Transforming growth factor-β1 in congenital ureteropelvic junction obstruction: diagnosis and follow-up

OBJECTIVE: To assess the role of transforming growth factor-β1 (TGF-β1) in congenital ureteropelvic junction obstruction at diagnosis and during postoperative follow-up. MATERIAL AND METHODS: We conducted a case-control study including 19 patients with a mean age of 6.7 years and 19 matched controls. All patients presented negative voiding cystourethrography, obstructive diuretic renogram and underwent dismembered pyeloplasty. Urinary TGF-β1 and other markers were measured pre-, intra- and postoperatively. RESULTS: The mean bladder urine TGF-β1 concentration in obstructed patients prior to pyeloplasty was higher than in controls (92.5 pg/mL ± 16.8 vs. 35.8 pg/mL ± 16.2; p = 0.0001). The mean renal pelvic urine TGF-β1 concentration in the hydronephrotic kidney was higher than in the preoperative bladder urine sample (122.3 pg/mL ± 43.9 vs. 92.5 pg/mL ± 16.8; p = 0.036). Postoperative mean TGF-β1 concentration was significantly lower than preoperative TGF-β1 (48.7 pg/mL ± 13.1 vs. 92.5 pg/mL ± 16.8; p = 0.0001). CONCLUSION: TGF-β1 is a cytokine leading to renal fibrosis. The measurement of urinary TGF-β1 could become a useful tool for the diagnosis of obstructive hydronephrosis and the evaluation of the parenchyma function status, pre and postoperatively

Neuroplasticity and dysfunction after gastrointestinal inflammation

The gastrointestinal tract is innervated by several distinct populations of neurons, whose cell bodies either reside within (intrinsic) or outside (extrinsic) the gastrointestinal wall. Normally, most individuals are unaware of the continuous, complicated functions of these neurons. However, for patients with gastrointestinal disorders, such as IBD and IBS, altered gastrointestinal motility, discomfort and pain are common, debilitating symptoms. Although bouts of intestinal inflammation underlie the symptoms associated with IBD, increasing preclinical and clinical evidence indicates that infection and inflammation are also key risk factors for the development of other gastrointestinal disorders. Notably, a strong correlation exists between prior exposure to gut infection and symptom occurrence in IBS. This Review discusses the evidence for neuroplasticity (structural, synaptic or intrinsic changes that alter neuronal function) affecting gastrointestinal function. Such changes are evident during inflammation and, in many cases, long after healing of the damaged tissues, when the nervous system fails to reset back to normal. Neuroplasticity within distinct populations of neurons has a fundamental role in the aberrant motility, secretion and sensation associated with common clinical gastrointestinal disorders. To find appropriate therapeutic treatments for these disorders, the extent and time course of neuroplasticity must be fully appreciated.Stuart M. Brierley and David R. Linde