A STUDY OF SO-CALLED ESSENTIAL RENAL HEMATURIA

Abstract

The clinical and experimental studies of so-called idiopathic renal hemorrhage havegiven the following results.
(1) The clinical and statistical observation revealed no significant differences from the reports by previous many authors.
(2) The historical review of etiology of so-called idiopathic renal hemorrhage was performed in order to collect and arrange the knowledge and explanation of the genesis and nature of this disease accumulated by previous authors.
(3) The electron microscopic observation of urinary colloid and the renal tissue can contribute to the differentiation between so-called idiopathic renal hemorrhage and hematuria due to another causes. In detail, the region of cellular disorder in the kidney can be supposed by observing the change in urinary colloids, because morphologically the ability of protein in take is determined by the athrocytotic activity in the apical cell zone and the reabsorbility is decided by the function of vesicicles, Palade's particles, etc.
(4) Renal hemorrhage due to anomaly of the autonomic nervous system is explained by the glomerular hemorrhage due to the increase in capillary permeability after the hypoxia which resulted from the intrarenal circulatory disturbance by an excess stimulation of the autonomic nervous system. At the same time, the distal tubular cells reveal the cellular degeneration caused by the blood stagnation, and the communication between tublar veins and pelvic veins may be taken place. All these changes are supposed to be belonged to the irritation syndrome (Reilly).
(5) Renal hemorrhage due to the increase in intrapelvic pressure is supposed to be the bleeding from the degenerate capillary endothelial cells in the papillary region. This degeneration is presumably caused by the venous dilation and the hypoxia due to the peritubular blood stagnation which resulted from the dilation of the tubules.
(6) Renal hemorrhage by hypoxemia is probably explained by the filtration of the erythrocyte from the glomerular capillaries with a remarkable increase in permeability. This change in permeability of glomerular capillaries is caused by bothe the hypoxemia followed by renal circulatory disturbances and the increase in intrapelvic pressure. Long persistence of the change may result in the bleeding through histological changes in the interstitial blood capillaries and collecting tubules.
(7) It was clarified by the histological observation that the kidney, which clinically showed hematuria as its chief complaint and was resistant to various treatments, revealed a figure of cryptic chronic pyelonephritis and that renal hemorrhage by the inflammation of the kidney was essentially caused by chronic pyelonephritis.
(8) It wa also clarified that the hemorrhage from small pathological foci included the bleeding by minute calculi in major part. The hematuria by minute calculi can be interpreted by the vicious circle that the existence of stones causes the pericapillapillary degeneration by the local circulatory disturbances at the paillary portions which in reverse results in the increase in minute calculi in size and number. The degeneration and sequential dilation of blood capillaries or small veins at the parillary apex and collecting tubule make the rupture and the exfoliation of microliths.
(9) Renal hemorrhage during pregnancy may be interpreted by the combination of the change in capillary endothelial cells due to the increase in permeability by the toxin with the increase in capillary permeabilty by the circulatory disorder such as a mechanical pressure to the perirenal blood vessels, the degeneration of tubular cells, and the incyease in intrapelvic pressure by the increase of the pregnant uterus.