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British Journal of Anaesthesia Nov 2022Acid-base status in full-term pregnant women is characterised by hypocapnic alkalosis. Whether this respiratory alkalosis is primary or consequent to changes in CSF...
BACKGROUND
Acid-base status in full-term pregnant women is characterised by hypocapnic alkalosis. Whether this respiratory alkalosis is primary or consequent to changes in CSF electrolytes is not clear.
METHODS
We enrolled third-trimester pregnant women (pregnant group) and healthy, non-pregnant women of childbearing age (controls) undergoing spinal anaesthesia for Caesarean delivery and elective surgery, respectively. Electrolytes, strong ion difference (SID), partial pressure of carbon dioxide ( [Formula: see text] ), and pH were measured in simultaneously collected CSF and arterial blood samples.
RESULTS
All pregnant women (20) were hypocapnic, whilst only four (30%) of the controls (13) had an arterial [Formula: see text] <4.7 kPa (P<0.001). The incidence of hypocapnic alkalosis was higher in the pregnant group (65% vs 8%; P=0.001). The CSF-to-plasma Pco difference was significantly higher in pregnant women (1.5 [0.3] vs 1.0 [0.4] kPa; P<0.001), mainly because of a decrease in arterial Pco (3.9 [0.3] vs 4.9 [0.5] kPa; P<0.001). Similarly, the CSF-to-plasma difference in SID was less negative in pregnant women (-7.8 [1.4] vs -11.4 [2.3] mM; P<0.001), mainly because of a decreased arterial SID (31.5 [1.2] vs 36.1 [1.9] mM; P<0.001). The major determinant of the reduced plasma SID of pregnant women was a relative increase in plasma chloride compared with sodium.
CONCLUSIONS
Primary hypocapnic alkalosis characterises third-trimester pregnant women leading to chronic acid-base adaptations of CSF and plasma. The compensatory SID reduction, mainly sustained by an increase in chloride concentration, is more pronounced in plasma than in CSF, as the decrease in Pco is more marked in this compartment.
CLINICAL TRIAL REGISTRATION
NCT03496311.
Topics: Female; Humans; Pregnancy; Acid-Base Equilibrium; Alkalosis; Bicarbonates; Carbon Dioxide; Chlorides; Electrolytes; Hydrogen-Ion Concentration; Pregnancy Trimester, Third; Sodium
PubMed: 36096944
DOI: 10.1016/j.bja.2022.07.048 -
Iranian Journal of Kidney Diseases May 2022Bartter syndrome (BS) is a salt losing tubulopathy due to impairment of the transport mechanisms at the thick ascending limb of the Henle's loop. The aim of this study...
INTRODUCTION
Bartter syndrome (BS) is a salt losing tubulopathy due to impairment of the transport mechanisms at the thick ascending limb of the Henle's loop. The aim of this study was to report the clinical course of patients with BS.
METHODS
Patients with BS were followed from 1996 to 2020 and enrolled to a systematic protocol to confirm primary BS by evaluating the metabolic derangements, nephrolithiasis and nephrocalcinosis. Treatment was based on standard guidelines. Comparisons were made between data at baseline and at the last visit.
RESULTS
A total of 13 patients (7 males) with primary BS were analyzed. Two patients had a mutation of the KCNJ1 gene. Age at diagnosis was 3 ± 4.5 years and the follow-up period was 11.19 ± 6.76 years. Metabolic alkalosis was initially detected in 76.92% and remained stable at the last visit (P > .05). Hypokalemia was present in 61.5% of patients at diagnosis, but sustained in 38.46% at the last visit (P < .05). Urine calcium level was 13.3 ± 9.6 mg/ kg/d at the first visit, and significantly reduced to 3.7 ± 2.0 mg/ kg/d at the last visit (P < .05). Nephrocalcinosis was detected by first kidney ultrasonography in 53.8% of patients. Kidney function was preserved, with a glomerular filtration rate of 120.1 ± 28.7 mL/min/ 1.73m2 at last visit. Growth was completely recovered in 71.42% and partially improved in 14.28% of patients after treatment, respectively. All patients received indomethacin and potassium chloride salts.
CONCLUSIONS
Long-term follow-up of this cohort of BS showed favorable outcomes after treatment resulting in metabolic normalization and growth catch-up in most patients. DOI: 10.52547/ijkd.6657.
Topics: Alkalosis; Bartter Syndrome; Humans; Hypokalemia; Male; Nephrocalcinosis; Potassium
PubMed: 35714210
DOI: No ID Found -
Kidney International May 2016Metabolic acidosis is a common complication of chronic kidney disease; it is typically caused by the accumulation of sulfate, phosphorus, and organic anions. Metabolic... (Review)
Review
Metabolic acidosis is a common complication of chronic kidney disease; it is typically caused by the accumulation of sulfate, phosphorus, and organic anions. Metabolic acidosis is correlated with several adverse outcomes, such as morbidity, hospitalization, and mortality. Thus, correction of metabolic acidosis is fundamental for the adequate management of many systemic complications of chronic kidney disease. In patients undergoing hemodialysis, acid-base homeostasis depends on many factors including the following: net acid production, amount of alkali given by the dialysate bath, duration of the interdialytic period, and residual diuresis, if any. Recent literature data suggest that the development of metabolic alkalosis after dialysis may contribute to adverse clinical outcomes. Our review is focused on the potential effects of different dialysate bicarbonate concentrations on hard outcomes such as mortality. Unfortunately, no randomized studies exist about this issue. Acid-base equilibrium is a complex and vital system whose regulation is impaired in chronic kidney disease. We await further studies to assess the extent to which acid-base status is a major determinant of overall survival in patients undergoing hemodialysis. For the present, the clinician should understand that target values for predialysis serum bicarbonate concentration have been established primarily based on observational studies and expert opinion. Based on this, we should keep the predialysis serum bicarbonate level at least at 22 mmol/l. Furthermore, a specific focus should be addressed by the attending nephrologist to the clinical and nutritional status of the major outliers on both the acid and alkaline sides of the curve.
Topics: Acid-Base Equilibrium; Acidosis; Bicarbonates; Hemodialysis Solutions; Humans; Hydrogen-Ion Concentration; Male; Models, Biological; Practice Guidelines as Topic; Renal Dialysis; Renal Insufficiency, Chronic; Risk Assessment; Risk Factors; Treatment Outcome
PubMed: 26924048
DOI: 10.1016/j.kint.2016.01.010 -
Cureus Sep 2023In a patient with persistent hypokalemia, it is important to consider Gitelman syndrome, a rare, salt-wasting tubulopathy inherited in an autosomal recessive pattern....
In a patient with persistent hypokalemia, it is important to consider Gitelman syndrome, a rare, salt-wasting tubulopathy inherited in an autosomal recessive pattern. Gitelman syndrome leads to electrolyte abnormalities like hypokalemia, hypomagnesemia, and metabolic alkalosis. Typical clinical features include muscle cramps, fatigue, polydipsia, and salt cravings. Our case involves a female patient in her early 40s who visited the endocrinology clinic with symptoms of polyuria, constipation, muscle weakness, and fatigue. Electrolyte abnormalities included hypokalemia, hypomagnesemia, hypochloremia, and hyperreninemia. Initial tests, such as renal function tests, renal ultrasound, and CT scan, yielded normal results. Differential diagnosis of Gitelman syndrome and Bartter syndrome was considered due to the mutual electrolyte abnormalities of hypokalemia and metabolic alkalosis. Bartter syndrome was ruled out in our patient due to the presence of hypomagnesemia, which indicates a different defective receptor. Ultimately, genetic testing would be necessary to confirm the diagnosis of Gitelman syndrome considering the characteristic electrolyte disturbances and classic clinical presentation of fatigue, weakness, and salt craving.
PubMed: 37795074
DOI: 10.7759/cureus.44590 -
Mathematical Biosciences and... Jun 2020Precise maintenance of acid-base homeostasis is fundamental for optimal functioning of physiological and cellular processes. The presence of an acid-base disturbance can...
Precise maintenance of acid-base homeostasis is fundamental for optimal functioning of physiological and cellular processes. The presence of an acid-base disturbance can affect clinical outcomes and is usually caused by an underlying disease. It is, therefore, important to assess the acid-base status of patients, and the extent to which various therapeutic treatments are effective in controlling these acid-base alterations. In this paper, we develop a dynamic model of the physiological regulation of an HCO/CO buffering system, an abundant and powerful buffering system, using Henderson-Hasselbalch kinetics. We simulate the normal physiological state and four cardinal acidbase disorders: Metabolic acidosis and alkalosis and respiratory acidosis and alkalosis. We show that the model accurately predicts serum pH over a range of clinical conditions. In addition to qualitative validation, we compare the in silico results with clinical data on acid-base homeostasis and alterations, finding clear relationships between primary acid-base disturbances and the secondary adaptive compensatory responses. We also show that the predicted primary disturbances accurately resemble clinically observed compensatory responses. Furthermore, via sensitivity analysis, key parameters were identified which could be the most effective in regulating systemic pH in healthy individuals, and those with chronic kidney disease and distal and proximal renal tubular acidosis. The model presented here may provide pathophysiologic insights and can serve as a tool to assess the safety and efficacy of different therapeutic interventions to control or correct acid-base disorders.
Topics: Acid-Base Equilibrium; Acid-Base Imbalance; Acidosis, Respiratory; Alkalosis; Humans; Hydrogen-Ion Concentration; Models, Theoretical
PubMed: 33120513
DOI: 10.3934/mbe.2020246 -
Clinical Practice and Cases in... Aug 2022Patients with history of abdominal aortic aneurysm (AAA) undergoing surgical repair can have a myriad of surgical complications including compromise to large arteries...
INTRODUCTION
Patients with history of abdominal aortic aneurysm (AAA) undergoing surgical repair can have a myriad of surgical complications including compromise to large arteries branching from the aorta. Secondary hyperaldosteronism, characterized by high levels of aldosterone and renin, can be due to a multitude of causes, including renal artery stenosis, and presents with nonspecific symptoms of fatigue, increased thirst, and muscle spasms. While it can initially be difficult to diagnose given its multitude of metabolic abnormalities, secondary hyperaldosteronism is important to consider in patients presenting with uncontrolled hypertension, hypokalemia, and metabolic alkalosis.
CASE REPORT
This report explores the case of a 65-year-old male with a complicated medical history presenting to the emergency department with hypokalemia and hypertension six months after undergoing endovascular repair for an AAA and was found to have metabolic abnormalities including hypokalemia and metabolic alkalosis consistent with secondary hyperaldosteronism, likely secondary to renal artery stent stenosis. He was admitted to the hospital for four days and made a full recovery.
CONCLUSION
This case highlights the need to understand, identify, and accurately diagnose hyperaldosteronism and recognize post-AAA repair complications of renal artery stenosis as a cause of this metabolic derangement.
PubMed: 36049207
DOI: 10.5811/cpcem2022.6.56522 -
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 -
Journal of Medical Virology Jan 2021
Topics: Alkalosis; COVID-19; Fever; Humans; SARS-CoV-2
PubMed: 32639623
DOI: 10.1002/jmv.26276 -
Acta Medica (Hradec Kralove) 2020Primary hyperaldosteronism (PA) is the most common cause of secondary arterial hypertension and is frequently undiagnosed. It affects all ages but is more frequent...
Primary hyperaldosteronism (PA) is the most common cause of secondary arterial hypertension and is frequently undiagnosed. It affects all ages but is more frequent between 20 and 60 years old. The clinical presentation is variable, and the diagnosis is based on screening and, in equivocal cases, confirmatory tests. A 19-year-old student presented with complaints of extreme fatigue, arterial hypertension, hypokalemia and metabolic alkalosis, raising a high index of suspicion for PA. Screening tests were performed and its expressiveness excluded the need of confirmatory tests. CT-scan showed a unilateral adrenal adenoma and the patient was submitted to laparoscopic adenectomy without complications. Prompt diagnosis and treatment are essential to avoid long term complications of PA.
Topics: Adrenal Cortex Neoplasms; Adrenalectomy; Adrenocortical Adenoma; Alkalosis; Fatigue; Humans; Hyperaldosteronism; Hypertension; Hypokalemia; Male; Tomography, X-Ray Computed; Treatment Outcome; Young Adult
PubMed: 33002402
DOI: 10.14712/18059694.2020.32 -
Indian Journal of Nephrology 2022Gitelman syndrome (GS) is a rare autosomal recessive disorder characterized by the loss of function mutation of the solute carrier family-12 member-3 () gene, encoding...
Gitelman syndrome (GS) is a rare autosomal recessive disorder characterized by the loss of function mutation of the solute carrier family-12 member-3 () gene, encoding for sodium-chloride cotransporter of the distal convolute tubule. GS is characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. GS-like syndrome has been described rarely. Hyperthyroidism due to Grave's disease (GD) is characterized by the presence of autoantibodies to thyrotropin receptors. Concurrent occurrence of GS and GD is rarely reported, that too exclusively from far-east Asian populations. We describe a case of a 45-year-old man who presented with severe muscle weakness; the evaluation showed volume depletion, hypokalemia, hypomagnesemia, renal potassium and magnesium wasting, metabolic alkalosis, and hypocalciuria. He was also detected to have GD at the time of presentation. Genetic evaluation revealed a mutation in transient receptor potential melastatin 4 () gene. The clinical significance of this mutation in our patient remains unclear.
PubMed: 35814325
DOI: 10.4103/ijn.IJN_532_20