Dietary Sodium Restriction Reduces Nocturnal Urine Volume and Nocturnal Polyuria Index in Renal Allograft Recipients With Nocturnal Polyuria.

OBJECTIVE: To investigate whether sodium restriction alters the nocturnal urine volume (NUV) and the ratio of NUV to 24-hour urine of renal allograft recipients (RARs). MATERIALS AND METHODS: This prospective, single-center study analyzed 38 of the 59 RARs who were followed up for more than 6 months in our hospital. All patients underwent 3 sessions of dietary counseling performed by a board-certified dietitian. Before and after these 3 sessions, 24-hour urine samples were collected, along with voiding frequency volume charts. RESULTS: Of the 38 included RARs, 23 (60.5%) were diagnosed as having nocturnal polyuria (NP, NUV >10 mL/kg). After counseling the RARs with NP, their 24-hour sodium excretion was reduced from 169.5 to 125.6 mEq (P = .0066), their NUV from 862 to 709 mL (P = .021), and the ratio of NUV to 24-hour urine volume from 38.9% to 33.0% (P = .023). In contrast, these parameters were not significantly changed by dietary counseling in RARs without NP. Reduced sodium excretion and decreased NUV were significantly correlated (Spearman rho = 0.45, P = .005). CONCLUSION: Excess intake of sodium is considered a cause of NP in RARs. Dietary counseling on sodium restriction is effective in reducing NUV in RARs. Prospective studies are needed to evaluate the general population with NP.

The Short-Term Impact of Dietary Counseling on Sodium Intake and Blood Pressure in Renal Allograft Recipients.

BACKGROUND: Sodium retention causes posttransplant hypertension, and sodium restriction is recommended in kidney allograft recipients. However, there have been few studies on the impact of dietary counseling on sodium intake and blood pressure (BP) in this population. OBJECTIVE: To determine the effect of dietary counseling on sodium intake and consequent BP control in kidney allograft recipients. DESIGN, SETTING, AND PARTICIPANTS: A prospective single-arm study to determine the effect of dietary counseling on sodium intake. Enrolled were renal allograft recipients with sodium intake >100 mEq/d, BP >130/80, antihypertensive use, or body mass index >25 kg/m2. Of 53 renal transplant recipients who met the criteria, 48 participated in the present study. Sodium intake was estimated based on 24-hour urinary sodium excretion before and after 3 sessions of dietary counseling by a board-certified dietitian. RESULTS: Sodium intake was significantly decreased after dietary counseling (158.7 vs 129.6 mEq/d; P = .005). Systolic BP was significantly decreased from 124 mm Hg (interquartile range: 122-134) before counseling to 121 mm Hg (interquartile range: 117-128) after counseling ( P < .001). The number of patients with systolic BP >130 mm Hg was decreased by 30% (n = 19-13; P = .07). Among 34 patients on antihypertensive medications, 8 (23.5%) ceased or reduced their drugs due to improvement in BP, whereas 2 increased or changed the drugs due to poor control of BP. CONCLUSION: Dietary counseling showed a short-term efficacy of reducing sodium intake and clinically relevant BP improvement in renal allograft recipients.

Carbohydrate intake is associated with time spent in the euglycemic range in patients with type 1 diabetes.

AIMS/INTRODUCTION: Greater glycemic variability and lack of predictability are important issues for patients with type 1 diabetes. Dietary factors are one of the contributors to this variability, but how closely diet is linked to glycemic fluctuation on a daily basis has not been investigated. We examined the association between carbohydrate intake and glycemic excursion in outpatients. MATERIALS AND METHODS: A total of 33 patients with type 1 diabetes were included in the analyses (age 44.5 ± 14.7 years, diabetes duration 15.1 ± 8.3 years, 64% female, 30% using insulin pump, glycated hemoglobin 8.1 ± 1.3%). Time spent in euglycemia (70-180 mg/dL), hyperglycemia (>180 mg/dL) and hypoglycemia (<70 mg/dL) of consecutive 48-h periods of continuous glucose monitoring data were collected together with simultaneous records of dietary intake, insulin dose and physical activity. Correlation analyses and multiple regression analyses were used to evaluate the contribution of carbohydrate intake to time spent in the target glycemic range. RESULTS: In multiple regression analyses, carbohydrate intake (ß = 0.53, P = 0.001), basal insulin dose per kg per day (ß = -0.31, P = 0.034) and diabetes duration (ß = 0.30, P = 0.042) were independent predictors of time spent in euglycemia. Carbohydrate intake (ß = -0.51, P = 0.001) and insulin pump use (ß = -0.34, P = 0.024) were independent predictors of time spent in hyperglycemia. Insulin pump use (ß = 0.52, P < 0.001) and bolus insulin dose per kg per day (ß = 0.46, P = 0.001) were independent predictors of time spent in hypoglycemia. CONCLUSIONS: Carbohydrate intake is associated with time spent in euglycemia in patients with type 1 diabetes.

Transgenic mice overexpressing glia maturation factor-ß, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation.

Glia Maturation Factor-ß (GMF), a brain specific protein, is induced by proteinuria in renal tubules. Ectopic GMF overexpression causes apoptosisin vitro via cellular vulnerability to oxidative stress. In order to examine the roles of GMF in non-brain tissue, we constructed transgenic mice overexpressing GMF (GMF-TG). The GMF-TG mice exhibited appearance phenotypes associated with premature aging. The GMF-TG mice also demonstrated short lifespans and reduced hair regrowth, suggesting an accelerated aging process. The production of an abnormal lamin A, a nuclear envelope protein, plays a causal role in both normal aging and accelerated aging diseases, known as laminopathies. Importantly, we identified the abnormal lamin A (prelamin A), accompanied by a down-regulation of a lamin A processing enzyme (Zmpste24) in the kidney of the GMF-TG mice. The GMF-TG mice showed accelerated aging in the kidney, compared with wild-type mice, showing increased TGF-ß1, CTGF gene and serum creatinine. The gene expression of p21/waf1 was increased at an earlier stage of life, at 10 weeks, which was in turn down-regulated at a later stage, at 60 weeks. In conclusion, we propose that GMF-TG mice might be a novel mouse model of accelerated aging, due to the abnormal lamin A.