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A semiquantitative glomerular damage index (GDI) was determined for overall (O), superficial (S), and juxtamedullary (JM) glomeruli in four models of experimental hypertension in the rat to assess the severity and distribution of injury in light of present day knowledge of glomerular hemodynamics. After a four week period of similar hypertension, comparison of Group 1 (renal ablation) with Group 2 (aortic ligature) revealed OGDIs of 0.420 +/- 0.064 (SEM) vs. 0.062 +/- 0.019, P less than 0.0001, SGDIs of 0.250 +/- 0.071 vs. 0.035 +/- 0.007, P less than 0.0089, and JGDIs of 0.455 +/- 0.071 vs. 0.155 +/- 0.036, P less than 0.002. Within Group 1 the SGDI and JMGDI were not significantly different but within Group 2 the SGDI was less (P less than 0.005) than the JMGDI. Arterial/arteriolar damage was comparable in both groups. After an eight week period of similar hypertension, comparison of Group 3 (deoxycorticosterone-saline) with Group 4 (stroke-prone spontaneously hypertensive rats) showed OGDIs of 0.301 +/- 0.065 vs. 0.128 +/- 0.023, P less than 0.025, SGDIs of 0.289 +/- 0.096 vs. 0.072 +/- 0.015, P less than 0.044, and JMGDIs of 0.394 +/- 0.083 vs. 0.307 +/- 0.062, NS. Within Group 3 the SGDI and JMGDI were not significantly different, but within Group 4 the SGDI was less (P less than 0.002) than the JMGDI. Vascular damage in the two groups was comparable. Taking into account known physiologic data, the findings are consistent with the idea that increased preglomerular resistance is protective of glomeruli, whereas decreased resistance with increased pressure and/or flow is injurious.(ABSTRACT TRUNCATED AT 250 WORDS)

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The examination of a piece of kidney cortex taken during sympathectomy for hypertension affords a method of studying the pathological changes during life. The present study has been undertaken to see if the severity of the vascular changes influenced the response to sympathectomy and other surgical methods for the lowering of blood pressure in patients with hypertension. Several other features that emerged in this investigation are also described.MATERIAL AND METHOD Portions of renal cortex were obtained from 50 patients with hypertension at the same time as the operations of sympathectomy and/or adrenalectomy were performed. In 5, biopsies were performed on both kidneys, and in the remainder, on one side only. The size of the specimen was of the order of 0.8 x 0 4 x 0 3 cm., and it was taken from the superficial part of the cortex after incising and partially reflecting the capsule. No untoward effects could be attributed to this. The material was fixed in 10 per cent formal-saline and sections cut at 5-it thickness in the long axis of the specimen at right angles to the subcapsular surface. Sections were stained routinely with hematoxylin and eosin, hamatoxylin and van Gieson's stain, and the Hart-Sheridan method for elastic tissue. Where necessary the following stains were used-periodic acid-Schiff, Mallory's phosphotungstic acid himatoxylin, 1 per cent toluidine blue, and Gordon and Sweet's method for reticulin.

The X-linked enzyme, glucose-6-phosphate dehydrogenase (G-6-PD) was used as a cellular marker to study the clonal characteristics of human atherosclerotic lesions from females heterozygous for G-6-PD isoenzymes. Portions of uninvolved aortic wall contained both isoenzyme types (A and B), and their isoenzyme patterns were used to establish criteria for polyclonal lesions. Portions of uterine leiomyomas contained predominantly one isoenzyme type (either all A or all B) and their isoenzyme patterns were used to establish criteria for monoclonal lesions. These techniques were used to address three questions concerning atherogenesis. First, evidence for the monoclonal origin of fibrous-capped plaques was provided by the findings that small plaques had G-6-PD isoenzyme distributions similar to those of leimyomas; that in large plaques with multiple portions assayed for G-6-PD, a large proportion (25 of 26, 96%) of plaques had monoclonal characteristics; and that multiple monoclonal portions were present in the same plaque. Second, the role of the fatty streak as a precursor of fibrous plaques was supported by the demonstration that a proportion (11 of 66, 16.7%) of fatty streaks contained isoenzyme patterns intermediate between those of polyclonal uninvolved aortic wall and monoclonal leiomyomas. Increased cellularity of fatty streaks correlated with increased deviation of isoenzyme pattern toward monoclonality. Third, the assay of portions of both small and large plaques provided no evidence for clonal selection as plaques increase in size.

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