The cystic fibrosis transmembrane conductance regulator (CFTR) and aquaporin-9 (AQP-9) are present in the luminal membrane of the epididymis, where they play an important role in formation of the epididymal fluid. Evidence is accumulating that CFTR regulates other membrane transport proteins besides functioning as a cAMP-activated chloride channel. We have explored the possible interaction between epididymal CFTR and AQP-9 by cloning them from the rat epididymis and expressing them in Xenopus oocytes. The effects of the expressed proteins on oocyte water permeability were studied by immersing oocytes in a hypo-osmotic solution, and the ensuing water flow was measured using a gravimetric method. The results show that AQP-9 alone caused an increase in oocyte water permeability, which could be further potentiated by CFTR. This potentiation was markedly reduced by phloretin and lonidamine (inhibitors of AQP-9 and CFTR, respectively). The regulation of water permeability by CFTR was also demonstrated in intact rat epididymis luminally perfused with a hypo-osmotic solution. Osmotic water reabsorption across the epididymal tubule was reduced by phloretin and lonidamine. Elevation of intracellular cAMP with 3-isobutyl-1-methylxanthine increased osmotic water permeability, whereas inhibiting protein kinase A with H-89 (N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide hydrochloride) reduced it. These results are consistent with a role for CFTR in controlling water permeability in the epididymis in vivo. We conclude that this additional role of CFTR in controlling water permeability may have an impact on the genetic disease cystic fibrosis, in which men with a mutated CFTR gene have abnormal epididymis and infertility.
Background There were limited data on the association of adipose microRNA expression with body composition and adverse clinical outcomes in patients with advanced chronic kidney disease (CKD). We aimed to evaluate the association of adipose miR-130b and miR-17–5p expressions with body composition, functional state, cardiovascular outcome and mortality in incident dialysis patients. Methods We performed a single-centre prospective cohort study. Patients who were planned for peritoneal dialysis were recruited. MiR-130b and miR-17–5p expressions were measured from subcutaneous and pre-peritoneal fat tissue obtained during peritoneal dialysis catheter insertion. Body composition and physical function were assessed by bioimpedance spectroscopy and Clinical Frailty Scale. Primary outcome was 2-year survival. Secondary outcomes were 2-year technique survival and major adverse cardiovascular event (MACE) rate. Results Adipose expression of miR-130b and miR-17–5p correlated with parameters of muscle mass including intracellular water (miR-130b: r = 0.191, P = 0.02; miR-17–5p: r = 0.211, P = 0.013) and lean tissue mass (miR-130b: r = 0.180, P = 0.03; miR-17–5p: r = 0.176, P = 0.004). miR-130b expression predicted frailty significantly (P = 0.016). Adipose miR-17–5p expression predicted 2-year all-cause survival (P = 0.020) and technique survival (P = 0.036), while miR-130b expression predicted incidence of major adverse cardiovascular events (P = 0.015). Conclusions Adipose miR-130b and miR-17–5p expressions correlated with body composition parameters, frailty, and predicted cardiovascular events and mortality in advanced CKD patients.
A 72-year-old patient reported a sudden development of poor outflow from his Tenckhoff catheter; he had been performing continuous ambulatory peritoneal dialysis for 3 years because of diabetic nephropathy and hypertensive nephrosclerosis.There was a slow outflow rate, and the effluent volume was only 400e600 mL after an instillation of 2 L of dialysate; the inflow rate was variable. He reported neither constipation symptoms nor the presence of fibrin in the dialysate effluent. Examination confirmed a right inguinal hernia, which had been known for 6 months, and the patient was scheduled to undergo surgical repair. Drainage volume and flow rate showed no improvement with addition of heparin to the dialysate.Several possibilities of outflow failure (drainage volume being significantly less than the inflow volume) in peritoneal dialysis were considered. Common examples include bowel trapping (mostly due to constipation) and catheter migration (frequently to the subdiaphragmatic location with subsequent omental trapping). In the case of fibrin encasement and catheter kink, the dialysate inflow rate would have been slow as well. Another important consideration is subcutaneous dialysate leakage; however, this condition is accompanied by a reduction in the volume drained but a normal outflow rate. Furthermore, no pitting edema at the lower abdomen was observed in this patient to suggest subcutaneous leakage of dialysate.An abdominal radiograph was taken to confirm the position of the Tenckhoff catheter tip and to rule out kinking of the catheter. Two striking features in this case are the presence of a preexisting right inguinal hernia and the apparently extraperitoneal location of the catheter tip from the abdominal radiograph (Fig. 1). The catheter appeared to have passed down on the right side, via a point approximately midway between the patient's right anterior superior iliac spine and the right pubic tubercle, and extended beyond the pubic bone.A computed tomography of the abdomen and pelvis confirmed that the catheter was located within the enlarged right scrotal sac containing bowel loops and mesenteric fat (Fig. 2). Surgical exploration after incision down to the right external oblique aponeurosis identified the indirect inguinal hernia sac containing the Tenckhoff catheter and 1 L of clear peritoneal dialysate fluid. Hernia mesh repair and repositioning of the Tenckhoff catheter allowed the resumption of smooth peritoneal dialysis.Despite a relatively high prevalence (10e25%) of hernia in peritoneal dialysis patients, 1 the complication of catheter migration into an indirect inguinal hernia is relatively uncommon. To our knowledge, only one similar case of flow obstruction secondary to misplaced Tenckhoff catheter at
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