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Chronic kidney disease is one of the most serious complications of diabetes. One of the challenges in the follow-up of patients with diabetes is to discover signs of kidney disease. Recent research shows that several drugs have renal protective effects. In this clinical review article we present markers used in the follow-up of patients with diabetes and chronic kidney disease, and new treatment options.

Background: Measurement of glycated haemoglobin A1 in whole blood (b-HbA1c) can be used in both diagnosing and following up patients with diabetes. Correct interpretation of analytical results is contingent on agreement between average plasma glucose (p-glucose) and b-HbA1c. This article provides an overview of factors that may result in a discrepancy between average glucose concentration and b-HbA1c., Method: Literature search in PubMed to identify scientific articles that describe strengths and weaknesses of b-HbA1c., Results: The b-HbA1c reading usually provides a good picture of average p-glucose for the preceding two to three months. Patients who are being treated with iron/vitamin B12 supplements, have liver failure, haemolytic anaemia or bleeding usually have a lower b-HbA1c than their p-glucose level would suggest. With increasing patient age, B12 deficiency or iron deficiency anaemia, higher values of b-HbA1c are seen for the same p-glucose level. Some ethnic groups have a higher b-HbA1c than their average p-glucose would suggest, but the risk of long-term complications appears generally to be more closely associated with b-HbA1c than with the glucose level. Pregnancy, renal failure or haemoglobinopathies may make the b-HbA1c value unreliable as an expression of average p-glucose., Interpretation: Correct interpretation of b-HbA1c is conditional on the requisitioner being aware of possible sources of error. If the patient is suspected to have a condition that leads to lack of consistency between b-HbA1c and average p-glucose, glucose-based criteria must be used in diagnosing diabetes.

Background and Methods: An overview of primary adrenal failure with emphasis on replacement therapy is presented. The article is based on a review of recent literature and authors' personal experience., Results and Conclusions: Addison's disease is usually caused by an autoimmune destruction of the adrenal cortex. It is relatively rare (prevalence 14 per 100,000 inhabitants), but often considered as a differential diagnosis when evaluating fatigue, tiredness and loss of weight. Addison's disease is treated by repletion of glucocorticoids and mineralocorticoids. The recommended starting dose is 25 mg cortisone acetate per day divided into three (12.5 + 6.25 + 6.25 mg) or two doses (12,5 mg x 2). Mineralocorticoid replacement is given as fludrocortisone 0.05 - 0.2 mg in one dose per day. Treatment with 20 - 50 mg dehydroepiandrosterone has been studied in adrenal failure, but the evidence for positive effects is weak, and it can not be recommended as standard treatment in primary adrenal failure.