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Six kidney biopsies of patients in different phases of leptospirosis were analyzed using both light and electron microscopy.
Electron microscopy disclosed a definite glomerular lesion in human leptospirosis, characterized by focal thickening of the basal membrane and fusion of the foot process of the glomerular epithelial cell, which is in agreement with the proteinuria seen in the disease.
The tubular lesion was characterized by a total or partial brush border loss, disjunction of the cellular limits, mitochondrial depletion and increased number of dense bodies. Brush border absence, also seen in the experimental disease, explains why alkaline phosphatase activity is not demonstrated focally in the kidney cortex of infected guinea pigs.
Although Leptospira icterohaemorrhagiae has not been conclusively demonstrated to possess a toxin, clinical, histological and now cellular changes strongly suggest a toxin acting in the mechanism of leptospiral pathogenicity.
Among the many factors able to contribute to the picture of tubular failure, the cellular disjunction could be basic in leptospirosis, acting through a shunt mechanism between glomerular filtrate and the kidney interstitium.
Mitochondrial depletion and the origin of the increased number of dense bodies seen mainly in the tubular cell is discussed.