Calculated estimates of GFR are an improvement over ClCr estimation. On balance, the MDRD formula does not improve the estimate of GFR compared with the Cockcroft and Gault formula in older Caucasian patients with chronic renal insufficiency.

Summary Background There are few studies that directly compare the variation in incidence of venous thromboembolism (VTE) according to ethnicity. Objective The aim of this study was to compare the rates of VTE, deep venous thrombosis (DVT) and pulmonary embolism (PE) among different ethnic groups. Method The cases diagnosed with VTE, DVT and PE for a period between March 2004 and June 2009 were identified through the hospital‐based database system. The 2006 New Zealand Census data were used to calculate the rate of diagnosis. Results The observed annual incidence of VTE during this period was 81.6 per 100 000 population. The relative risks of VTE when comparing European subjects with Maori, Pacific Island and Asian subjects after age standardization were 1.98 (95% confidence interval [CI], 1.63–2.41), 3.22 (95% CI, 2.60–3.99) and 4.02 (95% CI, 3.34–4.84), respectively. Relative risks of DVT after age standardization when comparing European subjects with Maori, Pacific Island and Asian subjects, were 2.14 (95% CI, 1.72–2.66), 3.20 (95% CI, 2.46–4.17) and 4.75 (95% CI, 3.80–5.94), respectively. Indirect age standardization was used for comparison of the diagnosis of PE. The ratio between the calculated expected number of cases and the actual number of cases was 1.32 (95% CI, 0.89–1.75) for Maori subjects, 2.96 (95% CI, 1.89–4.03) for Pacific Islanders and 3.89 (95% CI, 3.00–4.78) for Asians. Conclusion Europeans have a significantly higher incidence of VTE compared with Maori, Pacific Island and Asian populations.

Defects in induction signaling and response underlie the nucleocytoplasmic incompatibility between two evolutionarily distant frog species, while specific treatments partially restore this response in explants and whole embryos.

SUMMARYAim: To establish whether bone disease is present at diagnosis in inflammatory bowel disease and to identify contributory metabolic abnormalities. Methods: Newly diagnosed patients with inflammatory bowel disease (19 males, 15 females; mean age, 44 years; range, 17-79 years; 23 ulcerative colitis, 11 Crohn's disease) were compared against standard reference ranges and a control group with irritable bowel syndrome (eight males, 10 females; mean age, 40 years; range, 19-64 years). Bone mineral density (g ⁄ cm 2 , dual-energy X-ray absorptiometry: lumbar spine and femoral neck) and biochemical bone markers were measured. Results: Femoral neck bone mineral density, T-and Z-scores (mean ± s.d., respectively) were lower in inflammatory bowel disease patients than in irritable bowel syndrome controls (0.78 ± 0.12 vs. 0.90 ± 0.16, P ¼ 0.0046; ) 0.88 ± 0.92 vs. 0.12 ± 1.17, P ¼ 0.0018; ) 0.30 ± 0.89 vs. 0.61 ± 1.10, P ¼ 0.0030). Lumbar spine bone mineral density and T-scores were also significantly lower in patients than controls (0.98 ± 0.15 vs. 1.08 ± 0.13, P ¼ 0.0342; ) 1.05 ± 1.39 vs. ) 0.14 ± 1.19, P ¼ 0.0304). Compared with controls, the urinary deoxypyridinoline : creatinine ratio was increased (7.66 vs. 5.70 nmol ⁄ mmol, P ¼ 0.0163) and serum 25-hydroxy vitamin D was decreased (18.7 vs. 28.5 lg ⁄ L, P ¼ 0.0016); plasma osteocalcin and serum parathyroid hormone did not differ (P > 0.05). Conclusions: The bone mineral density is reduced at diagnosis, prior to corticosteroid treatment, in both Crohn's disease and ulcerative colitis. Our data suggest that this is attributable to increased resorption rather than decreased bone formation.