Chronic kidney disease (CKD) has been shown to result in profound changes in the composition and functions of the gut microbial flora which by disrupting intestinal epithelial barrier and generating toxic by-products contributes to systemic inflammation and the associated complications. On the other hand, emerging evidence points to the role of the gut microbiota in the development and progression of CKD by provoking inflammation, proteinuria, hypertension, and diabetes. These observations demonstrate the causal interconnection between the gut microbial dysbiosis and CKD. The gut microbiota closely interacts with the inflammatory, renal, cardiovascular, and endocrine systems via metabolic, humoral, and neural signaling pathways, events which can lead to chronic systemic inflammation, proteinuria, hypertension, diabetes, and kidney disease. Given the established role of the gut microbiota in the development and progression of CKD and its complications, favorable modification of the composition and function of the gut microbiome represents an appealing therapeutic target for prevention and treatment of CKD. This review provides an overview of the role of the gut microbial dysbiosis in the pathogenesis of the common causes of CKD including hypertension, diabetes, and proteinuria as well as progression of CKD.

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Metabolic syndrome and diabetes are main health problems of modern life in the twenty-first century. Alarming ratios of global prevalence lead to conduct more and more researches about etiological factors and pathogenesis. Disease mechanism is elementary for advancing more efficient and practicable treatment methods. Concurrent increase in both fructose consumption with Western diet and metabolic syndrome has revealed fructose hypothesis that suggests fructose as one of etiological factor of metabolic syndrome (insulin resistance, central obesity, hypertension, etc.). Recent studies have increasingly lightened the unknowns about role of fructose on pathogenesis. This review discusses fructose hypothesis by exploring current studies and their results in wide perspective. Potential mechanisms covering low-grade inflammation or de novo lipogenesis, etc., in the development of insulin resistance and obesity are explained. Clinical trials have revealed connection of fructose-induced hyperuricemia with insulin resistance and chronic inflammatory state leading to hepatosteatosis or obesity. Further, novel hypothesizes suggesting role of fructose-induced modifications in epigenetics, gut microbiota and oxidative stress on disease pathogenesis are reviewed based on recent clinical trials. More innovative theories including fructose-induced malignancy; decreased satiety feeling, and unfavorable bone health are argued covering fructose-induced neurotransmitter changes in central nervous system, more aggressive malignancy phenotype and impaired calcium absorption.

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Organ crosstalk pathways represent the next frontier for target-mining in molecular medicine for existing syndromes. Pulmonary hypertension and resistant essential hypertension are syndromes that have been proven elusive in etiology, and frequently refractory to first-line management. Underlying crosstalk mechanisms, not yet considered in these treatments, may hinder outcomes or unlock novel treatments. This review focuses systematically on erythropoietin, a synthesizable molecule, as a mediator of brain-kidney crosstalk. Insights gained from this review will be applied to cardiovascular diseases in a clinician-directed fashion.

Chronic non-communicable diseases have become a pandemic public problem in the 21st century, causing enormous burden on the economy, health and quality of life of societies. The role of a chronic inflammatory state in the pathogenesis of chronic disease has been more comprehensively recognized by recent findings. The new paradigm ‘metaflammation’ focuses on metabolism-induced (high fat or fructose-based diet or excessive calorie intake) chronic inflammation. There is a close correlation between the increased incidence of chronic kidney disease (CKD) and chronic heart failure with both increased inflammatory marker levels and western-type diet. In this review we describe the concept of metaflammation, its role in the development of CKD and chronic heart disease, the molecular and signalling pathways involved and the therapeutic consequences.

There is evidence that serum iron levels, regardless of the presence of anemia, directly impact outcomes in congestive heart failure (CHF) including quality of life, hospitalization rate and overall survival. Despite modern medical treatments, the prognosis of CHF remains grim. Ironically, simple iron replenishment may serve as a powerful tool in the armamentarium. This review will start from fundamental concepts of iron in oxygen delivery and analyze evidence-based outcomes in CHF iron-directed therapeutic trials. Imaging rationale that dovetails with this pathophysiology will also be detailed in a clinician-directed fashion.

We described clinical course and outcome of a patient with Listeria monocytogenes meningitis and rhombencephalitis (RE). A 65-year-old woman with past medical history of chemotherapy and radiotherapy for cervical cancer applied to emergency room with the history of fever and headache for three days. Clinical course indicating meningitis evolved to RE over time. We present this case because of the significance of early diagnosis and adequate antimicrobial therapy targeted to the pathogen. At the end, we suggested an algorithm for the case management.