Vol 86, No 6 (2014)

The paper shows the value of chronic kidney disease as a population-wide determinant of vascular dementia, including moderate cognitive impairments. It discusses the role of risk factors of cardiovascular events, including those associated with chronic kidney disease, in the development of vascular dementia and moderate cognitive impairments.

AIM: To determine the levels of 70-kDa heat shock protein (HSP70) in urine and anti-HPS70 antibodies (Abs) in serum and to assess their clinical and prognostic value in patients with different forms of chronic glomerulonephritis (CGN)/MATERIAL AND METHODS: Seventy-nine patients with CGN, including 15 with inactive nephritis (Group 1), 35 with active CGN and preserved renal function (Group 2), 14 with the highest CGN activity and transient creatininemia (Group 3), and 15 with persistent proteinuria and chronic renal failure (Group 4) were examined. ELISA was used to estimate urinary HSP70 levels and serum anti-HSP70 Abs in the examined groups/RESULTS: The patients with active CGN were found to have higher excretions of urinary HSP70 and serum anti-HSP70 Abs. Urinary HSP70 excretion was significantly higher in the patients with transient renal function (Group 3) than in those from the other groups. At the same time, there was a decrease in serum anti-HSP70 Abs, which was a poor factor of persistent nephrotic syndrome despite immunosuppressive therapy (IST). Despite long-term IST, the nephrotic syndrome was persistent in 9 (60%) of the 15 patients with low serum Ab titers. At the same time, 8 (80%) of the 10 patients with higher serum Ab titers responded to IST during 9 months/CONCLUSION: The investigation demonstrates the great value of HSP70 as an index of the severity of lesion and the activation of kidney self-defense mechanisms in patients with CGN. Determination of serum anti-HSP70 Abs may be used to assess the prognosis of CGN.

AIM: To investigate alterations of the complement system in patients with catastrophic antiphospholipid syndrome (CAPS)/MATERIAL AND METHODS: Four patients (2 men aged 23 and 40 years and 2 women aged 39 and 58 years) diagnosed as having CAPS, including 3 patients with systemic lupus erythematosus and secondary antiphospholipid syndrome (APS) and 1 patient with primary APS, were examined. The activity of the complement components C1-C5 and total hemolytic activity were determined in all the patients at the moment of an acute episode and in 1 patient after treatment/RESULTS: The activity of the studied complement components and total hemolytic complement activity proved to be significantly decreased in all the patients. That of complement components recovered after treatment using fresh frozen plasma. The possibility and mechanisms of complement system activation in the patients with CAPS are discussed/CONCLUSION: The preliminary results obtained by the examination of few cases may lead to the conclusion that the complement system may be involved in the development of CAPS.

AIM: To identify the risk factors of kidney injuries in hypertensive patients with uric acid (UA) metabolic disorders in order to choose the optimal management tactics, by analyzing the changes in markers for endothelial dysfunction (endothelin-1 (ET-1), microalbuminuria (MAU), intima-media thickness (IMT)) and tubulointerstitial tissue lesion (Β2-microglobulin (Β2-MG, monocyte chemotactic protein-1 (MCP-1))/MATERIAL AND METHODS: Eighty-one patients with grade 1 hypertension without associated diseases, diabetes mellitus, or metabolic syndrome were examined. There were 3 study groups: 1) hyperuricosuria (n=7); 2) hyperuricemia (n=53); 3) hyperuricemia and renal failure (n=6); and a control group of 15 hypertensive patients without UA metabolic disorders who were matched for age and gender with the patients of the study groups/RESULTS: The hypertensive patients with hyperuricemia, as compared with those without UA metabolic disorders, showed higher plasma concentrations of ET-1 (p=0.003) and MAU (p=0.009) and more marked increases in common carotid IMT (p=0.044), urinary excretion of Β2-MG (p=0.010), and MCP-1 (p=0.030). There were direct correlations between all the examined biomarkers and the degree of uricemia (Rs=0.453; р<0.001; Rs=0.411; р<0.001; Rs=0.322; р=0.067; Rs=0.537; р<0.001; and Rs=0.318; р=0.004, respectively) and between the markers of endothelial dysfunction and those of tubulointerstitial tissue lesion (Rs=0.295 for ET-1 and MCP-1; р=0.008; Rs=0.399 for ET-1 and Β2-MG; р<0.001; Rs=0.462 for MAU and Β2-MG; р<0.001; and Rs=0.188 for MAU and MCP-1; р=0.094). Multivariate analysis of the clinical and laboratory parameters under study confirmed the role of serum MCP-1, Β2-MG, MAU, creatinine levels as independent predictors for decreased relative urinary gravity, the clinical sign of tubulointerstitial tissue lesion/fibrosis, and that of a wider range of the indicators, such as MAU, ventricular septal thickness, glomerular filtration rate, relative urinary gravity, systolic blood pressure, MPC-1, low-density lipoproteins, as risk factors for renal filtrating dysfunction.

AIM: To analyze the prognostic value of the polymorphisms of the thrombophilic genes: plasminogen activator inhibitor type 1 (PAI-1) (–675 4G/5G), factor XIII (FXIII) (G485T), fibrinogen (FBG) (G(–455)A), glycoprotein Ia (GPIa) (C807T), glycoprotein IIIa (GPIIIa) (T106C), and p22phox (C242T), as well as protein genes involved in the pathogenesis of endothelial dysfunction: subunits of p22phox NADH-oxidase (p22phox) (C242T), endothelial NO-synthase (eNOS) (G894T), and methylenetetrahydrofolate reductase (MTHFR) (С677Т) for the development of antiphospholipid syndrome (APS) and a type of progressive lupous nephritis (LN) in patients with systemic lupus erythematosus (SLE)/MATERIAL AND METHODS: One hundred patients with SLE were examined and, according to the presence of clinical and laboratory signs of APS were divided into 2 groups: 1) 50 SLE patients with APS; 2) 50 SLE patients without APS who were matched for gender and age with Group 1 patients. The gene polymorphisms were analyzed using standard molecular genetic techniques. The frequency of clinical manifestations of APS and the type of progressive nephritis were analyzed in view of the genotypes of the patients/RESULTS: Comparison of SLE patients with and without SLE revealed no statistically significant differences in the rates of alleles and genotypes. The patients with arterial and/or venous thrombosis in the presence of APS more frequently displayed a minor allele (T) and genotype (TT) of the p22phox gene than those with APS without thrombosis: T, 64.5 and 34%, respectively (p=0.033); TT, 36 and 7% (p=0.021); odds ratio (OR), 2.1 at 95% confidence interval (CI), 1.5 to 22.7). In the APS patients with livedo reticularis, the minor allele (T) and genotype (TT) of the eNOS gene were more common than in those without livedo: T, 33 and 10%, respectively (p=0.019); TT, 15 and 0% (p=0.031); OR, 2.49 at 95% CI, 1.2 to 28.9). In the patients with AFS and rapidly progressive LN (RPLN), the minor allele (T) and genotype (TT) of the MTHFR gene were much more frequently encountered: T, 46 and 27%, respectively (p=0.038); TT, 30 and 0% (p=0.033); OR, 3.1 at 95% CI, 1.4 to 32.7). The group of patients without APS exhibited no relationship between the examined polymorphisms and kidney lesion/CONCLUSION: The mutant allele of the p22phox gene increases the risk of arterial and venous thrombosis; the polymorphism of the eNOS gene may be related to the higher incidence of impaired blood microcirculation in SLE concurrent with APS. The risk of RPLN in SLE patients with APS is probably associated with MTHFR gene mutation.

AIM: To elucidate whether and how tacrolimus affects the cumulative survival of patients after living related kidney donor transplantation/MATERIAL AND METHODS: The clinical materials of 246 related kidney transplant recipients, including 108 patients in whom tacrolimus (Prograf and Advagraf) Astellas Pharma US, Inc) was included in the immunodepression protocol (Group 1) and 138 patients who did not receive the agent (Group 2), were analyzed. Comparative analysis used the following tests: the Kaplan Meier test estimating the cumulative survival of recipients and transplants; the Cox test assessing the cumulative risk; and the log-rank test. Allorenal graft losses and mortality rates were also calculated./RESULTS: Mathematical analysis of the above indicators demonstrated that the allograft and survival rates were far higher (p<0.05) and the cumulative risk was much less in Group 1 (p<0.02). Graft losses and the recipients’ deaths were higher in Group 2/CONCLUSION: The analysis suggests that the incorporation of tacrolimus into the immunodepression therapy protocol positively impacts the results of lung related kidney donor transplantation.

The paper describes a case of severe preranal acute renal failure that was induced by the uncontrolled long-term use of furosemide and that was reversible after infusion therapy. Another case is a female patient with anorexia nervosa and end-stage uremia progressing to chronic tubulointerstitial nephritis. Some problems of the pathogenesis of kidney injury and its diagnostic difficulties in anorexia nervosa and diuretic abuse are discussed.

The problem of kidney dysfunction and its impact on outcomes in different groups of cardiac patients continue to being widely used. Kidney dysfunction is associated with a number of traditional cardiovascular risk factors. The use of new biomarkers, cystatin C in particular, to identify kidney injury can contribute to the improvement of early prediction of a risk for renal failure (RF). Cystatin C satisfies many characteristics as an ideal biomarker that can assist in not only detecting the early forms of kidney injury, but also in assessing the risk of RF, the needs for renal replacement therapy, and the risk of death in intensive care unit patients in cardiac clinics. Kidney involvement in many diseases, including those that are not initially regarded as renal, necessitates the elaboration of uniform approaches to managing patients with identified chronic RF, especially to the early prevention and treatment of its complications, such as anemia, phosphorus-calcium metabolic disorders, which substantially worsen the prognosis of other diseases.