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Anemia of chronic kidney disease is a multifactorial condition secondary to various etiologies, including nutritional deficiencies, chronic inflammation, erythropoietin deficiency or resistance, bone marrow suppression, iron deficiency and adverse drug effects. The major therapeutic intervention for anemia among chronic kidney disease patients is erythropoiesis-stimulating agents. However, a limitation of erythropoiesis-stimulating agents is the risk for thromboembolic events, hypertension, seizures, solid organ malignancies and hyporesponsiveness. A novel interleukin-6 monoclonal antibody, ziltivekimab, has been evaluated for managing anemia in chronic kidney disease patients in pilot clinical trials with promising outcomes, including an improvement in hemoglobin levels and reduction of inflammatory parameters. These trials have shown that ziltivekimab does not increase the risk for cytopenia or infectious complications as has been described for other interleukin-6-targeting monoclonal antibodies, like tocilizumab. Furthermore, potentially beneficial effects on serum lipid profile have been reported, leading to the hypothesis of a favorable impact of the drug on atherosclerotic complications. In addition, ziltivekimab has shown efficacy in improving anemia parameters, including hemoglobin levels and iron studies. Ziltivekimab deserves full scale clinical development, and to this aim, large-scale clinical trials are under way., (© 2024. The Author(s) under exclusive licence to Italian Society of Nephrology.)

As the number of patients living with kidney failure grows, the need also grows for kidney transplantation, the gold standard kidney replacement therapy that provides a survival advantage. This may result in an increased rate of transplantation from HLA-mismatched donors that increases the rate of antibody-mediated rejection (AMR), which already is the leading cause of allograft failure. Plasmapheresis, intravenous immunoglobulin therapy, anti-CD20 therapies (i.e., rituximab), bortezomib and splenectomy have been used over the years to treat AMR as well as to prevent AMR in high-risk sensitized kidney transplant recipients. Eculizumab and ravulizumab are monoclonal antibodies targeting the C5 protein of the complement pathway and part of the expanding field of anticomplement therapies, which is not limited to kidney transplant recipients, and also includes complement-mediated microangiopathic hemolytic anemia, paroxysmal nocturnal hemoglobinuria, and ANCA-vasculitis. In this narrative review, we summarize the current knowledge concerning the pathophysiological background and use of anti-C5 strategies (eculizumab and ravulizumab) and C1-esterase inhibitor in AMR, either to prevent AMR in high-risk desensitized patients or to treat AMR as first-line or rescue therapy and also to treat de novo thrombotic microangiopathy in kidney transplant recipients., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Cancer is the second leading cause of death among the adult population following cardiovascular diseases. Prevention and earlier diagnosis are among the cornerstones in the management of malignancies. Albuminuria is a diagnostic criterion for chronic kidney disease and has been associated with multiple conditions including cardiovascular diseases and systemic inflammation while the association between albuminuria and malignancy has been inadequately addressed. Large-scale observational studies with long follow-up periods demonstrate a statistically significant association between albuminuria and overall malignancy incidence, especially urothelial malignancy incidence. However, the underlying pathophysiology linking these two entities is not a straightforward causal relationship but most likely a multidirectional relationship including a causal link. In this narrative review, we evaluate the clinical studies investigating the association between albuminuria and malignancy along with potential underlying mechanisms linking them. We also summarize data on the impact of treatment modalities prescribed for albuminuria and/or proteinuria on the prevention or prognosis of malignancies., Competing Interests: Declaration of Competing Interest AO has received grants from Sanofi and consultancy or speaker fees or travel support from Adviccene, Alexion, Astellas, Astrazeneca, Amicus, Amgen, Boehringer Ingelheim, Fresenius Medical Care, GSK, Bayer, Sanofi-Genzyme, Menarini, Mundipharma, Kyowa Kirin, Lilly, Freeline, Idorsia, Chiesi, Otsuka, Novo-Nordisk, Sysmex and Vifor Fresenius Medical Care Renal Pharma and is Director of the Catedra UAM-Astrazeneca of chronic kidney disease and electrolytes. He has stock in Telara Farma. Other authors declare that they have no conflict of interest., (Copyright © 2023 European Federation of Internal Medicine. All rights reserved.)

Autism Spectrum Disorders (ASD) are a group of neurodevelopmental disorders characterized by repetitive behaviors, lack of social interaction and communication. CC2D1A is identified in patients as an autism risk gene. Recently, we suggested that heterozygous Cc2d1a mice exhibit impaired autophagy in the hippocampus. We now report the analysis of autophagy markers (Lc3, Beclin and p62) in different regions hippocampus, prefrontal cortex, hypothalamus and cerebellum, with an overall decrease in autophagy and changes in Beclin-1/p62 ratio in the hippocampus. We observed sex-dependent variations in transcripts and protein expression levels. Moreover, our analyses suggest that alterations in autophagy initiated in Cc2d1a heterozygous parents are variably transmitted to offspring, even when the offspring's genotype is wild type. Aberration in the autophagy mechanism may indirectly contribute to induce synapse alteration in the ASD brain., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest or other disclosures to report., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Objectives: The aim of the study was comparison of wet-type age-related macular degeneration in phakic and pseudophakic patients in terms of anatomical and functional success based on the real-life data of Türkiye., Methods: The multicenter retrospective real-life study data of the. retinal study group were used in this study. Among 867 eyes of 867 patients were included in the study. Patients were divided into two groups according to the status of the lens; phakic group and pseudophakic group. The follow-up period of the two groups, the number of injections at the 1 st , 2 nd , and 3 rd years, and changes in the central macular thickness (CMT, μ) and visual acuity (VA, logMAR) of the patients at the beginning, 6 th , 12 th , 24 th , and 36 th months were examined., Results: In our study, the number of injections in the 1 st , 2 nd , and 3 rd years, respectively, was 4.2±2.0, 1.8±1.9, and 1.0±1.7 in the phakic group, and 3.9±2.0, 1.7±1.9, and 0.8±1.4 in the pseudophakic group. When the two groups were compared in terms of the number of injections, there was a statistically significant difference in the 1st year, but there was no significant difference in the 2 nd and 3 rd years (p=0.001, p=0.350, and p=0.288, respectively). There was no statistically significant difference between the groups in terms of CMT in the baseline, 6 th , 12 th , 24 th , and 36 th months (p=0.991, p=0.327, p=0.652, p=0.599, and p=0.873, respectively). Although there was no difference in VA between groups at the beginning (p=0.052), the phakic group showed statistically better VA in controls at 3 rd , 6 th , 12 th , 24 th , and 36 th months (p=0.001, p=0.001, p=0.000, p=0.000, and p=0.003, respectively)., Conclusion: Differences in the number of injections and visual results between phakic and pseudophakic patients in wet type AMD may necessitate the creation of different treatment and follow-up protocols., Competing Interests: Conflict of Interest: None declared., (Copyright: © 2023 by Beyoglu Eye Training and Research Hospital.)

Osteopetrosis is a rare genetic disorder caused by osteoclast failure. Dominant negative mutations of the ClCN7 gene cause the so-called, autosomal dominant osteopetrosis type II, which represents the most frequent and heterogeneous form of osteopetrosis, ranging from asymptomatic to intermediate-severe, thus suggesting additional genetic and environmental determinants affecting penetrance. Here, we present a case a 46 year-old woman complained low back pain for 15 years. The patient lacked any history of direct trauma and her pain was radiating to her left leg, increasing with physical activity, she had no pain at nights. The patient was diagnosed with autosomal dominant osteopetrosis on the basis of the presence of typical radiological appearance. Were present a case report of osteopetrosis type II (an autosomal dominantly inherited disease) as a cause for low back pain without any familial penetrance of the disease.

In this study, we aimed to compare the effects of a single bout of acute moderate and strenuous running exercise on the production of interleukin-17 (IL-17), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra) and inflammatory response of skeletal muscles in regularly trained rats. Eight week old rats were trained by treadmill running 5 days per week for 13 weeks at the durations of 30 min (moderate) and 60 min (strenuous). Two days after the last training session, the animals were subjected to a single bout of moderate or strenuous exercise and serum samples were analyzed for IL-17, IL-6, IL-1ra levels and myeloperoxidase (MPO) activity of gastrocnemius muscle were determined. IL-17 level significantly increased in strenuous exercise group when compared to that of sedentary controls (p < 0.01), On the other hand, only in the moderate exercise group, there was a negative correlation between IL-6 and IL-17 levels (r = - 0.857 and p = 0.014). In conclusion, acute single bout of strenuous exercise increased IL-17 production in trained rats and, this cytokine may be involved in inflammatory process of skeletal muscles. Key pointsA single bout of acute strenuous running exercise markedly elevated IL-17 production.This preliminary result should be supported by forthcoming studies that investigate the role of IL-17 in acute inflammatory process of skeletal muscle.