[Update on Research and Treatment of Chronic Kidney Disease].

The kidney and brain share strain vessels, which are short and small arterioles that branch out of larger arteries. These vessels are vulnerable to risk factors such as atherosclerosis, old age, hypertension, diabetes, dyslipidemia, and smoking. The nervous system and the kidneys interact to maintain homeostasis.

Organelle communication maintains mitochondrial and endosomal homeostasis during podocyte lipotoxicity.

Organelle stress exacerbates podocyte injury, contributing to perturbed lipid metabolism. Simultaneous organelle stresses can occur in the kidney in the diseased state; therefore, a thorough analysis of organelle communication is crucial for understanding the progression of kidney diseases. Although organelles closely interact with one another at membrane contact sites, limited studies have explored their involvement in kidney homeostasis.

Uremia Impedes Skeletal Myocyte Myomixer Expression and Fusogenic Activity: Implication for Uremic Sarcopenia.

In patients with chronic kidney disease (CKD), skeletal muscle mass and function are known to occasionally decline. However, the muscle regeneration and differentiation process in uremia has not been extensively studied. In mice with CKD induced by adenine-containing diet, the tibialis anterior muscle injured using a barium chloride injection method recovered poorly as compared to control mice.

Acetate attenuates kidney fibrosis in an oxidative stress-dependent manner.

Short-chain fatty acids (SCFAs) are the end products of the fermentation of dietary fibers by the intestinal microbiota and reported to exert positive effects on host physiology. Acetate is the most abundant SCFA in humans and is shown to improve acute kidney injury in a mouse model of ischemia-reperfusion injury. However, how SCFAs protect the kidney and whether SCFAs have a renoprotective effect in chronic kidney disease (CKD) models remain to be elucidated.

Organelle Communication: Joined in Sickness and in Health.

Organelles are membrane-lined structures that compartmentalize subcellular biochemical functions. Therefore, interorganelle communication is crucial for cellular responses that require the coordination of such functions. Multiple principles govern interorganelle interactions, which arise from the complex nature of organelles: position, multilingualism, continuity, heterogeneity, proximity, and bidirectionality, among others.

Good and evil, more reasons to study UPR.

The unfolded protein response (UPR) pathway, launched by endoplasmic reticulum, maintains endoplasmic reticulum homeostasis. Dysregulated UPR pathway links disease phenotypes, such as proteinuria, inflammation, and fibrosis, in kidney disease. Although accumulating evidence indicates the beneficial impact of the UPR pathway as a therapeutic target for various diseases, including kidney disease, the control of adaptive UPR status is still difficult for disease treatment.

Bone marrow stromal cell antigen-1 (CD157) regulated by sphingosine kinase 2 mediates kidney fibrosis.

Chronic kidney disease is a progressive disease that may lead to end-stage renal disease. Interstitial fibrosis develops as the disease progresses. Therapies that focus on fibrosis to delay or reverse progressive renal failure are limited.

Potential progression biomarkers of diabetic kidney disease determined using comprehensive machine learning analysis of non-targeted metabolomics.

Diabetic kidney disease is the main cause of end-stage renal disease worldwide. The prediction of the clinical course of patients with diabetic kidney disease remains difficult, despite the identification of potential biomarkers; therefore, novel biomarkers are needed to predict the progression of the disease. We conducted non-targeted metabolomics using plasma and urine of patients with diabetic kidney disease whose estimated glomerular filtration rate was between 30 and 60 mL/min/1.

Early Identification of CKD-A Scoping Review of the Global Populations.

Introduction: Decisions on whether to screen for chronic kidney disease (CKD) or not remain contentious in nephrology. This study provides a global overview of early CKD identification efforts.

Methods: Guidelines for scoping reviews were followed and studies were identified by searching MEDLINE, EMBASE, Cochrane Library, CINAHL, ISI Web of Science, and PsycINFO.

Organelle Stress and Metabolic Derangement in Kidney Disease.

Advanced multiomics analysis has revealed novel pathophysiological mechanisms in kidney disease. In particular, proteomic and metabolomic analysis shed light on mitochondrial dysfunction (mitochondrial stress) by glycation in diabetic or age-related kidney disease. Further, metabolic damage often results from organelle stress, such as mitochondrial stress and endoplasmic reticulum (ER) stress, as well as interorganelle communication, or "organelle crosstalk", in various kidney cells.

Activation of α7 nicotinic acetylcholine receptors attenuates monocyte-endothelial adhesion through FUT7 inhibition.

Cholinergic anti-inflammatory pathway (CAP) describes a neuronal-inflammatory reflex centered on systemic cytokine regulation by α7 nicotinic acetylcholine receptor (α7nAChR) activation of spleen-residue macrophage. However, the CAP mechanism attenuating distal tissue inflammation, inducing a low level of systemic inflammation, is lesser known. In this study, we hypothesized that CAP regulates monocyte accessibility by influencing their adhesion to endothelial cells.

Assessing the impact of screening, early identification and intervention programmes for chronic kidney disease: protocol for a scoping review.

Introduction: Chronic kidney disease (CKD) is a major threat to public health, especially in low-income and lower middle-income countries, where resources for treating patients with advanced CKD are scarce. Although early CKD identification and intervention hold promise for reducing the burden of CKD and risk factors, it remains unclear if an uniform strategy can be applicable across all income groups. The aim of this scoping review is to synthesise available evidence on early CKD identification programmes in all world regions and income groups.

Lysophosphatidylcholine mediates fast decline in kidney function in diabetic kidney disease.

Some patients with diabetic kidney disease (DKD) show a fast progression of kidney dysfunction and are known as a "fast decliner" (FD). Therefore, it is critical to understand pathomechanisms specific for fast decline. Here, we performed a comprehensive metabolomic analysis of patients with stage G3 DKD and identified increased urinary lysophosphatidylcholine (LPC) in fast decline.

Metabolic Changes and Oxidative Stress in Diabetic Kidney Disease.

Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease, and it is crucial to understand the pathophysiology of DKD. The control of blood glucose levels by various glucose-lowering drugs, the common use of inhibitors of the renin-angiotensin system, and the aging of patients with diabetes can alter the disease course of DKD. Moreover, metabolic changes and associated atherosclerosis play a major role in the etiology of DKD.

Favorable therapeutic efficacy of low-density lipoprotein apheresis for nephrotic syndrome with impaired renal function.

Many reports have shown the therapeutic efficacy of LDL apheresis (LDL-A) in drug-resistant nephrotic syndrome (NS) for improvement of heavy proteinuria and severely impaired renal function. To obtain comprehensive results in a large number of cases, a post hoc analysis of the Prospective Observational survey on the Long-Term Effects of the LDL-Apheresis on the Drug Resistant Nephrotic Syndrome (POLARIS) study was performed by stratifying enrolled cases according to the pretreatment estimated glomerular filtration rate (eGFR) levels indicating normal (N) (≥60 ml/min/1.73 m ), moderately impaired (M) (≥30 to <60 ml/min/1.

Harnessing Metabolomics to Describe the Pathophysiology Underlying Progression in Diabetic Kidney Disease.

Purpose Of Review: Diabetic kidney disease (DKD), a leading cause of end-stage kidney disease, is the result of metabolic network alterations in the kidney. Therefore, metabolomics is an effective tool for understanding its pathophysiology, finding key biomarkers, and developing a new treatment strategy. In this review, we summarize the application of metabolomics to DKD research.

β2-adrenergic receptor agonist counteracts skeletal muscle atrophy and oxidative stress in uremic mice.

In patients with chronic kidney disease, skeletal muscle dysfunction is associated with mortality. Uremic sarcopenia is caused by ageing, malnutrition, and chronic inflammation, but the molecular mechanism and potential therapeutics have not been fully elucidated yet. We hypothesize that accumulated uremic toxins might exert a direct deteriorative effect on skeletal muscle and explore the pharmacological treatment in experimental animal and culture cell models.

Activation of Sympathetic Signaling in Macrophages Blocks Systemic Inflammation and Protects against Renal Ischemia-Reperfusion Injury.

Background: The sympathetic nervous system regulates immune cell dynamics. However, the detailed role of sympathetic signaling in inflammatory diseases is still unclear because it varies according to the disease situation and responsible cell types. This study focused on identifying the functions of sympathetic signaling in macrophages in LPS-induced sepsis and renal ischemia-reperfusion injury (IRI).