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Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 14330

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Dr. Shuo-Ming Ou

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Guest Editor

Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
Interests: chronic kidney disease; kidney transplantation; diabetic nephropathy; acute kidney injury; bioinformatics; artificial intelligence

Dr. Shang-Feng Yang

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Guest Editor

Division of Nephrology, Department of Medicine, Cheng Hsin General Hospital, Taipei, Taiwan
Interests: chronic kidney disease; acute kidney injury; renal fibrosis; cardiorenal syndrome

Special Issue Information

Dear Colleagues,

Kidney disease is an important public health problem as its prevalence continues to increase. Researchers have made advancements in research and management strategies for either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI is a heterogeneous clinical syndrome that can be caused by multiple etiologies, such as ischemia, hypoxia, or nephrotoxicity. AKI impairs the energetics of the highly metabolically active nephron segments and involved pathomechanisms and repair mechanisms through targeting the apoptosis of tubular and endothelial cells and/or angiogenic and mitogenic pathways. Currently, there are few effective therapeutic strategies available for AKI, and CKD is becoming increasingly recognized as being closely related to AKI. CKD manifests as a progressive decline in GFR due to the ongoing destruction of the renal parenchyma and the loss of functional nephrons (and ultimately end-stage renal disease). The loss of functional nephrons characterized by interstitial fibrosis and tubular atrophy may be the key contributors of CKD. Therefore, it is crucial to explore the mechanisms that lead to AKI or CKD in order to find therapeutic targets which can prevent or reverse functional nephron loss or the process of renal fibrosis.

We hope that this Special Issue will provide interesting insights into the pathophysiology and new therapeutic strategies to AKI or CKD and explore potential therapeutic strategies that prevent future risks of end-stage renal disease. It is acceptable to submit research addressing novel pathomechanisms related to AKI or CKD. Additionally, targeted therapeutics and novel approaches to managing AKI or CKD are also encouraged.

Dr. Shuo-Ming Ou
Dr. Shang-Feng Yang
Guest Editors

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Keywords

acute kidney injury
chronic kidney disease
inflammation
pathophysiological mechanisms
renal fibrosis renal function progression
therapeutic targets
tubular atrophy
renal recovery

Published Papers (11 papers)

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Research

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14 pages, 4508 KiB

Open AccessArticle

An Approach for Personalized Dynamic Assessment of Chronic Kidney Disease Progression Using Joint Model

by Chen-Mao Liao, Yi-Wei Kao, Yi-Ping Chang and Chih-Ming Lin

Biomedicines 2024, 12(3), 622; https://doi.org/10.3390/biomedicines12030622 - 11 Mar 2024

Viewed by 695

Abstract

Chronic kidney disease (CKD) poses significant challenges to public health and healthcare systems, demanding a comprehensive understanding of its progressive nature. Prior methods have often fallen short in capturing the dynamic and individual variability of renal function. This study aims to address this gap by introducing a novel approach for the individualized assessment of CKD progression. A cohort of 1042 patients, comprising 700 with stage 3a and 342 with stage 3b to stage 5 CKD, treated at a veteran general hospital in Taiwan from 2006 to 2019, was included in the study. A comprehensive dataset spanning 12 years, consisting of clinical measurements, was collected and analyzed using joint models to predict the progression to hemodialysis treatment. The study reveals that the estimated glomerular filtration rate (eGFR) can be considered an endogenous factor influenced by innate biochemical markers. Serum creatinine, blood pressure, and urinary protein excretion emerged as valuable factors for predicting CKD progression. The joint model, combining longitudinal and survival analyses, demonstrated predictive versatility across various CKD severities. This innovative approach enhances conventional models by concurrently incorporating both longitudinal and survival analyses and provides a nuanced understanding of the variables influencing renal function in CKD patients. This personalized model enables a more precise assessment of renal failure risk, tailored to each patient’s unique clinical profile. The findings contribute to improving the management of CKD patients and provide a foundation for personalized healthcare interventions in the context of renal diseases. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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12 pages, 1334 KiB

Open AccessArticle

Altered Expression of Intestinal Tight Junctions in Patients with Chronic Kidney Disease: A Pathogenetic Mechanism of Intestinal Hyperpermeability

by Georgia-Andriana Georgopoulou, Marios Papasotiriou, Pinelopi Bosgana, Anne-Lise de Lastic, Eleni-Evangelia Koufou, Evangelos Papachristou, Dimitrios S. Goumenos, Periklis Davlouros, Eleni Kourea, Vasiliki Zolota, Konstantinos Thomopoulos, Athanasia Mouzaki and Stelios F. Assimakopoulos

Biomedicines 2024, 12(2), 368; https://doi.org/10.3390/biomedicines12020368 - 5 Feb 2024

Viewed by 793

Abstract

Background: Systemic inflammation in chronic kidney disease (CKD) is associated (as a cause or effect) with intestinal barrier dysfunction and increased gut permeability, with mechanisms not yet fully understood. This study investigated different parameters of the intestinal barrier in CKD patients, especially tight junction (TJ) proteins and their possible association with systemic endotoxemia and inflammation. Methods: Thirty-three patients with stage I–IV CKD (n = 17) or end-stage kidney disease (ESKD) (n = 16) and 11 healthy controls underwent duodenal biopsy. Samples were examined histologically, the presence of CD3+ T-lymphocytes and the expression of occludin and claudin-1 in the intestinal epithelium was evaluated by means of immunohistochemistry, circulating endotoxin concentrations were determined by means of ELISA and the concentrations of the cytokines IL-1β, IL-6, IL-8, IL-10 and TNF-α in serum were measured using flow cytometry. Results: Patients with stage I–IV CKD or ESKD had significantly higher serum endotoxin, IL-6, IL-8 and IL-10 levels compared to controls. Intestinal occludin and claudin-1 were significantly decreased, and their expression was inversely correlated with systemic endotoxemia. Regarding occludin, a specific expression pattern was observed, with a gradually increasing loss of its expression from the crypt to the tip of the villi. Conclusion: The expression of occludin and claudin-1 in enterocytes is significantly reduced in patients with CKD, contributing to systemic endotoxemia and inflammatory responses in these patients. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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12 pages, 3024 KiB

Open AccessArticle

Adiponectin C1q/Tumor Necrosis Factor-Related Protein 13 (CTRP13) Protects against Renal Inflammation and Fibrosis in Obstructive Nephropathy

by Yongxia Li, Wenzhe Wang, Changxuan Liu, Min Zeng, Li Xu, Rong Du and Cheng Wang

Biomedicines 2024, 12(1), 51; https://doi.org/10.3390/biomedicines12010051 - 25 Dec 2023

Viewed by 858

Abstract

Renal inflammation and fibrosis are the important pathological phenomena associated with obstructive nephropathy. However, the underlying mechanism associated with this disease has yet to be fully elucidated. The present study, therefore, aimed to investigate the effects mediated by C1q/tumor necrosis factor-related protein 13 (CTRP13) on renal inflammation and fibrosis in addition to elucidating the underlying mechanism. To meet this aim, a mouse unilateral ureteral obstruction (UUO)-mediated renal dysfunction model was established. In addition, hematoxylin–eosin staining (H&E) staining and immunofluorescence experiments as well as Western blotting and reverse transcription quantitative (RT q) PCR analyses were performed. Recombinant CTRP13 was used to investigate the role of CTRP13 in chronic renal inflammation and fibrosis. A decreased expression level of CTRP13 was identified in the plasma of patients with renal fibrosis and in UUO-model mice. The renal histopathological and functional analyses revealed that CTRP13 could both reverse UUO mediated renal dysfunction and ameliorate the conditions of tubulointerstitial fibrosis and tubular injury. Additionally, CTRP13 was found to inhibit the expression levels of extracellular matrix proteins and proinflammatory mediators. In terms of the underlying mechanism, the protective effects on inflammation and fibrosis of the kidneys of CTRP13-treated mice undergoing UUO were found to be associated with the inactivation of the TGF β/Smad and NF κB p65 signaling pathways. Taken together, these findings have suggested that CTRP13 fulfills a vital role in the progression of obstructive nephropathy, thereby uncovering brand new insights into possible leads for the therapeutic treatment of chronic kidney disease (CKD). Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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14 pages, 1972 KiB

Open AccessArticle

Safety and Metabolic Tolerance of Citrate Anticoagulation in Critically Ill Polytrauma Patients with Acute Kidney Injury Requiring an Early Continuous Kidney Replacement Therapy

by Filippo Mariano, Alberto Mella, Paolo Randone, Fulvio Agostini, Daniela Bergamo, Maurizio Berardino and Luigi Biancone

Biomedicines 2023, 11(9), 2570; https://doi.org/10.3390/biomedicines11092570 - 19 Sep 2023

Viewed by 761

Abstract

For severe polytrauma patients with an early AKI requiring renal replacement therapy, anticoagulation remains a great challenge. Due to a high bleeding risk, hemodynamic instability, and increased lactate levels, continuous modality (CKRT) and citrate anticoagulation seem to be the most appropriate. However, their safety with regard to the potential risk of impaired citrate metabolism is not documented. A retrospective study of 60 severe polytrauma patients admitted to the emergency department between January 2000 and December 2021 was conducted; the patients requiring CKRT during the first 72 h were treated with citrate (n. 46, group Citrate) or with heparin (n. 14, group Heparin). Out of 60 patients, 31 survived (51.7%). According to logistic regression analysis, age and SOFA score were significant predictors of mortality. The incidence of rhabdomyolysis was more common in the survivors (77.4 vs. 51.7%), and Kaplan–Meyer analysis showed a better trend towards survival at 90 days for the group Citrate than the group Heparin (p 0.0956). In the group Citrate, hemorrhagic episodes were significantly less common (0.045 vs. 0.273 episodes/day, p < 0.001); the effective duration (h/day) of CKRT was longer; and the effective net ultrafiltration rate (mL/kg/h) and blood flow rate were lower. For severe polytrauma patients, early, soft CKRT with citrate anticoagulation at a low blood flow rate and circuit citratemia showed a better safety and hemodynamic stability, suggesting that citrate should be the first choice anticoagulant in this subset of patients. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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11 pages, 2585 KiB

Open AccessArticle

Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport

by Yanhua Wang, Lauren M. LaRocque, Joseph A. Ruiz, Eva L. Rodriguez, Jeff M. Sands and Janet D. Klein

Biomedicines 2023, 11(7), 1844; https://doi.org/10.3390/biomedicines11071844 - 27 Jun 2023

Viewed by 1229

Abstract

Hyponatremia (hypo-osmolality) is a disorder of water homeostasis due to abnormal renal diluting capacity. The body limits the degree to which serum sodium concentration falls through a mechanism called “vasopressin escape”. Vasopressin escape is a process that prevents the continuous decrease in serum sodium concentration even under conditions of sustained high plasma vasopressin levels. Previous reports suggest that aldosterone may be involved in the vasopressin escape mechanism. The abilities of aldosterone synthase (Cyp11b2) knockout and wild-type mice to escape from vasopressin were compared. Wild-type mice escaped while the aldosterone synthase knockout mice did not. Both the water channel aquaporin 2 (AQP2) and the urea transporter UT-A1 protein abundances were higher in aldosterone synthase knockout than in wild-type mice at the end of the escape period. Vasopressin escape was also blunted in rats given spironolactone, a mineralocorticoid receptor blocker. Next, the role of the phosphatase, calcineurin (protein phosphatase 2B, PP2B), in vasopressin escape was studied since aldosterone activates calcineurin in rat cortical collecting ducts. Tacrolimus, a calcineurin inhibitor, blunted vasopressin escape in rats compared with the control rats, increased UT-A1, AQP2, and pS256-AQP2, and decreased pS261-AQP2 protein abundances. Our results indicate that aldosterone regulates vasopressin escape through calcineurin-mediated protein changes in UT-A1 and AQP2. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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13 pages, 277 KiB

Open AccessArticle

Clinical Considerations for Patients Experiencing Acute Kidney Injury Following Percutaneous Nephrolithotomy

by Daniel A. Reich, Esra Adiyeke, Tezcan Ozrazgat-Baslanti, Andrew K. Rabley, Shahab Bozorgmehri, Azra Bihorac and Vincent G. Bird

Biomedicines 2023, 11(6), 1712; https://doi.org/10.3390/biomedicines11061712 - 14 Jun 2023

Viewed by 1165

Abstract

Acute kidney injury (AKI) is a common postoperative outcome in urology patients undergoing surgery for nephrolithiasis. The objective of this study was to determine the prevalence of postoperative AKI and its degrees of severity, identify risk factors, and understand the resultant outcomes of AKI in patients with nephrolithiasis undergoing percutaneous nephrolithotomy (PCNL). A cohort of patients admitted between 2012 and 2019 to a single tertiary-care institution who had undergone PCNL was retrospectively analyzed. Among 417 (n = 326 patients) encounters, 24.9% (n = 104) had AKI. Approximately one-quarter of AKI patients (n = 18) progressed to Stage 2 or higher AKI. Hypertension, peripheral vascular disease, chronic kidney disease, and chronic anemia were significant risk factors of post-PCNL AKI. Corticosteroids and antifungals were associated with increased odds of AKI. Cardiovascular, neurologic complications, sepsis, and prolonged intensive care unit (ICU) stay percentages were higher in AKI patients. Hospital and ICU length of stay was greater in the AKI group. Provided the limited literature regarding postoperative AKI following PCNL, and the detriment that AKI can have on clinical outcomes, it is important to continue studying this topic to better understand how to optimize patient care to address patient- and procedure-specific risk factors. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

13 pages, 2773 KiB

Open AccessArticle

Decreased MARCKS Protein Expression in Kidney Cortex Membrane Fractions of Cathepsin B Knockout Mice Is Associated with Reduced Lysophosphatidylcholine and Protein Kinase C Activity

by Tamim Kawakibi, Niharika Bala, Lauren P. Liu, Louis A. Searcy, Nancy D. Denslow and Abdel A. Alli

Biomedicines 2023, 11(5), 1489; https://doi.org/10.3390/biomedicines11051489 - 20 May 2023

Viewed by 1400

Abstract

Cathpesin B is a multi-functional protease that plays numerous roles in physiology and pathophysiology. We hypothesized that actin cytoskeleton proteins that are substrates of cathepsin B, various lipids, and kinases that are regulated by lipids would be down-regulated in the kidney of cathepsin B knockout mice. Here, we show by Western blot and densitometric analysis that the expression and proteolysis of the actin cytoskeleton proteins myristoylated alanine-rich C-kinase substrate (MARCKS) and spectrin are significantly reduced in kidney cortex membrane fractions of cathepsin B knockout mice compared to C57B6 wild-type control mice. Lipidomic results show that specific lipids are increased while other lipids, including lysophosphatidylcholine (LPC) species LPC (16:0), LPC (18:0), LPC (18:1), and LPC (18:2), are significantly decreased in membrane fractions of the kidney cortex from Cathepsin B null mice. Protein Kinase C (PKC) activity is significantly lower in the kidney cortex of cathepsin B knockout mice compared to wild-type mice, while calcium/calmodulin-dependent protein kinase II (CaMKII) activity and phospholipase D (PLD) activity are comparable between the two groups. Together, these results provide the first evidence of altered actin cytoskeleton organization, membrane lipid composition, and PKC activity in the kidneys of mice lacking cathepsin B. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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13 pages, 1351 KiB

Open AccessArticle

Metformin Alleviates Diabetes-Associated Hypertension by Attenuating the Renal Epithelial Sodium Channel

by Yogesh M. Scindia, Mohammed F. Gholam, Alina Waleed, Lauren P. Liu, Kevin M. Chacko, Dhruv Desai, Juliana Pena Lopez, Zeeshan Malik, Whitney C. Schramm, Angelica G. Morales, Morgan Carson-Marino and Abdel A. Alli

Biomedicines 2023, 11(2), 305; https://doi.org/10.3390/biomedicines11020305 - 21 Jan 2023

Cited by 3 | Viewed by 1971

Abstract

Diabetic nephropathy is the primary cause of morbidity in type 2 diabetes mellitus (T2DM) patients. New data indicate that hypertension, a common comorbidity in T2DM, can worsen outcomes of diabetic nephropathy. While metformin is a commonly prescribed drug for treating type 2 diabetes, its blood pressure regulating ability is not well documented. The aim of this study was to investigate the effect of metformin on normalizing blood pressure in salt-loaded hypertensive diabetic db/db mice. Sixteen-week-old male and female diabetic db/db mice were individually placed in metabolic cages and then randomized to a control vehicle (saline) or metformin treatment group. We evaluated the blood pressure reducing ability of metformin in salt-induced hypertension and progression of nephropathy in db/db mice. We observed that metformin- normalized systolic blood pressure in hypertensive diabetic mice. Mechanistically, metformin treatment reduced renal cathepsin B expression. Low cathepsin B expression was associated with reduced expression and activity of the epithelial sodium channel (ENaC), sodium retention, and thus control of hypertension. In addition, we identified that urinary extracellular vesicles (EVs) from the diabetic mice are enriched in cathepsin B. Compared to treatment with urinary EVs of vehicle-treated hypertensive diabetic mice, the amiloride-sensitive transepithelial current was significantly attenuated upon exposure of renal collecting duct cells to urinary EVs isolated from metformin-treated db/db mice or cathepsin B knockout mice. Collectively, our study identifies a novel blood pressure reducing role of metformin in diabetic nephropathy by regulating the cathepsin B-ENaC axis. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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Review

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15 pages, 1219 KiB

Open AccessReview

Wall Tension and Tubular Resistance in Kidney Cystic Conditions

by Michele Della Corte and Davide Viggiano

Biomedicines 2023, 11(6), 1750; https://doi.org/10.3390/biomedicines11061750 - 18 Jun 2023

Cited by 1 | Viewed by 1423

Abstract

The progressive formation of single or multiple cysts accompanies several renal diseases. Specifically, (i) genetic forms, such as adult dominant polycystic kidney disease (ADPKD), and (ii) acquired cystic kidney disease (ACKD) are probably the most frequent forms of cystic diseases. Adult dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by multiple kidney cysts and systemic alterations. The genes responsible for the condition are known, and a large amount of literature focuses on the molecular description of the mechanism. The present manuscript shows that a multiscale approach that considers supramolecular physical phenomena captures the characteristics of both ADPKD and acquired cystic kidney disease (ACKD) from the pathogenetic and therapeutical point of view, potentially suggesting future treatments. We first review the hypothesis of cystogenesis in ADPKD and then focus on ACKD, showing that they share essential pathogenetic features, which can be explained by a localized obstruction of a tubule and/or an alteration of the tubular wall tension. The consequent tubular aneurysms (cysts) follow Laplace’s law. Reviewing the public databases, we show that ADPKD genes are widely expressed in various organs, and these proteins interact with the extracellular matrix, thus potentially modifying wall tension. At the kidney and liver level, the authors suggest that altered cell polarity/secretion/proliferation produce tubular regions of high resistance to the urine/bile flow. The increased intratubular pressure upstream increases the difference between the inside (Pi) and the outside (Pe) of the tubules (∆P) and is counterbalanced by lower wall tension by a factor depending on the radius. The latter is a function of tubule length. In adult dominant polycystic kidney disease (ADPKD), a minimal reduction in the wall tension may lead to a dilatation in the tubular segments along the nephron over the years. The initial increase in the tubule radius would then facilitate the progressive expansion of the cysts. In this regard, tubular cell proliferation may be, at least partially, a consequence of the progressive cysts’ expansion. This theory is discussed in view of other diseases with reduced wall tension and with cysts and the therapeutic effects of vaptans, somatostatin, SGLT2 inhibitors, and potentially other therapeutic targets. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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20 pages, 1328 KiB

Open AccessReview

Acute Kidney Injury in Kidney Transplant Patients in Intensive Care Unit: From Pathogenesis to Clinical Management

by Marco Fiorentino, Francesca Bagagli, Annamaria Deleonardis, Alessandra Stasi, Rossana Franzin, Francesca Conserva, Barbara Infante, Giovanni Stallone, Paola Pontrelli and Loreto Gesualdo

Biomedicines 2023, 11(5), 1474; https://doi.org/10.3390/biomedicines11051474 - 18 May 2023

Cited by 5 | Viewed by 2684

Abstract

Kidney transplantation is the first-choice treatment for end-stage renal disease (ESRD). Kidney transplant recipients (KTRs) are at higher risk of experiencing a life-threatening event requiring intensive care unit (ICU) admission, mainly in the late post-transplant period (more than 6 months after transplantation). Urosepsis and bloodstream infections account for almost half of ICU admissions in this population; in addition, potential side effects related to immunosuppressive treatment should be accounted for cytotoxic and ischemic changes induced by calcineurin inhibitor (CNI), sirolimus/CNI-induced thrombotic microangiopathy and posterior reversible encephalopathy syndrome. Throughout the ICU stay, Acute Kidney Injury (AKI) incidence is common and ranges from 10% to 80%, and up to 40% will require renal replacement therapy. In-hospital mortality can reach 30% and correlates with acute illness severity and admission diagnosis. Graft survival is subordinated to baseline estimated glomerular filtration rate (eGFR), clinical presentation, disease severity and potential drug nephrotoxicity. The present review aims to define the impact of AKI events on short- and long-term outcomes in KTRs, focusing on the epidemiologic data regarding AKI incidence in this subpopulation; the pathophysiological mechanisms underlying AKI development and potential AKI biomarkers in kidney transplantation, graft and patients’ outcomes; the current diagnostic work up and management of AKI; and the modulation of immunosuppression in ICU-admitted KTRs. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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8 pages, 5629 KiB

Open AccessCase Report

Management of Double-Seropositive Anti-Glomerular Basement Membrane and Anti-Neutrophil Cytoplasmic Antibodies with 100% Crescentic Glomerulonephritis and Nephrotic Range Proteinuria in a Young Female

by Lalida Kunaprayoon, Emily T. C. Scheffel and Emaad M. Abdel-Rahman

Biomedicines 2024, 12(4), 906; https://doi.org/10.3390/biomedicines12040906 - 19 Apr 2024

Viewed by 471

Abstract

Nephrotic range proteinuria in the setting of dual-positive anti-glomerular basement membrane (AGBM) and anti-neutrophil cytoplasmic antibodies (ANCAs) is rare. Furthermore, using rituximab as a primary immunosuppressant along with steroids and plasmapheresis has not been widely studied. We present a case of dual AGBM [...] Read more.

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Disease: Pathophysiology and New Therapeutic Strategies)

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