Abstract
Altho the etiologic incitant of “lipoid nephrosis” is not known, it is likely that a host mechanism mediates the glomerular permeability changes. As a first step in examining the role of the kinin-generating system, plasma prekal1ikrein was assayed by means of its esterolytic action on a synthetic substrate. Kailikrein inhibitor was quantitated in arbitrary units. The results in 19 children, during an overt nephrotic episode (Active) and after corticosteroid-induced remission are given in the table:
After cessation of corticosteroids in 11 patients, plasma pre-kallikrein was 100.4 μmoles/ml/hr.; and kallikrein inhibitor, 0.84 units. Conclusions: 1)Plasma prekal1ikrein and kallikrein inhibitor are depressed during the active nephrotic syndrome but rise toward normal during remission; 2)Kinins may be the host mechanism mediating increased glomerular capillary permeability. Studies of urinary kallikrein are currently in progress.
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Lee, S., Kallen, R. & Spector, S. THE KININ-GENERATING SYSTEM IN LIPOID NEPHROSIS. Pediatr Res 8, 457 (1974). https://doi.org/10.1203/00006450-197404000-00702
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DOI: https://doi.org/10.1203/00006450-197404000-00702