Morphological study of congenital megaureter.

Congenital anomalies of the kidney and urinary tract are frequent. They can be detected once every 500 ultrasonography fetal examinations. Causes that determine a dilated ureter compared to the rest of the urinary tract are still partly unknown. If concerning the exploration and the clinical diagnosis of these anomalies important progresses have been made, the morphological research is still able to bring forth data that, together with genetic researches, may help reveal the pathogeny of the disease and may ease the planning of the screening genetic tests for early diagnosis. Material and methods. During the surgical operations realized in order to recalibrate the ureter, ureter fragments have been harvested, colored with 1% tionin, in sections thinner then 1 micron and examinated through immersion, ob. 100x. Other fragments have been prepared and examinated through electronic microscope. We have followed the structural modifications of the muscular tissue, nervous tissue, connective tissue and the rapports between these components. Results. Congenital megaureter presents qualitative and quantitative anomalies of the connective tissue and muscular tissue, and also structural modifications of the nervous tissue. Connective tissue. We have noticed the abundance of the connective tissue in congenital megaureter. Connective tissue, with an important representation of typical elements, such as fibroblasts, mastocytes and plasmocytes is partly hyalinated, dissociating muscular fiber bundles and nervous fiber bundles. Connective tissue/muscular tissue report is evidently increased. Muscular tissue. Muscular fibers are hypoplasic, smooth endoplasmic reticulum is present in the tubular form, rare mitochondria are vacuolized. Dense corps are increased in number, plasmatic membranes are folded. Sarcoplasm contains vacuolized organites. The nuclei are rigged with visible nucleoli. Nervous structures. We have noticed varied alterations of the axons and myelin. In some axons there are multiple cavities that may produce the opacifiation of the entire axonal structure. The proliferation of the myelin sheath under the nodular form or vortex form produces the destruction of the axonal structure. Mitochondria are condensed, partially vacuolized. The modifications in the axonal structure and those of the myelin sheath determine modifications of the nervous excitability and conductibility. All the lesions we have pointed out in congenital megaureter participate in compromising of the peristaltic. Nervous and muscular structures lesions indicate a process of incomplete development of the ureter. They are structures that do not achieve functional maturation. We may consider congenital megaureter as a digenesis with hypoplasia.