A prospective cohort study of two predictor models for 30-day emergency readmission in older patients.

AIM: To undertake a prospective study of the accuracy of two models (LACE and BOOST) in predicting unplanned hospital readmission in older patients (>75 years). METHODS: Data were collected from a single centre prospectively on 110 patients over 75 years old admitted to the acute medical unit. Follow-up was conducted at 30 days. The primary outcome was the c-statistic for both models. RESULTS: The readmission rate was 32.7% and median age 82 years, and both BOOST and LACE scores were significantly higher in those readmitted compared with those who were not. C-statistics were calculated for both tools with BOOST score 0.667 (95% CI 0.559-0.775, P = .005) and LACE index 0.685 (95% CI 0.579-0.792, P = .002). CONCLUSION: In this prospective study, both the BOOST and LACE scores were found to be significant yet poor, predictive models of hospital readmission. Recent hospitalisation (within the previous 6 months) was found to be the most significant contributing factor.

Clinical, biochemical, and pathophysiological analysis of SLC34A1 mutations.

Mutations in SLC34A1, encoding the proximal tubular sodium-phosphate transporter NaPi-IIa, may cause a range of clinical phenotypes including infantile hypercalcemia, a proximal renal Fanconi syndrome, which are typically autosomal recessive, and hypophosphatemic nephrolithiasis, which may be an autosomal dominant trait. Here, we report two patients with mixed clinical phenotypes, both with metabolic acidosis, hyperphosphaturia, and renal stones. Patient A had a single heterozygous pathogenic missense mutation (p.I456N) in SLC34A1, consistent with the autosomal dominant pattern of renal stone disease in this family. Patient B, with an autosomal recessive pattern of disease, was compound heterozygous for SLC34A1 variants; a missense variant (p.R512C) together with a relatively common in-frame deletion p.V91A97del7 (91del7). Xenopus oocyte and renal (HKC-8) cell line transfection studies of the variants revealed limited cell surface localization, consistent with trafficking defects. Co-expression of wild-type and I456N and 91del7 appeared to cause intracellular retention in HKC-8, whereas the R512C mutant had a less dominant effect. Expression in Xenopus oocytes failed to demonstrate a significant dominant negative effect for I456N and R512C; however, a negative impact of 91del7 on [32 P]phosphate transport was found. In conclusion, we have investigated pathogenic alleles of SLC34A1 which contribute to both autosomal dominant and autosomal recessive renal stone disease.

Activation energies of selenoxide elimination from Se-substituted selenocysteine.

Transition states for selenoxide elimination have been determined for a series of Se-substituted selenocysteine (RSeCys) derivatives that have potential use in the prevention and treatment of cancer, either directly or in conjunction with cisplatin (to reduce its nephrotoxic effects). Reduced activation barriers vs R=Me and R=Ph are found when the alkyl chain length is increased or when activating groups are para to the selenide. Ortho substitution of Lewis bases stabilizes the transition state by directly donating electron density to the selenoxide. The results suggest that RSeCys derivatives incorporating the properties of glutathione peroxidase mimics will, upon oxidation, rapidly eliminate selenenic acid, a precursor to chemopreventative selenols.