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Children with chronic kidney disease (CKD) are affected by cardiovascular complications, including disturbances in the intraventricular conduction system. Body surface potential mapping (BSPM) is a non-invasive method of assessing the cardioelectrical field. Our aim was to investigate conduction disturbances in young CKD patients using ventricular activation time (VAT) maps. Our study comprised 22 CKD children (mean age: 13.1 ± 2.5 years) treated conservatively and 29 control patients. For each child 12-lead electrocardiogram (ECG) readings were taken, and blood pressure and serum concentrations of iPTH, Pi, t-Ca, creatinine, Fe+3, ferritin, and Hb, as well as eGFR were measured. All children underwent registration in the 87-lead BSPM system, and group-mean VAT maps and a difference map, which presents statistically significant differences between the groups, were created. The VAT map distribution in CKD patients revealed abnormalities specific to left anterior fascicle block. The difference map displays the areas of intergroup VAT changes, which are of discriminative value in detecting intraventricular conduction disturbances. Intraventricular conduction impairments in the left bundle branch may occur in children with CKD. BSPM enables conduction disturbances in CKD children to be detected earlier than using 12-lead ECG. The difference map derived from the group-mean isochrone maps precisely localizes the sites of disturbed conduction in the heart intraventricular conduction system.

Sirtuins, silent information regulator 2 (Sir 2) proteins, belong to the family of NAD(+)-dependent enzymes with deacetylase or mono-ADP-ribosyltransferase activity. These enzymes are responsible for processes of DNA repair or recombination, chromosomal stability and gene transcription. In mammals, sirtuins occur in seven varieties, from 1 to 7 (SIRT1-SIRT7), differing among themselves with location. SIRT1, the best known variety, exerts its effects on proteins via NAD(+) coenzymes, being thus associated with cellular energetic metabolism and the 'red-ox' state. Its deficits are, among others, concomitant with stressful situations and associated with pathophysiologies of many medical conditions, including diabetes mellitus, cardiovascular diseases, neurodegenerative syndromes and kidney diseases. In kidney disorders, it promotes (stimulates) the survival of cells in an affected kidney by modulating their responses to various stress stimuli, takes part in arterial blood pressure control, protects against cellular apoptosis in renal tubules by catalase induction and triggers autophagy. More and more available in vitro and in vivo data indicate SIRT1 activity to be oriented, among others, towards nephroprotection. Thus, SIRT1 may become a novel element in the therapy of age-related renal diseases, including diabetic nephropathy.

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Aim of the study was to assess the effect of KT on heart conduction in HD children. Non-invasive electrocardiographic method of BSPM was used. Isochrone maps, presenting a VAT distribution, were taken from eight HD patients and 26 normal subjects. Patients were divided into two groups: I--three children were HD <12 months prior to KT; II--five children were HD >12 months prior to KT. After KT, the groups were marked as IP and IIP. Serum iPTH and phosphate levels were significantly higher in both HD groups than in controls, with a considerable normalization after transplantation. HD patients demonstrated neither conduction abnormalities on ECG nor left ventricular hypertrophy. Group-mean VAT maps revealed: I and II--similar patterns of complete LBBB; IP--partial normalization to a pattern of anterior fascicle block; IIP--preserved pattern of LBBB. Intraventricular conduction disturbances found in HD children using BSPM were alleviated by KT. Short HD therapy increases a chance of conduction disturbances regression after KT, contrary to the longer HD treatment. BSPM is more sensitive than standard ECG in detecting heart conduction impairments in the HD patients.

The intracellular Ca(i)(2+) homeostasis is disturbed in children with CKD and aggravates the deterioration of renal function as well. The reasons for the progressing increase of erythrocyte calcium concentration are multifactorial. Undoubtedly, the decreased PMCA activity, the calmodulin deficiency and the dysregulated CANP-CAST system are responsible for that phenomenon. The impact of many other biological modulators, creating a network defending the cell against the calcium accumulation, cannot be excluded.

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