Objective: to evaluate the occurrence of single nucleotide polymorphisms (SNPs) in transforming growth factor beta 1 (TGFB1) – rs1800469, rs1800470, rs1800471 – and their haplotypes in children with biliary atresia (BA).Materials and methods. We studied 106 pediatric liver recipients aged 4 to 150 (median 8) months, of whom 44 were boys, and 199 healthy individuals aged 32.7 ± 9.6 years, of whom 79 were boys. The indication for pediatric liver transplantation was BA. Genomic DNA was isolated from peripheral blood using a commercial QIAamp DNA Blood Mini Kit on a QIAcube automated analyzer. SNPs rs1800469, rs1800470, and rs1800471 in the TGFB1 gene were determined by real-time polymerase chain reaction using TaqMan probes on a CFX96 amplifier.Results. In children with BA, the occurrence of the investigated SNPs in TGFB1 was as follows: rs1800469 – 38% GG homozygotes, 50% AG heterozygotes and 12% AA homozygotes; rs1800470 – 39% AA, 44% AG, 17% GG; rs1800471 – 88% CC, 12% GC, 0% GG. The distributions of all the three SNPs followed the Hardy–Weinberg principle. For rs1800469 and rs1800470, the genotype and allele frequencies in children with BA did not differ from those in healthy individuals, whereas for rs1800471, the heterozygous GC genotype was three-fold more frequent in children with BA than in healthy individuals. Haplotype analysis showed the presence of 6 major combinations: 2 most frequent were present in a total of about 66% of patients and 91% of healthy individuals, each of the frequencies practically did not differ between the comparison groups. Significant differences were found in the frequency of 3 rarer haplotypes, A-A-C, G-G-C and G-A-G at position rs1800469, rs1800470, rs1800471, which were observed more frequently in patients with BA by 3.10 (CI 1.59 to 6.04) (p = 0.001), 3.10 (CI 1.55 to 6.17) (p = 0.0015), and 17.02 (CI 1.94 to 149.30) (p = 0.011) times, respectively, than in healthy individuals.Conclusion. In children with BA, the occurrence of CG heterozygotes in rs1800471 and the distribution of three rare haplotypes A-A-C, G-G-C and G-A-G of the rs1800469, rs1800470 and rs1800471 SNPs in the TGFB1 gene significantly differs from that in healthy individuals. It is possible that carriage of rare genotypes and haplotypes of TGFB1 may predispose to BA in children.

One of the most pressing issues in contemporary transplantology is the ongoing search for less invasive methods that would identify potential complications that recipients of solid organ transplants may encounter. Profibrogenic factor galectin-3 (Gal-3) is a potential marker of such complications. It is presumed that it may be involved in regulatory processes in both physiological and pathological conditions; Gal-3 is of particular importance in diseases associated with chronic inflammation and fibrosis.Objective: to assess the predictive significance of Gal-3, determined in the recipients’ serum, in the pathology of a transplanted kidney.Materials and methods. The study included 138 kidney recipients aged from 5 to 68 years and a group of healthy individuals (n = 11). Recipients’ serum Gal-3 levels were measured by immunoenzymatic method.Results. Among the kidney recipients, 91 patients had kidney graft dysfunction according to laboratory and clinical data, which served as an indication to perform a graft biopsy with morphologic examination of the samples. In kidney recipients, Gal-3 levels were significantly different and higher than in healthy individuals, p = 0.017; it did not correlate with most blood test parameters, but there was an inverse correlation with graft glomerular filtration rate (GFR) (r = –0.174; p = 0.043). Recipients’ Gal-3 levels were independent of their tacrolimus blood levels. Kidney recipients with graft dysfunction had considerably higher Gal-3 levels (p = 0.0003) compared to those without. Comparative analysis significantly showed higher Gal-3 concentrations in recipients with acute cellular rejection (ACR, p = 0.005), antibody-mediated rejection (AMR, p = 0.016) and сalcineurin inhibitor (CNI) nephrotoxicity (p = 0.006) compared to recipients without dysfunction. Recipients with signs of CNI nephrotoxicity tended to have higher Gal-3 levels when compared to recipients with graft dysfunction of other etiology (p = 0.08). Kidney recipients with Gal-3 levels above the calculated threshold value of 7.63 ng/mL had a 2.89-fold higher risk of developing chronic graft dysfunction and/or requiring hemodialysis compared with the rest of the kidney recipients (RR = 2.89 ± 0.46 [95% CI 1.17–7.11]), with 76.2% sensitivity and 56.1% specificity of the test.Conclusion. The threshold serum Gal-3 level in kidney recipients can be considered a predictor of an unfavorable graft outcome (chronic graft dysfunction and/or a need for renal replacement therapy).

Objective: to examine the relationship between native liver fibrosis and TGFB1 gene polymorphism in pediatric liver recipients. Materials and methods. Fibrosis of varying severity was diagnosed (METAVIR scale) based on histological analysis of the native liver of children (45 boys and 62 girls aged 3 to 73 months). Genomic DNA was genotyped by real-time polymerase chain reaction using TaqMan probes. Results. The prevalence of the TGFB1 single nucleotide polymorphisms (SNPs) rs1800469, rs1800470, and rs1800471 was examined in both children with liver fibrosis of varying severity and in healthy individuals. The distribution of rs1800470 in children with fibrosis was 50% homozygotes of major allele, 29% heterozygotes and 21% homozygotes of minor allele. This distribution was not consistent with the Hardy-Weinberg principle (p = 0.00026). Conclusion. Liver fibrosis in pediatric liver recipients is linked to the rs1800470 polymorphism of the TGFB1 gene. Carriage of the heterozygous rs1800470 genotype may be a protective factor against liver fibrosis in children with liver failure.

Growth hormone (GH) plays a leading role in the regulation of cell and tissue metabolism and growth. Its effects are mediated through the so-called somatomedins, among which the most important is the liver-produced insulinlike growth factor 1 (IGF-1). It has been reported that serum GH levels in liver recipients is related to the clinical transplant outcomes. Objective: to evaluate the prognostic significance of GH in pediatric liver transplantation (LT). Materials and methods . The study enrolled 148 children (61 boys) aged 2 to 60 months (median, 8) with end-stage liver disease resulting from biliary atresia (n = 86), biliary hypoplasia (n = 14), Byler disease (n = 15), Alagille syndrome (n = 12), Caroli syndrome (n = 5), and other liver diseases (n = 16, cryptogenic cirrhosis, fulminant and autoimmune hepatitis, Crigler–Najjar and Budd–Chiari syndromes, alpha-1 antitrypsin deficiency, glycogenosis and hepatoblastoma). All the patients were transplanted with the left lateral segment of the liver from a living related donor. GH concentrations were measured by enzyme immunoassay before, at one month and at one year after transplantation. Results. Median plasma GH levels in children with liver disease were 4.3 [1.6–7.2] ng/mL, significantly higher than in healthy children of the same age at 1.2 [0.3–2.4] ng/mL, p = 0.001, while mean height and body weight were lower than in healthy controls. GH levels decreased significantly after transplantation. At one month and one year later, the levels did not differ from those of healthy children (p = 0.74, p = 0.67, respectively). One month after transplantation, GH concentrations were lower in 1-year survivors than in non-survivors (p = 0.02); the diagnostically significant threshold GH level was 1.8 ng/mL. Prior to LT, plasma GH levels did not differ between 1-year survivors and non-survivors. Children with GH levels below 1.8 ng/mL post-LT were 9 times more likely to survive one year post-transplant than patients with levels above the threshold. Conclusion. GH concentrations in pediatric liver recipients is a positive prognostic indicator of pediatric LT outcomes.

Development of minimally invasive diagnosis techniques for complications in recipients, based on analysis of the levels of molecular and genetic biomarkers, is an urgent task facing modern transplantology. Transforming growth factor beta 1 (TGF-β1), which has multiple effects in the body, among the potential indicators of complications.Objective: to assess the diagnostic significance of serum TGF-β1 in kidney recipients with graft dysfunction.Materials and methods. The study included 129 kidney recipients aged 17 to 68 years and 35 healthy subjects. Serum TGF-β1 levels in the recipients were determined by immunoenzyme technique.Results. Kidney recipients included 95 patients with laboratory and clinical signs of graft dysfunction, who underwent biopsy of the transplanted kidney, followed by morphological examination, and 34 recipients with normal graft function. Serum TGF-β1 levels in the kidney recipients were significantly higher than in their healthy counterparts (p = 0.00001); it did not correlate with most blood test parameters; with the glomerular filtration rate (GFR). Kidney recipients with graft dysfunction had significantly higher TGF-β1 levels than other recipients (p = 0.018). In recipients with graft dysfunction, morphological study revealed the following: acute tubular necrosis (ATN, n = 11), acute T-cell mediated rejection (ACR, n = 26), acute antibody-mediated rejection (AMR, n = 35), non-immune-mediated nephrosclerosis with signs of calcineurin inhibitor nephrotoxicity (CNI nephrotoxicity, n = 13), and recurrent glomerulonephritis (chronic graft rejection, n = 10). Recipients with immune-mediated graft injury (ACR, AMR and chronic rejection) had higher serum TGF-β1 levels than recipients with graft dysfunction resulting from other causes, p < 0.0001. Kidney recipients with serum TGF-β1 levels above the threshold value of 94.3 ng/mL had a higher risk of immune-mediated graft dysfunction than other kidney recipients (RR = 2.2 ± 0.22 [95% CI 1.46–3.46]) with 77.5% test sensitivity and 60.3% specificity.Conclusion. The calculated threshold serum TGF-β1 level in kidney recipients can be considered as an auxiliary indicator of graft dysfunction resulting from acute or chronic rejection.

Transforming growth factor-1 (TGF-1), a cytokine with immunosuppressive and pro-fibrogenic activity, is a potential marker of infection, liver transplant rejection, and fibrosis. Its levels in the blood and tissues depend on many factors; however, the role of gene polymorphism is still unclear. In this work, the distribution frequency of three single nucleotide polymorphism (SNP) variants of the Tgfb1 gene, namely rs1800469, rs1800470, and rs1800471, was studied in children with end-stage liver disease (ESLD). The study included 225 pediatric liver recipients aged 1 month to 16 years (median, 8 months), including 100 boys and 125 girls, and 198 healthy individuals aged 32.7 9.6 years, including 78 men and 120 women. The indication for liver transplantation in children was ESLD, which was mostly caused by congenital and inherited liver diseases. SNPs were detected by real-time polymerase chain reaction using TaqMan probes and DNA isolated from peripheral blood. SNP frequency distribution was in HardyWeinberg equilibrium and did not differ between children with liver diseases and the healthy ones. Analysis of the SNPs frequency based on allelic interaction models did not reveal any differences between patients and the healthy individuals. Evaluation of linkage disequilibrium for Tgfb1 polymorphic variant pairs revealed a statistically significant linkage between all studied variants. Seven haplotypes, which are variants of SNP combinations, were observed in the studied groups of patients and healthy individuals. A total of 80% of the group had three haplotypes, whose frequencies did not differ between patients and the healthy individuals. Significant differences were found in the frequency of the haplotypes A-A-C, G-G-C, and G-A-G (at rs1800469, rs1800470, and rs1800471, respectively), which were observed up to 11 times more often in recipients compared to the healthy individuals. It is possible that these haplotypes are ESLD-predisposing variants, which may also contribute to the development of complications after liver transplantation in children.

The paper analyzes the literature on physical rehabilitation in transplantology. The medical and social aspects of rehabilitation and peculiarities of physical rehabilitation in child organ recipients are reflected. A rise in the number of organ recipients, including children, is noted. The role of physical rehabilitation in increasing the body’s adaptive reserves at the pre- and postoperative stage and improving the quality of life is described.

Introduction: The acute rejection and bacterial infections are the main risk factors of primary graft dysfunction and high mortality after heart transplantation (HTx). The search for new minimally invasive diagnostic methods and biomarkers of graft damage is extremely relevant. MicroRNAs are widely known as small molecules, regulating gene expression. Some of them (miR-27, -101, and -424) are involved in the mechanisms of cardiovascular diseases. The aim of the study is to determine the diagnostic value of miR-27, miR-101 and miR-424 levels for early post-transplant complications – heart graft acute rejection and gram-negative bacterial infections. Methods: The study enrolled 83 heart transplant recipients, aged 16 to 70 (48.6±10.9) years. The expression levels of miR-27, -101, and -424 were measured by PCR (Qiagen, USA) in plasma after HTx. Graft rejection was verified through morphological analysis of endomyocardial biopsy specimens; infection – through microbiological identification in blood culture. Results: The miR-424 level didn’t differ (p=0.47) in recipients with (n=39) and without acute graft rejection (n=44), however miR-27 and miR-101 levels are significantly lower in recipients with acute graft rejection than in recipients without (p=0.01 and p=0.02 resp.). By the way the diagnostic value of miR-27 and -101 and its’ threshold value for heart transplant acute rejection was found: when miR-27 expression level is below threshold value the relative risk of acute rejection is RR=1.8 [95% CI 1.13–3.01]; miR-101 – below threshold value RR=1.9 [95% CI 1.13–3.37]. For miR-27 the sensitivity (Se) and specificity (Sp) were 53.6% and 79.2%; for miR-101 – 64.3% and Sp=70.8% resp. (Fig. 1). MiR-27, -101 and -424 levels were determined in heart transplant recipients with bacterial infections after HTx (n=20). More than 50% of bacteria spectrum were gram-negative pathogenes: Аcinetobacter baumannii (55%), and Klebsiella pneumoniae (40%). MiR-27 and -101 didn’t differ in recipients with and without infection (p>0.05), but miR-424 level was significantly higher in heart transplant recipients with gram-negative bacteremia (p=0.02). When miR-424 level is above -5.72 fold change, the relative risk of bacteremia is RR=3.9 [95% CI 1.94–7.61]; Se=60.0%; Sp=89.2% (Fig. 2). Conclusion: The measurement of miR-27, -101, and -424 expression levels can be used as complex tests for monitoring the risk of acute rejection and bacterial infections after HTx.

Introduction: Myocardial fibrosis is one of the factors that have a negative impact on long-term prognosis after heart transplantation. Its development is most often accompanied by a violation of the structure and function of the cardiac allograft in recipients. Transforming growth factor β1 is a pleiotropic cytokine involved in the formation of fibrosis. Single nucleotide polymorphisms in the regulatory regions of the TGFB1 gene affect the level of expression and, accordingly, mediate various biological effects of the encoded protein. The aim: to estimate polymorphisms rs1800469, rs1800470, rs1800471 of the TGFB1 gene and their relationship with myocardial fibrosis in heart transplant recipients. Materials and Methods: 110 heart transplant recipients were examined, including 99 (84%) men; the average age of the recipients was 44±14 (from 16 to 70) years. Polymorphisms rs1800469, rs1800470, rs1800471 of the TGFB1 gene were determined using real-time polymerase chain reaction (TaqMan probes). Fibrosis of the cardiac allograft was verified by the results of endomyocardial biopsy; thin sections of endomyocardial tissue were stained with Masson’s trichrome. Results: In 49 heart transplant recipients with verified fibrosis, the following distribution of the studied polymorphisms was observed: rs1800469 - 11% AA homozygotes, 35% AG heterozygotes, and 54% GG homozygotes; rs1800470 - 98% AA homozygotes, 2% AG heterozygotes, and 0% GG homozygotes, rs1800471 - 0% GG homozygotes, 2% GC heterozygotes and 98% CC homozygotes. In heart transplant recipients without fibrosis: rs1800469 - 25% AA homozygotes, 46% AG heterozygotes and 29% GG homozygotes, rs1800470 - 82% AA homozygotes, 11% AG heterozygotes, and 7% GG homozygotes, rs1800471 - 100% CC homozygotes. There were no differences in the distribution of genotypes and alleles of polymorphisms rs1800469, rs1800471 of the TGFB1 gene in recipients with and without fibrosis. In heart transplant recipients with the AA genotype of the rs1800470 polymorphism of the TGFB1 gene, myocardial fibrosis was detected more often than in the carriers of the G allele (OR=10.4, 95% CI:1.152-94.538, p=0.013). There were no differences in the distribution of genotypes and alleles of investigated polymorphisms TGFB1 gene in recipients with and without transplant rejection. Conclusion: The presence of the AA rs1800470 genotype of the TGFB1 gene in heart transplant recipients may be associated with a predisposition to the development of graft myocardial fibrosis.

Fibrosis is one of the causes of kidney allograft loss, especially late after transplantation (up to 65% incidence after 2 years). The purpose of this literature review is to analyze studies examining noninvasive monitoring techniques for renal graft fibrosis.

Introduction: Investigation of new prognostic biomarkers for posttransplant complications is an important issue in today's transplantology. It has been shown that the blood plasma level of transforming growth factor β1 (TGFβ1) may correlate with graft dysfunction development in pediatric liver recipients. However, it is unknown whether these associations are causal and which factors can determine the cytokine plasma levels. The aim was to access the relations of TGFβ1 blood plasma concentrations before and after liver transplantation (LT) with TGFB1 gene polymorphism in pediatric recipients. Materials: 136 children (62 boys) with LT; aged from 3 to 192 (median - 11) months and 64 healthy donors (27 men) aged from 27 to 64 (median - 31) years were included in the study. Concentrations of TGFβ1 were measured in blood plasma before, one month and one year after LT by ELISA. The three types (rs1800469, rs1800470 and rs1800471) of single nucleotide polymorphism (SNP) of TGFB1 was studied by TaqMan SNP genotyping assay. Results: In the liver recipients, the median level of TGF-β1 was 4.17 (1.28-9.29), 6.25 (1.35–15.52) and 7.57 (1.86–13.50) ng/ml before, one month and one year after LT, respectively; frequencies of the SNPs: rs1800469 - 21% AA homozygotes, 35% AG heterozygotes, and 44% GG homozygotes; rs1800470 – 77% AA, 15% AG, 7% GG; rs1800471 – 0% GG, 12% GC, 88% CC. In the donors, the median level of TGF-β1 was 6.65 (3.77 – 17.77), the SNPs frequencies: rs1800469 - 15% AA, 34% AG and 51% GG; rs1800470 - 85% AA, 15% AG and 0% GG, and rs1800471 – 0% GG, 6% GC, 94% CC. A comparative analysis reviled that the cytokine level in pts. with GG genotype rs1800469 was significantly higher than with AG: 1.87 (0.60-7.25) vs 5.25 (2.86–9.45), p=0.038. Differences in levels of TGF-β1 in pts. or donors with other SNPs were not found. Conclusion: Higher plasma level of TGF-β1 may be associated with genotype GG rs1800469 TGFB1 in pediatric liver recipients. Further investigation should be carried out to evaluate whether this polymorphism may impact on posttransplant complications.

Introduction: Chronic cardiovascular disease (CVD) is the most common cause of death in many countries around the world. The genetic mechanisms underlying the pathogenesis of CVD are not fully understood. It has been shown that transforming growth factor β1 regulates the production of the intracellular matrix, inhibits the proliferation of vascular smooth muscle cells, disrupts the division and migration of endothelial cells, which can contribute to the development of coronary heart disease. The aim was to estimate the impact of three types of TGFB1 gene polymorphism (rs1800469, rs1800470, rs1800471) in patients with terminal heart failure who waiting cardiac transplantation. Materials and Methods: The study included 110 patients (99 men; 44±14 years) with heart failure caused by dilated (57 cases) or ischemic (53 cases) cardiomyopathy. The comparison group was healthy blood donors (n=64). Single nucleotide polymorphism (SNP) (rs1800469, rs1800470 and rs1800471) of TGFB1 gene was studied by TaqMan SNP genotyping assay. Results: The pts. had next frequencies of the investigated alleles: rs1800469 - 20% AA homozygotes, 38% AG heterozygotes, and 42% GG homozygotes; rs1800470 – 83% AA, 13% AG, 4% GG; rs1800471 – 3% GG, 13% GC, 84% CC. The SNPs frequencies in the donors had next profile: rs1800469 - 15% AA, 34% AG and 51% GG; rs1800470 - 85% AA, 15% AG and 0% GG, and rs1800471 – 0% GG, 6% GC, 94% CC. There was deviation from Hardy-Weinberg equilibrium in distribution of SNPs rs1800469 and rs1800470 in cardiac pts. In healthy donors all the investigated SNPs were in Hardy-Weinberg equilibrium. Carriers of the genotype CC (p = 0.037, OR = 0.23, 95% CI: 0.054-1.031) and more often the allele G of rs1800471 (p = 0.037, OR = 4,2, 95% CI: 0.970-18.55) were found in patients less often than in healthy individuals. In patients with ischemic heart disease, the genotype GG was less common (p = 0.035, OR = 2.68, 95% CI: 1.061-6.793) and more often the allele A of rs1800469 (p = 0.035, OR = 0.37 95% CI: 0.148-0.942) than in patients with dilated cardiomyopathy. Conclusion: The frequency of rs1800471 TGFB1 differs between patients and healthy individuals. Allele A rs1800469 TGFB1 is associated with ischemic heart disease in potential heart transplant candidates.

Introduction: Transforming growth factor beta 1 (TGF-beta1) is a pleiotropic cytokine produced by almost all cells of the body and has multidirectional autocrine and paracrine effects. Current research indicates a possible role for TGF beta1 in the development of cardiac allograft rejection and fibrosis after heart transplantation. The aim: to evaluate the level and dynamics of TGF-beta1 in patients with chronic heart failure and in cardiac recipients and it is relationship with HLA mismatch. Methods: 161 patients were examined before and after heart transplantation, aged 49±12 (from 16 to 78) years, 141 (87%) of them were men. Initial diagnosis was dilated cardiomyopathy in 89 (55%) patients. The comparison group consisted of healthy adults (n=12) - liver donors aged 30 ± 6 years, including 5 men (42%). All patients underwent heart transplantation from an identical or AB0 matched donor. Before transplantation, all patients had their blood group determined, and HLA typing of the A, B, DR loci was performed using the polymerase chain reaction. The concentration of TGF beta1 was determined in blood plasma samples before, one month and one year after transplantation by ELISA. Results: The average plasma level of TGFbeta1 in the patients with terminal heart failure was 27.2± 18.8 ng/ml and was significantly higher than in healthy individuals 8.7 ± 7.5 ng/ml (p= 0.00). The level of TGF-beta1 did not differ in men and women (p=0.7), and did not depend on the initial diagnosis (p=0.27) and blood type (p=0.8). Heart transplantations identical in blood type were performed in 86% of cases, compatible - in 14%. The proportion of mismatch (MM) according to the HLA system was: ММ6=14%, ММ5=35%, ММ4=32%, ММ3=14%, ММ2=5%. One month after heart transplantation, the plasma level of TGF-beta1 decreased to 11.1 ± 7.7 ng/ml (p = 0.00) and did not differ from the amount of MM. A year after transplantation, the plasma level of TGFbeta1 was 10.2 ± 10.5 ng/ml and significantly differed from the level before transplantation (p=0.00). In patients with MM4, the level of TGF beta1 was significantly higher than with MM6 (12.7±11.0 ng/ml vs 5.5±4.5 ng/ml, p=0.048). It was found correlation between plasma level of TGF-beta1 and blood concentration of tacrolimus a year after HTx (r=0.148, p=0.04). However, the plasma level of TGF-beta1 didn’t differ in recipients with and without myocardial fibrosis (p=0.42). Conclusion: In patients with chronic heart failure the plasma concentration of TGF-beta1 is higher than in healthy individuals, and significantly decreases in recipients after heart transplantation. A relationship was found between the level of TGFbeta1 and the amount of MM, which requires further research.

Aims: Early post-transplant complications such as acute graft rejection and infections are associated with high morbidity and mortality of heart and lung transplant recipients who are in vital need of immunosuppressive therapy. MiR-424 is a member of the miR-16 family, which plays an important physiological role in the development of cardiovascular and respiratory pathology, is involved in the regulation of monocyte and macrophage differentiation, and has an immunosuppressive potential. The aim of the study was to determine the diagnostic value of circulating miR-424 as a potential biomarker of post-transplant complications in heart and lung transplant recipients.Methods: The study enrolled 83 heart transplant recipients, aged 18 to 70 (48 +/- 13) years; 26 lung transplant recipients, aged 10 to 74 (36 +/- 16) years. The miR-424 plasma expression was detected by real-time PCR (Qiagen, USA). Significance of miR-424 level was assessed through the Delta Ct method. Acute graft rejection was verified by the results of endomyocardial or transbronchial biopsy. Post-transplant infectious complications were verified through microbiological identification of bacteremia from blood cultures.Results: Our study shows miR-424 upregulation in plasma of patients with chronic heart or respiratory failure in comparison with healthy individuals (p = 0.003 and p = 0.04 resp.). There was a direct correlation of miR-424 expression with red blood cells and hemoglobin levels in patients before heart transplantation (p = 0.01 and p = 0.03 resp.). After transplantation the expression of plasma miR-424 correlated with the level of C-reactive protein (CRP) both in heart (r = 0.75; p = 0.02) and lung (r = 0.50; p = 0.04) transplant recipients. The expression of plasma miR-424 correlated with tacrolimus blood concentration after heart transplantation (r = 0.38; p = 0.04). The miR-424 level didn't differ in heart or lung transplant recipients with and without acute graft rejection (p = 0.47 and p = 0.78 resp.), but was significantly higher in heart and lung transplant recipients with gram-negative bacteremia (p = 0.002). When the miR-424 level is above a threshold value (-5.72 fold change), the relative risk of bacteremia is RR = 3.84 [95% CI 1.94-7.61]; Se = 60.0%; Sp = 89.2%. CRP concentration above 7 mg/L in duplex test with miR-424 improves the diagnostic characteristics of miR-424 for post-transplant gram-negative bacteremia in heart and lung transplant recipients up to RR = 9.17 [95% CI 1.37-61.46]; Se = 83.3% and Sp = 90.1%. Conclusion: MiR-424 plasma expression was upregulated in patients with chronic heart and respiratory failure and in heart and lung transplant recipients in the early post-transplant period. The duplex test, including miR424 and CRP, has a diagnostic value for detecting the high risk of post-transplant gram-negative bacteremia in heart and lung transplant recipients.