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Acid–base homeostasis is fundamental for maintaining life. This article reviews a stepwise method for the physiological approach to evaluation of acid–base status. Internal acid–base homeostasis is fundamental for maintaining life. Accurate and timely interpretation of an acid–base disorder can be lifesaving, but the establishment of a correct diagnosis may be challenging. 1 The three major methods of quantifying acid–base disorders are the physiological approach, the base-excess approach, and the physicochemical approach (also called the Stewart method). 2 This article reviews a stepwise method for the physiological approach. The physiological approach uses the carbonic acid–bicarbonate buffer system. Based on the isohydric principle, this system characterizes acids as hydrogen-ion donors and bases as hydrogen-ion acceptors. The carbonic acid–bicarbonate system is important in maintaining homeostatic control. In . . .

Although pH is a fundamental property of Earth’s oceans, critical to our understanding of seawater biogeochemistry, its long-timescale geologic history is poorly constrained. We constrain seawater pH through time by accounting for the cycles of the major components of seawater. We infer an increase from early Archean pH values between ~6.5 and 7.0 and Phanerozoic values between ~7.5 and 9.0, which was caused by a gradual decrease in atmospheric pCO₂ in response to solar brightening, alongside a decrease in hydrothermal exchange between seawater and the ocean crust. A lower pH in Earth’s early oceans likely affected the kinetics of chemical reactions associated with the origin of life, the energetics of early metabolisms, and climate through the partitioning of CO₂ between the oceans and atmosphere.

Forages commonly used in dry cow rations contain high K concentrations. This results in a high dietary cation–anion difference (DCAD), which can compromise the calcium homeostasis of periparturient cows. The aim of this study was to determine the effect of 2 types of hay, fed during the prepartum period and differing in their K concentrations, on the peripartum acid–base status and mineral balance of dairy cows. During the prepartum period, the cows of group K33 (n=6) received a diet based on hay with a high K concentration (33g/kg of DM), whereas the cows of group K13 (n=6) received a diet based on hay with a low K concentration (13g/kg of DM). Both experimental diets were formulated to be isoenergetic and isonitrogenous. After calving, all cows received the same diet based on hay K33. Blood and urine samples were taken on d 14, 7, and 3 before parturition, at parturition, and then daily during the first 8 d after calving. Concentrations of minerals were analyzed in both blood and urine. Creatinine was also measured in urine for the calculation of the mineral:creatinine ratio. The acid–base parameters in blood (pH and HCO3− concentration) and urine (pH, net acid–base excretion, and base–acid quotient) were determined on d 14, 7, and 3 before parturition, at parturition, and on d 1 after parturition. The use of hay K13 reduced the DCAD value of the prepartum diet by half (195 vs. 514mEq/kg of DM). No significant differences between the 2 groups were observed for blood acid–base indicators or plasma minerals except for the Mg plasma concentration, which tended to be higher in group K13 from d 3 prepartum to d 2 after calving. In group K13, urinary Ca excretion tended to be higher from d 3 prepartum to d 1 after parturition than that in group K33. On d 3 before parturition, urinary pH and net acid–base excretion were significantly lower in group K13 than in group K33. On d 14, 7, and 3 before parturition, base–acid quotient was significantly lower in group K13 than in group K33. In group K13, daily feed intake and hence daily intake of Ca, P, and Mg during d 3 and 4 after parturition were higher than in group K33. The decrease of the DCAD in positive ranges by feeding a low-K hay before parturition induced a reduction of the metabolic alkalotic charge, as observed in acid–base parameters in urine, and increased the availability of Ca and P as a result of higher feed intake at the onset of lactation.

Hydration is one of the most significant issues for combat sports as athletes often use water restriction for quick weight loss before competition. It appears that alkaline water can be an effective alternative to sodium bicarbonate in preventing the effects of exercise-induced metabolic acidosis. Therefore, the main aim of the present study was to investigate, in a double blind, placebo controlled randomized study, the impact of mineral-based highly alkaline water on acid-base balance, hydration status, and anaerobic capacity. Sixteen well trained combat sport athletes (n = 16), were randomly divided into two groups; the experimental group (EG; n = 8), which ingested highly alkaline water for three weeks, and the control group (CG; n = 8), which received regular table water. Anaerobic performance was evaluated by two double 30 s Wingate tests for lower and upper limbs, respectively, with a passive rest interval of 3 minutes between the bouts of exercise. Fingertip capillary blood samples for the assessment of lactate concentration were drawn at rest and during the 3rd min of recovery. In addition, acid-base equilibrium and electrolyte status were evaluated. Urine samples were evaluated for specific gravity and pH. The results indicate that drinking alkalized water enhances hydration, improves acid-base balance and anaerobic exercise performance.

The kidneys filter large amounts of glucose. To prevent the loss of this valuable fuel, the tubular system of the kidney, particularly the proximal tubule, has been programmed to reabsorb all filtered glucose. The machinery involves the sodium-glucose cotransporters SGLT2 and SGLT1 on the apical membrane and the facilitative glucose transporter GLUT2 on the basolateral membrane. The proximal tubule also generates new glucose, particularly in the post-absorptive phase but also to enhance bicarbonate formation and maintain acid-base balance. The glucose reabsorbed or formed by the proximal tubule is primarily taken up into peritubular capillaries and returned to the systemic circulation or provided as an energy source to further distal tubular segments that take up glucose by basolateral GLUT1. Recent studies provided insights on the coordination of renal glucose reabsorption, formation, and usage. Moreover, a better understanding of renal glucose transport in disease states is emerging. This includes the kidney in diabetes mellitus, when renal glucose retention becomes maladaptive and contributes to hyperglycemia. Furthermore, enhanced glucose reabsorption is coupled to sodium retention through the sodium-glucose cotransporter SGLT2, which induces secondary deleterious effects. As a consequence, SGLT2 inhibitors are new anti-hyperglycemic drugs that can protect the kidneys and heart from failing. Recent studies discovered unique roles for SGLT1 with implications in acute kidney injury and glucose sensing at the macula densa. This review discusses established and emerging concepts of renal glucose transport, and outlines the need for a better understanding of renal glucose handling in health and disease.

CO 2 , HCO 3 , SID , and total weak acids have been defined as pH’s independent variables. However, according to Gamble, HCO 3 should be equal to the difference between the sum of cations and the sum of anions besides HCO 3 . Therefore, if this mathematical expression is substituted for HCO 3 in the Henderson-Hasselbalch equation, all independent variables of pH can be demonstrated. Our aim is to test this theory in this study. This prospective observational study was conducted between 2019 and 2020. All admitted patients to the intensive care unit who were >18 years old were included. Demographic data, blood gas parameters, albumin, magnesium, and inorganic phosphorus levels, and outcomes were recorded twice (at admission and at the 24 th hour). The multivariate linear regression model was used to determine pH’s independent variables. In the multivariate linear regression model, pH was significantly increased by each unit increase in Na, K, Ca, and Mg (mmol L -1 ). In contrast, pH was significantly decreased by each unit increase in CO 2 , Cl, lactate, albumin (g dL -1 ), inorganic phosphorus (mg dL -1 ), and the strong ion gap. Ten independent variables can accurately predict the changes in pH. For this reason, all ten independent variables should be separately evaluated when interpreting the acid-base status. With this understanding, all algorithms regarding acid-base evaluation may become unnecessary.

The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na + -dependent Cl − /HCO 3 − exchanger AE4 ( Slc4a9 ). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl − /HCO 3 − exchanger pendrin ( Slc26a4 ) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status. Maintaining systemic acid-base balance is a central task of the kidneys, but it is still undetermined how acid-base alterations are perceived by the kidney. Here, the authors show that the solute transporter AE4 in β-intercalated cells is an essential part of the renal acid-base sensing mechanism

For the past 300 years, hydrogen sulfide (H 2 S) has been considered a toxic gas. Nowadays, it has been found to be a novel signaling molecule in plants involved in the regulation of cellular metabolism, seed germination, plant growth, development, and response to environmental stresses, including high temperature (HT) and low temperature (LT). As a signaling molecule, H 2 S can be actively synthesized and degraded in the cytosol, chloroplasts, and mitochondria of plant cells by enzymatic and non-enzymatic pathways to maintain homeostasis. To date, plant receptors for H 2 S have not been found. It usually exerts physiological functions through the persulfidation of target proteins. In the past 10 years, H 2 S signaling in plants has gained much attention. Therefore, in this review, based on that same attention, H 2 S homeostasis, protein persulfidation, and the signaling role of H 2 S in plant response to HT and LT stress were summarized. Also, the common mechanisms of H 2 S-induced HT and LT tolerance in plants were updated. These mechanisms involve restoration of biomembrane integrity, synthesis of stress proteins, enhancement of the antioxidant system and methylglyoxal (MG) detoxification system, improvement of the water homeostasis system, and reestablishment of Ca 2+ homeostasis and acid-base balance. These updates lay the foundation for further understanding the physiological functions of H 2 S and acquiring temperature-stress-resistant crops to develop sustainable food and agriculture.

Inorganic phosphate (Pi) is an abundant element in the body and is essential for a wide variety of key biological processes. It plays an essential role in cellular energy metabolism and cell signalling, e.g. adenosine and guanosine triphosphates (ATP, GTP), and in the composition of phospholipid membranes and bone, and is an integral part of DNA and RNA. It is an important buffer in blood and urine and contributes to normal acid-base balance. Given its widespread role in almost every molecular and cellular function, changes in serum Pi levels and balance can have important and untoward effects. Pi homoeostasis is maintained by a counterbalance between dietary Pi absorption by the gut, mobilisation from bone and renal excretion. Approximately 85% of total body Pi is present in bone and only 1% is present as free Pi in extracellular fluids. In humans, extracellular concentrations of inorganic Pi vary between 0.8 and 1.2 mM, and in plasma or serum Pi exists in both its monovalent and divalent forms (H2PO4− and HPO42−). In the intestine, approximately 30% of Pi absorption is vitamin D regulated and dependent. To help maintain Pi balance, reabsorption of filtered Pi along the renal proximal tubule (PT) is via the NaPi-IIa and NaPi-IIc Na+-coupled Pi cotransporters, with a smaller contribution from the PiT-2 transporters. Endocrine factors, including, vitamin D and parathyroid hormone (PTH), as well as newer factors such as fibroblast growth factor (FGF)-23 and its coreceptor α-klotho, are intimately involved in the control of Pi homeostasis. A tight regulation of Pi is critical, since hyperphosphataemia is associated with increased cardiovascular morbidity in chronic kidney disease (CKD) and hypophosphataemia with rickets and growth retardation. This short review considers the control of Pi balance by vitamin D, PTH and Pi itself, with an emphasis on the insights gained from human genetic disorders and genetically modified mouse models.

The mechanism of Long Covid (Post-Acute Sequelae of COVID-19; PASC) is currently unknown, with no validated diagnostics or therapeutics. SARS-CoV-2 can cause disseminated infections that result in multi-system tissue damage, dysregulated inflammation, and cellular metabolic disruptions. The tissue damage and inflammation has been shown to impair microvascular circulation, resulting in hypoxia, which coupled with virally-induced metabolic reprogramming, increases cellular anaerobic respiration. Both acute and PASC patients show systemic dysregulation of multiple markers of the acid-base balance. Based on these data, we hypothesize that the shift to anaerobic respiration causes an acid-base disruption that can affect every organ system and underpins the symptoms of PASC. This hypothesis can be tested by longitudinally evaluating acid-base markers in PASC patients and controls over the course of a month. If our hypothesis is correct, this could have significant implications for our understanding of PASC and our ability to develop effective diagnostic and therapeutic approaches.