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Acid–Base Metabolism, and Human Physiology and Pathophysiology
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Acid–Base Metabolism, and Human Physiology and Pathophysiology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 4222

Special Issue Editors

Prof. Dr. Lynda A. Frassetto

E-Mail Website
Guest Editor
Division of Nephrology, School of Medicine, University of California, 505 Parnassus Ave, Campus Box 0126, San Francisco, CA 94143, USA
Interests: paleo diet and health; acid-base balance; uremic toxins; artificial kidney; HIV-transplant drug interactions; cell membrane transporter-metabolizing enzyme interactions
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Thomas Remer

E-Mail Website
Guest Editor
DONALD Study Center Dortmund, Nutritional Epidemiology, Institute of Nutritional and Food Sciences, University of Bonn, Heinstück 11, 44225 Dortmund, Germany
Interests: acid-base metabolism and its interrelationships with nutrition, hormones, and health-relevant outcomes; steroid metabolome (cortisol metabolism, prepubertal sex hormones), adrenarche and their interrelations with nutrition and growth; identification and characterization of non-invasive biomarkers of nutrition and growth; iodine nutrition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acid–base metabolism plays a pivotal role in numerous body functions and thus in human health. Kidney function and nutrition are important determinants of acid base status.

Over the last decades, researchers from different disciplines have substantially contributed to our understanding of the short- and long-term impact of certain diets and nutritional habits on acid base status, its balance and its buffering systems including hemoglobin and bicarbonate levels in blood and ammonium, phosphate, and organic acid anion excretion in urine.

The effects of diet on acid–base metabolism are at least partly mediated by hormones or are closely related to changes in major endocrine systems, mostly with significant consequences for kidney health.

Against this background the current Special Issue “Acid–Base Metabolism in Human Pathophysiology” invites authors working in relevant areas to submit original research articles as well as reviews on hormonal interactions between acid–base metabolism, nutrition and kidney function.

We welcome manuscripts that cover experimental work and human studies into all stages of human life, from young childhood to old adulthood. Potential topics include, but are not limited to, the following endocrine foci related to renal nutrition and acid–base metabolism:

  • Insulin secretion and resistance;
  • Growth hormone-insulin like growth factor axis;
  • Adrenal gland activity, glucocorticoids, cortisol and cortisone;
  • Renin–angiotensin system, aldosterone secretion, potassium balance;
  • Parathyroid hormone, FGF-23-Klotho axis potentially related to kidney stone risk along with circulating and renally excreted phosphate and calcium;
  • Adipo-renal axis, leptin;
  • Thyroid gland activity, thyroid hormones and TSH.

Prof. Dr. Lynda A. Frassetto
Prof. Dr. Thomas Remer
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • ammoniagenesis
  • FGF-23-Klotho axis
  • growth hormone–IGF axis
  • hormones
  • kidney physiology and function
  • NAE
  • nutrition
  • potassium balance
  • PRAL
  • renin–angiotensin aldosterone system

Published Papers (5 papers)

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Research

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11 pages, 1055 KiB  
Article
Higher Renal Net Acid Excretion, but Not Higher Phosphate Excretion, during Childhood and Adolescence Associates with the Circulating Renal Tubular Injury Marker Interleukin-18 in Adulthood
by Seyedeh-Masomeh Derakhshandeh-Rishehri, Luciana Peixoto Franco, Yifan Hua, Christian Herder, Hermann Kalhoff, Lynda A. Frassetto, Stefan A. Wudy and Thomas Remer
Int. J. Mol. Sci. 2024, 25(3), 1408; https://doi.org/10.3390/ijms25031408 - 24 Jan 2024
Cited by 1 | Viewed by 564
Abstract
High dietary phosphorus intake (P-In) and high acid loads may adversely affect kidney function. In animal models, excessive phosphorus intake causes renal injury, which, in humans, is also inducible by chronic metabolic acidosis. We thus examined whether habitually high P-In and endogenous acid [...] Read more.
High dietary phosphorus intake (P-In) and high acid loads may adversely affect kidney function. In animal models, excessive phosphorus intake causes renal injury, which, in humans, is also inducible by chronic metabolic acidosis. We thus examined whether habitually high P-In and endogenous acid production during childhood and adolescence may be early indicators of incipient renal inflammatory processes later in adulthood. P-In and acid–base status were longitudinally and exclusively determined by biomarker-based assessment in 277 healthy children, utilizing phosphate and net acid excretion (NAE) measurements in 24 h urine samples repeatedly collected between the ages of 3 and 17 years. Standard deviation scores (by sex and age) were calculated for anthropometric data and for the urinary biomarkers available within age range 3–17 years. Multivariable linear regression was used to analyze the relations of phosphate excretion and NAE with the adulthood outcome circulating interleukin-18 (IL-18), a marker of inflammation and kidney dysfunction. After adjusting for growth- and adulthood-related covariates and pro-inflammatory biomarkers to rule out confounding by non-renal inflammatory processes, regression models revealed a significant positive relationship of long-term NAE (p = 0.01), but not of long-term phosphate excretion with adult serum IL-18. Similar significant positive regression results were obtained after replacing NAE with 24 h urinary ammonium excretion as the exposition variable. Our results suggest that even moderate elevations in renal ammonia production, as caused by habitually higher acid loading during growth, may affect the intrarenal pro-inflammatory system in the long-term, known to be boosted by acidosis-induced raised ammoniagenesis. Full article
(This article belongs to the Special Issue Acid–Base Metabolism, and Human Physiology and Pathophysiology)
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Review

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9 pages, 929 KiB  
Review
Effects of Alterations in Acid–Base Effects on Insulin Signaling
by Lynda A. Frassetto and Umesh Masharani
Int. J. Mol. Sci. 2024, 25(5), 2739; https://doi.org/10.3390/ijms25052739 - 27 Feb 2024
Viewed by 530
Abstract
Insulin tightly regulates glucose levels within a narrow range through its action on muscle, adipose tissue and the liver. The activation of insulin receptors activates multiple intracellular pathways with different functions. Another tightly regulated complex system in the body is acid–base balance. Metabolic [...] Read more.
Insulin tightly regulates glucose levels within a narrow range through its action on muscle, adipose tissue and the liver. The activation of insulin receptors activates multiple intracellular pathways with different functions. Another tightly regulated complex system in the body is acid–base balance. Metabolic acidosis, defined as a blood pH < 7.35 and serum bicarbonate < 22 mmol/L, has clear pathophysiologic consequences including an effect on insulin action. With the ongoing intake of typical acid-producing Western diets and the age-related decline in renal function, there is an increase in acid levels within the range considered to be normal. This modest increase in acidosis is referred to as “acid stress” and it may have some pathophysiological consequences. In this article, we discuss the effects of acid stress on insulin actions in different tissues. Full article
(This article belongs to the Special Issue Acid–Base Metabolism, and Human Physiology and Pathophysiology)
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19 pages, 1128 KiB  
Review
The Role of the Endocrine System in the Regulation of Acid–Base Balance by the Kidney and the Progression of Chronic Kidney Disease
by Glenn T. Nagami and Jeffrey A. Kraut
Int. J. Mol. Sci. 2024, 25(4), 2420; https://doi.org/10.3390/ijms25042420 - 19 Feb 2024
Cited by 1 | Viewed by 1129
Abstract
Systemic acid–base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate filtered by the kidney. In chronic [...] Read more.
Systemic acid–base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate filtered by the kidney. In chronic kidney disease (CKD), acid retention may occur when dietary acid production is not balanced by bicarbonate generation by the diseased kidney. Hormones including aldosterone, angiotensin II, endothelin, PTH, glucocorticoids, insulin, thyroid hormone, and growth hormone can affect acid–base balance in different ways. The levels of some hormones such as aldosterone, angiotensin II and endothelin are increased with acid accumulation and contribute to an adaptive increase in renal acid excretion and bicarbonate generation. However, the persistent elevated levels of these hormones can damage the kidney and accelerate progression of CKD. Measures to slow the progression of CKD have included administration of medications which inhibit the production or action of deleterious hormones. However, since metabolic acidosis accompanying CKD stimulates the secretion of several of these hormones, treatment of CKD should also include administration of base to correct the metabolic acidosis. Full article
(This article belongs to the Special Issue Acid–Base Metabolism, and Human Physiology and Pathophysiology)
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16 pages, 1216 KiB  
Review
Pathophysiology of Diet-Induced Acid Stress
by Nimrit Goraya and Donald E. Wesson
Int. J. Mol. Sci. 2024, 25(4), 2336; https://doi.org/10.3390/ijms25042336 - 16 Feb 2024
Viewed by 703
Abstract
Diets can influence the body’s acid–base status because specific food components yield acids, bases, or neither when metabolized. Animal-sourced foods yield acids and plant-sourced food, particularly fruits and vegetables, generally yield bases when metabolized. Modern diets proportionately contain more animal-sourced than plant-sourced foods, [...] Read more.
Diets can influence the body’s acid–base status because specific food components yield acids, bases, or neither when metabolized. Animal-sourced foods yield acids and plant-sourced food, particularly fruits and vegetables, generally yield bases when metabolized. Modern diets proportionately contain more animal-sourced than plant-sourced foods, are, thereby, generally net acid-producing, and so constitute an ongoing acid challenge. Acid accumulation severe enough to reduce serum bicarbonate concentration, i.e., manifesting as chronic metabolic acidosis, the most extreme end of the continuum of “acid stress”, harms bones and muscles and appears to enhance the progression of chronic kidney disease (CKD). Progressive acid accumulation that does not achieve the threshold amount necessary to cause chronic metabolic acidosis also appears to have deleterious effects. Specifically, identifiable acid retention without reduced serum bicarbonate concentration, which, in this review, we will call “covert acidosis”, appears to cause kidney injury and exacerbate CKD progression. Furthermore, the chronic engagement of mechanisms to mitigate the ongoing acid challenge of modern diets also appears to threaten health, including kidney health. This review describes the full continuum of “acid stress” to which modern diets contribute and the mechanisms by which acid stress challenges health. Ongoing research will develop clinically useful tools to identify stages of acid stress earlier than metabolic acidosis and determine if dietary acid reduction lowers or eliminates the threats to health that these diets appear to cause. Full article
(This article belongs to the Special Issue Acid–Base Metabolism, and Human Physiology and Pathophysiology)
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14 pages, 2065 KiB  
Review
The Effects of Acid on Calcium and Phosphate Metabolism
by Juan D. Salcedo-Betancourt and Orson W. Moe
Int. J. Mol. Sci. 2024, 25(4), 2081; https://doi.org/10.3390/ijms25042081 - 08 Feb 2024
Viewed by 962
Abstract
A variety of changes in mineral metabolism aiming to restore acid–base balance occur in acid loading and metabolic acidosis. Phosphate plays a key role in defense against metabolic acidosis, both as an intracellular and extracellular buffer, as well as in the renal excretion [...] Read more.
A variety of changes in mineral metabolism aiming to restore acid–base balance occur in acid loading and metabolic acidosis. Phosphate plays a key role in defense against metabolic acidosis, both as an intracellular and extracellular buffer, as well as in the renal excretion of excess acid in the form of urinary titratable acid. The skeleton acts as an extracellular buffer in states of metabolic acidosis, as the bone matrix demineralizes, leading to bone apatite dissolution and the release of phosphate, calcium, carbonate, and citrate into the circulation. The renal handling of calcium, phosphate and citrate is also affected, with resultant hypercalciuria, hyperphosphaturia and hypocitraturia. Full article
(This article belongs to the Special Issue Acid–Base Metabolism, and Human Physiology and Pathophysiology)
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