STUDIES ON UNEXPLAINED RENAL HEMATURIA
II. Experimental Studies on Changes in Fibrinolytic Enzyme Systems of Dogs Due to Renal Venous Congestion and Ischemia
1981 Volume 72 Issue 1 Pages 60-73
Details
1981 Volume 72 Issue 1 Pages 60-73
The author performed experimental studies on mongrel dogs to elucidate the mechanism of abnormalities in the urinary fibrinolytic enzyme systems of patients with renal hematuria. Renal venous congestion and ischemia which are considered to be the cause of renal hematuria were induced in dogs by constriction of the renal vein and occlusion of the renal artery. Changes of fibrinolytic enzyme activity in blood and urine by these manipulations were measured. Furthermore, the secretion site of urokinase (UK) and urinary trypsin inhibitor (UTI) were studied by the stop-flow technique.
The results are as follows:
1) Microscopic hematuria was noted in the urine from the treated side during and/or after constriction of the vein and occlusion of the artery, the degree of hematuria being more marked in the former.
2) Significant increases in the UK and UTI levels on the treated side were recognized, whereas significant changes of the fibrinolytic activity were not observed in the blood of treated renal vein and femoral artery. A difference in the secretion modes of both urinary enzymes was noted.
3) UK activity was observed only in fractions with the highest PAH concentration, which was considered to be at the level of the proximal tubule as determined by the stop flow technique. UTI activity was recognized in all fractions and presented a pattern similar to that of urinary protein concentration, and its highest activity was noted in the site which was considered to be the proximal tubule.
On the basis of these results, it is considered that renal venous congestion and ischemia are the causes of renal hematuria. It is also assumed that these abnormalities of renal hemodynamics give rise to UK secretion, and that the site of such secretion is the proximal tubule of the nephron.
