This study suggests that avoidance of major polypharmacy, use of nonpharmacological measures to improve lifestyle habits and decreasing the exposure of physicians to drug promotional material may reduce the risk of PIM use in older primary care outpatients. The only modifiable protective factors for PPOs were working environment of the patients chosen GPs and more frequent ambulatory visits to specialists.

The questionnaire about knowledge of ACE inhibitors' adverse effects is a reliable and probably valid instrument for measuring patients' knowledge about adverse effects of ACE inhibitors.

Summary Anemia is defined as blood hemoglobin concentration of less than 120 g/l in women and less than 130 g/l in men. The main cause of the development of anemia in patients treated with regular hemodialysis is the lack of endogenous erythropoietin, and its main clinical consequences are: progressive decline in residual renal function, development of cardiovascular disorders, disorders of cognitive functions and a decrease in the quality of life of these patients. Despite the administration of an appropriate dose of erythropoietin, in 5-10% of patients treated with regular hemodialysis, there is resistance to erythropoietin activity. The main risk factors for the development of resistance to the effects of erythropoietin are: iron deficiency, microinflammation, deficiency of vitamin D, secondary hyperparathyroidism, deficiency of vitamin C, and inadequate hemodialysis. The main side effects of erythropoietin are: hypertension, thrombosis of the vascular approach to hemodialysis, and the red blood cell precursor aplasia in the bone marrow. Early detection and elimination of risk factors, optimization and indi-vidualization of hemodialysis prescription prevent the development of resistance to erythropoietin activity, enable the achievement of target blood hemoglobin, reduce the development of cardiovascular morbidity, and improve the quality of life of these patients.

Acute damage to the kidney is a serious complication in patients in intensive care units. The causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the definition and classification of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifications are used. There is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insufficiency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have significant roles in the diagnosis of acute kidney damage. Prevention of the development of acute kidney damage in intensive care units includes maintaining an adequate haemodynamic status in patients and avoiding nephrotoxic drugs and agents (radiocontrast agents). The complications of acute kidney damage (hyperkalaemia, metabolic acidosis, hypervolaemia and azotaemia) are treated with medications, intravenous solutions, and therapies for renal function replacement. Absolute indications for acute haemodialysis include resistant hyperkalaemia, severe metabolic acidosis, resistant hypervolaemia and complications of high azotaemia. In the absence of an absolute indication, dialysis is indicated for patients in intensive care units at stage 3 of the AKIN/KDIGO classification and in some patients with stage 2. Intermittent haemodialysis is applied for haemodynamically stable patients with severe hyperkalaemia and hypervolaemia. In patients who are haemodynamically unstable and have liver insufficiency or brain damage, continuous modalities of treatment for renal replacement are indicated.

Secondary hypertension occurs in 5-