title: [Histological study of fetal hydronephrosis. Development background of prenatal treatment].
abstract: It is still unclear whether prenatal decompression of the dilated urinary tracts can preserve renal development and function. Following the previous report on the relationship between the nephrogenesis and the gestational weeks in normal fetuses, we studied the hydronephrotic kidneys to find the histological background of the fetal treatment. Of the fetuses autopsied in the Department of Pathology of our Institute from 1982 to 1992, 32 kidneys from 21 fetuses associated with dilatation of the upper urinary tracts irrespective of the presence of urethral obstruction on macroscopic inspections were reviewed. The underlying disorders causing hydronephrosis included urethral obstruction in 7, vesico-intestinal fissure in 3, hydrometrocolpos in 2 and double ureter in 1. The etiology of the hydronephrosis was not clarified in another 8. The position and configuration of the ureteral orifices were not described in the autopsy reports. Microscopic examination was done to define the radial glomerular count (RGC), presence or absence of the nephrogenic zone, cortical cysts and dysplastic elements, changes of the collecting tubules and interstitium. Of the kidneys 19 had cortical cysts of various sizes. In some kidneys, the normal cortex was mixed with pathological segments where there were subcapsular small cysts and tubular dilatation. Nephrogenic zone, which was observed in specimens of 33-weeks fetus with moderate hydronephrosis, was already missing by 28 weeks in severe hydronephrosis. Collecting tubules were dilated in 12 kidneys with mild to moderate hydronephrosis. Tubular atrophy and increase in the interstitium were seen in 12 kidneys, eleven of which were of the fetus over 30 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Division of Urology, Osaka Medical Center and Research Institute for Maternal and Child Health.
authors.forename: K
authors.initials: K
authors.lastname: Shimada
authors.forename: S
authors.initials: S
authors.lastname: Hosokawa
authors.forename: A
authors.initials: A
authors.lastname: Tohda
mesh_terms: D005314:Embryonic and Fetal Development; D005315:Fetal Diseases / Q000473:pathology* / Q000628:therapy; D005865:Gestational Age; D006801:Humans; D006869:Hydronephrosis / Q000473:pathology* / Q000628:therapy