Metabolic Acidosis

2016 ◽  
Author(s):  
Steve Krywawych
Keyword(s):  
Metabolic Acidosis ◽  
Cardiac Function ◽  
Hydrogen Concentration ◽  
Metabolic Diseases ◽  
Hydrogen Ion ◽  
Variable Degree ◽  
Ion Balance ◽  
Essential Requirement ◽  
Underlying Causes ◽  
Per Se

Hydrogen ion turnover in resting adults exceeds 500 mole/24 hours and maintenance of hydrogen ion balance is an essential requirement for normal cellular, organ and body function. A variety of mechanisms co-operate to ensure that the hydrogen concentration in plasma can be tightly controlled between 35 to 46 nano moles per litre and any deviation being rapidly compensated. Inherited metabolic diseases can to a variable degree impact to disturb this equilibrium. The underlying causes responsible for this outcome are disease dependent and may occur due to generation of overwhelming quantities of hydrogen per se, or at the level of renal reabsorption or generation of bicarbonate or due to tissue hypoxia resulting from either poor pulmonary or cardiac function.

Adaptive changes in renal acidification in response to chronic respiratory acidosis

1985 ◽  
Vol 248 (4) ◽  
pp. F492-F499 ◽  
Author(s):  
R. L. Tannen ◽  
B. Hamid
Keyword(s):  
Metabolic Acidosis ◽  
Proton Transport ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Chronic Metabolic Acidosis ◽  
Adaptive Changes ◽  
Secretory Capacity

To examine whether chronic respiratory acidosis results in adaptive changes in renal acidification, rats were housed for 3 days in an environmental chamber with an ambient CO2 content of 10% and their kidneys were perfused in vitro according to two protocols. To assess hydrogen ion secretory capacity of the distal nephron, perfusions were carried out with a low bicarbonate concentration, in the absence of ammoniagenic substrate, and with saturating quantities of the buffer creatinine. Under these conditions, the titration of creatinine at a pH less than 6.0 (TA pH 6.0) reflects the H+ secretory capacity of a discrete functional segment of the distal nephron. Kidneys from rats with chronic respiratory acidosis exhibited a significantly lower urine pH and higher rate of TA pH 6.0 than controls perfused in this fashion, indicative of an adaptive increase in the distal nephron capacity for proton transport. This adaptation was comparable with that reported previously for rats exposed to chronic metabolic acidosis. Furthermore, evidence of adaptation persisted in the presence of amiloride (10(-5) M), suggesting that it reflects, at least in part, a sodium-independent mechanism of proton transport. Hydrogen ion secretion by the proximal nephron was assessed by performing standard bicarbonate titration curves with kidneys from rats with chronic respiratory acidosis, chronic metabolic acidosis, and controls using a perfusate equilibrated with 95% O2/5% CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Imidazole propionate is increased in diabetes and associated with dietary patterns and altered microbial ecology

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Antonio Molinaro ◽  
◽  
Pierre Bel Lassen ◽  
Marcus Henricsson ◽  
Hao Wu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Microbial Ecology ◽  
Metabolic Diseases ◽  
Elevated Serum ◽  
Bacterial Gene ◽  
Host Diet ◽  
Per Se ◽  
Gene Richness

AbstractMicrobiota-host-diet interactions contribute to the development of metabolic diseases. Imidazole propionate is a novel microbially produced metabolite from histidine, which impairs glucose metabolism. Here, we show that subjects with prediabetes and diabetes in the MetaCardis cohort from three European countries have elevated serum imidazole propionate levels. Furthermore, imidazole propionate levels were increased in subjects with low bacterial gene richness and Bacteroides 2 enterotype, which have previously been associated with obesity. The Bacteroides 2 enterotype was also associated with increased abundance of the genes involved in imidazole propionate biosynthesis from dietary histidine. Since patients and controls did not differ in their histidine dietary intake, the elevated levels of imidazole propionate in type 2 diabetes likely reflects altered microbial metabolism of histidine, rather than histidine intake per se. Thus the microbiota may contribute to type 2 diabetes by generating imidazole propionate that can modulate host inflammation and metabolism.

Importance of medullary events in ammonium excretion: studies in acute respiratory and acute metabolic acidosis

1983 ◽  
Vol 61 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Andre Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
Marc Goldstein ◽  
Bobby Stinebaugh ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Respiratory Acidosis ◽  
Renal Medulla ◽  
Hydrogen Ion ◽  
Ammonium Excretion ◽  
Urine Ph ◽  
Ion Secretion ◽  
Medullary Collecting Duct ◽  
Acute Metabolic Acidosis

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary [Formula: see text]. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, [Formula: see text], and the urine minus blood [Formula: see text] difference (U-B [Formula: see text]) were lower during acute hypercapnia. In these experiments, the urine [Formula: see text] was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B [Formula: see text] was 5 ± 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary [Formula: see text] can modify this relationship.

Gaspirali v. Il'Minskii: Two Identity Projects for the Muslims of the Russian Empire

2002 ◽  
Vol 30 (2) ◽  
pp. 265-289 ◽  
Author(s):  
Mustafa Özgür Tuna
Keyword(s):  
Russian Empire ◽  
Russian Orthodox ◽  
Literary Language ◽  
Islamic Studies ◽  
The Past ◽  
Underlying Causes ◽  
Per Se ◽  
Points Of View ◽  
The Russian Empire

In 1913, an article in a Russian missionary journal compared two “very typical representatives” of Islamic studies in Russia: İsmail Bey Gaspıralı (1851–1914) and Nikolai Ivanovich Il'minskii (1822–1891). Nothing could better symbolize the two opposing points of view about the past, present and future of the Muslims of Russia in 1913. Il'minskii was a Russian Orthodox missionary whose ideas and efforts had formed the imperial perceptions and policies about the Muslims of the Russian empire in the late Tsarist period, while Gaspıralı was a Muslim educator and publisher whose ideas and efforts had shaped the Muslim society per se in the same period. Il'minskii, beginning in the 1860s, and Gaspıralı, beginning in the 1880s, developed two formally similar but inherently contradictory programs for the Muslims of the Russian empire. Schooling and the creation of a literary language or literary languages constituted the hearts of both of their programs. Besides their own efforts, both Gaspıralı and Il'minskii had a large number of followers that diligently worked to put their programs into practice among the Muslims of Russia. As a result of the inherent contradiction of these programs, a bitter controversy developed between what we may call the Il'minskii and Gaspıralı groups, which particularly intensified after the revolution of 1905. In this article, I will discuss the underlying causes and development of this controversy by focusing on the role of language in the programs of Gaspıralı and Il'minskii. Then, I will conclude my article with an evaluation of the legacies of these two individuals in their own time and beyond.

scholarly journals ASIDOSIS TUBULAR RENAL DISTAL

2020 ◽  
Vol 5 (1) ◽  
pp. 265
Author(s):  
Ayu Pathya ◽  
Harnavi Harun
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Bone Growth ◽  
Hydrogen Ion ◽  
Genetic Mutations ◽  
Growth Disorders ◽  
Urine Ph ◽  
Renal Tubular ◽  
Hands And Feet

<p><em>Asidosis tubular renal (ATR) merupakan tubulopati ginjal yang jarang terjadi, dimana terdapat ketidakmampuan ginjal untuk menjaga perbedaan pH normal antara darah dan lumen tubulus ginjal. Pada kondisi ini terjadi gangguan pengasaman urin disebabkan gangguan reabsorbsi bikarbonat, gangguan ekskresi ion hidrogen, atau keduanya sehingga mengakibatkan asidosis metabolik. ATR ditandai dengan adanya asidosis metabolik dengan senjang anion plasma yang normal, hiperkloremik dan laju filtrasi glomerulus normal. ATR terbagi menjadi 3 tipe utama, yaitu ATR tipe 1 (ATR distal), tipe-2 (ATR proksimal), dan tipe 4 (ATR hiperkalemia). ATR distal merupakan ATR yang disebabkan oleh defek pada tubulus distal ginjal, dimana defek ini menyebabkan gangguan pada sekresi ion hidrogen. Beberapa penelitian menunjukkan bahwa ATR tipe 1 dikaitkan dengan mutasi genetik. Mutasi genetik herediter dapat autosomal dominan atau autosomal resesif. Gambaran klinis dapat mencakup kelainan pertumbuhan tulang, kelemahan atau kelumpuhan otot, deposit kalsium di ginjal, anoreksia, muntah, konstipasi, diare, dehidrasi, dan poliuria. Telah dilaporkan kasus pasien wanita usia 19 tahun dengan keluhan utama kelemahan di kedua tangan dan kaki. Dari penelusuran klinis dan laboratorium  didapatkan hipokalemia dan berdasarkan pendekatan hipokalemia dengan HCO3- rendah dan pH urine &gt;5,5, diagnosis pada pasien ini ditegakkan sebagai asidosis tubulus renal distal (ATRd).</em></p><p><strong><em>Kata kunci:</em></strong><em> </em><em>ATR, ATRd,  asidosis metabolik, hiperkloremik, hipokalemia </em><em></em></p><p><strong><em>Abstract</em></strong></p><p><em>Renal tubular acidosis (RTA) is a condition caused by the inability of the kidneys to maintain normal pH differences between the blood and tubules lumen of the kidney. Renal tubular acidosis is a rare kidney tubulopathy. In this condition, urine acidification is caused by bicarbonate reabsorption, disruption of hydrogen ion excretion, or both, resulting in metabolic acidosis. RTA is characterized by metabolic acidosis with normal plasma anion, hyperchloremic gaps and normal glomerular filtration rates. RTA is divided into 3 main types, namely type 1 RTA (distal RTA), type-2 (proximal RTA), and type 4 (hyperkalemia RTA). Distal RTA caused by defects in the distal tubules of the kidney, where these defects cause interference with the hydrogen ion secretion. Several studies have shown that type 1 RTA is associated with genetic mutations. Hereditary genetic mutations can be autosomal dominant or autosomal recessive. Clinical features can include bone growth disorders, muscle weakness or paralysis, calcium deposits in the kidneys, anorexia, vomiting, constipation, diarrhea, dehydration, and polyuria. There has been a reported case of a 19-year-old female patient with a chief complaint weakness in both hands and feet. From clinical and laboratory investigations, it was found that hypopotassium and based on the hypokalemia approach with low HCO3- and urine pH &gt;5,5, the diagnosis in this patient was established as a distal renal tubular acidosis (RTAd)</em> <strong><em> </em></strong></p><p><strong><em>Keywords: </em></strong><em>RTA, RTAd ,metabolic acidosis, hypopotassium, hiperchloremic</em></p><p><em> </em></p>

Anaerobic Glycolysis and Glycogenolysis do not Release Protons and do not Cause Acidosis

2020 ◽  
Vol 7 (1) ◽  
pp. 6-10
Author(s):  
Rossana Pesi ◽  
Francesco Balestri ◽  
Piero L. Ipata
Keyword(s):  
Metabolic Acidosis ◽  
Atpase Activity ◽  
Muscle Contraction ◽  
Metabolic Network ◽  
Metabolic Pathway ◽  
Short Review ◽  
Present Knowledge ◽  
Anaerobic Glycolysis ◽  
Per Se ◽  
Biochemical Features

Background: A metabolic pathway is composed of a series of enzymatic steps, where the product of each reaction becomes the substrate of the subsequent one. We can summarize the single reactions to obtain the overall equation of the metabolic pathway, suggesting its role in the metabolic network. Objective: In this short review, we aim at presenting our present knowledge on the biochemical features underlying the interrelation between acidosis occurring during anaerobic muscle contraction and the glycolytic and glycogenolytic pathways. We emphasize that both pathways per se are not acidifying processes. Conclusions: The review emphasizes the following points: i) The importance that single reactions, as well as the overall equation of a metabolic pathway, are balanced; ii) Unbalanced reactions lead to unbalanced overall equations, whose functions cannot be correctly understood; iii) Glycogen acts as the major fuel for muscle anaerobic contraction. Anaerobic glycogenolysis not only does not release protons, but it also consumes one proton; iv) When dealing with metabolic acidosis, it should be always recalled that protons are released by muscle ATPase activity, not by glycolysis or glycogenolysis.

scholarly journals Effects of Lysine on Ammonia Formation, Hydrogen Ion, and Potassium Ion Balance: A Review and an Hypothesis

1973 ◽  
Vol 19 (9) ◽  
pp. 943-949 ◽  
Author(s):  
Jack I Zweig
Keyword(s):  
Amino Acids ◽  
Potassium Ion ◽  
Hydrogen Ion ◽  
Potassium Excretion ◽  
Ion Balance ◽  
Disease States ◽  
Dibasic Amino Acids ◽  
Ammonia Formation

Abstract Evidence is assembled that lysine acts as an intracellular hydrogen ion acceptor, causing increased ammonia formation and increased potassium excretion in certain disease states. It is suggested that other intracellular dibasic amino acids may have the same effects.

Inherited metabolic disease

2020 ◽  
pp. 489-512
Keyword(s):  
Metabolic Disease ◽  
Differential Diagnosis ◽  
Metabolic Acidosis ◽  
Liver Dysfunction ◽  
Diagnostic Tests ◽  
Metabolic Diseases ◽  
Laboratory Diagnosis ◽  
Initial Management ◽  
Organ Specific ◽  
Elevated Lactate

Although individually rare, inherited metabolic diseases (IMDs) are a diverse and increasing number of recognized disorders. This chapter gives a practical overview of IMDs, concentrating on the approach to recognition, laboratory diagnosis, and initial management. Common presenting modalities of IMDs are described, including the acutely unwell child, elevated lactate, hypoglycaemia, hyperammonaemia, and metabolic acidosis. A systems-based approach is used to enable the reader to consider IMD in the differential diagnosis of organ-specific disease, as well as a description of the commoner diagnostic tests to consider. These include neurological (seizures, developmental delay), hepatic (hepatomegaly and liver dysfunction), and cardiac systems (cardiomyopathy). The IMDs causing dysmorphic syndromes are also considered.

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