EXPERIMENTAL ATRESIA OF THE URETER.

Area of Science:

• Nephrology and Urology
• Renal Physiology
• Pathology

Background:

• Complete ureteral occlusion is known to cause either hydronephrosis or renal atrophy.
• Previous studies, including Lindemann's work on dogs and rabbits, have shown variable outcomes and proposed mechanisms involving intrapelvic pressure and collateral blood supply.
• The compensatory mechanisms and resulting fluid accumulation or atrophy are not fully understood.

Purpose of the Study:

• To investigate the effects of ureteral occlusion on kidney structure and fluid composition.
• To analyze the chemical characteristics of accumulated fluid in hydronephrosis.
• To compare findings in animal models with a human case.

Main Methods:

• Induction of complete ureteral occlusion in dogs and rabbits.
• Observation of resulting hydronephrosis or atrophy.
• Chemical analysis of accumulated renal pelvic fluid, including specific gravity, total solids, proteids, urea, and chloride content.
• Histological examination of renal tissue.

Main Results:

• All dogs in the study developed hydronephrosis after the initial operation.
• The accumulated fluid showed a uniform chemical composition, resembling dilute lymph with significantly higher chloride content than serum or lymph.
• Histological examination revealed renal cell necrosis, glomerular obliteration, increased connective tissue, and vascular changes (endarteritis, periarteritis).

Conclusions:

• The high chloride content in the renal fluid is a key characteristic, likely due to slow absorption from the kidney pelvis.
• Histological changes indicate significant renal damage following ureteral occlusion.
• The findings provide insights into the pathophysiology of hydronephrosis and the composition of non-urinary renal fluid.