The respiratory burst activity of peripheral leukocytes from 17 patients with chronic renal failure and 12 healthy individuals was assessed using the technique of whole-blood chemiluminescence (CL). Luminol- and lucigenin-dependent CL was measured in two dilutions of venous blood following stimulation with serum-treated zymosan or phorbol myristate acetate, and the CL peaks associated with a polymorphonuclear leukocyte count of 104 /ml were calculated. The mean CL peaks for the patients were significantly higher than those for the controls in all experimental designs (p < 0.05). This enhanced leukocyte respiratory burst activity was not associated with the underlying renal abnormality or with the type of dialysis treatment, but may have been related to the induction of tissue enzymes which is known to occur in uremia.
Thirteen of 20 female Wistar rats developed perihilar kidney scars 6 weeks after ascending infection with Escherichia coli 078. After removal of the lesser scarred kidney from 6 of the aminals, all animals were followed for 54 weeks. Proteinuria ( > 18 mg/24 h) developed at 20 weeks in the uninephrectomised infected rats and at 34 weeks in the 2-kidney infected model. In 10 uninephrectomised controls significant proteinuria did not appear until 52 weeks. In 9 2-kidney controls proteinuria did not develop at all. The speed of onset and severity of proteinuria was related to the extent of the renal parenchymal loss. Pyelonephritic scars did not show macroscopic progression over the 54-week observation period, even though the original renal infection persisted. Uninephrectomised animals with infected scars developed a highly significant rise of creatinine/body weight (p < 0.02) and of heart weight/body weight p < 0.02) ratios compared with the non-infected controls. Their kidneys showed focal and segmental hyalinosis and sclerosis of the glomeruli adjacent to the scars. Immunofluorescent staining for serum proteins was negative, but mesangial deposits of Tamm-Horsfall protein were found in the glomeruli between the scars in animals with renal impairment. These findings establish that progressive renal impairment in rats with infected kidney scars is associated with the development of proteinuria and a glomerulopathy. The cause of the glomerulopathy is not clear, both glomerular hyperfiltration and deposition of Tamm-Horsfall protein in glomerular mesangial cells may be involved.
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