The role of blood testing in prevention, diagnosis, and management of chronic diseases: A review.

Blood tests are vital to prevention, diagnosis, and management of chronic diseases. Despite this, it can be challenging to construct a comprehensive view of the clinical importance of blood testing because relevant literature is typically fragmented across different disease areas and patient populations. This lack of collated evidence can also make it difficult for primary care providers to adhere to best practices for blood testing across different diseases and guidelines.

Autoregulatory mission impossible: when afferent arterioles lose contractility.

The myogenic response of afferent arterioles is a key autoregulatory mechanism that protects the glomeruli from barotrauma. Afferent arteriolar smooth muscle cells contract to increased intraluminal pressure through mechanosensitive cation channels and interactions between integrin and extracellular matrix that trigger calcium-dependent actomyosin contraction. The study by Feng et al.

Sex differences in blood pressure regulation and hypertension: renal, hemodynamic, and hormonal mechanisms.

The teleology of sex differences has been argued since at least as early as Aristotle's controversial more than 300 years BC, which reflects the sex bias of the time to contemporary readers. Although the question "why are the sexes different" remains a topic of debate in the present day in metaphysics, the recent emphasis on sex comparison in research studies has led to the question "how are the sexes different" being addressed in health science through numerous observational studies in both health and disease susceptibility, including blood pressure regulation and hypertension. These efforts have resulted in better understanding of differences in males and females at the molecular level that partially explain their differences in vascular function and renal sodium handling and hence blood pressure and the consequential cardiovascular and kidney disease risks in hypertension.

Extracellular Vesicles in Kidney Diseases: Moving Forward.

Extracellular vesicles (EVs) are evolving as novel cell mediators, biomarkers, and therapeutic targets in kidney health and disease. They are naturally derived from cells both within and outside the kidney and carry cargo which mirrors the state of the parent cell. Thus, they are potentially more sensitive and disease-specific as biomarkers and messengers in various kidney diseases.

The Clinicopathologic Spectrum of Membranous Nephropathy with Lupus-Like Features.

Introduction: The pathologic features of membranous lupus nephritis (MLN) are occasionally encountered in secondary membranous nephropathy (sMN) without overt clinical evidence of systemic lupus erythematosus. Moreover, some sMN with lupus-like features (lupus-like membranous nephropathy [LL-MN]) have a clinical presentation more typical of primary membranous nephropathy (pMN). Based on the confounding clinical and pathologic presentation, it is unclear how to categorize and treat these patients.

Role of in Hypertension, CKD, and Related Diseases across the Life Span.

Over 20 years after the introduction of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, CKD remains a major public health burden with limited therapeutic options to halt or slow kidney disease progression at all ages. The consensus is that oxidative stress contributes to CKD development and progression. Yet, to date, there is no clear evidence that broad use of antioxidant therapy provides a beneficial effect in CKD.

TMEM27 expression and clinical characteristics and survival in clear cell renal cell carcinoma.

Background: Transmembrane protein 27 (TMEM27/collectrin), a glycoprotein and homolog of angiotensin-converting enzyme 2 (ACE2), is a regulator of renal amino acid uptake in the proximal tubule and may have a protective role in hypertension. Two previous reports have shown that the absence of TMEM27 expression in clear cell renal cell carcinoma (ccRCC) correlates with poorer cancer-related survival. We report our findings of TMEM27 expression in ccRCC and clinical outcomes in an independent third cohort.

Collectrin ( deficiency in proximal tubules causes hypertension in mice and a variant associates with blood pressure in males in a Latino cohort.

Collectrin (), an angiotensin-converting enzyme 2 homologue, is a chaperone of amino acid transporters in the kidney and endothelium. Global collectrin knockout (KO) mice have hypertension, endothelial dysfunction, exaggerated salt sensitivity, and diminished renal blood flow. This phenotype is associated with altered nitric oxide and superoxide balance and increased proximal tubule (PT) Na/H exchanger isoform 3 (NHE3) expression.

Development of a Vietnamese version of the Revised Hasegawa's Dementia scale.

As the aging population grows worldwide, the problem of age-related health is becoming an important public health concern. Dementia is a devastating disease that places a significant physical, emotional, and financial burden on patients, their caregivers, and society. It is predicted to increase in developing countries.

The spectrum of renal diseases with lupus-like features: a single-center study.

Background: A subset of patients without overt systemic lupus erythematosus (SLE) present with biopsy findings typically seen in lupus nephritis (LN). Although a minority eventually develops SLE, many do not. It remains unclear how to classify or treat these patients.

Association of GSTM1 Deletion With Progression of CKD in Children: Findings From the Chronic Kidney Disease in Children (CKiD) Study.

Rationale & Objective: Loss of function of the product of the GSTM1 gene has been implicated in rapid progression of adult chronic kidney disease (CKD). Its role in pediatric CKD has not been previously described.

Study Design: Secondary analysis of a prospective observational cohort examining the association between deletions in GSTM1 and progression of CKD.

Gene, Diet, and Kidney Disease: Implication for Precision Medicine?: Recent Advances in Hypertension.

In the United States, the prevalence of chronic kidney disease in adults is ≈14%. The mainstay of therapy for chronic kidney disease is angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, but many patients with chronic kidney disease still progress to end-stage kidney disease. Increased oxidative stress is a major molecular underpinning of chronic kidney disease progression.

Eat Your Broccoli: Oxidative Stress, NRF2, and Sulforaphane in Chronic Kidney Disease.

The mainstay of therapy for chronic kidney disease is control of blood pressure and proteinuria through the use of angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) that were introduced more than 20 years ago. Yet, many chronic kidney disease (CKD) patients still progress to end-stage kidney disease-the ultimate in failed prevention. While increased oxidative stress is a major molecular underpinning of CKD progression, no treatment modality specifically targeting oxidative stress has been established clinically.

T cell-derived extracellular vesicles are elevated in essential HTN.

Extracellular vesicles (EVs) are novel mediators of cell-to-cell communication and appear to mediate the pathogenesis of hypertension (HTN). However, the mechanisms underlying the involvement of EVs in HTN remain unclear. The adaptive and innate immune systems play an important role affecting the kidney and vasculature in animal models of HTN.

Vitamin K deficiency: an emerging player in the pathogenesis of vascular calcification and an iatrogenic consequence of therapies in advanced renal disease.

Vascular calcification is a known complication of chronic kidney disease (CKD). The prevalence of vascular calcification in patients with non-dialysis-dependent CKD stages 3-5 has been shown to be as high as 79% (20). Vascular calcification has been associated with increased risk for mortality, hospital admissions, and cardiovascular disease (6, 20, 50, 55).

Ethical challenges in nephrology: a call for action.

The American Society of Nephrology, the European Renal Association-European Dialysis and Transplant Association and the International Society of Nephrology Joint Working Group on Ethical Issues in Nephrology have identified ten broad areas of ethical concern as priority challenges that require collaborative action. Here, we describe these challenges - equity in access to kidney failure care, avoiding futile dialysis, reducing dialysis costs, shared decision-making in kidney failure care, living donor risk evaluation and decision-making, priority setting in kidney disease prevention and care, the ethical implications of genetic kidney diseases, responsible advocacy for kidney health and management of conflicts of interest - with the aim of highlighting the need for ethical analysis of specific issues, as well as for the development of tools and training to support clinicians who treat patients with kidney disease in practising ethically and contributing to ethical policy-making.

Pannexin 1 channels in renin-expressing cells influence renin secretion and blood pressure homeostasis.

Kidney function and blood pressure homeostasis are regulated by purinergic signaling mechanisms. These autocrine/paracrine signaling pathways are initiated by the release of cellular ATP, which influences kidney hemodynamics and steady-state renin secretion from juxtaglomerular cells. However, the mechanism responsible for ATP release that supports tonic inputs to juxtaglomerular cells and regulates renin secretion remains unclear.

Rigorous characterization of urinary extracellular vesicles (uEVs) in the low centrifugation pellet - a neglected source for uEVs.

Urinary extracellular vesicles (uEVs) provide bio-markers for kidney and urogenital diseases. Centrifugation is the most common method used to enrich uEVs. However, a majority of studies to date have focused on the ultracentrifugation pellet, potentially losing a novel source of important biomarkers that could be obtained at lower centrifugation.

Circulating Extracellular Vesicles in Normotension Restrain Vasodilation in Resistance Arteries.

Extracellular vesicles (EVs) have been described as novel biomarkers and bioactivators in vascular dysfunction in hypertension. However, the mechanism(s) by which EVs affect vascular function is unknown. To examine the effects of EVs on endothelial-dependent vasodilation (acetylcholine), we isolated circulating EVs from platelet-poor plasma using a low centrifugation speed (17 000) and mesenteric resistance arteries from 12-week-old normotensive WKYs (Wistar-Kyoto rats) and SHRs (spontaneously hypertensive rats).

Extracellular vesicles as a novel diagnostic and research tool for patients with HTN and kidney disease.

Hypertension (HTN) affects one in three adults in the United States and is a major risk factor for cardiovascular disease and kidney failure. There is emerging evidence that more intense blood pressure lowering reduces mortality in patients with kidney disease who are at risk of cardiovascular disease and progression to end-stage renal disease. However, the ideal blood pressure threshold for patients with kidney disease remains a question of debate.

Loss of reticulocalbin 2 lowers blood pressure and restrains ANG II-induced hypertension in vivo.

Hypertension affects over 1 billion people worldwide and increases the risk for heart failure, stroke, and chronic kidney disease. Despite high prevalence and devastating impact, its etiology still remains poorly understood for most hypertensive cases. , which encodes reticulocalbin 2, is a candidate gene for atherosclerosis that we have previously reported in mice.

Trans-ethnic kidney function association study reveals putative causal genes and effects on kidney-specific disease aetiologies.

Chronic kidney disease (CKD) affects ~10% of the global population, with considerable ethnic differences in prevalence and aetiology. We assemble genome-wide association studies of estimated glomerular filtration rate (eGFR), a measure of kidney function that defines CKD, in 312,468 individuals of diverse ancestry. We identify 127 distinct association signals with homogeneous effects on eGFR across ancestries and enrichment in genomic annotations including kidney-specific histone modifications.

Adrenal Tissue-Specific Deletion of TASK Channels Causes Aldosterone-Driven Angiotensin II-Independent Hypertension.

The renin-angiotensin system tightly controls aldosterone synthesis. Dysregulation is evident in hypertension (primary aldosteronism), low renin, and resistant hypertension) but also can exist in normotension. Whether chronic, mild aldosterone autonomy can elicit hypertension remains untested.