Does the A9285G Polymorphism in Collagen Type XII α1 Gene Associate with the Risk of Anterior Cruciate Ligament Ruptures?

One of the most severe injuries sustained by athletes is rupture of the anterior cruciate ligament (ACL). Recent investigations suggest that a predisposition for ACL rupture may be the result of specific genetic sequence variants. In light of this, we decided to investigate whether the COL12A1 A9285G polymorphism was associated with ACL ruptures in Polish football players. We compared genotypic and allelic frequencies of the COL12A1 A9285G polymorphism in two groups of athletes: 91 male football players (23 ± 3 years) with surgically diagnosed primary ACL ruptures who qualified for ligament reconstruction (cases) and 143 apparently healthy, male football players of the same ethnicity, a similar age category, and a comparable level of exposure to ACL injury, who were without any self-reported history of ligament or tendon injury (controls). DNA samples extracted from the oral epithelial cells were genotyped by using a real-time polymerase chain reaction (Ri-Ti-PCR) method. The genotype distribution in the cases were not different from those in controls (p = 0.70). The frequency of the G allele was lower in the cases (18.1%) but not statistically significant (p = 0.40) when compared with controls (21.3%). Our results are in contradiction to the hypothesis that the COL12A1 A9285G polymorphism is associated with a predisposition for ACL injury. However, these conclusions should be supported with more experimental studies on COL12A1 polymorphisms.

THE GSTP1 c.313A>G POLYMORPHISM MODULATES THE CARDIORESPIRATORY RESPONSE TO AEROBIC TRAINING.

The GSTP1 c.313A>G polymorphism is a candidate to explain some of the individual differences in cardiorespiratory fitness phenotypes' responses to aerobic exercise training. We aim to explore the association between the GSTP1 c.313A>G polymorphism and the response to low-high impact aerobic exercise training. Sixty-six Polish Caucasian women were genotyped for the GSTP1 c.313A>G polymorphism; 62 of them completed 12-week aerobic (50-75% HRmax) exercise training and were measured for selected somatic features (body mass and BMI) and cardiorespiratory fitness indices - maximal oxygen uptake (VO2max, maximum heart rate (HRmax), maximum ventilation (VEmax) and anaerobic threshold (AT) - before and after the training period. Two-factor analysis of variance revealed a main training effect for body mass reduction (p=0.007) and BMI reduction (p=0.013), improvements of absolute and relative VO2max (both p<0.001), and increased VEmax (p=0.005), but not for changes in fat-free mass (FFM) (p=0.162). However, a significant training x GSTP1 c.313A>G interaction was found only for FFM (p=0.042), absolute and relative VO2max (p=0.029 and p=0.026), and VEmax (p=0.005). As the result of training, significantly greater improvements in VO2max, VEmax and FFM were gained by the GG+GA group compared to the AA genotype group. The results support the hypothesis that heterogeneity in individual response to training stimuli is at least in part determined by genetics, and GSTP1 c.313A>G may be considered as one (of what appear to be many) target polymorphisms to influence these changes.

MBL2, MASP2, AMELX, and ENAM gene polymorphisms and dental caries in Polish children.

OBJECTIVE: The aim of the study was to examine whether the MBL2 C(-290)G and G161A, MASP2 A359G, AMELX C287T and C522T, and ENAM C2452T polymorphisms are associated with dental caries. SUBJECTS AND METHODS: Genomic DNA of 95 Polish children with 'higher caries experience' (HC) and 84 subjects with 'lower caries experience' (LC) belonging to two age-groups (5 and 13 years old) was extracted from the buccal mucosa. SNPs were genotyped with PCR-RFLP methods. RESULTS: Among 5-year-old children, we found significantly higher percentage of subjects carrying MBL2 (-290)G allele in HC group compared with LC group (43.2%vs 17.6%, P = 0.023). MBL2 C(-290)G-G161A C-G haplotype was overrepresented in LC group in 5-year-olds (P = 0.01), while the opposite association was observed in 13-year-olds, where C-G was overrepresented in HC group (P = 0.028). In 5-year-old children, the frequency of MBL2 G-G haplotype was higher in HC group compared with LC subjects (P = 0.045), while the opposite association (with borderline significance) was observed in 13-year-old children (P = 0.057). SNPs in MASP2, AMELX, and ENAM were not associated with dental caries. CONCLUSION: MBL2 gene polymorphism is associated with caries experience in Polish children, but the direction of this association seems to be opposite in primary and permanent dentition.

C677T polymorphism of the methylenetetrahydrofolate reductase gene and the risk of ischemic stroke in Polish subjects.

Hyperhomocysteinemia is reported to be an independent risk factor for the development of ischemic stroke. Several studies on genetic variants of methylenetetrahydrofolate reductase (MTHFR, which plays a crucial role in regulation of plasma homocysteine concentration) reported an association between C677T gene polymorphism and stroke in some Asian populations. No study but one detected this association in Caucasians. The purpose of the present case-control study was to find a relationship between MTHFR genotypes and stroke in a Polish population. MTHFR genotypes were determined by PCR in 152 patients with ischemic stroke from northwestern Poland and in 135 consecutive newborns from the same population. The TT genotype and the T allele were significantly more frequent in patients than in the control group (11.8% vs. 4.4%, and 34.5% vs. 21.5%, P<0.01). When males and females were analyzed separately, the differences were statistically significant in both genders. It is concluded that presence of the T allele is a risk factor for ischemic stroke in Polish subjects.

Sequence variants of chemokine receptor genes and susceptibility to HIV-1 infection.

Genetic susceptibility to HIV infection was previously proven to be influenced by some chemokine receptor polymorphisms clustering on chromosome 3p21. Here the influence of 5 genetic variants was studied: Delta32 CCR5, G(-2459)A CCR5, G190A CCR2, G744A CX3CR1 and C838T CX3CR1. They were screened in a cohort of 168 HIV-1 positive adults [HIV(+) group] and 151 newborns [control group] from northwestern Poland. PCR-RFLP was performed to screen for the variants (except for Delta32 CCR5 polymorphism, where PCR fragment size was sufficient to identify the alleles) and then electrophoresed on agarose gel to determine fragment size. Distribution of genotypes and alleles was not significantly different between the groups except for the CCR5 polymorphisms, with the Delta32 allele and the (-2459)A CCR5 allele more frequent among neonates than in the HIV(+) group. No Delta32/Delta32 homozygotes were found in the HIV(+) group, but 16.1 percent were Delta32/wt heterozygotes. In the control group, 1.3 percent; were Delta32/Delta32 homozygotes and 26.0percent were Delta32/wt heterozygotes. Linkage between the chemokine polymorphisms was calculated using the most informative loci for haplotype reconstruction. Haplotypes containing Delta32 CCR5, 190G CCR2 and 744A CX3CR1 were found to be significantly more common in the control group. This suggests an association between these haplotypes and resistance to HIV-1 infection.

Experience with autosomal dominant polycystic kidney disease in patients before and after renal transplantation: a 7-year observation.

OBJECTIVE: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the presence of multiple cysts in both kidneys. Symptoms of the disease may arise either from the presence of cysts or from increasing loss of kidney function. First symptoms usually appear in the third decade of life: lumbar pain, urinary tract infections, arterial hypertension, or renal colic due to cyst rupture or coexistent nephrolithiasis. An early diagnosis, male gender, large kidneys by sonography, arterial hypertension, hematuria, and urinary tract infections are predictive factors of a faster progression of the disease. Our aim was to establish the indications for nephrectomy among symptomatic ADPKD patients before kidney transplantation and to assess the risks of posttransplantation complications among ADPKD patients without nephrectomy. PATIENTS AND METHODS: The observed group consisted of 183 patients with ADPKD among whom 50 (27.3%) underwent kidney transplantation during a 7-year observation period (2000-2007). Among those subjects were 3 groups: (I) nephrectomy preceding transplantation; (II) nephrectomy during kidney transplantation; and (III) without nephrectomy. RESULTS: Among group I before transplantation we observed: arterial hemorrhage, wound infections, and splenectomy 4 weeks after ADPKD nephrectomy; afterward we observed: urinary tract infections and contralateral cyst infection. Among group II we only observed 1 case of wound infection. Among group III we observed: ascending urinary tract infections, cyst infections, and cyst hemorrhage. Cyst hemorrhage and cyst infections led mainly to ADPKD kidney nephrectomy. During the observation time, 80.95% of grafts were functioning. CONCLUSIONS: Unilateral nephrectomy is a well-founded preliminary surgical treatment before kidney transplantation. Bilateral nephrectomy before or during transplantation eliminates ADPKD complications and does not significantly increase general complications. The greatest numbers of complications and of graft losses were observed among the group without pretransplantation nephrectomy.

Major depression and atrial natriuretic peptide: The role of adverse childhood experiences.

Atrial natriuretic peptide (ANP) exerts anxiolytic effects in animals and humans. Patients with anxiety, trauma-associated and depressive disorders exhibit lower ANP plasma levels compared to healthy individuals. However, the role of ANP in patients with major depressive disorder (MDD) with and without concomitant adverse childhood experiences (ACE) and in healthy individuals with and without ACE is not clear. We recruited a total of 93 women: 23 women with MDD and ACE, 24 women with MDD without ACE, 22 women with ACE but no current or lifetime MDD, and 24 healthy women without ACE. ANP plasma levels were measured with a radioimmunoassay. The four groups did not differ in demographic and clinical variables. We found a positive correlation between age and plasma levels of ANP (r = .39; p < .001). After controlling for age, there was no significant main effect of MDD or ACE on ANP plasma levels, but a significant interaction between MDD and ACE such that ACE was associated with reduced basal ANP levels in the absence of MDD. We assume that low plasma ANP might be a consequence of ACE in the absence of current psychopathology. Therefore, future studies are needed to replicate our findings and to characterize the influencing factors of ACE on ANP more comprehensively, for example by including a comprehensive trauma and comorbidity anamnesis as well as cardiovascular state and risk factors.

Do estrogens regulate lipid status in testicular steroidogenic Leydig cell?

In this study mouse Leydig cell (MA-10) were treated with G-protein coupled membrane estrogen receptor antagonist (G-15; 10 nM). Cells were analyzed by Western blotting for expression of estrogen-related receptors (ERRα, ß and γ), steroidogenic markers (lutropin receptor; LHR and 3ß-hydroxysteroid dehydrogenase; 3ß-HSD) and lipid droplet markers (perilipin; PLIN and microtubule-associated protein 1 A/1B-light chain 3; LC3). Concomitantly, microscopic analyses by light microscope (immunofluorescent staining for lipid droplets, PLIN and LC3) as well as by electron microscope (for lipid droplet ultrastructure) were utilized. For analysis of cholesterol content, cAMP level and progesterone secretion, G-15, estrogen receptor (ER) antagonist (ICI 182,780; 10 µM), 17ß-estradiol (10 mM) and, bisphenol A (BPA; 10 nM) were used alone or in combinations. We revealed no changes in ERRs expression but alterations in ERRß and γ localization in G-15-treated cells when compared to control. Partial translocation of ERRß and γ from the cell nucleus to cytoplasm was observed. Decreased expression of LHR, 3ß-HSD, PLIN and LC3 was detected. Moreover, in treated cells large lipid droplets and differences in their distribution were found. Very strong signal of co-localization for PLIN and LC3 was found in treated cells when compared to control. In ultrastructure of treated cells, degenerating lipid droplets and double membrane indicating on presence of lipophagosome were observed. We found, that only (i) BPA and G-15 did not effect on cholesterol content, (ii) BPA, G-15 and ICI did not effect on cAMP level and (iii) BPA, ICI alone and in combination, and BPA with G-15 did not modulate progesterone secretion. These findings showed complex and diverse estrogen effects on mouse Leydig cells at various steps of steroid hormone production (cholesterol storage, release and processing). Lipid homeostasis and metabolism in these cells were affected by endogenous and exogenous estrogen, interactions of receptors (GPER, ER and ERR) and GPER and ER antagonists.

Prenatal exposure to an environmentally relevant mixture of Canadian Arctic contaminants decreases male reproductive function in an aging rat model.

Elevated levels of organochlorines (OC) have been reported in Inuit populations in the Arctic. We hypothesized that prenatal exposure to a Canadian Arctic OC mixture adversely affects male reproductive function and health with age. Sprague-Dawley female rats (F0) were gavaged with an environmentally relevant concentration of an Arctic OC mixture or corn oil (Control) during mating with untreated males until parturition (F1 litters). After postnatal day (PND) 90, the weights of the OC F1 males differed dramatically relative to Controls (P<0.05; n=10) and they exhibited respiratory distress. Except for possible thinning of the alveolar barrier, histological observation of the lungs revealed no apparent pathology to explain the respiratory distress. At PND 365, OC F1 males had reduced relative reproductive organ weights and lower sperm quality than Controls (P<0.05). At PND 90, OC F1 males were subfertile (P<0.05), but were infertile at PND 365. In conclusion, environmentally relevant prenatal OC exposure reduced reproductive function and health in aging male rats, providing new insight into the effects of early-life exposures to these contaminants.

Dynamics of core body temperature cycles in long-term measurements under real life conditions in women.

Studies under real life conditions become more and more relevant in chronobiological and chronomedical research. The present study aims to analyze one of the most prominent biological rhythms: the core body temperature (CBT) rhythm in the real world outside the laboratory. CBT was recorded continuously in 37 healthy women (age between 21 and 44 years, median 29 years) with a newly developed intravaginal temperature sensor for up to 102 days. Sleep logs were available from 23 participants. To quantify the daily dynamics of each individual CBT-curve, novel measurement parameters are introduced which permit the quantification of the phase and shape of the CBT rhythms as well as their relation to the sleep-wake cycle. In addition to the classical phase markers (i.e. nadir and peak), the daily curves were segmented into quartiles by introducing the t25/t50/t75-values which can be used as phase and shape markers. At variance to previous studies, a conspicuous day-to-day variation was shown not only for the time point of the peak, but also for the time point of the nadir. However, the t-values, particularly the t75-value were relatively closely locked to external time and thus represent more reliable phase markers than the nadir. The (variable) time point of the nadir determined the period length, phase and shape of the subsequent CBT cycle. If a nadir occurred close to the wake-up time, the following cycle was considerably shorter than 24 hours, while a nadir distant from the wake-up time was followed by a longer cycle. Thus, the period lengths of the daily CBT cycles of each individual were characterized by an "expand/contract" rhythm. The analyses of the novel phase markers (t25/t50/t75) of the CBT curves allowed to identify "early" and "late" participants who may differ in their phase-response curves with regard to the entraining effect of light. In addition, the novel phase markers mirrored the different social entrainment conditions on weekends and workdays.

Risk factors for uterine rupture and neonatal consequences of uterine rupture: a population-based study of successive pregnancies in Sweden.

OBJECTIVE: Uterine rupture is a rare but a catastrophic event. The aim of the present study was to explore the risk factors for uterine rupture and associated neonatal morbidity and mortality among a cohort of Swedish women attempting vaginal birth in their second delivery. DESIGN: Population-based cohort study. SETTING: Sweden. POPULATION: A total of 300,200 Swedish women delivering two single consecutive births between 1983 and 2001. METHODS: Swedish population-based registers were used to obtain information concerning demographics, pregnancy and birth characteristics, and neonatal outcomes. Logistic regression was used to analyse potential risk factors for uterine rupture and risk of neonatal mortality associated with uterine rupture. Odds ratios were used to estimate relative risks using 95% CI. MAIN OUTCOME MEASURE: Uterine rupture and neonatal mortality in the second pregnancy. RESULTS: Compared with women who delivered vaginally in their first birth, women who underwent a caesarean delivery were, during their second delivery, at increased risk of uterine rupture (adjusted OR 41.79; 95% CI 29.73-57.00). Induction of labour, high (> or = 4000 g) birthweight, postterm (> or = 42 weeks) births, high (> or = 35 years) maternal age, and short (< or = 164 cm) maternal stature were also associated with increased risk of uterine rupture. Uterine rupture was associated with a substantially increased risk in neonatal mortality (adjusted OR 65.62; 95% CI 32.60-132.08). CONCLUSION: The risk of uterine rupture in subsequent deliveries is not only markedly increased among women with a previous caesarean delivery but also influenced by induction of labour, birthweight, gestational age, and maternal characteristics.

HRV Influence During Renal Transplantation Procedure on Long-Term Mortality.

BACKGROUND: The autonomic nervous system plays an important role in heart function regulation. One of the most acknowledged methods for noninvasive measurement of autonomic system activity is to determine heart rate variability (HRV). Reduced HRV parameters-heart rate rigidity/stiffness-are an independent prognostic factor of sudden cardiac death risk because of arrhythmia. Renal transplantation is an important factor in HRV changes because of hemodynamic and ion disturbances. The main purpose of this study was to determine the influence of HRV disturbances during renal transplantation procedures on long-term mortality in patients with chronic kidney disease. METHODS: A prospective observation study was performed in the Department of Anesthesiology, Intensive Care, and Acute Poisoning, Pomeranian Medical University, Szczecin, Poland. There were 75 patients (mean age, 47 ± 12 years; 42 men) treated with renal transplantation between 2008 and 2010. Patients were monitored with electrocardiographic tracing with the use of 7 electrodes in position type B. The final stage of analysis was to determine the possible relationship between HRV parameters during the perioperative period and the number of deaths within a 5-year follow-up. RESULTS: HRV parameters during the perioperative period of renal transplantation and the number of deaths within a 5-year follow-up, measured by use of the Holter method, did not differ among patients in the studied population. CONCLUSIONS: HRV is a noninvasive and confirmed tool used for the evaluation of autonomic function and mortality risk in patients with end-stage renal disease. HRV parameters recorded in the perioperative period are not optimal stratification tools for estimating the risk of cardiac deaths in patients with end-stage renal disease.

Spatial differences of matrix metalloproteinase-2 and matrix metalloproteinase-9 within abdominal aortic aneurysm wall and intraluminal thrombus.

Formation of an abdominal aortic aneurysm is a complex process involving aortic wall degradation. The matrix metalloproteinases (MMPs) mainly involved in this process are MMP-2 and MMP-9. Most aneurysms contain an intraluminal thrombus. It is suggested that the thrombus' thickness correlates with the risk of aneurysm rupture and may be a new prognostic factor. The purpose of the present study was to investigate enzyme protein levels in thick (A1) and thin (B1) segments of the thrombus and aneurysm wall sections A (adjacent to A1) and B (adjacent to B1). Aneurysm samples from one aneurism sac were collected from 36 patients that underwent aneurysm repair. MMP-2, MMP-9 and a tissue inhibitor of metalloproteinases (TIMP-1) were measured using enzyme-linked-immunosorbent assay of protein extract. MMP-9 concentrations were significantly higher in B1 samples compared with A1 (113.4 ± 118.0 versus 63.0 ± 61.2, P = 0.004), A(113.4 ± 118.0 versus 31.7 ± 30.0, P < 0.001) or B (113.4 ± 118.0 versus 39.5 ± 41.5, P < 0.001). Likewise MMP-9/TIMP-1 ratio was elevated in B1 compared with A1 (18.9 ± 27.8 versus 9.1 ± 10.6, P = 0.017), A (18.9 ± 27.8 versus 2.5 ± 2.2, P < 0.001) or B (18.9 ± 27.8 versus 3.6 ± 4.5, P < 0.001). MMP-2 and TIMP-1 were higher in A compared with A1 (18.4 ± 8.5 versus 7.2 ± 7.6, P < 0.001; 14.3 ± 5.9 versus 8.5 ± 5.4, P < 0.001, respectively) and B1 (18.4 ± 8.5 versus 5.2 ± 2.9, P < 0.001; 14.3 ± 5.9 versus 8.9 ± 4.9, P < 0.001, respectively) as well as in B compared with A1 (15.9 ± 7.3 versus 7.2 ± 7.6, P < 0.001; 13.0 ± 5.0 versus 8.5 ± 5.4, P < 0.001, respectively) and B1 (15.9 ± 7.3 versus 5.2 ± 2.9, P < 0.001; 13.0 ± 5.0 versus 8.9 ± 4.9, P = 0.003, respectively). There were significant correlations between thin thrombus TIMP-1 and thrombus thickness (ß = -0.24, P = 0.021) and between thin thrombus MMP-9/TIMP-1 ratio and thrombus thickness (ß = 1.75, P = 0.003). Our study has revealed that the presence of thrombi with thin segments in the aneurysm sac, associated with higher proteolytic activity, could possibly be used as a potential indicator of a rupture site.

Selective inhibition by probucol of vascular cell adhesion molecule-1 (VCAM-1) expression in human vascular endothelial cells.

An early event in atherogenesis is the adhesion of monocytes to endothelium via adhesion molecules, such as VCAM-1 and intracellular adhesion molecule-1 (ICAM-1). It has been suggested that VCAM-1 plays a very important role in the recruitment of monocytes in atherosclerosis. Probucol is a potent inhibitor of atherosclerosis in animal models. However, the mechanism of its antiatherogenic effect is poorly understood. The aim of our study was to evaluate whether probucol can influence the expression of endothelial cell adhesion molecules and endothelial adhesiveness. The study was performed on cultured human umbilical vein endothelial cells (HUVEC). HUVEC were pretreated with probucol (50 microM) at different time periods before stimulation with TNFalpha (100 U ml(-1)) or IL-1beta (100 U ml(-1)). The protein expression of VCAM-1 and ICAM-1 was measured by flow cytometry. VCAM-1 mRNA expression was measured by reverse transcription polymerase chain reaction (RT PCR). Probucol time dependently reduced agonist-induced VCAM-1 ( approximately 45%, 48 h) surface protein and mRNA expression ( approximately 40%, 48 h) in HUVEC, but not ICAM-1 surface protein expression. Decreased VCAM-1 expression was associated with reduction ( approximately 40%) of adherence between cytokine-stimulated HUVEC and peripheral blood mononuclear leukocytes (PBMC). Our results suggest that the antiatherogenic effect of probucol may, in part, be due to a downregulation of VCAM-1 expression.

Simvastatin modulates TNFalpha-induced adhesion molecules expression in human endothelial cells.

Adhesion and transendothelial migration of leukocytes into the vascular wall is a crucial step in atherogenesis. Expression of cell adhesion molecules by endothelial cells plays a leading role in this process. We investigated the effect of simvastatin, an inhibitor of HMG-CoA reductase administered to reduce plasma levels of LDL-cholesterol, on the expression of vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1) by human umbilical vein endothelial cells (HUVEC) stimulated with tumor necrosis factor alpha (TNFalpha). We found the expression to be significantly inhibited by the drug in a time and concentration-dependent manner and to a greater extent in the case of VCAM-1 as compared with ICAM-1. In TNFalpha-stimulated HUVEC, simvastatin decreased VCAM-1 and ICAM-1 mRNA levels, inhibited TNFalpha-induced activation of nuclear factor kappaB (NF-kappaB) and enhanced expression of peroxisome proliferator-activated receptor alpha (PPARalpha). These effects were associated with reduction of adherence of monocytes and lymphocytes to HUVEC. The present findings suggest that the benefits of statins in vascular disease may include the inhibition of expression of VCAM-1 and ICAM-1 through effects on NF-kappaB.

Rapid derivative spectrophotometric method for the determination of platinum in Pt-Ru/C catalyst using iodide media.

A rapid spectrophotometric method for the determination of platinum in 20% Pt-Ru (Pt:Ru (1:1)) carbon-supported catalyst has been developed. The samples of catalyst (0.85-12.60 mg) have been digested 1) in aqua regia after preliminary separation of carbon by burning or 2) directly in aqua regia in the presence of carbon. The detection of platinum was carried out in the obtained solutions after conversion of the metal into the iodide complex. The interfering effect of ruthenium on the detection of platinum was eliminated by the use of derivative spectrophotometry. Platinum was selectively determined by numerical calculation of the 4th-order-derivative absorption spectrum of the mixture of iodide complexes of both metals.

Influence of the hemodynamic status of multiorgan donors on long-term kidney graft survival--a multivariable analysis.

BACKGROUND: The quality of transplanted organ and timing of the initiation of its effective function depends on many factors potentially causing graft dysfunction. The aim of this study was to evaluate the influence of the cardiovascular status of multiorgan donors on the long-term kidney graft survival over a 15-year observation period. METHODS: In 2007, the authors of this study published a multicenter prospective study evaluating the influence of the hemodynamic status of multiorgan donors on the early function of transplanted kidney. The results of that study showed that mean arterial pressure, central venous pressure, and pulmonary capillary wedge pressure values of the donor importantly influence the frequency of delayed graft function after renal transplantation. The present analysis covers the effect of the donor's hemodynamic status parameters on graft function time within the 15-year observation period. Univariate and multivariate analyses using the Cox regression proportional hazard model were performed to evaluate the prognostic parameters for overall survival and renal graft survival time. P < .05 was considered to be significant. RESULTS: The univariate analysis showed a significantly shorter time of graft survival in the group of recipients who had a kidney retrieved from donors with lower pulmonary capillary wedge pressure values (P = .038) and lower cardiac index values (P = .039). The same results were obtained for the multifactorial Cox logistic regression analysis. CONCLUSIONS: The filling of the intravascular bed of the donor as determined by pulmonary capillary wedge pressure and maintained donor tissue perfusion as determined by cardiac index, impose important factors influencing long-term kidney graft survival.

Influence of selected factors on long-term kidney graft survival--a multivariable analysis.

BACKGROUND: Long-term function of transplanted kidney is the factor determining quality of life for transplant recipients. The aim of this study was to evaluate the effect of selected factors on time of graft function after renal transplantation within 15 years of observation. METHODS: Preoperative and intraoperative factors were analyzed in 232 kidney recipients within a 15-year observation period. Analysis included age, sex, cause of recipient's renal failure, length of hemodialyses before transplantation, peak panel reactive antibodies test, human leukocyte antigen compatibility, cold ischemia time, delayed graft function occurrence, length and time of hemodialyses after transplantation, early graft rejection, creatinine level at days 1, 3, 7, 30, 90, and 180 after transplantation, and influence of these factors on the time of graft function. Statistical analysis was performed with the use of univariate and multivariate Kaplan-Meier test and Cox regression proportional hazards model, with P < .05 considered to be significant. RESULTS: Univariate analysis showed significantly shorter renal graft function in the group of recipients with higher creatinine levels in all of the analyzed time periods and in patients experiencing delayed graft function. Length of time of hemodialyses after transplantation and number of dialyses had significant impact on worsening of late transplant results. Multivariate analysis reported that early graft rejection in the postoperative period is an independent factor improving late graft function: P = .002; hazard ratio (HR), 0.49 (95% confidence interval [CI], 0.31-0.78). Higher creatinine level at day 90 after kidney transplantation is a predictive factor of late graft dysfunction: P = .002; HR, 1.68 (95% CI 1.2-2.35). CONCLUSIONS: Creatinine level at day 90 after renal transplantation is the prognostic factor of long-term kidney function. Early transplant rejection leads to introduction of more aggressive immunosuppression protocol, which improves long-term transplant results.

Effect of recipient sensitization (peak panel reactive antibodies) on 15-year survival after kidney transplantation.

BACKGROUND: Despite dynamic development within the field of transplantology, the immunization of a potential organ recipient remains an important issue for transplant teams. Panel reactive antibodies (PRA) identification in the serum of the recipient remains routine practice in the majority of transplantation centers. The influence of peak PRA levels on graft function is a well known fact. The aim of this study was to determine the effect of peak PRA on long-term survival after renal transplantation. METHODS: The study was conducted on a group of 232 kidney recipients from multiorgan donors, transplanted in 6 transplant centers in Poland from 1995 to 1997. Data analyzed in this study included recipients' age, sex, PRA, HLA, number and time of hemodialyses after the transplantation, cold ischemia time, and etiology of end-stage renal disease. The effect of data examined in this study on mortality was evaluated at set time points at 5, 10, and 15 years after transplantation. The statistical methods included monofactorial and multifactorial Kaplan-Meier survival analysis and Cox proportional hazards model for mortality prediction. A P value of <.05 was considered to be statistically significant. RESULTS: Among all of the analyzed factors, only peak PRA concentrations significantly correlated with increased mortality among renal transplant recipients. The results were analyzed in all of the set time points: P = .007 at 5 years, P = .014 at 10 years, and P = .05 at 15 years after transplantation. CONCLUSIONS: The increased level of PRA in kidney recipients is a risk factor increasing mortality after the transplantation.

Impact of graft infection on long-term survival after kidney transplant.

BACKGROUND: Patients undergoing transplantation procedures are at a high risk of developing infections because of the need for immunosuppression. Infections presenting directly after renal transplantation greatly influence the overall success of the procedure. The aim of this study was to evaluate the influence of postoperative infection on the length of survival after renal transplant. METHODS: In 2009 a multicenter prospective trial evaluating the factors that influence the occurrence of postoperative infective complications was published by the authors. That study reported that 25 out of 232 recipients of a renal transplant were diagnosed with an infection. The present study shows the effect of postoperative infection on the length of survival after renal transplantation during a 15-year observation period. Statistical methods involved monofactorial and multifactorial Kaplan-Meier analysis for the length of survival and the Cox proportional hazards model for mortality prediction. A P value of <.05 was considered to indicate statistical significance. RESULTS: The analysis demonstrated that the lifespan of renal transplant recipients was decreased in those with postoperative infection, at both year 10 of the observation period (P = .013) and 15 years after transplantation (P = .012). Moreover, it was ascertained that an infection in the postoperative period was an independent risk factor increasing the mortality after renal transplantation: P = .026; hazard ratio 2.90 (95% confidence interval, 1.13-7.41). CONCLUSIONS: The occurrence of an infection in the postoperative period significantly decreases the lifespan of a renal transplantation recipient.