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Diagnostics
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Kidney Disease: Biomarkers, Diagnosis, and Prognosis: 3rd Edition
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Kidney Disease: Biomarkers, Diagnosis, and Prognosis: 3rd Edition

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Pathology and Molecular Diagnostics".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 2829

Special Issue Editor

Prof. Dr. Akito Maeshima

E-Mail Website
Guest Editor
Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, 1981 Tsujido, Kamoda, Kawagoe 350-8550, Saitama, Japan
Interests: nephrology; acute kidney injury; regenerative medicine; renal stem/progenitor cell; biomarker; activin-follistatin system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are a worldwide public health problem, with ;increasing incidence and prevalence, high costs and poor outcomes. To overcome this problem, it is indispensable for us to explore or establish early detection methods/techniques and better treatment options for various kidney diseases such as primary/secondary glomerulonephritis, rapidly progressive glomerulonephritis, nephrotic syndrome, acute kidney injury, diabetic nephropathy/diabetic kidney disease, chronic renal failure, renal fibrosis and polycystic kidney disease.

Biochemical parameters such as serum creatinine and blood urea nitrogen levels and/or urinalysis are generally used for the early detection of kidney diseases. Kidney biopsy samples enable us to perform a histological diagnosis of kidney diseases. However, serum/urinary biomarkers, techniques and approaches for the early diagnosis of kidney diseases, the evaluation of kidney disease activity and renal prognosis are still lacking.

This Special Issue offers an open-access forum that aims to bring together a collection of original research and review articles addressing novel biomarkers, techniques and approaches that will be valuable and helpful for the diagnosis or analysis of kidney diseases, assessment of kidney disease activity, and renal prognosis.

We hope that this Special Issue will help us in the diagnosis, evaluation and treatment of kidney diseases in the clinical setting, and will provide essential and insightful clues to further our understanding of the development and progression of kidney diseases.

Prof. Dr. Akito Maeshima
Guest Editor

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. Diagnostics 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

  • primary/secondary glomerulonephritis
  • rapidly progressive glomerulonephritis
  • nephrotic syndrome
  • acute kidney injury
  • chronic kidney disease
  • diabetic nephropathy/diabetic kidney disease
  • chronic renal failure
  • kidney transplantation
  • renal fibrosis
  • polycystic kidney

Published Papers (2 papers)

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Research

9 pages, 812 KiB  
Article
Real-Life Experience on the Effect of SGLT2 Inhibitors vs. Finerenone vs. Combination on Albuminuria in Chronic Kidney Disease
by Mohamad Hanouneh, Dustin Le, Bernard G. Jaar, Christina Tamargo and C. Elena Cervantes
Diagnostics 2024, 14(13), 1357; https://doi.org/10.3390/diagnostics14131357 - 26 Jun 2024
Viewed by 1885
Abstract
Background: There have been several recent advances in the care of patients with chronic kidney disease (CKD), including the use of sodium glucose cotransporter 2 (SGLT2) inhibitors and selective mineralocorticoid receptor antagonists (MRAs). There are very few data reporting the outcomes of these [...] Read more.
Background: There have been several recent advances in the care of patients with chronic kidney disease (CKD), including the use of sodium glucose cotransporter 2 (SGLT2) inhibitors and selective mineralocorticoid receptor antagonists (MRAs). There are very few data reporting the outcomes of these treatments in real-world experience. The aim of this retrospective study is to report the effects of SGLT2 inhibitors, finerenone, and their combination in CKD patients in our community-based setting. Methods: Ninety-eight patients with CKD with an estimated glomerular filtration rate (eGFR) between 25 and 90 mL/min per 1.73 m2 and a urine albumin-to-creatinine ratio (UACR) ≥ 30 mg/g were included. Patients were divided into three groups: two monotherapy groups of SGLT2 inhibitors or finerenone and a third combination group of therapy with SGLT2 inhibitors for the first 4 months and SGLT2 inhibitors and finerenone subsequently. The primary outcomes were the timing and percentage of patients achieving a >50% reduction in UACR from baseline. Results: Group 1 comprised 52 patients on SGLT2i, group 2 had 22 patients on finerenone, and group 3 had 24 patients on combination therapy. The baseline median UACR and mean eGFR were 513 mg/g and 47.9 mL/min per 1.73 m2 in group 1, 548.0 mg/g and 50.5 mL/min per 1.73 m2 in group 2, and 800 mg/g and 60 mL/min per 1.73 m2 in group 3. At baseline, 71 (72.4%) patients were on the angiotensin-converting enzyme inhibitor (ACEi) or the angiotensin receptor blocker (ARB), and 78 (79.5%) patients had type 2 diabetes. After 8 months of follow-up, a >50% decrease in albuminuria was achieved in 96% of patients in group 3, compared to 50% in group 1 and 59% in group 2 (p-values were <0.01 and <0.01, respectively). There was a statistically but not clinically significant change in mean potassium levels in group 2 (+0.4 mmol/L) compared to either group 1 (0.0 mmol/L with p-value: <0.01) or group 3 (−0.01 mmol/L with p-value: <0.01). However, there was no difference in potassium levels when comparing groups 1 and 3. At the end of the follow-up, the average difference in eGFR was −3.4 (8.8), −5.3(10.1), and −7.8 (11.2) mL/min per 1.73 m2 in groups 1, 2, and 3, respectively, without a statistically significant difference between groups. Conclusions: In this real-world experience in our community setting, the combination of SGLT2 inhibitors and finerenone in our adult patients with CKD was associated with a very significant and clinically relevant reduction in UACR, without an increased risk of hyperkalemia. Combination therapy of SGLT2 inhibitor and finerenone regarding background use of ACEi/ARB is feasible and should be encouraged for further albuminuria reductions in CKD patients. Full article
(This article belongs to the Special Issue Kidney Disease: Biomarkers, Diagnosis, and Prognosis: 3rd Edition)
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15 pages, 2123 KiB  
Article
Sodium–Glucose Cotransporter 2 Inhibitor Combined with Conventional Diuretics Ameliorate Body Fluid Retention without Excessive Plasma Volume Reduction
by Maki Asakura-Kinoshita, Takahiro Masuda, Kentaro Oka, Ken Ohara, Marina Miura, Masato Morinari, Kyohei Misawa, Yasuharu Miyazawa, Tetsu Akimoto, Kazuyuki Shimada and Daisuke Nagata
Diagnostics 2024, 14(11), 1194; https://doi.org/10.3390/diagnostics14111194 - 5 Jun 2024
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Abstract
We previously reported that sodium–glucose cotransporter 2 (SGLT2) inhibitors exert sustained fluid homeostatic actions through compensatory increases in osmotic diuresis-induced vasopressin secretion and fluid intake. However, SGLT2 inhibitors alone do not produce durable amelioration of fluid retention. In this study, we examined the [...] Read more.
We previously reported that sodium–glucose cotransporter 2 (SGLT2) inhibitors exert sustained fluid homeostatic actions through compensatory increases in osmotic diuresis-induced vasopressin secretion and fluid intake. However, SGLT2 inhibitors alone do not produce durable amelioration of fluid retention. In this study, we examined the comparative effects of the SGLT2 inhibitor dapagliflozin (SGLT2i group, n = 53) and the combined use of dapagliflozin and conventional diuretics, including loop diuretics and/or thiazides (SGLT2i + diuretic group, n = 23), on serum copeptin, a stable, sensitive, and simple surrogate marker of vasopressin release and body fluid status. After six months of treatment, the change in copeptin was significantly lower in the SGLT2i + diuretic group than in the SGLT2i group (−1.4 ± 31.5% vs. 31.5 ± 56.3%, p = 0.0153). The change in the estimated plasma volume calculated using the Strauss formula was not significantly different between the two groups. Contrastingly, changes in interstitial fluid, extracellular water, intracellular water, and total body water were significantly lower in the SGLT2i + diuretic group than in the SGLT2i group. Changes in renin, aldosterone, and absolute epinephrine levels were not significantly different between the two groups. In conclusion, the combined use of the SGLT2 inhibitor dapagliflozin and conventional diuretics inhibited the increase in copeptin levels and remarkably ameliorated fluid retention without excessively reducing plasma volume and activating the renin–angiotensin–aldosterone and sympathetic nervous systems. Full article
(This article belongs to the Special Issue Kidney Disease: Biomarkers, Diagnosis, and Prognosis: 3rd Edition)
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