Complications of Chronic Kidney Disease

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Uremic Toxins".

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 4215

Special Issue Editor


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Guest Editor
Division of Nephrology, Department of Internal Medicine, Shinmatsudo Central General Hospital, Matsudo, Chiba, Japan
Interests: sepsis; acute kidney injury; chronic kidney disease; hemodialysis therapy; diabetic nephropathy; aquaporin 2
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Special Issue Information

Dear Colleagues,

Chronic kidney disease is a systemic disease that causes many complications that seem to be unrelated to the kidneys. These complications contribute to the high morbidity and mortality of those affected and their poor quality of life. Above all, life-threatening complications require early detection and early responses. We aim to provide readers of this Special Issue with information about the complications of chronic kidney disease, including basic features and the latest knowledge in this field.

This Special Issue is devoted to publishing original research and high-quality review articles related to recent advances in the complications of chronic kidney disease. Original investigations, including both clinical and basic sciences studies, as well meta-analyses and scholarly review papers will be considered.

Dr. Eiichi Sato
Guest Editor

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Keywords

  • chronic kidney disease
  • uremic toxins
  • renal anemia
  • mineral and bone disease

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Published Papers (2 papers)

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Research

16 pages, 4798 KiB  
Article
Factors Regulating Fluid Restitution and Plasma Volume Reduction over the Course of Hemodialysis
by Jen-shih Lee and Lian-pin Lee
Toxins 2023, 15(1), 31; https://doi.org/10.3390/toxins15010031 - 31 Dec 2022
Cited by 2 | Viewed by 1613
Abstract
Over the course of hemodialysis, fluid and protein are restituted from the tissue compartment to the circulation compartment through the endothelia. Our previous model analysis on fluid and protein transport during hemodialysis is expanded to account for changes occurring in the tissue. The [...] Read more.
Over the course of hemodialysis, fluid and protein are restituted from the tissue compartment to the circulation compartment through the endothelia. Our previous model analysis on fluid and protein transport during hemodialysis is expanded to account for changes occurring in the tissue. The measured initial and end plasma protein concentration (PPC, Cp and Cp’) for six hemodialysis studies are analyzed by this expanded model. The computation results indicate that the total driving pressure to restitute fluid from the tissue to the circulation ranges from 5.4 to 20.3 mmHg. The analysis identifies that the increase in plasma colloidal osmotic pressure (COP) contributes 78 ± 6% of the total driving pressure, the decrease in microvascular blood pressure 32 ± 4%, the increase in the COP of interstitial fluid −6 ± 3%, and the decrease in interstitial fluid pressure −5 ± 2%. Let this ratio (Cp’ − Cp)/Cp’ be termed the PPC increment. The six HDs can be divided into three groups which are to have these PPC increments 25.7%, 14.5 ± 2.6(SD)% and 8.3%. It is calculated that their correspondent filtration coefficients are 0.43, 1.29 ± 0.28 and 5.93 mL/min/mmHg and the relative reductions in plasma volume (RRPV) −22.1%, −13.1 ± 6% and −9.4%. The large variations in PPC increments and RRPV show the filtration coefficient is a key factor to regulate the hemodialysis process. Full article
(This article belongs to the Special Issue Complications of Chronic Kidney Disease)
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8 pages, 2016 KiB  
Article
Effects of Zinc Acetate Hydrate Supplementation on Renal Anemia with Hypozincemia in Hemodialysis Patients
by Eiichi Sato, Shohei Sato, Manaka Degawa, Takao Ono, Hongmei Lu, Daisuke Matsumura, Mayumi Nomura, Noriaki Moriyama, Mayuko Amaha and Tsukasa Nakamura
Toxins 2022, 14(11), 746; https://doi.org/10.3390/toxins14110746 - 31 Oct 2022
Cited by 6 | Viewed by 2008
Abstract
Introduction and Aims: This study examined whether zinc supplementation with zinc acetate hydrate improved renal anemia with hypozincemia in patients undergoing hemodialysis. Methods: The study participants included 21 patients undergoing hemodialysis who presented with a serum zinc level < 60 mg/dL and who [...] Read more.
Introduction and Aims: This study examined whether zinc supplementation with zinc acetate hydrate improved renal anemia with hypozincemia in patients undergoing hemodialysis. Methods: The study participants included 21 patients undergoing hemodialysis who presented with a serum zinc level < 60 mg/dL and who were administered zinc acetate hydrate at 50 mg (reduced to 25 mg, as appropriate) for 6 months. Patients with a hemorrhagic lesion, acute-phase disease (pneumonia or cardiac failure), or hematologic disease and those whose treatment was switched from peritoneal dialysis to hemodialysis were excluded. The changes in the erythropoietin resistance index (ERI) before and after zinc acetate hydrate administration were examined. ERI was defined as the dose (IU) of erythropoiesis-stimulating agent (ESA)/week/body weight (kg)/hemoglobin content (g/dL). The differences between the two groups were analyzed using the Wilcoxon signed rank sum test, and p < 0.05 was considered statistically significant. Results: The study participants included 19 men and 2 women aged 41–95 years (mean ± standard deviation (SD): 67.1 ± 13.6). The changes in the values of parameters measured before and after zinc acetate hydrate administration were as follows: Blood Hb did not change significantly, from 10.0–13.6 g/dL (11.5 ± 1.0 g/dL) to 10.2–12.4 g/dL (11.4 ± 0.7 g/dL); serum zinc concentration significantly increased, from 33.0–59.0 mg/dL μg/dL (52.4 ± 7.6 mg/dL μg/dL) to 57.0–124.0 mg/dL μg/dL (84.1 ± 16.3 mg/dL μg/dL; p < 0.01); the ESA dose significantly decreased, from 0–12,000 IU/week (5630 ± 3351 IU/week) to 0–9000 IU/week (4428 ± 2779; p = 0.04); and ERI significantly decreased, from 0.0–18.2 (8.1 ± 5.1) to 0.0–16.0 (6.3 ± 4.3; p = 0.04). Conclusions: Zinc supplementation increased the serum zinc concentration and significantly reduced the ESA dose and ERI, suggesting that a correction of hypozincemia contributes to lessening renal anemia in these patients. Full article
(This article belongs to the Special Issue Complications of Chronic Kidney Disease)
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