Imlifidase in kidney transplantation.

Kidney transplantation, the gold-standard therapeutic approach for patients with end-stage kidney disease, offers improvement in patient survival and quality of life. However, broad sensitization against human leukocyte antigens often resulting in a positive crossmatch against the patient's living donor or the majority of potential deceased donors in the allocation system represents a major obstacle due to a high risk for antibody-mediated rejection, delayed graft function and allograft loss. Kidney-paired donation and desensitization protocols have been established to overcome this obstacle, with limited success. Imlifidase, a novel immunoglobulin G (IgG)-degrading enzyme derived from Streptococcus pyogenes and recombinantly produced in Escherichia coli, is a promising agent for recipients with a positive crossmatch against their organ donor with high specificity towards IgG, rapid action and high efficacy in early pre-clinical and clinical studies. However, the rebound of IgG after a few days can lead to antibody-mediated rejection, making the administration of potent immunosuppressive regimens in the early post-transplant phase necessary. There is currently no comparative study evaluating the efficiency of imlifidase therapy compared with conventional desensitization protocols along with the lack of randomized control trials, indicating the clear need for future large-scale clinical studies in this field. Besides providing a practical framework for the clinical use of the agent, our aim in this article is to evaluate the underlying mechanism of action, efficiency and safety of imlifidase therapy in immunologically high-risk kidney transplant recipients.

Demographic, clinical and laboratory characteristics of adult-onset minimal change disease in Turkey: Turkish Society of Nephrology-Glomerular Diseases (TSN-GOLD) Working Group.

PURPOSE: In our study, diagnostic and demographic characteristics of patients diagnosed with minimal change disease (MCD) by biopsy, clinical and laboratory findings in our country were investigated. METHODS: Data were obtained from the Turkish Society of Nephrology Glomerular Diseases (TSN-GOLD) Working Group database. Demographic characteristics, indications for biopsy, diagnosis of the glomerular diseases, comorbidities, laboratory and biopsy findings of all patients were recorded. The data presented are cross-sectional and includes application data for the biopsy period. RESULTS: Of 3875 patients, 233 patients with MCD (median age 35.0 years) were included in the study, which constitutes 6.0% of the total glomerulonephritis database. Renal biopsy was performed in 196 (84.1%) patients due to nephrotic syndrome. Median serum creatinine was 0.7 (0.6-1.0) mg/dl, mean eGFR was 104 ± 33 ml/min/1.73 m2 and median proteinuria 6000 mg/day. The number of patients under the age of 40 years was 139 (59.7%) (Group A), and the number of patients aged 40 years and over was 94 (40.3%) (Group B). Compared to Group A, global sclerotic glomeruli (24 vs. 43, p < 0.001) interstitial inflammation (15 vs. 34, p < 0.001), interstitial fibrosis (20 vs. 31, p = 0.001, vascular changes (10 vs. 25, p < 0.001) and tubular atrophy (18 vs. 30, p < 0.001) were found to be significantly higher in Group B. There was no difference in immunofluorescent staining properties between the two groups. CONCLUSION: Our data are generally compatible with the literature. Chronic histopathological changes were more common in patients aged 40 years and older than younger patients. Studies investigating the effects of these different features on renal survival are needed.

Aldosterone Resistance Due to Tacrolimus: A Case Report.

Although more common with tacrolimus, it is known that calcineurin inhibitors may induce the development of electrolyte disorders such as hyponatremia and hyperkalemia by causing a hyporeninemic hypoaldosteronism-like syndrome. We present a 32-year-old female renal transplant patient who admitted to clinic with hyponatremia and hyperkalemia. Normal anion gap metabolic acidosis and renal tubular dysfunction were detected and after other reasons were excluded, it was considered as electrolyte disorder due to tacrolimus. No response was detected after tacrolimus conversion to everolimus and considering tubular dysfunction due to aldosterone resistance, we initiated fludrocortisone therapy and electrolyte disorders rapidly improved. Fludrocortisone therapy should be considered when hyponatremia and/or hyperkalemia due to tacrolimus are detected in renal transplant patients.

Serum uric acid levels and inflammatory markers with respect to dipping status: A retrospective analysis of hypertensive patients with or without chronic kidney disease.

BACKGROUND: The aim of this study was to evaluate serum uric acid levels, inflammatory markers [C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR)] and mean platelet volume (MPV) among hypertensive patients with or without chronic kidney disease (CKD) with respect to dipping status. METHODS: A total of 432 hypertensive patients with (n = 340) or without (n = 92) CKD who had ambulatory blood pressure monitoring recordings were included. Correlation of serum uric acid levels with inflammatory markers (CRP, PLR, NLR) was evaluated as was the logistic regression analysis for determinants of nondipper pattern. RESULTS: Nondipper pattern was noted in 65.2% and 79.7% of non-CKD and CKD patients, respectively. Multivariate logistic regression analysis revealed that only serum uric acid (OR, 2.69; 95% CI, 1.60 to 4.52; p = 0.000), MPV (OR, 1.81; 95% CI, 1.30 to 2.53; p = 0.000), PLR (OR, 0.98; 95% CI, 0.97 to 0.99; p = 0.000), and serum albumin (OR, 0.42; 95% CI, 0.19 to 0.93; p = 0.031) were significant determinants of nondipper pattern in the overall study population. CONCLUSION: In conclusion, our findings revealed higher prevalence of nondipper pattern in hypertensive patients with than without CKD and significantly higher levels for uric acid, CRP, MPV, PLR, and NLR among nondipper than dipper hypertensive patients with CKD. High levels for uric acid and MPV and lower levels for PLR and serum albumin were noted as significant determinants of nondipper pattern among hypertensive patients.

Guillain-Barre Syndrome in a Patient with Primary Extranodal Intestinal Non-Hodgkin's Lymphoma: Paraneoplastic, Drug Induced or Coincidental?

Neurological involvement is observed in 5%-25% of patients with lymphoma being either the first presentation of the disease or emerging during its course. However, Guillain-Barré syndrome is rarely reported. In this article, we present a case with intestinal lymphoma developing Guillain-Barré syndrome during the course of the disease. A 66-year-old male patient with primary extranodal intestinal lymphoma developed quadriparesis, sensory deficits and autonomic dysfunction while receiving chemotherapy. The findings of clinical, electrophysiological and laboratory examinations were consistent with Guillain-Barré syndrome. Guillain-Barré syndrome can potentially be fatal and mimic chemotherapy-induced neurotoxicity, especially in patients with lymphoma, and therefore, must be considered in the differential diagnosis.

Pleomorphic carcinoma of the lung with high serum beta-human chorionic gonadotropin level and gynecomastia.

Although gynecomastia is a well-defined paraneoplastic syndrome in patients with non-small cell lung cancer, the association with pleomorphic carcinoma has not been reported. A 50-yr-old man presented with bilateral gynecomastia and elevated serum beta-human chorionic gonadotropin (ßhCG) level. Chest tomography showed a mass in the right middle lobe. Right middle lobectomy and mediastinal lymph node dissection were performed. ßhCG levels decreased rapidly after surgery. Histological examination revealed pleomorphic carcinoma with positive immunostaining for ßhCG. Serum ßhCG levels began to increase gradually on postoperatively 4th month. Computed tomography detected recurrence and chemotherapy was started. After second cycle of chemotherapy, ßhCG levels decreased dramatically again and tomography showed regression in mass. Patient died 6 months later due to brain metastasis. ßhCG expression may be associated with aggressive clinical course and increased risk of recurrence, also ßhCG levels may be used to evaluate therapy response in patients with pleomorphic carcinoma.