Effect of acute metabolic acidosis on ammonia metabolism in kidney

Bogusky, Ronald T.; Dietrich, R.

doi:10.1152/ajprenal.1989.256.2.f321

Cited by 5 publications

(27 citation statements)

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“…Increased Glud1 expression with experimental metabolic acidosis is consistent with previous reports (Lombardo et al. ; Bogusky and Dietrich ; Mu and Welbourne ) and likely contributes to the increased ammonia generation that occurs during metabolic acidosis. The lack of Glud1 increase in the spontaneously acidotic NBCe1 KO mice is consistent with the generalized disturbance in proximal tubule ammonia metabolism reported recently (Handlogten et al.…”

Section: Resultssupporting

confidence: 91%

Effect of NBCe1 deletion on renal citrate and 2-oxoglutarate handling

et al. 2016

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The bicarbonate transporter, NBCe1 (SLC4A4), is necessary for at least two components of the proximal tubule contribution to acid‐base homeostasis, filtered bicarbonate reabsorption, and ammonia metabolism. This study's purpose was to determine NBCe1's role in a third component of acid‐base homeostasis, organic anion metabolism, by studying mice with NBCe1 deletion. Because NBCe1 deletion causes metabolic acidosis, we also examined acid‐loaded wild‐type adult mice to determine if the effects of NBCe1 deletion were specific to NBCe1 deletion or were a non‐specific effect of the associated metabolic acidosis. Both NBCe1 KO and acid‐loading decreased citrate excretion, but in contrast to metabolic acidosis alone, NBCe1 KO decreased expression of the apical citrate transporter, NaDC‐1. Thus, NBCe1 expression is necessary for normal NaDC‐1 expression, and NBCe1 deletion induces a novel citrate reabsorptive pathway. Second, NBCe1 KO increased 2‐oxoglutarate excretion. This could not be attributed to the metabolic acidosis as experimental acidosis decreased excretion. Increased 2‐oxoglutarate excretion could not be explained by changes in plasma 2‐oxoglutarate levels, the glutaminase I or the glutaminase II generation pathways, 2‐oxoglutarate metabolism, its putative apical 2‐oxoglutarate transporter, OAT10, or its basolateral transporter, NaDC‐3. In summary: (1) NBCe1 is necessary for normal proximal tubule NaDC‐1 expression; (2) NBCe1 deletion results in stimulation of a novel citrate reabsorptive pathway; and (3) NBCe1 is necessary for normal 2‐oxoglutarate metabolism through mechanisms independent of expression of known transport and metabolic pathways.

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Section: Resultssupporting

confidence: 91%

Effect of NBCe1 deletion on renal citrate and 2-oxoglutarate handling

et al. 2016

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“…Bogusky et al added two different forms of radioactively labeled glutamine 27 . One in which nitrogen of the amido and one in which the nitrogen from the amino group was labeled.…”

Section: Resultsmentioning

confidence: 99%

“…Bogusky et al added two different forms of radioactively labeled glutamine. 27 One in which nitrogen of the amido and one in which the nitrogen from the amino group was labeled. They found that lowering perfusate pH increases the rate of glutamine deamidation.…”

Section: Amino Acid Metabolismmentioning

confidence: 99%

“…35,38,48,51,55 Performance bias was rated as high in three studies, 31,34,40 low in one study, 42 and unclear in all others (26/30, 87%). [27][28][29][30]32,33,[35][36][37][38][39]41,[43][44][45][46][47][48][49][50][51][52][53][54][55] Random housing of animals was not performed in two studies (2/30, 7%) 31,40 and was not reported in the remaining st udies. [27][28][29][30][32][33][34][35][36][37][38][39][41][42][43]…”

Section: Quality and Risk Of Bias Assessmentmentioning

confidence: 99%

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Unraveling metabolism during kidney perfusion using tracer studies: a systematic review

et al. 2022

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Background Understanding kidney metabolism during perfusion is vital to further develop the technology as a preservation, viability assessment, and resuscitation platform. We reviewed the evidence on the use of labeled metabolites (tracers) to understand “on‐pump” kidney behavior. Methods PubMed, Embase, Web of Science, and Cochrane databases were systematically searched for studies evaluating metabolism of (non)radioactively labeled endogenous compounds during kidney perfusion. Results Of 5899 articles, 30 were included. All were animal studies [rat (70%), dog (13%), pig (10%), rabbit (7%)] perfusing but not transplanting kidneys. Perfusion took place at hypothermic (4–12°C) (20%), normothermic (35–40°C) (77%), or undefined temperatures (3%). Hypothermic perfusion used albumin or a clinical kidney preservation solution, mostly in the presence of oxygen. Normothermic perfusion was mostly performed with oxygenated crystalloids often containing glucose and amino acids with unclear partial oxygen tensions. Active metabolism of carbohydrate, amino acid, lipids, and large molecules was shown in hypothermic and normothermic perfusion. Production of macromolecules, such as prostaglandin, thromboxane, and vitamin D, takes place during normothermic perfusion. No experiments compared differences in metabolic activity between hypothermic and normothermic perfusion. One conference abstract showed increased anaerobic metabolism in kidneys donated after circulatory death by adding labeled glucose to hypothermically perfused human kidneys. Conclusions Tracer studies during kidney perfusion contribute to unraveling kidney metabolic behavior in pre‐clinical models. Whether findings are truly translational needs further investigation in large animal models of human kidneys. Furthermore, it is essential to better understand how ischemia changes this metabolic behavior.

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“…In metabolic acidosis, both the quantity of new HCO 3 − produced in the proximal tubule is increased and the intertubular transport of NH 3 /NH 4 + is altered such that a greater percentage of total NH 4 + produced is excreted in the urine (less being delivered to the renal veins) thereby significantly increasing the effective new HCO 3 − delivery to the systemic circulation (101, 535, 686, 687). By altering the total new HCO 3 − production rate and renal vein/urine NH 4 + partitioning, the kidney possesses powerful mechanisms for compensating for the loss of HCO 3 − due to dietary metabolic H + generation and in the urea cycle.…”

Section: Whole Body Acid-base Balancementioning

confidence: 99%

Molecular Mechanisms and Regulation of Urinary Acidification

Kurtz

2014

Comprehensive Physiology

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The H+ concentration in human blood is kept within very narrow limits, ~ 40 nM, despite the fact that dietary metabolism generates acid and base loads that are added to the systemic circulation throughout the life of mammals. One of the primary functions of the kidney is to maintain the constancy of systemic acid-base chemistry. The kidney has evolved the capacity to regulate blood acidity by performing three key functions: 1) reabsorb HCO3− that is filtered through the glomeruli to prevent its excretion in the urine; 2) generate a sufficient quantity of new HCO3− to compensate for the loss of HCO3− resulting from dietary metabolic H+ loads and loss of HCO3− in the urea cycle; and 3) excrete HCO3− (or metabolizable organic anions) following a systemic base load. The ability of the kidney to perform these functions requires that various cell types throughout the nephron respond to changes in acid-base chemistry by modulating specific ion transport and/or metabolic processes in a coordinated fashion such that the urine and renal vein chemistry is altered appropriately. The purpose of the article is to provide the interested reader with a broad review of a field that began historically ~ 60 years ago with whole animal studies, and has evolved to where we are currently addressing questions related to kidney acid-base regulation at the single protein structure/function level.

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Effect of acute metabolic acidosis on ammonia metabolism in kidney

Cited by 5 publications

References 0 publications

Effect of NBCe1 deletion on renal citrate and 2-oxoglutarate handling

Effect of NBCe1 deletion on renal citrate and 2-oxoglutarate handling

Unraveling metabolism during kidney perfusion using tracer studies: a systematic review

Molecular Mechanisms and Regulation of Urinary Acidification

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