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Electrolyte & Blood Pressure : E & BP Jun 2023Metabolic alkalosis is a common acid-base imbalance frequently observed in intensive care unit (ICU) patients and is associated with increased mortality.... (Review)
Review
Metabolic alkalosis is a common acid-base imbalance frequently observed in intensive care unit (ICU) patients and is associated with increased mortality. Post-hypercarbia alkalosis (PHA) is a type of metabolic alkalosis caused by sustained high serum bicarbonate levels following a rapid resolution of hypoventilation in patients with chronic hypercapnia due to prolonged respiratory disturbance. Common causes of chronic hypercapnia include chronic obstructive pulmonary disease (COPD), central nervous system disorders, neuromuscular disorders, and narcotic abuse. Rapid correction of hypercapnia through hyperventilation leads to a swift normalization of pCO, which lacks renal compensation, consequently causing an increase in plasma HCO levels and severe metabolic alkalosis. Most of PHA occurs in the ICU setting requiring mechanical ventilation and can progress severe alkalemia due to secondary mineralocorticoid excess from volume depletion or decreased HCO excretion from decreased glomerular filtration rate and increased proximal tubular reabsorption. PHA is associated with increased ICU stay, ventilator dependency, and mortality. Acetazolamide, a carbonic anhydrase inhibitor, has been utilized for managing PHA by inducing alkaline diuresis and reducing tubular reabsorption of bicarbonate. While acetazolamide effectively improves alkalemia, its impact on hard outcomes may be limited by factors such as patient complexity, co-administered medications, and underlying conditions contributing to alkalosis.
PubMed: 37434801
DOI: 10.5049/EBP.2023.21.1.18 -
Annals of Hepatology 2022In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the... (Review)
Review
In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the regulation of ABE is crucial because of its role in lactic acid metabolism, urea production and in protein homeostasis. The main acid-base imbalance that occurs in patients with liver cirrhosis is Respiratory Alkalosis (RAlk). Due to the fact that in these patients additional pathophysiological mechanisms that affect the ABE are present, other disorders may appear which compensate or enhance the primary disorder. Conventional ABE reading models fail to identify and assess the underlying disorders in patients with liver cirrhosis. This weakness of the classical models led to the creation of new physicochemical mathematical models that take into account all the known parameters that develop and affect the ABE. In addition to the RAlk, in patients with liver cirrhosis, metabolic alkalosis (due to hypoalbuminemia), hyponatremic metabolic acidosis, hyperchloremic metabolic acidosis, lactic acidosis and metabolic alkalosis due to urea metabolism are some of the pathophysiological mechanisms that affect the ABE.
Topics: Acidosis; Alkalosis; Humans; Liver Cirrhosis; Liver Diseases; Urea
PubMed: 35074477
DOI: 10.1016/j.aohep.2022.100675 -
Nature Communications May 2023The 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...
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 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 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.
Topics: Mice; Animals; Kidney; Membrane Transport Proteins; Acid-Base Equilibrium; Nephrons; Sulfate Transporters; Bicarbonates; Chloride-Bicarbonate Antiporters
PubMed: 37236964
DOI: 10.1038/s41467-023-38562-x -
F1000Research 2020The global pandemic secondary to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is leading to unprecedented global morbidity and mortality. With a... (Review)
Review
The global pandemic secondary to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is leading to unprecedented global morbidity and mortality. With a bewildering array of complications, renal involvement in various forms is common, including serum electrolyte derangements. Hypokalaemia secondary to SARS-CoV-2 was common in a reported Chinese cohort. Here we review the emerging evidence on hypokalaemia and SARS-CoV-2 infection, the potential pathophysiological mechanisms based on early clinical and histopathological data and important clinical implications. Mechanisms of hypokalaemia are multifactorial and so the electrolyte disturbance can be difficult to avoid. We provide further support to the theory of renin-angiotensin-aldosterone (RAS) activation, discuss the strengths and weaknesses of implicating RAS involvement and highlight the importance of calculating the transtubular potassium gradient to identify those at risk of hypokalaemia and its complications.
Topics: Humans; Aldosterone; Betacoronavirus; Coronavirus Infections; COVID-19; Electrolytes; Hypokalemia; Pandemics; Pneumonia, Viral; Potassium; Renin-Angiotensin System; SARS-CoV-2
PubMed: 33093945
DOI: 10.12688/f1000research.24441.2 -
BMJ Case Reports Dec 2019Congenital chloride diarrhoea is one of the rare causes of diarrhoea during infancy and it is infrequently reported throughout the world. It is an autosomal recessive...
Congenital chloride diarrhoea is one of the rare causes of diarrhoea during infancy and it is infrequently reported throughout the world. It is an autosomal recessive condition which is more prevalent in Poland, Finland, Saudi Arabia and Kuwait while rarely reported in Pakistan. Our patient was 7.5-month-old baby boy who presented with diarrhoea since neonatal period. He had consanguineous parents. On examination, baby had distended abdomen, hypotonia and hyporeflexia. Investigations revealed hypochloremic hypokalemic metabolic alkalosis. Urinary electrolytes were normal. Stool electrolytes revealed increased stool chloride excretion that confirmed our diagnosis of congenital chloride diarrhoea. Patient was treated with intravenous fluids and electrolyte replacement, followed by oral potassium and sodium replacement. He was also started on butyrate, cholestyramine and proton-pump inhibitors. He started gaining weight during his hospital admission and is being followed up in clinic.
Topics: Consanguinity; Diarrhea; Electrolytes; Feces; Fluid Therapy; Humans; Infant; Infant, Newborn; Male; Metabolism, Inborn Errors; Pakistan; Potassium; Sodium; Treatment Outcome; Weight Gain
PubMed: 31826900
DOI: 10.1136/bcr-2018-229012