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International Journal of Molecular... Feb 2024A variety of changes in mineral metabolism aiming to restore acid-base balance occur in acid loading and metabolic acidosis. Phosphate plays a key role in defense... (Review)
Review
A variety of changes in mineral metabolism aiming to restore acid-base balance occur in acid loading and metabolic acidosis. Phosphate plays a key role in defense against metabolic acidosis, both as an intracellular and extracellular buffer, as well as in the renal excretion of excess acid in the form of urinary titratable acid. The skeleton acts as an extracellular buffer in states of metabolic acidosis, as the bone matrix demineralizes, leading to bone apatite dissolution and the release of phosphate, calcium, carbonate, and citrate into the circulation. The renal handling of calcium, phosphate and citrate is also affected, with resultant hypercalciuria, hyperphosphaturia and hypocitraturia.
Topics: Humans; Calcium; Kidney; Acidosis; Citric Acid; Kidney Diseases; Citrates; Calcium, Dietary; Phosphates
PubMed: 38396761
DOI: 10.3390/ijms25042081 -
Critical Care (London, England) Feb 2021Metabolic acidosis is a major complication of critical illness. However, its current epidemiology and its treatment with sodium bicarbonate given to correct metabolic... (Observational Study)
Observational Study
BACKGROUND
Metabolic acidosis is a major complication of critical illness. However, its current epidemiology and its treatment with sodium bicarbonate given to correct metabolic acidosis in the ICU are poorly understood.
METHOD
This was an international retrospective observational study in 18 ICUs in Australia, Japan, and Taiwan. Adult patients were consecutively screened, and those with early metabolic acidosis (pH < 7.3 and a Base Excess < -4 mEq/L, within 24-h of ICU admission) were included. Screening continued until 10 patients who received and 10 patients who did not receive sodium bicarbonate in the first 24 h (early bicarbonate therapy) were included at each site. The primary outcome was ICU mortality, and the association between sodium bicarbonate and the clinical outcomes were assessed using regression analysis with generalized linear mixed model.
RESULTS
We screened 9437 patients. Of these, 1292 had early metabolic acidosis (14.0%). Early sodium bicarbonate was given to 18.0% (233/1292) of these patients. Dosing, physiological, and clinical outcome data were assessed in 360 patients. The median dose of sodium bicarbonate in the first 24 h was 110 mmol, which was not correlated with bodyweight or the severity of metabolic acidosis. Patients who received early sodium bicarbonate had higher APACHE III scores, lower pH, lower base excess, lower PaCO, and a higher lactate and received higher doses of vasopressors. After adjusting for confounders, the early administration of sodium bicarbonate was associated with an adjusted odds ratio (aOR) of 0.85 (95% CI, 0.44 to 1.62) for ICU mortality. In patients with vasopressor dependency, early sodium bicarbonate was associated with higher mean arterial pressure at 6 h and an aOR of 0.52 (95% CI, 0.22 to 1.19) for ICU mortality.
CONCLUSIONS
Early metabolic acidosis is common in critically ill patients. Early sodium bicarbonate is administered by clinicians to more severely ill patients but without correction for weight or acidosis severity. Bicarbonate therapy in acidotic vasopressor-dependent patients may be beneficial and warrants further investigation.
Topics: APACHE; Acidosis; Aged; Australia; Female; Humans; Incidence; Intensive Care Units; Internationality; Japan; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate; Taiwan
PubMed: 33531020
DOI: 10.1186/s13054-020-03431-2 -
BMJ Case Reports Jan 2021A 75-year-old woman was admitted to a regional hospital with an acute kidney injury (AKI) and nausea on a background of recent treatment for bacteraemia secondary to...
A 75-year-old woman was admitted to a regional hospital with an acute kidney injury (AKI) and nausea on a background of recent treatment for bacteraemia secondary to pneumonia. The treatment thereof resulted in a high anion gap metabolic acidosis (HAGMA). The pneumonia was initially treated with intravenous piperacillin and tazobactam and the patient transferred to a tertiary hospital. There, the diagnosis of bacteraemia secondary to a pulmonary source was confirmed and treatment was changed to intravenous flucloxacillin and the patient was discharged to hospital in the home (HITH is a service that allows short-term healthcare at home to be provided to people who would otherwise need to be in hospital) to complete the antibiotic course. Five weeks after commencing flucloxacillin, the patient was referred back to hospital with nausea and worsening kidney function with an associated significant HAGMA. The patient has a background of chronic kidney disease and chronic back pain for which she was taking long-term paracetamol. The HAGMA was determined to be due to a pyroglutamic acidosis (PGA), deemed secondary to the combined use of paracetamol and flucloxacillin. This was subsequently confirmed with a plasma pyroglutamic acid concentration level of 7467 µmol/L (reference range 20-50 µmol/L) and a urinary level of 1700 mmol/mol creatinine (<110 mmol/mol creatinine). To our knowledge, this is the highest plasma and urinary levels published to date. Furthermore, considering the common use of paracetamol and penicillins, it is important to recognise HAGMA as a potential complication of co-administration of paracetamol and iso-oxylopenicillin. The HAGMA resolved after cessation of flucloxacillin despite the continuation of paracetamol and without administration of N-acetylcysteine. PGA-related HAGMA appears to be a unique potential side effect of iso-oxylopenicillin rather than other beta-lactams.
Topics: Acetaminophen; Acidosis; Acute Kidney Injury; Aged; Anti-Bacterial Agents; Antipyretics; Bacteremia; Female; Floxacillin; Humans; Pyrrolidonecarboxylic Acid; Staphylococcal Infections
PubMed: 33419747
DOI: 10.1136/bcr-2020-237536 -
Frontiers in Endocrinology 2022Hypoaldosteronism can be congenital or acquired, isolated or part of primary adrenal insufficiency, and caused by an aldosterone deficit, resistance, or a combination of...
INTRODUCTION
Hypoaldosteronism can be congenital or acquired, isolated or part of primary adrenal insufficiency, and caused by an aldosterone deficit, resistance, or a combination of both. Reduced mineralocorticoid action can induce a decrease in urine K+ and H+ excretion and an increase in urine Na+ excretion, leading to hyperkalemia, and/or hyponatremia, often combined with metabolic acidosis. We aimed to characterize the clinical manifestations of hypoaldosteronism, and their associated factors.
METHODS
Retrospective analysis of 112 episodes of hypoaldosteronism diagnosed in 86 adult patients from 2012-2019 by the Endocrinology and Nutrition Department of a tertiary hospital. The frequency of hyperkalemia, hypovolemic hyponatremia (HH) and metabolic acidosis (MA), and their associated factors were evaluated.
RESULTS
Patients had a median age of 77 [65 - 84], 55.4% were male. 94.6% cases showed hyperkalemia, 54.5% HH, and 60.3% MA. The mean serum K+ of all cases was 5.4 ± 0.5 mmol/L, Na+: 132.1 ± 6.3 mmol/L, HCO3: 22.6 ± 3.3 mmol/L. Hypoaldosteronism was isolated in the majority of cases: only 6/112 (5%) had primary adrenal insufficiency. Hypovolemia was associated with hyponatremia and a more florid clinical presentation. HH was associated with a combined presence of aldosterone-lowering and mineralocorticoid resistance factors. MA was associated with the presence of mineralocorticoid resistance factors.
CONCLUSIONS
Hypoaldosteronism in adult endocrinological clinical practice is primarily isolated, and acquired. It predisposes not only to the development of hyperkalemia and MA, but also to that of HH. Hypoaldosteronism must be considered in the differential diagnosis of HH with urinary sodium wasting.
Topics: Adult; Humans; Male; Female; Hypoaldosteronism; Hyperkalemia; Aldosterone; Hyponatremia; Mineralocorticoids; Addison Disease; Retrospective Studies; Sodium; Acidosis
PubMed: 36303866
DOI: 10.3389/fendo.2022.990148 -
Andrology Jan 2022Intracavernous pressure measurement following cavernous nerve electrostimulation has been extensively adopted for the evaluation of erectile function in animals....
BACKGROUND
Intracavernous pressure measurement following cavernous nerve electrostimulation has been extensively adopted for the evaluation of erectile function in animals. However, the effect of measurement time and acidosis during anesthesia is still lacking.
OBJECTIVE
To explore the effect of measurement time and acidosis during anesthesia.
MATERIALS AND METHODS
Fifty-six male Sprague-Dawley rats were used and anesthetized by a spontaneous inhalation of isoflurane. In the first step, rats were randomly divided into four groups: a control group and three time-delayed measurement groups (intracavernous pressure measurement beginning at 15, 30, and 45 min after cavernous nerve exposure). In the second step, rats were randomly divided into three groups: a control group and two time-delayed measurement groups. Two intravenous fluid support strategies were used in time-delayed measurement groups: a normal saline solution and an isotonic Na CO solution.
RESULTS
Isoflurane-anesthetized rats developed systemic acidosis that worsens with time during intracavernous pressure measurement, which results in a significant decrease in the maximum intracavernous pressure value, intracavernous pressure/mean arterial pressure ratio, and total intracavernous pressure measured. The Na CO infusion could effectively correct acidosis. The decrease in intracavernous pressure was related to the reduced nitric oxide synthase activity, decreased cyclic guanosine monophosphate concentration, and reactive oxygen species activation in rat penis under acidosis conditions.
DISCUSSION AND CONCLUSION
Prolonged isoflurane anesthesia-induced acidosis markedly depresses the erectile response to cavernous nerve electrostimulation in rats. In this situation, it is recommended to supplement with a Na CO infusion to maintain a normal acid-base balance.
Topics: Acidosis; Anesthetics, Inhalation; Animals; Arterial Pressure; Disease Models, Animal; Electric Stimulation; Erectile Dysfunction; Isoflurane; Male; Penile Erection; Penis; Rats; Rats, Sprague-Dawley
PubMed: 34333872
DOI: 10.1111/andr.13085 -
BMJ Case Reports Dec 2021Starvation ketoacidosis (SKA) is a rarer cause of ketoacidosis. Most patients will only have a mild acidosis, but if exacerbated by stress can result in a severe...
Starvation ketoacidosis (SKA) is a rarer cause of ketoacidosis. Most patients will only have a mild acidosis, but if exacerbated by stress can result in a severe acidosis. We describe a 66-year-old man admitted with reduced consciousness and found to have a severe metabolic acidosis with raised anion gap. His body mass index (BMI) was noted to be within the healthy range at 23 kg/m; however, it was last documented 1 year previously at 28 kg/m with no clear timeframe of weight loss. While his acidosis improved with intravenous fluids, he subsequently developed severe electrolyte imbalance consistent with refeeding during his admission. Awareness of SKA as a cause for high anion gap metabolic acidosis is important and knowledge of management including intravenous fluids, thiamine, dietetic input and electrolyte replacement is vital.
Topics: Acid-Base Equilibrium; Acidosis; Aged; Humans; Ketosis; Male; Refeeding Syndrome; Starvation; Water-Electrolyte Imbalance
PubMed: 34880037
DOI: 10.1136/bcr-2021-245065 -
British Journal of Hospital Medicine... Aug 2022Metabolic acidosis is a common complication among acutely unwell hospitalised patients. Untreated, it can result in undesirable cardiovascular, respiratory and...
Metabolic acidosis is a common complication among acutely unwell hospitalised patients. Untreated, it can result in undesirable cardiovascular, respiratory and neurological consequences. Metabolic acidosis can occur as an isolated entity or coexist with other acid-base disorders, making diagnosing the aetiology difficult. Accurate identification of the underlying cause is imperative for proper and timely management. A systematic approach can help simplify the assessment of patients and can aid in establishing the correct diagnosis, even in more complex cases. This article provides a practical, step-by-step guide for the assessment of adult patients with metabolic acidosis.
Topics: Acid-Base Equilibrium; Acidosis; Adult; Humans
PubMed: 36066292
DOI: 10.12968/hmed.2021.0582 -
Clinical Medicine (London, England) Mar 2024This review concerns the rare, acquired, usually iatrogenic, high-anion-gap metabolic acidosis, pyroglutamic acidosis. Pyroglutamate is a derivative of the amino acid... (Review)
Review
This review concerns the rare, acquired, usually iatrogenic, high-anion-gap metabolic acidosis, pyroglutamic acidosis. Pyroglutamate is a derivative of the amino acid glutamate, and is an intermediate in the 'glutathione cycle', by which glutathione is continuously synthesized and broken down. The vast majority of pyroglutamic acidosis cases occur in patients on regular, therapeutic doses of paracetamol. In about a third of cases, flucloxacillin is co-prescribed. In addition, the patients are almost always seriously unwell in other ways, typically with under-nourishment of some form. Paracetamol, with underlying disorders, conspires to divert the glutathione cycle, leading to the overproduction of pyroglutamate. Hypokalaemia is seen in about a third of cases. Once the diagnosis is suspected, it is simple to stop the paracetamol and change the antibiotic (if flucloxacillin is present), pending biochemistry. N-acetyl-cysteine can be given, but while the biochemical justification is compelling, the clinical evidence base is anecdotal.
Topics: Humans; Pyrrolidonecarboxylic Acid; Acetaminophen; Acidosis; Floxacillin; Anti-Bacterial Agents
PubMed: 38431210
DOI: 10.1016/j.clinme.2024.100030 -
Journal of Ayub Medical College,... 2020Blood gases can provide information about the perinatal, natal and postnatal condition of newborn. Severity of metabolic acidosis has deleterious effect on the outcome...
BACKGROUND
Blood gases can provide information about the perinatal, natal and postnatal condition of newborn. Severity of metabolic acidosis has deleterious effect on the outcome of babies. When the cord blood gases are not available the arterial blood gases are used for interpreting the status of newborn. The purpose of study was to determine the relationship between severity of metabolic acidosis at admission with the stage of hypoxic ischemic encephalopathy, and its outcome in asphyxiated neonates.
METHODS
This was descriptive cross-sectional study of 384 neonates born at ≥35 weeks to <42 weeks from June to December 2018, admitted in Neonatology department of the Children's hospital & the Institute of Child Health, Lahore within first 6 hours of birth. The neonates with history of delayed cry at birth and arterial pH ≤7.30 and base deficit ≥10 were included in the study. The pH and base deficit of babies was analyzed in relation to the stage of HIE, duration of stay and death or discharge of the babies using SPSS-20. The p-value was calculated using chi-square test.
RESULTS
Total of 470 neonates were eligible. Eighty-four neonates were excluded. Finally, 384 neonates were included and analyzed for the outcome variables. With severe metabolic acidosis pH <7.01, all the babies developed HIEII/III. Majority (82.1%) of the babies expired and 27.9% had prolonged hospital stay.
CONCLUSIONS
Increasing severity of metabolic acidosis at admission increases the likelihood of adverse outcome in asphyxiated neonates.
Topics: Acidosis; Asphyxia Neonatorum; Cross-Sectional Studies; Humans; Infant, Newborn; Patient Admission; Treatment Outcome
PubMed: 32583992
DOI: No ID Found -
Endocrine Journal Jul 2023Pseudohypoaldosteronism (PHA) type II (PHA2) is a genetic disorder that leads to volume overload and hyperkalemic metabolic acidosis. PHA2 and PHA type I (PHA1) have... (Review)
Review
Pseudohypoaldosteronism (PHA) type II (PHA2) is a genetic disorder that leads to volume overload and hyperkalemic metabolic acidosis. PHA2 and PHA type I (PHA1) have been considered to be genetic and pediatric counterparts to type IV renal tubular acidosis (RTA). Type IV RTA is frequently found in adults with chronic kidney disease and is characterized by hyperchloremic hyperkalemic acidosis with normal anion gap (AG). However, we recently observed that PHA1 was not always identical to type IV RTA. In this study, we focused on the acid-base balance in PHA2. Through a literature search published between 2008-2020, 46 molecularly diagnosed cases with PHA2 were identified (median age of 14 years). They comprised 11 sets of familial and 16 sporadic cases and the pathology was associated with mutations in WNK 4 (n = 1), KLHL3 (n = 17), and CUL3 (n = 9). The mean potassium (K) level was 6.2 ± 0.9 mEq/L (n = 46, range 4.0-8.6 mEq/L), whereas that of chloride (Cl) was 110 ± 3.5 mEq/L (n = 41, 100-119 mEq/L), with 28 of 41 cases identified as hyperchloremic. More than half of the cases (18/35) presented with metabolic acidosis. Although AG data was obtained only in 16 cases, all but one cases were within normal AG range. Both Cl and HCO3 levels showed significant correlations with K levels, which suggested that the degree of hyperchloremia and acidosis reflect the clinical severity, and is closely related to the fundamental pathophysiology of PHA2. In conclusion, our study confirmed that PHA2 is compatible with type IV RTA based on laboratory findings.
Topics: Adult; Humans; Child; Adolescent; Pseudohypoaldosteronism; Hypoaldosteronism; Acidosis; Mutation; Hyperkalemia
PubMed: 37081692
DOI: 10.1507/endocrj.EJ22-0607