RESUMEN
BACKGROUND: Kidney transplantation is the best treatment method for end-stage renal disease. Technically, left kidney transplantation is easier than right kidney, and the complication rates in the right are higher than the left kidney. We performed 28 kidney transplantations from 14 deceased donors between November 2010 and May 2016. Our aim was to share our outcomes and experiences about these 28 patients. METHODS: We performed 182 kidney transplantations between November 2010 and May 2016. Fifty-four kidney transplantations were performed from deceased donors. Thirty-two of these were performed from 16 of the same donors. These 32 recipients' data were collected and retrospectively analyzed. We excluded the transplantations from two same-donors to their four recipients in this study. The remaining 28 recipients were included in the study. RESULTS: The left and right kidney recipients' numbers were equal (14:14). The left kidney:right kidney rate was 11:3 in the first kidney transplantation recipient group; in the second kidney transplantation recipient group, the rate was 3:11. The difference was statistically significant (P = .002). We found no statistical differences for sex, mean age, and body mass index of recipients, total ischemic time of grafts, hospitalization times, creatinine levels at discharge time, and current ratio of postoperative complications of recipients (P > .05). CONCLUSIONS: There were no differences in the left or the right kidneys or in the first and the second kidney transplantations during the long follow-up period.
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Trasplante de Riñón/métodos , Adulto , Cadáver , Femenino , Supervivencia de Injerto , Humanos , Fallo Renal Crónico/cirugía , Masculino , Persona de Mediana Edad , Complicaciones Posoperatorias , Estudios Retrospectivos , Donantes de TejidosRESUMEN
OBJECTIVE: We designed the present study to test the hypothesis that urinary biomarkers might predict acute kidney injury (AKI) development in non-septic and non-asphyxiated critically ill preterm infants. We evaluated urine (u) sistatin-C (uCys-C), kidney injury molecule-1 (uKIM-1) and neutrophil gelatinase associate lipocaline (uNGAL) as markers of AKI. METHODS: Sixty-four preterm infants with gestational age between 28 and 32 weeks were included in this study. Biomarkers were measured on day of life (DOL) 1, 3, and 7. RESULTS: uNGAL levels in the AKI group were significantly higher than in no-AKI group on DOL 1, 3 and 7 (p = 0.016, p = 0.007 and p = 0.0014, respectively). CONCLUSIONS: uNGAL is sensitive, early, and noninvasive AKI biomarkers, increasing significantly in non-septic and non-asphyxiated critically ill preterm neonates.
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Lesión Renal Aguda/diagnóstico , Cistatina C/orina , Receptor Celular 1 del Virus de la Hepatitis A/metabolismo , Enfermedades del Prematuro/diagnóstico , Lipocalina 2/orina , Lesión Renal Aguda/orina , Biomarcadores/orina , Estudios de Casos y Controles , Enfermedad Crítica , Ensayo de Inmunoadsorción Enzimática , Femenino , Humanos , Recién Nacido , Recien Nacido Prematuro , Enfermedades del Prematuro/orina , Masculino , Estudios Prospectivos , Sensibilidad y EspecificidadRESUMEN
The aim of this study is to investigate Arg753Gln allele polymorphisms of toll-like receptor-2 (TLR2) gene distribution, allele frequency in urinary tract infection (UTI) and genotype-phenotype association of TLR2 gene in children with UTI. The polymorphism was investigated in 124 children with UTI (22 boys and 102 girls; mean age 5.81 +/- 3.47 years) with direct DNA sequencing-based method. TLR2 gene Arg753Gln allele frequency was higher in the patient group when compared with control group (OR 3.14, 95%CI 1.53-6.44, P < 0.001). The frequency of the Arg753Gln allele was significantly higher in gram-positive group than in gram-negative group (OR 7.64, 95%CI 2.80-20.81, P < 0.001). The frequency of UTI was found significantly higher in the Arg753Gln allele carriers of TLR2 gene than the non-carriers (OR 4.94, 95%CI 1.09-22.33, P < 0.05). Similarly, the incidence of asymptomatic UTI was also found significantly higher in the group carrying Arg753Gln allele (OR 3.73, 95%Cl 1.54-9.04, P < 0.05). As a result, we suggest that TLR2 gene could be the predisposing factor for urinary tract infection. Additionally, we observed that subjects carrying the TLR2 Arg753Gln allele had higher risk of urinary tract infection with gram-positive pathogens, history of more than two attacks of UTI and asymptomatic UTI.
Asunto(s)
Infecciones Bacterianas/genética , Polimorfismo Genético , Receptor Toll-Like 2/genética , Infecciones Urinarias/genética , Alelos , Niño , Preescolar , Femenino , Frecuencia de los Genes , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Masculino , Fenotipo , Receptor Toll-Like 2/sangre , Receptor Toll-Like 2/inmunología , TurquíaRESUMEN
OBJECTIVE: Acute rheumatic fever (ARF) is a multisystem inflammatory disease process that follows nasopharyngeal infection caused by group A streptococcus (GAS) (Streptococcus pyogenes). Recent studies have demonstrated that allelic variations at the tumour necrosis factor alpha (TNFalpha) locus are involved in the nature of rheumatic diseases such as juvenile idiopathic arthritis and rheumatic heart disease. Thus, TNFalpha polymorphisms at -308 in ARF patients might be useful in contributing to identification of the primary factors associated with pathogenesis of ARF. METHODS: We performed a case-control association study between the common G/A promoter polymorphism at position -308 in the TNFalpha gene and ARF in Turkish patients, investigating whether this locus acts as a risk factor or has a modifying effect. RESULTS AND CONCLUSION: Previous studies have reported that TNFalpha plays a major role in the pathogenesis of a number of autoimmune and inflammatory diseases. Moreover, significantly elevated TNFalpha levels were reported in patients with ARF. However, in our sample of patients with ARF (n = 66), no such association was found. No interactive effect was found between the TNFalpha polymorphism at position -308 and no association was detected with disease progression. These findings suggest that the role of TNFalpha in ARF may be in linkage disequilibrium with some other severity genes not yet genetically determined.