Magnetic resonance imaging (MRI) was used to study vascular anatomy in 3 patients with the nutcracker syndrome and in 10 healthy volunteers. From these studies an abnormal branching of the superior mesenteric artery from the aorta was identified as being the cause of the nutcracker syndrome. Consequently, surgical transposition of the left renal vein to achieve an unobstructed renal venous backflow was performed successfully in 2 patients, while 1 underwent nephrectomy. In 1 patient adjuvant ureteral instrumentation became necessary to aid occlusion of persisting shunts between peripelvic venous varicosities and the urinary tract. Awareness of the pathophysiology of the nutcracker syndrome ensures an early diagnosis, which should be confirmed by a combination of diagnostic procedures, including MRI.
Sacral foramen neuromodulation--initially applied for the treatment of urinary incontinence--has proved to be effective in patients with chronic urinary retention. Thus far, the underlying neurophysiological mechanisms have not been elucidated. In an experimental study on the neurophysiological basis of sacral neurostimulation, one objective was to investigate the mechanisms responsible for initiation of micturition in chronic urinary retention. In ten female cats anesthetized with alpha-chloralose the clinical situation of sacral foramen stimulation was experimentally reproduced by isolated S2 nerve stimulation after L6-S3 laminectomy. Stimulation responses were recorded from the bladder, peripheral nerves, and striated muscles of the foot and pelvic floor. The effect of sudden cessation of prolonged S2 stimulation, during which the bladder was completely inhibited, was evaluated in 70 stimulation sequences in 5 cats. Sacral nerve stimulation induced excitatory and inhibitory effects on the bladder, depending on the frequency and intensity of stimulation. With unilateral S2 stimulation, bladder excitation was best at frequencies of 2-5 Hz and at intensities ranging between 0.8 and 1.4 times the threshold for the M-response of the foot muscle. Inhibition was the dominating effect at frequencies of 7-10 Hz and at intensities exceeding 1.4 times the threshold. Prolonged S2 stimulation above the threshold produced complete bladder inhibition during stimulation but induced strong bladder contractions after sudden interruption of stimulation, with amplitudes being significantly higher than that of spontaneous contractions preceding the stimulation. These results confirm the hypothesis of a "rebound" phenomenon as the mechanism of action for induction of spontaneous voiding in patients with chronic urinary retention.
We report on 3 patients with tumor in a horseshoe kidney, 1 of whom had bilateral tumor (renal cell cancer on the right side and urothelial cancer on the left side). Tumors that arise predominantly in the bridge of a horseshoe kidney can mimic the symptoms of an intra-abdominal disease process. Besides routine diagnostic procedures, angiography is essential to plan the surgical approach, which in principle should be organ-sparing. The literature of the embryology of the horseshoe kidney was reviewed for a relationship between the abnormal renal development and the site of tumorigenesis, and for development of a key for the wide variation of blood supply. Recently reported data suggest that the theory of a mechanical fusion is valid only for horseshoe kidneys with a fibrous isthmus but that an abnormal migration of the posterior nephrogenic area causes the majority of horseshoe kidneys in which the isthmus consists of parenchyma. Development of the isthmus through abnormal migration could predispose this location for renal cell cancer and would explain the varying forms of blood supply. Additionally, this hypothesis supports the previously raised assumption that horseshoe kidneys may be the result of teratogenic factors, which also may be responsible for the known increased incidence of related congenital anomalies and of nephroblastoma.
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