Factors Influencing Lymphocele Development After Kidney Transplant: Single Center Experience.

OBJECTIVES: Lymphocele is a well-known postoperative surgical complication after kidney transplant. In this study, our aim was to analyze incidence, risk factors, and outcomes of posttransplant lymphocele in a large cohort. MATERIALS AND METHODS: This observational study included 395 consecutive patients (219 males and 176 females) who underwent kidney transplant procedures from 183 living and 212 deceased donors in our center between January 2007 and 2014. A lymphocele was diagnosed with ultrasonography. RESULTS: The incidence of lymphoceles in our cohort was 31.9% (n = 126). There were no significant dif-ferences with regard to body mass indexes, age of donors, deceased donor ratios, acute rejection episodes, and history of abdominal surgery between those with and without lymphoceles. The pre-transplant serum albumin levels (3.29 ± 0.67 vs 3.48 ± 0.69 g/dL; P = .009) in the lymphocele group and diabetes mellitus ratios (15.9% vs 4.5%; P < .001) in the nonlymphocele group were lower than levels shown in the other group. The lymphocele ratio in patients who received cyclosporine was higher than that shown in patients who did not received it (37.5% vs. 27.4%; P = .032). There was no difference in lymphocele incidence between patients who were taking and those who were not taking mammalian target of rapamycin inhibitors, mycophenolate mofetil, or mycophenolate sodium. In regression analysis, presence of diabetes mellitus, transplant from deceased donors, older age of donors, and lower albumin levels were independent risk factors for posttransplant lymphocele occurrence. CONCLUSIONS: Posttransplant lymphocele was a relatively common surgical complication in our cohort. We concluded that diabetes mellitus, use of kidneys from deceased donors, older donor age, and hypoalbuminemia were independent risk factors for lymphocele development.

Membranous Nephropathy with Lambda Light Chain Restriction: A Rare Form with Serum Negative and Tissue Positive PLA2R Ab.

Membranous nephropathy (MN) is the most common cause of nephrotic syndrome in adults. Subepithelial polyclonal immunoglobulin deposits and >70% M-type phospholipase A2 receptor antibody positivity are typical findings in idiopathic MN. A 58-year-old female patient was admitted with clinical presentation of nephrotic syndrome. Autoimmune diseases, infections, and malignancies were ruled out after clinical and laboratory evaluations. Diagnostic work-up revealed serum PLA2R antibody negativity and diffuse thickening of glomerular capillary wall on biopsy, while glomerular capillary wall IgG, C3, and Lambda monotypic light chain deposition and PLA2R1 positivity were detected by immunofluorescence and immunohistochemical examination, respectively. Following prednisolone treatment, creatinine and proteinuria were markedly regressed. The MN cases with a light chain deposits are rare and experience regarding their treatment are insufficient.

Serum fetuin-A is associated with the components of MIAC(malnutrition, inflammation, atherosclerosis, calcification) syndrome in different stages of chronic kidney disease

Background/aim: Fetuin-A, a circulating inhibitor of calcification, is a marker of inflammatory-nutritional state. We evaluated the association between serum fetuin-A levels and vascular calcification, intima-media thickness, and nutritional and inflammatory markers in different stages of chronic kidney disease (CKD). Materials and methods: CKD patients were sampled for calcium-phosphate parameters and nutritional and inflammatory markers [highly sensitive C-reactive protein (hs-CRP)], and serum fetuin-A levels. Intima-media thicknesses of the common carotid arteries (CIMT) were measured. Peripheral artery calcification scores were obtained. Results: A total of 238 patients were included in the study. Fetuin-A levels in patients with end-stage renal disease were significantly lower than those in patients with stage-3 and stage-4 CKD (stage-5 vs. stage-4, P < 0.001; stage-5 vs. stage-3, P < 0.001). Fetuin-A was negatively correlated with creatinine (P < 0.001), Ca × P product (P < 0.001), hs-CRP (P = 0.01), vascular calcification score (P < 0.001), and CIMT (P < 0.001), and positively correlated with BMI (P < 0.001, r = 0.30) and serum albumin (P < 0.001). Conclusion: Lower levels of fetuin-A were associated with higher vascular calcification scores, CIMT, hs-CRP levels, and lower BMI and albumin. Fetuin-A deficiency may be a key element for MIAC syndrome.

Relationship between Helicobacter pylori infection and metabolic syndrome.

BACKGROUND/AIMS: To investigate the prevalence of metabolic syndrome (MS) and its components in patients with Helicobacter pylori that was detected using histopathological diagnostic methods. MATERIALS AND METHODS: The study included 200 patients who presented with dyspeptic complaints and had indication for endoscopy. H. pylori-positive [HP (+)] and H. pylori-negative [HP (-)] patients were compared in terms of MS and its components. RESULTS: The prevalence of H. pylori in general patient population is 49.5%. When patients were examined using a diagnostic criteria of MS, MS was present in 78 patients (78.8%) in the HP (+) (n=99) group and in 22 patients (21.8%) in the HP (-) (n=101) group (p<0.01). Logistic regression analysis revealed that H. pylori infection enhances the risk of developing MS by approximately 3.6 times (Relative Risk - (RR)=3.617, 95% CI: 2.465-5.307, p<0.001). With regard to the MS criteria, mean systolic-diastolic blood pressures and body mass index were significantly higher in HP (+) individuals than in HP (-) individuals. Furthermore, fasting plasma glucose, insulin and homeostatic model assessment-insulin resistance, very low-density lipoproteins, and triglyceride levels were also higher in the HP (+) group, whereas high-density lipoproteins levels were lower. CONCLUSION: H. pylori infection is a risk factor for MS. H. pylori leads to insulin resistance by developing chronic inflammation and accordingly facilitates the development of MS.