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High lipoprotein(a) (LP(a)) level contributes as an independent risk factor to the development of cardiovascular diseases of atherosclerotic origin. The article contains data on the structural features of this particle, the genetic determination of its metabolism and content in blood plasma, and the pathogenic mechanisms of its proatherogenic, proinflammatory and prothrombotic effects. The authors analyzed epidemiological data on the frequency of elevated LP(a) levels in different population groups and its association with the risk of cardiovascular diseases. The data presented concern the indicators of LP(a) as a risk factor for the development of ischemic stroke (including recurrent stroke) and its individual pathogenetic subtypes, as well as the relationship between LP(a) levels and functional outcomes after cerebral accidents. Current recommendations for the treatment of patients with elevated LP(a) levels in the context of primary and secondary prevention of cardiovascular diseases are analyzed.

AIM: To study an association between clinical and morphological evidence and the serum and daily urinary levels of cystatin C (CysC) and neutrophil gelatinase-associated lipocalin (NGAL) in patients with primary glomerulopathies/MATERIAL AND METHODS: The investigation included 104 patients; morphological examination showed minimal change disease in 15 (14.4%) patients, focal segmental glomerulosclerosis in 24 (23.1%), membrane nephropathy in 32 (30.8%), and IgA nephropathy (mesangioproliferative glomerulonephritis) in 33 (31.7%). The investigators analyzed the clinical type of nephropathy, performed conventional laboratory and instrumental examinations, and determined the level of CysC (by immunoturbodimetry) and NGAL (by enzyme immunoassay) in the serum and daily urine taken before kidney biopsy. The degree of glomerulosclerosis, tubulointerstititial sclerosis, and tubular atrophy was semiquantitatively estimated/RESULTS: Urinary CysC and NGAL excretion correlated with the degree of glomerulosclerosis and proteinuria and the reduced glomerular filtration rate (GFR) regardless of the method of its determination. The urinary level of NGAL positively correlated with the degree of tubular atrophy. The GFR value determined from serum CysC and creatinine levels more precisely reflected the degree of glomerulosclerosis/CONCLUSION: The tubulointerstitial compartment in primary glomerulopathies should be determined not only by morphological changes, but also by tubular function parameters by estimating the urinary excretion of biomarkers. The urinary content of CysC reflects tubular epithelial dysfunction whereas that of NGAL also characterizes tubular atrophy. To estimate the degree of glomerulosclerosis, it is more preferable to use the GFR calculated from the blood concentrations of CysC and creatinine, by keeping in mind clinical findings (using Chronic Kidney Disease Epidemiology Collaboration formula, 2012).