Maja Vuckovic, Ingrid Prkacin, Gordana Cavric and Martina Zeljko
Ingrid Prkacin, Gordana Cavric and Nikolina Basic-Jukic
Clinical and laboratory findings of kidney disease in an adult may find an explanation in kidney functional and/or structural abnormalities that already existed during infancy and childhood, but that may have been missed or underdiagnosed. All the cardiovascular abnormalities that occur in adults with chronic kidney disease are also present in children with chronic kidney disease. Complications in childhood chronic kidney disease will have consequences well beyond pediatric age and influence outcomes of affected young adults with disease. Kidney dysfunction appears early in the course of kidney disease and has been observed in children and adults with chronic kidney disease, condition characterised with kidney fibrosis. Transforming growth factor beta is recognized as a major mediator of kidney fibrosis. New evidence illustrates the relationship between transforming growth factor beta signaling and microRNAs expression during kidney diseases development. MicroRNAs play important roles in kidney development and kidney diseases; they are naturally occurring, 22-nucleotide, noncoding RNAs that mediate posttranscriptional gene regulation. Dysregulation of miRNA expression is an indicator of several diseases including chronic kidney disease. Targeting microRNAs should be a therapeutic potential to ameliorate the disease related to fibrosis. The discovery that circulating miRNAs are detectable in serum and plasma, and that their expression varies as a result of disease, presents great potential to be used as biomarkers in kidney disease prevention and diagnosis.
Ingrid Prkacin, Petra Vrdoljak, Gordana Cavric, Damir Vazanic, Petra Pervan and Visnja-Nesek Adam
Studies have documented independent contribution of sympathetic activation to the cardiovascular disease continuum. Hypertension is one of the leading modifiable factors. Most if not all the benefit of antihypertensive treatment depends on blood pressure lowering, regardless how it is obtained. Resistant hypertension is defined as blood pressure that remains uncontrolled in spite of the concurrent use of three antihypertensive drugs of different classes. Ideally, one of the three drugs should be a diuretic, and all drugs should be prescribed at optimal dose amounts. Poor adherence to antihypertensive therapy, undiscovered secondary causes (e.g. obstructive sleep apnea, primary aldosteronism, renal artery stenosis), and lifestyle factors (e.g. obesity, excessive sodium intake, heavy alcohol intake, various drug interactions) are the most common causes of resistant hypertension. Cardio(reno)vascular morbidity and mortality are significantly higher in resistant hypertensive than in general hypertensive population, as such patients are typically presented with a long-standing history of poorly controlled hypertension. Early diagnosis and treatment is needed to avoid further end-organ damage to prevent cardiorenovascular remodeling. Treatment strategy includes lifestyle changes, adding a mineralocorticoid receptor antagonist, treatment adherence in cardiovascular prevention and, in case of failure to control blood pressure, renal sympathetic denervation or baroreceptor activation therapy. The comparative outcomes in resistant hypertension deserve better understanding. In this review, the most current approaches to resistant hypertension and cardiovascular risk based on the available literature evidence will be discussed.