Kidney Diseases
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Published By S. Karger Ag

2296-9357, 2296-9381

2022 ◽  
pp. 1-12
Author(s):  
Henry H.L. Wu ◽  
Rajkumar Chinnadurai

<b><i>Background:</i></b> Erythropoietin-stimulating agent (ESA) hyporesponsiveness is commonly observed in patients with anemia secondary to chronic kidney disease (CKD). Because of its complexity, a global consensus on how we should define ESA hyporesponsiveness remains unavailable. The reported prevalence and demographic information on ESA hyporesponsiveness within the CKD population are variable with no consensus definition. <b><i>Summary:</i></b> ESA hyporesponsiveness is defined as having no increase in hemoglobin concentration from baseline after the first month of treatment on appropriate weight-based dosing. The important factors associated with ESA hyporesponsiveness include absolute or functional iron deficiency, inflammation, and uremia. Hepcidin has been demonstrated to play an important role in this process. Mineral bone disease secondary to CKD and non-iron malnutrition among other factors are also associated with ESA hyporesponsiveness. There is continued debate toward determining a gold-standard treatment pathway to manage ESA hyporesponsiveness. The development of hypoxia-inducing factor-stabilizers brings new insights and opportunities in the management of ESA hyporesponsiveness. <b><i>Key Message:</i></b> Management of ESA hyporesponsiveness involves a comprehensive multidisciplinary team approach to address its risk factors. The progression of basic and clinical research on identifying risk factors and management of ESA hyporesponsiveness brings greater hope on finding solutions to eventually tackling one of the most difficult problems in the topic of anemia in CKD.


2022 ◽  
pp. 1-11
Author(s):  
Bo Wang ◽  
Zhuoshu Li ◽  
Longfei Mao ◽  
Mingyi Zhao ◽  
Bingchang Yang ◽  
...  

<b><i>Background:</i></b> Hydrogen is a chemical substance that has yet to be widely used in medicine. However, recent evidence indicates that hydrogen has multi-faceted pharmacological effects such as antioxidant, anti-inflammatory, and antiapoptotic properties. An increased number of studies are being conducted on the application of hydrogen in various diseases, especially those affecting the renal system. <b><i>Summary:</i></b> Hydrogen can be inhaled, as a gas or liquid, and can be administered orally, intravenously, or locally. Hydrogen can rapidly enter suborganelles such as mitochondria and nucleus by simple diffusion, producing reactive oxygen species (ROS) and triggering DNA damage. Hydrogen can selectively scavenge hydroxyl radical (•OH) and peroxynitrite (ONOO<sup>−</sup>), but not other reactive oxygen radicals with physiological functions, such as peroxyanion (O<sub>2</sub><sup>−</sup>) and hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). Although the regulatory effect of hydrogen on the signal transduction pathway has been confirmed, the specific mechanism of its influence on signal molecules remains unknown. Although many studies have investigated the therapeutic and preventive effects of H<sub>2</sub> in cellular and animal experiments, clinical trials are few and still far behind. As a result, more clinical trials are required to investigate the role of hydrogen in kidney disease, as well as the effect of its dose, timing, and form on the overall efficacy. Large-scale randomized controlled clinical trials will be required before hydrogen can be used to treat renal illnesses. <b><i>Key Messages:</i></b> This article reviews the mechanisms of hydrogen in the treatment of renal disease and explores the possibilities of its use in clinical practice.


2021 ◽  
pp. 1-8
Author(s):  
Xingji Lian ◽  
Li Fan ◽  
Xin Ning ◽  
Cong Wang ◽  
Yi Lin ◽  
...  

<b><i>Background:</i></b> Gestation complications have a recurrence risk and could predispose to each other in the next pregnancy. We aimed to evaluate the relationship between a history of adverse pregnancy and maternal-fetal outcomes in subsequent pregnancy in patients with Immunoglobulin A nephropathy (IgAN). <b><i>Methods:</i></b> A retrospective cohort study from a Chinese single center was conducted. Pregnant women with biopsy-proven primary IgAN and aged ≥18 years were enrolled and divided into the 2 groups by a history of adverse pregnancy. The primary outcome was adverse pregnancy outcome, which included maternal-fetal outcomes. Logistical regression model was used to evaluate the association of a history of adverse pregnancy with subsequent adverse maternal and fetal outcomes. <b><i>Results:</i></b> Ninety-one women with 100 pregnancies were included, of which 54 (54%) pregnancies had a history of adverse pregnancy. IgAN patients with adverse pregnancy history had more composite maternal outcomes (70.4% vs. 45.7%, <i>p</i> = 0.012), while there was no difference in the composite adverse fetal outcomes between the 2 groups (55.6% vs. 45.7%). IgAN patients with a history of adverse pregnancy were associated with an increased risk of subsequent adverse maternal outcomes (adjusted odds ratio [OR], 2.64; 95% CI, 1.07–6.47). Similar results were shown in those with baseline serum albumin &#x3c;3.5 g/dL, 24 h proteinuria ≥1 g/day, and a history of hypertension. There was no association between a history of adverse pregnancy and subsequent adverse fetal outcomes in IgAN patients (adjusted OR, 1.56; 95% CI, 0.63–3.87). <b><i>Conclusion:</i></b> A history of adverse pregnancy was associated with an increased risk of subsequent adverse maternal outcomes, but not for adverse fetal outcomes in IgAN patients.


2021 ◽  
pp. 1-13
Author(s):  
Haiyang Li ◽  
Jiachuan Xiong ◽  
Yu Du ◽  
Yinghui Huang ◽  
Jinghong Zhao

<b><i>Background:</i></b> Dual-specificity phosphatases (DUSPs) belong to the family of protein tyrosine phosphatases, which can dephosphorylate both serine/threonine and tyrosine residues. During the past decades, DUSPs have been implicated in various physiological and pathological activities. Besides mitogen-activated protein kinases (MAPKs) as the main substrates, other protein and nonprotein substrates can also be dephosphorylated by DUSPs. Aberrant regulations of DUSPs have been found in various diseases such as cancer, neurological disorders, and kidney diseases, suggesting the involvement of DUSPs in the pathogenesis of diseases. <b><i>Summary:</i></b> In this review, we summarize the general characteristics of DUSPs and the research progress made in the field of kidney diseases, including diabetic nephropathy, hypertensive nephropathy, chronic kidney disease, acute kidney injury, and lupus nephritis. As the main biochemical function of DUSPs is to dephosphorylate MAPKs activity, decreased DUSPs are found in kidney disease models, whereas forced DUSPs expression reverses the disease presentation, which was proved by using transgenic or gene knockout model. <b><i>Key Messages:</i></b> Mounting evidence demonstrates that DUSPs have essential physiological and pathological functions in kidney disease. Fully understanding the functions and mechanisms of DUSPs in kidney disease contributes to their clinical application in translation medicine.


2021 ◽  
pp. 1-11
Author(s):  
Yue Zhao ◽  
Yue Lang ◽  
Mingchao Zhang ◽  
Shaoshan Liang ◽  
Xiaodong Zhu ◽  
...  

<b><i>Background:</i></b> Mitochondria are dynamic organelles whose structure are maintained by continuous fusion and fission. During acute kidney injury (AKI) progression, mitochondrial fission in renal tubular cells was elevated, characterized by mitochondrial fragmentation. It is tightly associated with mitochondrial dysfunction, which has been proven as a critical mechanism responsible for AKI. However, the initiating factor for the disruption of mitochondrial dynamics in AKI was not well understood. <b><i>Objectives:</i></b> To explore the molecular mechanisms of mitochondrial disorders and kidney damage. <b><i>Methods:</i></b> We established cisplatin-induced AKI model in C57BL/6 mice and proximal tubular cells, and detected the expression of miR-125b by qPCR. Then we delivered miR-125b antagomir after cisplatin treatment in mice via hydrodynamic-based gene transfer technique. Subsequently, we performed luciferase reporter and immunoblotting ­assays to prove miR-125b could directly modulate mitofusin1 (MFN1) expression. We also tested the role of miR-125b in mitochondrial and renal injury through immunofluorescent staining, qPCR, and immunoblotting assays. <b><i>Results:</i></b> miR-125b levels were induced in cisplatin-challenged mice and cultured tubular cells. Anti-miR-125b could effectively alleviate cisplatin-induced mitochondrial fragmentation and kidney injury both in vitro and in vivo. Furthermore, miR-125b could directly regulate MFN1, which is a key regulator of mitochondrial fusion. Our study indicated that miR-125b is upregulated during cisplatin-induced AKI. Inhibition of miR-125b may suppress mitochondrial and renal damage through upregulating MFN1. This study suggests that miR-125b could be a potential therapeutic target in AKI.


2021 ◽  
pp. 1-7
Author(s):  
Ryohei Miyamoto ◽  
Akinari Sekine ◽  
Takuya Fujimaru ◽  
Tatsuya Suwabe ◽  
Hiroki Mizuno ◽  
...  

<b><i>Background:</i></b> Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary cystic kidney disease and is well known to have extrarenal complications. Cardiovascular complications are of particular clinical relevance because of their morbidity and mortality; however, unclear is why they occur so frequently in patients with ADPKD and whether they are related to the genotypes. <b><i>Methods:</i></b> We extracted and retrospectively analyzed clinical data on patients with ADPKD who underwent echocardiography and whose genotype was confirmed by genetic testing between April 2016 and December 2020. We used next-generation sequencing to compare cardiac function, structural data, and the presence of cardiac valvular disease in patients with 1 of 3 genotypes: <i>PKD1</i>, <i>PKD2</i>, and non-<i>PKD1</i>, <i>2</i>. <b><i>Results:</i></b> This retrospective study included 65 patients with ADPKD. Patients were divided into 3 groups: <i>PKD1</i>, <i>n</i> = 32; <i>PKD2</i>, <i>n</i> = 12; and non-<i>PKD1</i>, <i>2</i>, <i>n</i> = 21. The prevalence of mitral regurgitation (MR) was significantly higher in the <i>PKD1</i> group than in the <i>PKD2</i> and non-<i>PKD1</i>, <i>2</i> group (46.9% vs. 8.3% vs. 19.0%, respectively; <i>p</i> = 0.02). In contrast, no significant difference was found for other cardiac valve complications. <b><i>Conclusion:</i></b> This study found a significantly higher prevalence of MR in patients with the <i>PKD1</i> genotype than in those with the <i>PKD2</i> or non-<i>PKD1</i>, <i>2</i> genotypes. Physicians may need to perform echocardiography earlier and more frequently in patients with ADPKD and the <i>PKD1</i> genotype and to control fluid volume and blood pressure more strictly in these patients to prevent future cardiac events.


2021 ◽  
pp. 1-13
Author(s):  
Qiu-Yu Li ◽  
Fei Liu ◽  
Xiaoxiao Tang ◽  
Haidong Fu ◽  
Jianhua Mao

<b><i>Background:</i></b> The kidney requires abundant blood supply, and oxygen is transmitted by diffusion through blood vessels. Most physiological metabolism of the kidney depends on oxygen, so it is very sensitive to oxygen. An increasing pool of evidence suggests that hypoxia is involved in almost all acute and chronic kidney diseases (CKDs). Vascular damage, tubular injury, and fibrosis are the main pathologies associated during hypoxia. Hypoxia-inducible factors (HIFs) are the main mediators during hypoxia, but their functions remain controversial. This article reviewed recent studies and described its mechanisms on renoprotection. <b><i>Summary:</i></b> HIF is degraded rapidly during under normal oxygen. But under hypoxia, HIFs accumulate and many target genes are regulated by HIFs. Homeostasis during injury is maintained through these genes. Pretreatment of HIF can protect the kidney from acute hypoxia and can improve repair, but HIF’s role in CKD and in renal tumor is still controversial. Due to its mechanism in kidney disease, many drugs toward HIFs are widely researched, even some of which have been used in clinical or in clinical research. <b><i>Key Messages:</i></b> In this review, we described the known physiological mechanisms, target genes, and renal protective roles of HIFs, and we discussed several drugs that are researched due to such renal protective roles.


2021 ◽  
pp. 1-18
Author(s):  
Lin Tian ◽  
Anhua Lei ◽  
Tianyu Tan ◽  
Mengmeng Zhu ◽  
Li Zhang ◽  
...  

<b><i>Background:</i></b> Cells of the immune system can inhibit tumor growth and progression; however, immune cells can also promote tumor cell growth, survival, and angiogenesis as a result of the immunosuppressive microenvironments. In the last decade, a growing number of new therapeutic strategies focused on reversing the immunosuppressive status of tumor microenvironments (TMEs), to reprogram the TME to be normal, and to further activate the antitumor functions of immune cells. Most of the “hot tumors” are encompassed with M2 macrophages promoting tumor growth, and the accumulation of M2 macrophages into tumor islets leads to poor prognosis in a wide variety of tumors. <b><i>Summary:</i></b> Therefore, how to uncover more immunosuppressive signals and to reverse the M2 tumor-associated macrophages (TAMs) to M1-type macrophages is essential for reversing the immunosuppressive state. Except for reeducation of TAMs in the cancer immunotherapy, macrophages as central effectors and regulators of the innate immune system have the capacity of phagocytosis and immune modulation in macrophage-based cell therapies. <b><i>Key Messages:</i></b> We review the current macrophage-based cell therapies that use genetic engineering to augment macrophage functionalities with antitumor activity for the application of novel genetically engineered immune cell therapeutics. A combination of TAM reeducation and macrophage-based cell strategy may bring us closer to achieving the original goals of curing cancer. In this review, we describe the characteristics, immune status, and tumor immunotherapy strategies of macrophages to provide clues and evidences for future macrophage-based immune cell therapies.


2021 ◽  
pp. 1-7
Author(s):  
Xiaoling Hu ◽  
Jiahui Zhang ◽  
Yuan Lv ◽  
Xijing Chen ◽  
Guofang Feng ◽  
...  

<b><i>Background:</i></b> Alport syndrome (AS) is a hereditary renal basement membrane disease that can lead to end-stage renal disease in young adults. It can be diagnosed by genetic analysis, being mostly caused by mutations in <i>COL4A3</i>, <i>COL­4A4</i>, and <i>COL4A5</i>. To date, there is no radical cure for this disease. <b><i>Objectives:</i></b> The aim of this study was to avoid the transmission of AS within an affected family by selecting healthy embryos for uterine transfer. The embryos were identified by preimplantation genetic testing for monogenic disorders (PGT-M). <b><i>Methods:</i></b> We used next-generation sequencing (NGS) to identify mutations in the proband and his parents. The results of NGS were confirmed by Sanger sequencing. Targeted NGS combined with targeted single-nucleotide polymorphism haplotyping was used for the in vitro identification of <i>COL4A5</i> mutations in human embryos to prevent their intergenerational transmission. <b><i>Results:</i></b> The c.349_359delGGACCTCAAGG and c.360_361insTGC mutations in <i>COL4A5</i> were identified in a family affected by X-linked AS. Whole-genome sequencing by NGS with targeted haplotyping was performed on biopsied trophectoderm cells. A healthy baby was born after transfer of a single freeze-thawed blastocyst. <b><i>Conclusions:</i></b> The use of targeted NGS for identifying diagnostic markers combined with targeted haplotyping is an easy and efficient PGT-M method for preventing intergenerational transmission of AS.


2021 ◽  
pp. 1-14
Author(s):  
Mei Li ◽  
Zoran Popovic ◽  
Chang Chu ◽  
Bernhard K. Krämer ◽  
Berthold Hocher

Endostatin, a protein derived from the cleavage of collagen XVIII by the action of proteases, is an endogenous inhibitor known for its ability to inhibit proliferation and migration of endothelial cells, angiogenesis, and tumor growth. Angiogenesis is defined as the formation of new blood vessels from pre-existing vasculature, which is crucial in many physiological processes, such as embryogenesis, tissue regeneration, and neoplasia. <b><i>Summary:</i></b> Increasing evidence shows that dysregulation of angiogenesis is crucial for the pathogenesis of renal and cardiovascular diseases. Endostatin plays a pivotal role in the regulation of angiogenesis. Recent studies have provided evidence that circulating endostatin increases significantly in patients with kidney and heart failure and may also contribute to disease progression. <b><i>Key Message:</i></b> In the current review, we summarize the latest findings on preclinical and clinical studies analyzing the impact of endostatin on renal and cardiovascular diseases.


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