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Novel Clinical Updates in Uremia
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Novel Clinical Updates in Uremia

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Nephrology & Urology".

Deadline for manuscript submissions: closed (20 April 2023) | Viewed by 6936

Special Issue Editors

Dr. Grazia Maria Virzì

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Guest Editor
Department of Nephrol Dialysis and Transplant, San Bortolo Hospital, 36100 Vicenza, Italy
Interests: dialysis; uremia; cardiorenal syndrome; organ crosstalk; kidney; biomarkers; chronic kidney disease
Special Issues, Collections and Topics in MDPI journals
Dr. Anna Clementi

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Guest Editor
Nephrology and Dialysis Unit, Santa Marta and Santa Venera Hospital, 95024 Acireale, Catania, Italy
Interests: acute kidney injury; chronic kidney disease; cardio-renal syndromes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Uremia is a clinical disorder related with worsening renal function. It is characterized by fluid, electrolyte and metabolic anomalies, as well as hormonal imbalances. Patients presenting with uremic status typically complain of nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus or changes in mental status. The presence of toxins is believed to be a major problem in the progression of uremia in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). One of the earliest known toxins is urea.

The aim of this Special Issue is to investigate and highlight the updates about uremia, with particular attention to biological mechanisms, new biomarkers and dialysis innovations in order to improve the uremic status. In this Special Issue, we welcome the submission of original research and review articles to deepen the latest evidence in the field of uremia and dialysis.

Dr. Grazia Maria Virzi
Dr. Anna Clementi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • uremia
  • dialysis
  • biomarkers
  • biological mechanism
  • chronic kidney disease
  • uremic toxin

Published Papers (5 papers)

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Editorial

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2 pages, 167 KiB  
Editorial
Novel Clinical Updates in Uremia
by Anna Clementi and Grazia Maria Virzì
J. Clin. Med. 2022, 11(13), 3791; https://doi.org/10.3390/jcm11133791 - 30 Jun 2022
Cited by 1 | Viewed by 1129
Abstract
The progressive loss of kidney function is responsible for the retention of different metabolites due to a decrease in their renal clearance [...] Full article
(This article belongs to the Special Issue Novel Clinical Updates in Uremia)

Research

Jump to: Editorial

11 pages, 1602 KiB  
Article
Marinobufagenin, Left Ventricular Hypertrophy and Residual Renal Function in Kidney Transplant Recipients
by Davide Bolignano, Marta Greco, Pierangela Presta, Alfredo Caglioti, Nazareno Carullo, Mariateresa Zicarelli, Daniela Patrizia Foti, Francesco Dragone, Michele Andreucci and Giuseppe Coppolino
J. Clin. Med. 2023, 12(9), 3072; https://doi.org/10.3390/jcm12093072 - 23 Apr 2023
Cited by 3 | Viewed by 1059
Abstract
Background: Left ventricular hypertrophy (LVH), which is a pervasive complication of end-stage kidney disease (ESKD), persists in some uremic individuals even after kidney transplantation (Ktx), contributing to worsening CV outcomes. Marinobufagenin (MBG), an endogenous steroid cardiotonic hormone endowed with natriuretic and vasoconstrictive properties, [...] Read more.
Background: Left ventricular hypertrophy (LVH), which is a pervasive complication of end-stage kidney disease (ESKD), persists in some uremic individuals even after kidney transplantation (Ktx), contributing to worsening CV outcomes. Marinobufagenin (MBG), an endogenous steroid cardiotonic hormone endowed with natriuretic and vasoconstrictive properties, is an acknowledged trigger of uremic cardiomyopathy. However, its clinical significance in the setting of Ktx remains undefined. Methods: In a cohort of chronic Ktx recipients (n = 40), we assessed circulating MBG together with a thorough clinical and echocardiographic examination. Forty matched haemodialysis (HD) patients and thirty healthy subjects served as controls for MBG measurements. Patients were then prospectively followed up to 12 months and the occurrence of an established cardio-renal endpoint (death, CV events, renal events, graft rejection) was recorded. Results: Median MBG plasma levels were lower in Ktx as compared with HD patients (p = 0.02), but higher as compared with healthy controls (p = 0.0005). Urinary sodium (β = 0.423; p = 0.01) and eGFR (β = −0.324; p = 0.02) were the sole independent predictors of MBG in this cohort, while a strong correlation with left ventricular mass index (LVMi), found in univariate analyses (R = 0.543; p = 0.0007), gained significance only in multivariate models not including eGFR. Logistic regression analyses indicated MBG as a significant predictor of the combined endpoint (OR 2.38 [1.10–5.12] per each 1 nmoL/L increase; p = 0.01), as well as eGFR, LVMi, serum phosphate and proteinuria. Conclusions: Ktx recipients display altered MBG levels which are influenced by sodium balance, renal impairment and the severity of LVH. Thus, MBG might represent an important missing link between reduced graft function and pathological cardiac remodelling and may hold important prognostic value for improving cardio-renal risk assessment. Full article
(This article belongs to the Special Issue Novel Clinical Updates in Uremia)
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10 pages, 1562 KiB  
Article
Carotid–Femoral Pulse Wave Velocity Could Be a Marker to Predict Cardiovascular and All-Cause Mortality of Hemodialysis Patients
by Xin-Ning Ng, Jen-Pi Tsai, Chih-Hsien Wang and Bang-Gee Hsu
J. Clin. Med. 2023, 12(7), 2509; https://doi.org/10.3390/jcm12072509 - 26 Mar 2023
Cited by 2 | Viewed by 1437
Abstract
Among hemodialysis (HD) patients, cardiovascular disease (CVD) is recognized as a major contributor to the high risk of mortality, and emerging evidence has ascertained arterial stiffness as an independent predictor of adverse cardiovascular (CV) outcomes. We aimed to investigate the efficacy of arterial [...] Read more.
Among hemodialysis (HD) patients, cardiovascular disease (CVD) is recognized as a major contributor to the high risk of mortality, and emerging evidence has ascertained arterial stiffness as an independent predictor of adverse cardiovascular (CV) outcomes. We aimed to investigate the efficacy of arterial stiffness measurement in predicting CV and all-cause mortality in patients on HD (n = 130). Carotid–femoral pulse wave velocity (cfPWV) was measured by a validated tonometry system. A cfPWV of >10 m/s was used to assign patients to the arterial stiffness group (n = 64). Baseline and biochemical characteristics, as well as all-cause and CV mortality, were recorded. During the 3-year follow-up period, a total of 32 deaths (25%) occurred. The patients who died had clinically significant high cfPWV levels; were relatively old; and had hypoalbuminemia, low creatinine levels, and diabetes. After adjustment for the prognostic variables, patients with elevated cfPWV had significantly higher all-cause (p = 0.036) and CV mortality (p = 0.017), compared with the mortality rates in the normal group. In this study, cfPWV was found to be an independent predictor of all-cause and CV mortality in HD patients. Full article
(This article belongs to the Special Issue Novel Clinical Updates in Uremia)
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11 pages, 1412 KiB  
Article
Relationship between Residual Urine Output and Type of Dialysis with FGF23 Levels
by Valentina Corradi, Sara Samoni, Alice Mariotto, Carlotta Caprara, Elisa Scalzotto, Anna Chiara Frigo, Francesca K. Martino, Davide Giavarina, Claudio Ronco and Monica Zanella
J. Clin. Med. 2023, 12(1), 222; https://doi.org/10.3390/jcm12010222 - 28 Dec 2022
Viewed by 1354
Abstract
Several studies investigated the role of fibroblast growth factor 23 (FGF23) in the regulation of renal phosphate excretion in chronic kidney disease (CKD). However, patients with residual urine output (UO) seem to control their serum phosphorus levels better. Our aim was to determine [...] Read more.
Several studies investigated the role of fibroblast growth factor 23 (FGF23) in the regulation of renal phosphate excretion in chronic kidney disease (CKD). However, patients with residual urine output (UO) seem to control their serum phosphorus levels better. Our aim was to determine whether FGF23 levels are influenced by dialysis modality and UO. We performed a cross-sectional study in hemodialysis (HD) and peritoneal dialysis (PD) patients. The C-terminal FGF23 (cFGF23) levels were determined in plasma with a two-site enzyme-linked immunosorbent assay. The UO collection referred to an mL/day measurement. All p values were two-sided, and the statistical significance was set at p < 0.05. We enrolled 133 patients (58 HD, 75 PD, UO 70%). The median cFGF23 was significantly higher in HD vs. PD patients (p = 0.0017) and not significantly higher in patients without UO (p = 0.12). We found a negative correlation between cFGF23 and the UO volume (p = 0.0250), but the correlation was not significant when considering the type of dialysis treatment. Phosphorus (ß = 0.21677; p = 0.0007), type of dialysis (ß = −0.68392; p = 0.0003), and creatinine (ß = 0.08130; p = 0.0133) were significant and independent predictors of cFGF23 levels. In conclusion, cFGF23 was significantly higher in HD than in PD patients. We found a significant negative correlation between cFGF23 and the residual UO volume, but the correlation was not significant considering the type of dialysis. Our study reveals that dialysis modality is an independent predictor of FGF23 levels. In particular, PD is associated with lower FGF23 levels than HD. Full article
(This article belongs to the Special Issue Novel Clinical Updates in Uremia)
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10 pages, 1216 KiB  
Article
In Vitro Induction of Eryptosis by Uremic Toxins and Inflammation Mediators in Healthy Red Blood Cells
by Grazia Maria Virzì, Maria Mattiotti, Anna Clementi, Sabrina Milan Manani, Giovanni Giorgio Battaglia, Claudio Ronco and Monica Zanella
J. Clin. Med. 2022, 11(18), 5329; https://doi.org/10.3390/jcm11185329 - 10 Sep 2022
Cited by 7 | Viewed by 1339
Abstract
Eryptosis is the stress-induced RBC (red blood cell) death mechanism. It is known that eryptosis is largely influenced by plasma and blood composition, and that it is accelerated in patients affected by chronic kidney disease (CKD). The aim of this study is to [...] Read more.
Eryptosis is the stress-induced RBC (red blood cell) death mechanism. It is known that eryptosis is largely influenced by plasma and blood composition, and that it is accelerated in patients affected by chronic kidney disease (CKD). The aim of this study is to evaluate the eryptosis rate in healthy RBCs treated with different concentration of IL-6, IL-1β, urea and p-cresol, comparable to plasmatic level of CKD patients, at different time points. We exposed healthy RBCs to increasing concentrations of IL-6, IL-1β, urea and p-cresol. Morphological markers of eryptosis (cell membrane scrambling, cell shrinkage and PS exposure at RBC surface) were evaluated by flow cytometric analyses. The cytotoxic effect of cytokines and uremic toxins were analyzed in vitro on healthy RBCs at 4, 8 and 24 h. Morphology of treated RBCs was dramatically deranged, and the average cell volume was significantly higher in RBCs exposed to higher concentration of all molecules (all, p < 0.001). Furthermore, healthy RBCs incubated with each molecules demonstrated a significant increase in eryptosis. Cytofluorimetric analysis of eryptosis highlighted significantly higher cell death rate in RBCs incubated with a higher concentration of both cytokines compared with RBCs incubated with a lower concentration (all, p < 0.05). In conclusion, our data show that cytokines and uremic toxins have a harmful effect on RBCs viability and trigger eryptosis. Further studies are necessary to validate these results in vivo and to associate abnormal eryptosis with cytokine levels in CKD patients. The eryptosis pathway could, moreover, become a new promising target for anemia management in CKD patients. Full article
(This article belongs to the Special Issue Novel Clinical Updates in Uremia)
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