Background: Fatigue is an important symptom to patients with advanced chronic kidney disease (CKD). The aim of this study is to examine the prevalence and severity of fatigue among non-dialysis-dependent CKD and end-stage renal disease (ESRD) patients, to examine the association of fatigue with subjective and objective sleep quality, and to identify other modifiable factors associated with fatigue. Methods: A cross-sectional survey of 87 non-dialysis-dependent CKD (eGFR ≤45 ml/min/1.73 m²) and 86 ESRD patients was done using the Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-F) and 36-Item Short-Form (SF-36) vitality scale. Higher FACIT-F score denoted less fatigue. Objective sleep was assessed using in-home polysomnography. Predictors of fatigue were determined using a linear regression model. Results: The mean FACIT-F score among all participants was 34.5 ± 11.0. Mean scores were similar among CKD and ESRD groups (34.25 ± 11.28 vs. 34.73 ± 10.86; p = 0.73). On univariate analyses, patients with higher levels of fatigue were more likely to have cardiovascular disease, benzodiazepine use, depressive symptoms, and slightly lower hemoglobin and serum albumin levels. There was no significant association between severity of sleep apnea and level of fatigue (Apnea Hypopnea Index 20.1 ± 27.6 vs. 20.3 ± 22.0; p = 0.69). Presence of cardiovascular disease, low serum albumin, depressive symptoms, poor subjective sleep quality, excessive daytime sleepiness and restless legs syndrome were independently associated with greater fatigue in multivariable regression models. The FACIT-F score correlated closely with the SF-36 vitality score (r = 0.81, p < 0.0001). Conclusions: Patients with advanced CKD and ESRD experience profound fatigue. Depressive symptoms, restless legs syndrome, excessive daytime sleepiness, and low albumin levels may provide targets for interventions to improve fatigue in patients with advanced CKD.

Pouch-vaginal fistulas are a difficult problem in females following restorative proctocolectomy. However, local repair can be successful with good functional outcomes. Redo restorative proctocolectomy may also achieve healing if local repairs are not possible or have failed. A delayed diagnosis of Crohn's disease results in worse treatment outcome and higher pouch failure rates.

Background Peritoneal dialysis (PD) patients are at risk for 25(OH) vitamin D deficiency due to effluent loss in addition to traditional risk factors. Objectives To measure 25(OH) vitamin D deficiency in prevalent PD patients, to evaluate a replacement dose, and to determine the effects of correction. Methods 25(OH) vitamin D levels were drawn on prevalent PD patients. Patients deficient in 25(OH) vitamin D were given ergocalciferol, 50 000 IU orally once per week for 4 weeks. Patients scored muscle weakness, bone pain, and fatigue on a scale of 0 (none) to 5 (severe). Serum calcium, phosphate, parathyroid hormone (PTH), and 25(OH) vitamin D, and 1,25(OH)2 vitamin D levels were obtained before and after treatment. Results 25(OH) vitamin D levels were measured in 29 PD patients. Deficiency (<15 ng/mL) was found in 28/29 (97%); 25/29 (86%) had undetectable levels (<7 ng/mL). One course of ergocalciferol corrected the deficiency in all but 1 patient, who required a second course. Scores for muscle weakness and bone pain fell from pre- to posttreatment ( p < 0.001). 1,25(OH)2 vitamin D levels rose post ergocalciferol (from 20 to 26 pg/mL, n = 20, p = 0.09). Serum calcium, phosphate, and PTH levels did not change with ergocalciferol. Conclusions Most PD patients had marked 25(OH) vitamin D deficiency, which was readily and safely corrected with one course of 50000 IU ergocalciferol, having no effect on serum calcium, phosphorus, or PTH, but complaints of muscle weakness and bone pain decreased. A prospective, placebo-controlled double-blinded study is needed to determine whether replacement of 25(OH) vitamin D is beneficial in PD patients.

Children with the sepsis syndrome, particularly those patients with hypotension, have increased total serum nitrite and nitrate concentrations that likely reflect increased endogenous production of nitric oxide. Vascular hyporesponsiveness to norepinephrine during the sepsis syndrome may be, in part, a nitric oxide-mediated process.