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Kidney Response to the Spectrum of Diet-Induced Acid Stress

Chronic ingestion of the acid (H(+))-producing diets that are typical of developed societies appears to pose a long-term threat to kidney health. Mechanisms employed by kidneys to excrete this high dietary H(+) load appear to cause long-term kidney injury when deployed over many years. In addition,...

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Autores principales: Goraya, Nimrit, Wesson, Donald E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986476/
https://www.ncbi.nlm.nih.gov/pubmed/29751620
http://dx.doi.org/10.3390/nu10050596
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author Goraya, Nimrit
Wesson, Donald E.
author_facet Goraya, Nimrit
Wesson, Donald E.
author_sort Goraya, Nimrit
collection PubMed
description Chronic ingestion of the acid (H(+))-producing diets that are typical of developed societies appears to pose a long-term threat to kidney health. Mechanisms employed by kidneys to excrete this high dietary H(+) load appear to cause long-term kidney injury when deployed over many years. In addition, cumulative urine H(+) excretion is less than the cumulative increment in dietary H(+), consistent with H(+) retention. This H(+) retention associated with the described high dietary H(+) worsens as the glomerular filtration rate (GFR) declines which further exacerbates kidney injury. Modest H(+) retention does not measurably change plasma acid–base parameters but, nevertheless, causes kidney injury and might contribute to progressive nephropathy. Current clinical methods do not detect H(+) retention in its early stages but the condition manifests as metabolic acidosis as it worsens, with progressive decline of the glomerular filtration rate. We discuss this spectrum of H(+) injury, which we characterize as “H(+) stress”, and the emerging evidence that high dietary H(+) constitutes a threat to long-term kidney health.
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spelling pubmed-59864762018-06-05 Kidney Response to the Spectrum of Diet-Induced Acid Stress Goraya, Nimrit Wesson, Donald E. Nutrients Article Chronic ingestion of the acid (H(+))-producing diets that are typical of developed societies appears to pose a long-term threat to kidney health. Mechanisms employed by kidneys to excrete this high dietary H(+) load appear to cause long-term kidney injury when deployed over many years. In addition, cumulative urine H(+) excretion is less than the cumulative increment in dietary H(+), consistent with H(+) retention. This H(+) retention associated with the described high dietary H(+) worsens as the glomerular filtration rate (GFR) declines which further exacerbates kidney injury. Modest H(+) retention does not measurably change plasma acid–base parameters but, nevertheless, causes kidney injury and might contribute to progressive nephropathy. Current clinical methods do not detect H(+) retention in its early stages but the condition manifests as metabolic acidosis as it worsens, with progressive decline of the glomerular filtration rate. We discuss this spectrum of H(+) injury, which we characterize as “H(+) stress”, and the emerging evidence that high dietary H(+) constitutes a threat to long-term kidney health. MDPI 2018-05-11 /pmc/articles/PMC5986476/ /pubmed/29751620 http://dx.doi.org/10.3390/nu10050596 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Goraya, Nimrit
Wesson, Donald E.
Kidney Response to the Spectrum of Diet-Induced Acid Stress
title Kidney Response to the Spectrum of Diet-Induced Acid Stress
title_full Kidney Response to the Spectrum of Diet-Induced Acid Stress
title_fullStr Kidney Response to the Spectrum of Diet-Induced Acid Stress
title_full_unstemmed Kidney Response to the Spectrum of Diet-Induced Acid Stress
title_short Kidney Response to the Spectrum of Diet-Induced Acid Stress
title_sort kidney response to the spectrum of diet-induced acid stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986476/
https://www.ncbi.nlm.nih.gov/pubmed/29751620
http://dx.doi.org/10.3390/nu10050596
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