1962 Volume 53 Issue 4 Pages 291-307
Renal calcification was experimentally induced in one side kidney by the means of temporal ischemia (for one and two hours) while another side of kidney was removed prior to the experiment and variations both of volumes and concentrations of urinary, serum mucoprotein and protective colloids in urine were investigated, and comparison of these results were made between changes of both urinary and of serum calcium levels. In addition, the histochemical study of kidney was also carried out (by the method of PAS and Von Kossa stain).
Following results were obtained:
1) High Levels of the mucoprotein excretion in urine were maintained during the oliguric period caused by renal ischemia. When urinary volume was recovered to the normal, the concentration and daily output of urinary mucopratein increased and lasted for 10 days: This was more prominent in the ischemic group of 2 hours.
2) Serum mucoprotein also showed the high level after ischemia in many cases. In these cases these values were parallel with urinary mucoprotein.
3) Although the values of protective colloids in urine increased after ischemia in the many cases, it was variable and any difinite relationship was not found between these values and those of urinary mucoprotein.
4) Urinary calcium slightly increased in early stage. Any significant change was not seen in serum calcium value.
5) Calcium deposits were seen in many cases of which renal blood supply was stopped for 2 hours. The main site of renal involvement was evident in renal tubules, and its necrotic lesion and casts were positive by PAS stain. Calcium deposits were developed over these lesions.
On these results it was considered that the most of urinary mucoprotein appeared to be the sum of those which was originated from serum mucoprotein and from the epithelium of degenerated renal tubules, and that the changes of this substance in renal tubules were very important as a cause of calcium deposits in ischemic kidney of rabbit.
