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"Good clinical practice" (GCP) is an international guideline on how to conduct clinical trials on medical products involving human participants. Danish statute follows the EU trial directive (2001/20/EF) including the GCP guidelines. This article summarises the practical implementation of reporting adverse events and adverse reactions to the Danish Medicines Agency and the regional ethics committee based on the protocol of the ongoing Copenhagen Insulin and Metformin Therapy (CIMT) trial.

Monogenic forms of hypertension are very rare, but have a well-characterized heredity. Primary hypertension is very common with a complex and polygenic heredity. Primary hypertension arises due to an interaction between multiple genetic and environmental factors. Its heredity is unknown, although some candidate genes have been suggested. Intense research is ongoing and includes the use of modern genetics methods as genome wide association and linkage studies.

We evaluated the relationship between serum mannose-binding lectin (MBL) and mortality and incident albuminuria in 326 patients with type 2 diabetes mellitus (T2DM). During 15 years of follow-up, 169 patients died. In a multivariate analysis, MBL was a significant risk factor for death from any cause and added to the predictive power of CRP. Normoalbuminuric patients with both high MBL and high C-reactive protein (CRP) levels had a significantly increased risk of developing albuminuria. We conclude that MBL alone or in combination with CRP can provide prognostic information on mortality and the development of albuminuria in T2DM

The aim of the study was to evaluate the effect of an insertion/deletion polymorphism of the angiotensin converting enzyme (ACE) gene on progression of diabetic nephropathy. We performed an observational follow-up study of 35 patients with insulin-dependent diabetes and diabetic nephropathy. Patients were investigated during captopril treatment for a median of seven (range three to nine) years. Eleven patients were homozygous for the deletion allele (DD) and 24 were hetero- or homozygous for the insertion allele (ID + II). The two groups had comparable glomerular filtration rate, albuminuria and blood pressure at baseline and captopril induced nearly the same mean reduction in blood pressure--to 103 (SD 5) mm Hg in the DD-group and 102 (8) mm Hg in the ID + II-group. The rate of decline in glomerular filtration rate was significantly steeper in the DD group than in the other group (mean 5.7 (SD 3.7) versus 2.6 (2.8) ml/min/year, p = 0.01). In conclusion, the deletion polymorphism in the ACE gene reduces the long term beneficial effect of ACE inhibition on the progression of diabetic nephropathy in patients with insulin dependent diabetes.

It has been demonstrated that intrauterine growth retardation gives rise to a reduction in nephron number. Oligonephropathy has been suggested to enhance the risk for expression of renal disease following exposure to potentially injurious renal stimuli. In a case-control study we investigated if low birth weight is a risk factor for development of diabetic nephropathy in 184 IDDM patients with diabetic nephropathy (persistent albuminuria > 300 mg/24 hours) and 182 normoalbuminuric (< 30 mg/24 hours) patients. In women with birthweight < 10 th centile (< or = 2,700 g, n = 16) 75% had nephropathy compared to only 35% among patients > 90 th centile (> or = 4,000 g, n = 17) (p = 0.05). In men with birth-weight < 10th centile (< or = 2,910 g, n = 22) the prevalence of nephropathy: 50%, was similar to the prevalence among patients > 90th centile (> or = 4,200 g, n = 24) 54%. Mean weight at birth were similar in patients with and without diabetic nephropathy. Men with diabetic nephropathy were significantly shorter than men with normoalbuminuria (176.9 (7.1) vs 179.4 (6.5), p < 0.01). In conclusion, our study supports the hypothesis that genetic predisposition or factors operating in utero or early childhood, or both, contribute to the development of diabetic nephropathy.