formation between afferent and efferent arterioles mostly in autonephrectomized cases, Arteriolosclerosis was found in 17.2 % among nodular type, while 26.7% in ulcero-cavitary, variety, partly responsible for the histogenesis of glomerular obsolescence. Those cases with moderate arterio and arteriolar sclerosis showed a high tendency of transformation into stage III-IV obsolescence especially in ulcero-cavitary tuberculosis. Relative prevalence rate of systolic hypertension in ulcerocavitary tuberculosis was 5.8%, two times higher than nodular type, but in only one case the post -operative blood pressure returned to normal range. With the above findings it is assumed that glomerular oboslescence of so-called hypertensive glomerulopathy is a subtype of ischemic nature, and induced not only by vascular is chemic changes but also compromised through the intra-renal tubular obstruction and intraglomerular capillary shunt formaion may attribute to the development of secondary hypertension, though rare, in renal tuberculosis associated with arteriosclerot ic changes as well."
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