[Diabetic nephropathy is the main cause of chronic kidney disease affecting about one-third of type 2 diabetic patients. The exact pathomechanism is not known, therefore the treatment and the prevention is still unsolved. However appropriate glycemic control and lowering blood pressure significantly slow the progression of kidney damage these treatment options are still not enough to stop renal injury. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are the newest drugs in the treatment of diabetes. By inhibiting the glucose reabsorption in the proximal tubules SGLT2 inhibitors lower blood glucose level and facilitate glucosuria. This paper summarizes the effect of SGLT2 inhibitors currently approved in Europe paying particular attention to their possible renoprotective effects.]

[Introduction: There are inconsistent observations regarding the earlier studies of the connection between ACE gene I/D polymorphism and the cardiovascular mortality. In the case of hemodialyzed patients suffering from chronic kidney disease the DD polymorphism connected to the elevated ACE levels was pointed out to be connected to the mortality rate primarily in patients with diabetes. The previous observations were verified by us during the analyzation of the short-term (three year period) survival data. We hypothesized that the significance of the ACE gene I / D polymorphism in chronic kidney disease would be verified and that during long-term observations (10 year period) the previous results could be validated. Method: In our non-invasive, prospective and multicentre study clinical data was collected from 746 patients whose blood samples were genotyped for ACE gene I/D single nucleotide polymorphism. Three genotype groups (I/I, I/D és D/D) were created during the analyzation of the mortality that was done using multivariate Cox proportional hazard models. Results: The mean age of the HD patients was 54.9 years, 46,8% of all patients were female. The prevalence of diabetes was 19.3%. ACE inhibitor therapy was prescribed for 47.9% of all patients. The median duration of dialysis before the start of the study was 23.8 months (IQR 11.2-47.1). The most frequent genotype was I/D (42.6%), followed by D/D (37.7%) and I/I (19.7%) genotypes. During the ten year follow- up of patients, the median follow-up was 29.8 months (IQR 12.6-63.4). The D/D genotypes showed lower survivability (I/I vs. D/D: log-rank test: p=0.04) from the group of patients without ACE inhibitor therapy. In multivarite Cox regression models D/D genotype compared with I/I genotype only showed that it significantly determines mortality in patients with no ACE inhibitor therapy (HR 0.67, 95% CI 0.46-0.97, p=0.03). Conclusions: There was no difference in survival among unselected patients with different genotypes. Our data suggests that hemodialyzed patients with the D/D genotype might have inferior outcome, and ACE inhibitor therapy may be associated with improved survival in this subgroup.]

[A 48 year old male patient with hypertension, resistant to the combined administration of seven antihypertensive drugs had an associated hypertrophic nonobstructive cardiomyopathy. Bilateral renal denervation has been performed with the Symplicity catether of Medtronic after the exclusion of possible secondary forms of hypertension, but his blood pressure did not decrease. Preventive intracardiac cardioverter defibrillator implantation has also been performed because of progressive congestive heart failure. We planned a witnessed intake of antihypertensive medication before qualifying ABPM study but without success because of noncompliance of the patient. According to the database of the Hungarian National Health Insurance Fund (OEP) on request of his general practitioner, the patient payed for prescripted medicine only once in the previous year, on the day before his planned witnessed intake of antihypertensive medication. The witnessed intake of medication before qualifying ABPM study was finally successful two years after the renal denervation and both his office and ambulatory blood pressure decreased substantially. The witnessed intake of antihypertensive medication for the exclusion of nonadherence as a cause of therapy resistant hypertension is warranted, especially before device or operative interventions for the treatment of hypertension.]