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Sheng Li Xue Bao : [Acta Physiologica... Apr 2023Virtually all of the dietary potassium intake is absorbed in the intestine, over 90% of which is excreted by the kidneys regarded as the most important organ of... (Review)
Review
Virtually all of the dietary potassium intake is absorbed in the intestine, over 90% of which is excreted by the kidneys regarded as the most important organ of potassium excretion in the body. The renal excretion of potassium results primarily from the secretion of potassium by the principal cells in the aldosterone-sensitive distal nephron (ASDN), which is coupled to the reabsorption of Na by the epithelial Na channel (ENaC) located at the apical membrane of principal cells. When Na is transferred from the lumen into the cell by ENaC, the negativity in the lumen is relatively increased. K efflux, H efflux, and Cl influx are the 3 pathways that respond to Na influx, that is, all these 3 pathways are coupled to Na influx. In general, Na influx is equal to the sum of K efflux, H efflux, and Cl influx. Therefore, any alteration in Na influx, H efflux, or Cl influx can affect K efflux, thereby affecting the renal K excretion. Firstly, Na influx is affected by the expression level of ENaC, which is mainly regulated by the aldosterone-mineralocorticoid receptor (MR) pathway. ENaC gain-of-function mutations (Liddle syndrome, also known as pseudohyperaldosteronism), MR gain-of-function mutations (Geller syndrome), increased aldosterone levels (primary/secondary hyperaldosteronism), and increased cortisol (Cushing syndrome) or deoxycorticosterone (hypercortisolism) which also activate MR, can lead to up-regulation of ENaC expression, and increased Na reabsorption, K excretion, as well as H excretion, clinically manifested as hypertension, hypokalemia and alkalosis. Conversely, ENaC inactivating mutations (pseudohypoaldosteronism type 1b), MR inactivating mutations (pseudohypoaldosteronism type 1a), or decreased aldosterone levels (hypoaldosteronism) can cause decreased reabsorption of Na and decreased excretion of both K and H, clinically manifested as hypotension, hyperkalemia, and acidosis. The ENaC inhibitors amiloride and Triamterene can cause manifestations resembling pseudohypoaldosteronism type 1b; MR antagonist spironolactone causes manifestations similar to pseudohypoaldosteronism type 1a. Secondly, Na influx is regulated by the distal delivery of water and sodium. Therefore, when loss-of-function mutations in Na-K-2Cl cotransporter (NKCC) expressed in the thick ascending limb of the loop and in Na-Cl cotransporter (NCC) expressed in the distal convoluted tubule (Bartter syndrome and Gitelman syndrome, respectively) occur, the distal delivery of water and sodium increases, followed by an increase in the reabsorption of Na by ENaC at the collecting duct, as well as increased excretion of K and H, clinically manifested as hypokalemia and alkalosis. Loop diuretics acting as NKCC inhibitors and thiazide diuretics acting as NCC inhibitors can cause manifestations resembling Bartter syndrome and Gitelman syndrome, respectively. Conversely, when the distal delivery of water and sodium is reduced (e.g., Gordon syndrome, also known as pseudohypoaldosteronism type 2), it is manifested as hypertension, hyperkalemia, and acidosis. Finally, when the distal delivery of non-chloride anions increases (e.g., proximal renal tubular acidosis and congenital chloride-losing diarrhea), the influx of Cl in the collecting duct decreases; or when the excretion of hydrogen ions by collecting duct intercalated cells is impaired (e.g., distal renal tubular acidosis), the efflux of H decreases. Both above conditions can lead to increased K secretion and hypokalemia. In this review, we focus on the regulatory mechanisms of renal potassium excretion and the corresponding diseases arising from dysregulation.
Topics: Humans; Bartter Syndrome; Pseudohypoaldosteronism; Potassium; Aldosterone; Hypokalemia; Gitelman Syndrome; Hyperkalemia; Clinical Relevance; Epithelial Sodium Channels; Kidney Tubules, Distal; Sodium; Hypertension; Alkalosis; Water; Kidney
PubMed: 37089096
DOI: No ID Found -
Hypertension (Dallas, Tex. : 1979) Apr 2022Intercalated cells make up about a third of all cells within the connecting tubule and the collecting duct and are subclassified as type A, type B and non-A, non-B based... (Review)
Review
Intercalated cells make up about a third of all cells within the connecting tubule and the collecting duct and are subclassified as type A, type B and non-A, non-B based on the subcellular distribution of the H-ATPase, which dictates whether it secretes H or HCO. Type B intercalated cells mediate Cl absorption and HCO secretion, which occurs largely through the anion exchanger pendrin. Pendrin is stimulated by angiotensin II via the angiotensin type 1a receptor and by aldosterone through MR (mineralocorticoid receptor). Aldosterone stimulates pendrin expression and function, in part, through the alkalosis it generates. Pendrin-mediated HCO secretion increases in models of metabolic alkalosis, which attenuates the alkalosis. However, pendrin-positive intercalated cells also regulate blood pressure, at least partly, through pendrin-mediated Cl absorption and through their indirect effect on the epithelial Na channel, ENaC. This aldosterone-induced increase in pendrin secondarily stimulates ENaC, thereby contributing to the aldosterone pressor response. This review describes the contribution of pendrin-positive intercalated cells to Na, K, Cl and acid-base balance.
Topics: Aldosterone; Alkalosis; Anion Transport Proteins; Blood Pressure; Epithelial Sodium Channels; Humans; Sodium; Sulfate Transporters
PubMed: 35109661
DOI: 10.1161/HYPERTENSIONAHA.121.16492 -
Case Reports in Nephrology 2022Calcium regulation is tightly controlled in the body. Multiple causes of hypercalcemia have been studied including primary hyperparathyroidism, hypercalcemia of...
Calcium regulation is tightly controlled in the body. Multiple causes of hypercalcemia have been studied including primary hyperparathyroidism, hypercalcemia of malignancy, and chronic granulomatous disorders. Among the less studied causes is calcium-alkali syndrome. Here, we discuss a case of hypercalcemia secondary to calcium-alkali syndrome, presenting with hypercalcemia, metabolic alkalosis, and acute kidney injury as a result of ingestion of a large amount of calcium supplements. Hypercalcemia can result in impaired collecting duct system sensitivity to antidiuretic hormone, afferent arteriole constriction, and activation of calcium sensor receptors in multiple tissues. The net effect is an increase in calcium reabsorption with a salt and water diuresis which leads to volume depletion, acute kidney injury, and metabolic alkalosis.
PubMed: 35433065
DOI: 10.1155/2022/1320259 -
The Journal of Physiology Mar 2020It was unknown whether respiratory alkalosis impacts the global cerebral metabolic response as well as the cerebral pro-oxidation and inflammatory response in passive...
KEY POINTS
It was unknown whether respiratory alkalosis impacts the global cerebral metabolic response as well as the cerebral pro-oxidation and inflammatory response in passive hyperthermia. This study demonstrated that the cerebral metabolic rate was increased by ∼20% with passive hyperthermia of up to +2°C oesophageal temperature, and this response was unaffected by respiratory alkalosis. Additionally, the increase in cerebral metabolism did not significantly impact the net cerebral release of oxidative and inflammatory markers. These data indicate that passive heating of up to +2°C core temperature in healthy young men is not enough to confer a major oxidative and inflammatory burden on the brain, but it does markedly increase the cerebral metabolic rate, independently of .
ABSTRACT
There is limited information concerning the impact of arterial /pH on heat-induced alteration in cerebral metabolism, as well as on the cerebral oxidative/inflammatory burden of hyperthermia. Accordingly, we sought to address two hypotheses: (1) passive hyperthermia will increase the cerebral metabolic rate of oxygen (CMRO ) consistent with a combined influence of Q10 and respiratory alkalosis; and (2) the net cerebral release of pro-oxidative and pro-inflammatory markers will be elevated in hyperthermia, particularly in poikilocapnic hyperthermia. Healthy young men (n = 6) underwent passive heating until an oesophageal temperature of 2°C above resting was reached. At 0.5°C increments in core temperature, CMRO was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference (cannulation). Net cerebral glucose/lactate exchange, and biomarkers of oxidative and inflammatory stress were also measured. At +2.0°C oesophageal temperature, arterial was restored to normothermic values using end-tidal forcing. The primary findings were: (1) while CMRO was increased (P < 0.05) by ∼20% with hyperthermia of +1.5-2.0°C, this was not influenced by respiratory alkalosis, and (2) although biomarkers of pro-oxidation and pro-inflammation were systemically elevated in hyperthermia (P < 0.05), there were no differences in the trans-cerebral exchange kinetics. These novel data indicate that passive heating of up to +2°C core temperature in healthy young men is not enough to confer a major oxidative and inflammatory burden on the brain, despite it markedly increasing CMRO , irrespective of arterial pH.
Topics: Alkalosis, Respiratory; Brain; Cerebrovascular Circulation; Fever; Humans; Hyperthermia; Inflammation; Male
PubMed: 31900940
DOI: 10.1113/JP278889 -
Kidney International Reports Nov 2023Excessive dialytic potassium (K) and acid removal are risk factors for arrhythmias; however, treatment-to-treatment dialysate modification is rarely performed. We...
INTRODUCTION
Excessive dialytic potassium (K) and acid removal are risk factors for arrhythmias; however, treatment-to-treatment dialysate modification is rarely performed. We conducted a multicenter, pilot randomized study to test the safety, feasibility, and efficacy of 4 point-of-care (POC) chemistry-guided protocols to adjust dialysate K and bicarbonate (HCO3) in outpatient hemodialysis (HD) clinics.
METHODS
Participants received implantable cardiac loop monitors and crossed over to four 4-week periods with adjustment of dialysate K or HCO3 at each treatment according to pre-HD POC values: (i) K-removal minimization, (ii) K-removal maximization, (iii) Acidosis avoidance, and (iv) Alkalosis avoidance. The primary end point was percentage of treatments adhering to the intervention algorithm. Secondary endpoints included pre-HD K and HCO variability, adverse events, and rates of clinically significant arrhythmias (CSAs).
RESULTS
Nineteen subjects were enrolled in the study. HD staff completed POC testing and correctly adjusted the dialysate in 604 of 708 (85%) of available HD treatments. There was 1 K ≤3, 29 HCO3 <20 and 2 HCO3 >32 mEq/l and no serious adverse events related to study interventions. Although there were no significant differences between POC results and conventional laboratory measures drawn concurrently, intertreatment K and HCO3 variability was high. There were 45 CSA events; most were transient atrial fibrillation (AF), with numerically fewer events during the alkalosis avoidance period (8) and K-removal maximization period (3) compared to other intervention periods (17). There were no significant differences in CSA duration among interventions.
CONCLUSION
Algorithm-guided K/HCO3 adjustment based on POC testing is feasible. The variability of intertreatment K and HCO3 suggests that a POC-laboratory-guided algorithm could markedly alter dialysate-serum chemistry gradients. Definitive end point-powered trials should be considered.
PubMed: 38025214
DOI: 10.1016/j.ekir.2023.07.039 -
Neuroscience and Biobehavioral Reviews Dec 2023High Ventilation Breathwork (HVB) refers to practices employing specific volitional manipulation of breathing, with a long history of use to relieve various forms of... (Review)
Review
High Ventilation Breathwork (HVB) refers to practices employing specific volitional manipulation of breathing, with a long history of use to relieve various forms of psychological distress. This paper seeks to offer a consolidative insight into potential clinical application of HVB as a treatment of psychiatric disorders. We thus review the characteristic phenomenological and neurophysiological effects of these practices to inform their mechanism of therapeutic action, safety profiles and future clinical applications. Clinical observations and data from neurophysiological studies indicate that HVB is associated with extraordinary changes in subjective experience, as well as with profound effects on central and autonomic nervous systems functions through modulation of neurometabolic parameters and interoceptive sensory systems. This growing evidence base may guide how the phenomenological effects of HVB can be understood, and potentially harnessed in the context of such volitional perturbation of psychophysiological state. Reports of putative beneficial effects for trauma-related, affective, and somatic disorders invite further research to obtain detailed mechanistic knowledge, and rigorous clinical testing of these potential therapeutic uses.
Topics: Humans; Yoga; Respiration; Autonomic Nervous System; Mental Disorders; Psychophysiology
PubMed: 37923236
DOI: 10.1016/j.neubiorev.2023.105453 -
Effect of Intravenously Administered Crystalloid Solutions on Acid-Base Balance in Domestic Animals.Journal of Veterinary Internal Medicine Sep 2017Intravenous fluid therapy can alter plasma acid-base balance. The Stewart approach to acid-base balance is uniquely suited to identify and quantify the effects of the... (Review)
Review
Intravenous fluid therapy can alter plasma acid-base balance. The Stewart approach to acid-base balance is uniquely suited to identify and quantify the effects of the cationic and anionic constituents of crystalloid solutions on plasma pH. The plasma strong ion difference (SID) and weak acid concentrations are similar to those of the administered fluid, more so at higher administration rates and with larger volumes. A crystalloid's in vivo effects on plasma pH are described by 3 general rules: SID > [HCO3-] increases plasma pH (alkalosis); SID < [HCO3-] decreases plasma pH (alkalosis); and SID = [HCO3-] yields no change in plasma pH. The in vitro pH of commercially prepared crystalloid solutions has little to no effect on plasma pH because of their low titratable acidity. Appreciation of IV fluid composition and an understanding of basic physicochemical principles provide therapeutically valuable insights about how and why fluid therapy can produce and correct alterations of plasma acid-base equilibrium. The ideal balanced crystalloid should (1) contain species-specific concentrations of key electrolytes (Na , Cl , K , Ca , Mg ), particularly Na and Cl ; (2) maintain or normalize acid-base balance (provide an appropriate SID); and (3) be isosmotic and isotonic (not induce inappropriate fluid shifts) with normal plasma.
Topics: Acid-Base Equilibrium; Acidosis; Animals; Crystalloid Solutions; Fluid Therapy; Hydrogen-Ion Concentration; Infusions, Intravenous; Isotonic Solutions
PubMed: 28833697
DOI: 10.1111/jvim.14803 -
Cureus Jul 2022Background The high prevalence of pneumonia and renal involvement in coronavirus disease 2019 (COVID-19) leads to frequent acid-base abnormalities in serious patients...
Background The high prevalence of pneumonia and renal involvement in coronavirus disease 2019 (COVID-19) leads to frequent acid-base abnormalities in serious patients and affects prognosis. In this study, we aimed to assess the arterial blood gas (ABG) and acid-base patterns in COVID-19 patients admitted to a tertiary care hospital. Methodology A retrospective observational study was conducted in a designated COVID-19 hospital involving 267 reverse transcription-polymerasechain reaction-positive COVID-19 patients. Demographic and laboratory data including ABG data within the first day after admission and in patients with multiple ABG analyses, only the first measurement was collected and analyzed statistically, including its association with comorbidities. Results The most common age group of the patients was 51-60 years (30.8%), with a male predominance (male:female = 2.7:1). The most common comorbidities were hypertension, diabetes mellitus, and chronic obstructive pulmonary disease found in 147 (55%) COVID-19 patients. Alkalosis and acidosis were observed in 145 (54.3%) and 50 (18.7%) patients, respectively. The most common ABG abnormality observed was primary respiratory alkalosis with secondary metabolic acidosis in 67 (25.1%) patients, followed by primary respiratory alkalosis with secondary metabolic alkalosis in 54 (20.2%) patients. Statistically significant negative correlation was found with PaCO and pH (r = -0.530, p < 0.0001), statistically significant positive correlation was found between pH and base (r = 0.533, p < 0.0001), pH and TCO (r = 0.260, p < 0.0001), and pH and HCO (r = 0.354, p < 0.0001). Conclusions Acid-base abnormalities are commonly encountered in COVID-19 patients. Respiratory alkalosis as a part of a single or mixed pattern on ABG was the most common pattern found in critically ill COVID-19 patients. ABG on admission in moderate-to-severe COVID-19 patients can help in the early correction of metabolic abnormalities leading to improved patient outcomes.
PubMed: 35967170
DOI: 10.7759/cureus.26715 -
Clinical Kidney Journal Jan 2021The common finding of hypokalemic alkalosis in several unrelated disorders may confound the early diagnosis of salt-losing tubulopathy (SLT). Antenatal Bartter syndrome... (Review)
Review
The common finding of hypokalemic alkalosis in several unrelated disorders may confound the early diagnosis of salt-losing tubulopathy (SLT). Antenatal Bartter syndrome (BS) must be considered in idiopathic early-onset polyhydramnios. Fetal megabladder in BS may allow its distinction from third-trimester polyhydramnios that occurs in congenital chloride diarrhea (CCD). Fetal megacolon occurs in CCD while fecal chloride >90 mEq/L in infants is diagnostic. Failure-to-thrive, polydipsia and polyuria in early childhood are the hallmarks of classic BS. Unlike BS, there is low urinary chloride in hypokalemic alkalosis of intractable emesis and cystic fibrosis. Rarely, renal salt wasting may result from cystinosis, Dent disease, disorders of paracellular claudin-10b and Kir4.1 potassium-channel deficiency. Acquired BS may result from calcimimetic up-regulation of a calcium-sensing receptor or autoantibody inactivation of sodium chloride co-transporters in Sjögren syndrome. A relatively common event of heterozygous gene mutations for Gitelman syndrome increases the likelihood of its random occurrence in certain diseases of adult onset. Finally, diuretic abuse is the most common differential diagnosis of SLT. Unlike the persistent elevation in BS, urinary chloride concentration losses waxes and wanes on day-to-day assessment in patients with diuretic misuse.
PubMed: 33564404
DOI: 10.1093/ckj/sfaa172 -
Frontiers in Pediatrics 2023Bartter syndrome (BS) type III is a rare autosomal recessive genetic disease. Its clinical features are polyuria, hypokalemia, hypochloremia, metabolic alkalosis, and... (Review)
Review
BACKGROUND
Bartter syndrome (BS) type III is a rare autosomal recessive genetic disease. Its clinical features are polyuria, hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninaemia. A few BS type III can be complicated with chronic kidney disease.
CASE PRESENTATION
We report a 14-year-old boy with Bartter syndrome caused by a c.1792C > T (.Q598*) mutation in the CLCNKB gene. He was a no deafness and full-term baby, and he had renal dysplasia and chronic kidney disease (CKD). In addition, we summarize all cases of BS type III complicated with CKD.
CONCLUSIONS
We report a case of Bartter syndrome complicated by chronic kidney disease caused by a new mutation of CLCNKB. As we all know, BS type IV is usually combined with chronic kidney disease, and BS type III can also integrate with CKD. We don't find BS type III with glomerular dysplasia in the literature. So renal damage in BS type III is not only FSGS; clinicians must also be aware of glomerular dysplasia.
PubMed: 37063660
DOI: 10.3389/fped.2023.1169486