Subject(s)
Fetal Diseases/diagnostic imaging , Hydronephrosis/diagnostic imaging , Ultrasonography, Prenatal , Urethral Obstruction/diagnostic imaging , Algorithms , Female , Fetal Diseases/embryology , Fetal Diseases/therapy , Humans , Hydronephrosis/etiology , Hydronephrosis/therapy , Kidney/embryology , Kidney/physiology , Pregnancy , Urethral Obstruction/complications , Urethral Obstruction/embryology , Urethral Obstruction/therapyABSTRACT
PURPOSE: The aim of this study was to determine the risk factors for vesicoureteral reflux following ureteral reimplantation to identify a population that can be safely excluded from postoperative voiding cystography. MATERIALS AND METHODS: We retrospectively reviewed the medical records of 273 patients who underwent ureteroneocystostomy for vesicoureteral reflux between 1990 and 1998 and recorded the postoperative renal ultrasonography and voiding cystography results. RESULTS: There were 273 patients (534 ureters) who underwent ureteral reimplantation. We recorded the grade of preoperative hydronephrosis and vesicoureteral reflux and noted several preoperative and intraoperative variables, such as dysfunctional voiding, breakthrough infections, renal scarring, bladder trabeculations, type of reimplant, and postoperative urinary tract infections. With a mean follow-up of 20.6 months, persistent postoperative vesicoureteral reflux was noted in 11 patients (4%). Persistent postoperative reflux was noted in 11 patients (4%) or 12 renal units (2.2%). Reflux resolution rates for 534 renal units and 273 patients after routine follow-up voiding cystourethrogram (VCUG) was 97.8% (renal units) and 96% (patients), respectively. Contralateral vesicoureteral reflux developed in 4 (5.1%) of the 78 patients who underwent unilateral reimplantation. Two patients (0.7%) had postoperative ureteral obstruction. The risk factors for persistent postoperative reflux were identified as preoperative and postoperative hydronephrosis, renal scarring, and tapered reimplantations. The type of reimplant did not correlate with outcome. CONCLUSIONS: Vesicoureteral reflux after ureteral reimplantation is uncommon (4%). Because of the high success rate of ureteral reimplants and the benign course of those patients with persistent low-grade postoperative reflux, it is safe and efficient to eliminate postoperative VCUG in most patients who had a simple ureteral reimplantation for reflux. However, in some higher-risk patients, such as those with preoperative hydronephrosis, renal scarring, and ureteral tapering, postoperative voiding cystography may be indicated to assure resolution of vesicoureteral reflux.
Subject(s)
Cystostomy/adverse effects , Postoperative Care , Ureter/surgery , Vesico-Ureteral Reflux/diagnostic imaging , Vesico-Ureteral Reflux/etiology , Female , Follow-Up Studies , Humans , Male , Radiography , Retrospective Studies , UrinationABSTRACT
Atrial and brain natriuretic peptides (ANP and BNP, respectively) are potent pulmonary vasodilators that are upregulated in hypoxia-adapted rats and may protect against hypoxic pulmonary hypertension. To test the hypothesis that C-type natriuretic peptide (CNP) also modulates pulmonary vascular responses to hypoxia, we compared the vasodilator effect of CNP with that of ANP on pulmonary arterial rings, thoracic aortic rings, and isolated perfused lungs obtained from normoxic and hypoxia-adapted rats. We also measured CNP and ANP levels in heart, lung, brain, and plasma in normoxic and hypoxia-adapted rats. Steady-state CNP mRNA levels were quantified in the same organs by relative RT-PCR. CNP was a less potent vasodilator than ANP in preconstricted thoracic aortic and pulmonary arterial rings and in isolated lungs from normoxic and hypoxia-adapted rats. Chronic hypoxia increased plasma CNP (15 +/- 2 vs. 6 +/- 1 pg/ml; P < 0.05) and decreased CNP in the right atrium (35 +/- 14 vs. 65 +/- 17 pg/mg protein; P < 0.05) and in the lung (3 +/- 1 vs. 14 +/- 3 pg/mg protein; P < 0.05) but had no effect on CNP in brain or right ventricle. Chronic hypoxia increased ANP levels fivefold in the right ventricle (49 +/- 5 vs. 11 +/- 2 pg/mg protein; P < 0.05) but had no effect on ANP in lung or brain. There was a trend toward decreased ANP levels in the right atrium (2,009 +/- 323 vs. 2,934 +/- 397 pg/mg protein; P = not significant). No differences in CNP transcript levels were observed between the two groups of rats except that the right atrial CNP mRNA levels were lower in hypoxia-adapted rats. We conclude that CNP is a less potent pulmonary vasodilator than ANP in normoxic and hypoxia-adapted rats and that hypoxia raises circulating CNP levels without increasing cardiopulmonary CNP expression. These findings suggest that CNP may be less important than ANP or BNP in protecting against hypoxic pulmonary hypertension in rats.
