26 research outputs found
Renal outcome in adults with renal insufficiency and irregular asymmetric kidneys
BACKGROUND: The commonest cause of end-stage renal failure (ESRF) in children and young adults is congenital malformation of the kidney and urinary tract. In this retrospective review, we examine whether progression to ESRF can be predicted and whether treatment with angiotensin converting enzyme inhibitors (ACEI) can delay or prevent this. METHODS: We reviewed 78 patients with asymmetric irregular kidneys as a consequence of either primary vesico-ureteric reflux or renal dysplasia (Group 1, n = 44), or abnormal bladder function (Group 2, n = 34). Patients (median age 24 years) had an estimated GFR (eGFR) < 60 ml/min/1.73 m(2 )with at least 5 years of follow up (median 143 months). 48 patients received ACEI. We explored potential prognostic factors that affect the time to ESRF using Cox-regression analyses. RESULTS: At start, mean (SE) creatinine was 189 (8) μmol/l, mean eGFR 41 (1) ml/min 1.73 m(2), mean proteinuria 144 (14) mg/mmol creatinine (1.7 g/24 hrs). Of 78 patients, 36 (46%) developed ESRF, but none of 19 with proteinuria less than 50 mg/mmol and only two of 18 patients with eGFR above 50 ml/min did so. Renal outcome between Groups 1 and 2 appeared similar with no evidence for a difference. A benefit in favour of treatment with ACEI was observed above an eGFR of 40 ml/min (p = 0.024). CONCLUSION: The similar outcome of the two groups supports the nephrological nature of progressive renal failure in young men born with abnormal bladders. There is a watershed GFR of 40–50 ml/min at which ACEI treatment can be successful at improving renal outcome
Increased energy expenditure in growing adolescents with Crohn's disease
Undernutrition is considered to have a central role in the pathogenesis of growth retardation in Crohn's disease. This may occur as a consequence of inadequate food intake, increased energy expenditure, or both. Ten growing adolescents with inactive Crohn's disease were assessed with respect to anthropometric parameters and resting energy expenditure, measured by indirect calorimetry during remission, repeated in relapse (N = 5), and compared to that predicted from the Harris-Benedict formula. Mean energy intake was assessed with seven-day diaries in five patients and compared to recommended intake for age, sex, weight, and physical activity. Ten healthy, growing, age- and sex-matched adolescents served as controls. Nine patients with inactive Crohn's disease, who had ceased growing, were matched for disease site and duration and acted as disease controls. Patients and disease controls had lower body mass index (19.2 ± 0.6; 20.9 ± 0.7) than healthy controls (23.7 ± 0.6; P < 0.001). Percent body fat was lower in patients (13.2 ± 1.9%) compared to healthy controls (20.5 ± 2.4%; P < 0.05) but not to disease controls (17.0 ± 2.6%). Patients had higher resting energy expenditure per kilogram of fat-free mass than disease or healthy controls (36.9 ± 5.1; 32.9 ± 2.6; 30.9 ± 2.1 kcal; P < 0.02). Measured resting energy expenditure in patients, but not in disease or healthy controls, was higher than the predicted (measured: predicted 1.15, 1.03, 0.9, respectively; P < 0.03). Energy intake in patients was 97% of recommended intake but the measured ratio of energy intake/resting energy expenditure was lower than the predicted ratio (1.49 vs 1.71; P < 0.05). During subsequent relapse in five patients resting energy expenditure was unchanged. In growing adolescents with inactive Crohn's disease, there is increased energy expenditure that is not accompanied by an increase in energy intake; Relapse of disease does not appear to increase resting energy expenditure further but may 'divert' energy from growth to disease activity. This suggests that nutritional therapy should be directed towards increasing caloric intake to maximize growth potential