Treatment of idiopathic retroperitoneal fibrosis using cyclosporin. (33/384)

The main goal of traditional treatment of idiopathic retroperitoneal fibrosis is limitation of morbidity, and surgery of already formed fibrous masses has been the main therapeutic approach. More recently, the knowledge that the disorder may be the result of an allergic reaction to atherosclerotic lipids has prompted the use of corticosteroids and cytotoxic drugs, which proved efficacious, but also toxic. On the basis of data indicating a T cell pathogenesis of idiopathic retroperitoneal fibrosis, cyclosporin, a non-cytotoxic pretranscriptional inhibitor of proinflammatory cytokines, was used to treat the case reported here. A 65 year old man with aggressive retroperitoneal fibrosis and obstructive renal failure initially received steroids, which eventually lost their efficacy and led to vertebral collapse. He responded to 5 mg/kg/day cyclosporin, with radiological reduction of tissue deposition, relief of urether compression, and reduction in acute phase reactants in the blood. Chronic disease remission required stable drug concentrations. In conclusion, progress in research into the T cell pathogenesis of idiopathic retroperitoneal fibrosis may justify attempts with drugs such as cyclosporin to block the disease at its origin rather than treating the morbidity.  (+info)

Primary peritonitis in infancy and childhood. (34/384)

Primary peritonitis, rarely diagnosed preoperatively, is an uncommon disease accounting for 2.1% of all pediatric abdominal emergencies. It is often associated with urinary or hepatic pathology, the former the source of the infecting organism in the majority of cases, and presents with characteristic symptoms depending upon whether it occurs in infancy or childhood. The symptoms and signs which allow for a positive prospective diagnosis are illustrated by comparing this disease to those entities with which it is most often confused, e.g. diffuse peritonitis of other etiologies, and include a short duration of symptoms, associated urinary tract infection and an absence of free air on abdominal roentgenograms. In the past, gram positive organisms were the most common infecting agent; however, in this series gram negative bacteria accounted for 69% or the organisms. Antibiotics with a gram negative spectrum and exploratory laparotomy with appendectomy are the hallmarks of therapy, the latter replaced by abdominal tap only in the patient who satisfies the criteria for primary peritonitis and in whom an associated disease makes the risk of surgery prohibitive.  (+info)

Natural history of fetal hydronephrosis diagnosed on mid-trimester ultrasound. (35/384)

OBJECTIVES: Renal tract dilatation is a common finding in routine prenatal ultrasound. However, there is no consensus as to the criteria used for differentiating pathological from physiological dilatation. The aim of this study was to evaluate the natural history and postnatal outcome of fetal hydronephrosis in an unselected obstetric population. DESIGN: This was a prospective study of fetal hydronephrosis, detected at 18-23 weeks' gestation, in a routine obstetric population. Fetal hydronephrosis was diagnosed as 'mild' if the antero-posterior renal pelvic diameter (APRPD) measured >or = 4 mm and as 'moderate/severe' if the APRPD measured > or = 7 mm or if there was associated calyceal dilatation. The postnatal outcome of fetuses with persistent hydronephrosis (> or = 10 mm in the third trimester) was determined from a postal questionnaire. RESULTS: During the study period, 11 465 women underwent an anomaly scan at 18-23 weeks of gestation. Fetal hydronephrosis was identified in 2.3% (268/11 465) of women. Mild hydronephrosis was present in 80.6% (216/268) and moderate/severe hydronephrosis in 19.4% (52/268). The hydronephrosis resolved in the antenatal or early neonatal period in 88% of fetuses. None of the fetuses with mild hydronephrosis and approximately one in three fetuses with persistent moderate/severe hydronephrosis required postnatal surgery. Overall, only one in every 1000 total births in the study population required postnatal urological surgery. CONCLUSIONS: The current study highlights the natural history of antenatally detected hydronephrosis. Mild fetal hydronephrosis appears to be associated with an excellent prognosis and probably represents the group with physiological renal pelvic dilatation. Moderate/severe fetal hydronephrosis is associated with poorer outcome and is perhaps the group that will need more intense follow up both antenatally and postnatally.  (+info)

Teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice lacking the expression of EGF and/or TGF-alpha. (36/384)

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure produces hydronephrosis and cleft palate in mice. These responses are correlated with disruption of expression of epidermal growth factor (EGF) receptor ligands, primarily EGF and transforming growth factor-alpha (TGF-alpha), and altered epithelial cell proliferation and differentiation. This research examined the role of these growth factors in TCDD-induced teratogenicity by using wild type (WT) and knockout (-/-) mice that do not express EGF, TGF-alpha, or both EGF and TGF-alpha. Pregnant females were weighed on GD 12 and dosed by gavage with either corn oil or TCDD at 24 microg/kg, 5 ml/kg. On GD 17.5, the maternal parameters evaluated included body weight, body weight gain, liver weight (absolute and adjusted for body weight). The number of implantations, live and dead fetuses, early or late resorptions, the proportion of males, fetal body weight, fetal absolute and relative liver weight, placenta weight, incidence of cleft palate, and the severity and incidence of hydronephrosis were recorded. TCDD did not affect maternal weight gain, fetal weight, or survival, but maternal and fetal liver weights and liver-to-body weight ratios were increased in all genotypes. The WT and TGF-alpha (-/-), but not the EGF (-/-) and EGF + TGF-alpha (-/-) fetuses, developed cleft palate after exposure to 24 microg TCDD/kg. Hydronephrosis was induced by TCDD in all genotypes, with the incidence in EGF + TGF-alpha (-/-) fetuses comparable to that of the WT. The incidence and severity of this defect was substantially increased in EGF (-/-) and TGF-alpha (-/-). In conclusion, this study demonstrated that expression of EGF influences the induction of cleft palate by TCDD. Also, EGF and TGF-alpha are not required for the induction of hydronephrosis, but when either is absent the response of the fetal urinary tract to TCDD is enhanced.  (+info)

Diabetes-induced microvascular dysfunction in the hydronephrotic kidney: role of nitric oxide. (37/384)

BACKGROUND: Renal hemodynamics in early diabetes are characterized by preglomerular and postglomerular vasodilation and increased glomerular capillary pressure, leading to hyperfiltration. Despite intensive research, the etiology of the renal vasodilation in diabetes remains a matter of debate. The present study investigated the controversial role of nitric oxide (NO) in the renal vasodilation in streptozotocin-induced diabetic rats. METHODS: In the renal microcirculation, basal tone and response to NO synthase blockade were studied using the in vivo hydronephrotic kidney technique. L-arginine analog N-nitro-L-arginine methyl ester (L-NAME) was administered locally to avoid confounding by systemic blood pressure effects. The expression of endothelial NO synthase (eNOS) was investigated in total kidney by immunocytochemistry and in isolated renal vascular trees by Western blotting. Urinary excretion of nitrites/nitrates was measured. RESULTS: Diabetic rats demonstrated a significant basal vasodilation of all preglomerular and postglomerular vessels versus control rats. Vasoconstriction to L-NAME was significantly increased in diabetic vessels. After high-dose L-NAME, there was no difference in diameter between diabetic and control vessels, suggesting that the basal vasodilation is mediated by NO. Immunocytochemically, the expression of eNOS was mainly localized in the endothelium of preglomerular and postglomerular vessels and glomerular capillaries, and was increased in the diabetic kidneys. Immunoblots on isolated renal vascular trees revealed an up-regulation of eNOS protein expression in diabetic animals. The urinary excretion of nitrites/nitrates was elevated in diabetic rats. CONCLUSION: The present study suggests that an up-regulation of eNOS in the renal microvasculature, resulting in an increased basal generation of NO, is responsible for the intrarenal vasodilation characteristic of early diabetes.  (+info)

Candida infection associated with a solitary mycotic common iliac artery aneurysm. (38/384)

We report on a case of an isolated common iliac artery aneurysm infected by Candida albicans. To our knowledge, only one other case of this condition has been reported. The patient, a 49-year-old man with diabetes mellitus and a history of fungal urinary tract infections, had recurrent right knee pain and swelling. The knee effusion grew C albicans. Mild right hydronephrosis and a 4.6-cm aneurysm of the right common iliac artery without involvement of the aorta or iliac bifurcation was revealed by means of a computed tomography scan. The aneurysm wall was inflammatory, and there was associated purulence at the time of operation. The right ureter was densely adherent to the anterior aspect of the aneurysm, but could be palpated and dissected free because of a ureteral stent that was placed before the surgical incision. The aneurysm was resected, and the proximal and distal margins were oversewn without graft placement. C albicans was found in the resected aneurysm. The patient recovered without limb-threatening ischemia or claudication, but the distance he could walk remained limited because of right knee symptoms. The aneurysm may have formed by direct extension of infection from the right ureter or by hematogenous or lymphatic spread. This case raises interesting issues about operative strategies and etiology.  (+info)

Effect of T-type selective calcium antagonist on renal microcirculation: studies in the isolated perfused hydronephrotic kidney. (39/384)

Although calcium antagonists exert preferential vasodilation of renal afferent arterioles, we have recently demonstrated that nilvadipine and efonidipine, possessing both L-type and T-type calcium channel blocking action, reverse the angiotensin (Ang) II-induced afferent and efferent arteriolar constriction. In the present study, we investigated the role of T-type calcium channels in mediating the Ang II-induced efferent arteriolar tone using the selective T-type calcium channel blocker mibefradil. Isolated perfused hydronephrotic rat kidneys were used for direct visualization of renal microcirculation. Administration of Ang II (0.3 nmol/L) caused marked constriction of afferent (from 13.5+/-0.6 to 9.2+/-0.6 microm, P<0.01, n=6) and efferent (from 11.5+/-1.0 to 7.4+/-0.7 microm, P<0.01, n=5) arterioles. Mibefradil (1 micromol/L) dilated both vessels, with 82+/-11% and 72+/-7% reversal of afferent and efferent arterioles, respectively. Similarly, nickel chloride (100 micromol/L) caused dilation of both arterioles, similar in magnitude in afferent (68+/-10%, n=7) and efferent (80+/-7%, n=7) arterioles. To eliminate the possibility that the mibefradil-induced dilation was mediated by L-type channel blockade, mibefradil was administered in the presence of nifedipine (1 micromol/L). Thus, nifedipine caused modest efferent arteriolar dilation (30+/-6% reversal, n=9), and subsequent addition of mibefradil elicited further dilation of this vessel (80+/-4%, P<0.01 versus nifedipine). Furthermore, mibefradil reversed the Ang II-induced efferent arteriolar constriction even in the presence of nifedipine and phentolamine. These findings demonstrate that T-type calcium antagonists markedly dilate the Ang II-induced efferent arteriolar constriction, but the action is not mediated by inhibition of catecholamine release. This potent activity would contribute to the efferent arteriolar response to nilvadipine and efonidipine and may offer benefit in light of glomerular hemodynamics.  (+info)

Evaluation and follow-up of fetal hydronephrosis. (40/384)

OBJECTIVE: To determine the antenatal course and neonatal follow-up of isolated fetal hydronephrosis. METHODS: We reviewed our ultrasonography database from January 1989 to June 1999 for all cases of unilateral or bilateral fetal hydronephrosis that had at least 1 follow-up ultrasonographic examination. Cases were defined as mild, moderate, or severe depending on the renal pelvis anteroposterior diameter and gestational age. Data were analyzed using the chi2 test with the Fisher exact test where appropriate. Medical records were reviewed, and telephone interviews were performed to determine which infants received follow-up after birth. RESULTS: Of 57,966 ultrasonographic examinations in 20,049 women during the study period, 393 patients met criteria for evaluation. Of these, 347 (88%) had fetuses with mild hydronephrosis. Most of these had complete resolution during the pregnancy. Forty patients had fetuses classified as having moderate hydronephrosis, and 6 patients had fetuses with severe hydronephrosis. Of those classified as moderate hydronephrosis, 15% resolved, 25% improved, 48% remained unchanged, and 12% worsened during the pregnancy. There were no cases of in utero resolution in the severe group; however, 4 of 6 cases improved to moderate or mild, and 2 cases remained unchanged. Of the cases identified prenatally, 25 received consultation by a pediatric urologist in the newborn period, and 7 of these required surgical intervention. CONCLUSIONS: Our population-based data suggest that most cases of mild hydronephrosis will resolve before delivery. In contrast, cases of moderate or severe hydronephrosis are less likely to have resolution in utero and are more likely to worsen or remain unchanged. Of those fetuses with persistent hydronephrosis, only a small number required some surgical intervention after birth. This information is useful in counseling the patient whose fetus is noted to have isolated hydronephrosis.  (+info)