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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 -
Journal of Pediatric Intensive Care Jun 2019Alkalosis is a disorder of acid-base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum... (Review)
Review
Alkalosis is a disorder of acid-base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum bicarbonate. Due to several mechanisms, it is often associated with hypochloremia and hypokalemia and can only persist in the presence of factors causing and maintaining alkalosis. Respiratory alkalosis is a consequence of dysfunction of respiratory system's control center. There are no pathognomonic symptoms. History is important in the evaluation of alkalosis and usually reveals the cause. It is important to evaluate volemia during physical examination. Treatment must be causal and prognosis depends on a cause.
PubMed: 31093455
DOI: 10.1055/s-0038-1676061 -
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 -
Clinical Kidney Journal Jun 2015In this paper we present an interesting case of acute kidney injury and severe metabolic alkalosis in a patient with a history of heavy heroin abuse. Urine microscopy...
In this paper we present an interesting case of acute kidney injury and severe metabolic alkalosis in a patient with a history of heavy heroin abuse. Urine microscopy showed numerous broomstick-like crystals. These crystals are also identified in light and electron microscopy. We hypothesize that heroin crystalizes in an alkaline pH, resulting in tubular obstruction and acute kidney injury. Management is mainly supportive as there is no known specific therapy for this condition. This paper highlights the utility of urine microscopy in diagnosing the etiology of acute kidney injury and proposes a novel disease called heroin crystal nephropathy.
PubMed: 26034599
DOI: 10.1093/ckj/sfv018 -
Electrolyte & Blood Pressure : E & BP Dec 2022Bartter syndrome (BS) is one of the most well-known hereditary tubular disorders, characterized by hypokalemic, hypochloremic metabolic alkalosis, and... (Review)
Review
Bartter syndrome (BS) is one of the most well-known hereditary tubular disorders, characterized by hypokalemic, hypochloremic metabolic alkalosis, and polyuria/polydipsia. This disease usually presents before or during infancy, and adult nephrologists often inherit the patients from pediatric nephrologists since this is a life-long condition. Here, a few case scenarios will be presented to recount how they first got diagnosed and how their clinical courses were during childhood until adulthood, in addition to a brief review of the disease and its treatment.
PubMed: 36688207
DOI: 10.5049/EBP.2022.20.2.49 -
Cureus Jan 2021Metabolic alkalosis is an increase in blood pH to >7.45 due to a primary increase in serum bicarbonate (HCO ). Metabolic alkalosis results from alkali accumulation or... (Review)
Review
Metabolic alkalosis is an increase in blood pH to >7.45 due to a primary increase in serum bicarbonate (HCO ). Metabolic alkalosis results from alkali accumulation or acid loss, and it is associated with a secondary increase in carbon dioxide arterial pressure (PCO). Metabolic alkalosis is a common acid-base disorder, especially in critically ill patients. The pathogenesis of chronic metabolic alkalosis includes two derangements, generation of metabolic alkalosis via gain of alkali or loss of acid and maintenance of metabolic alkalosis by increased tubular HCO reabsorption (failure of the kidneys to excrete excess alkali). Metabolic alkalosis is the most common acid-base disorder in hospitalized patients, particularly in the surgical critical care unit. Mortality increases as pH increases.
PubMed: 33628696
DOI: 10.7759/cureus.12841 -
European Annals of Otorhinolaryngology,... May 2023
Topics: Humans; Hyperventilation; Hydrogen-Ion Concentration
PubMed: 36609116
DOI: 10.1016/j.anorl.2022.12.005 -
American Journal of Translational... 2022Gitelman syndrome (GS) is an autosomal recessive salt-losing tubulopathy caused by biallelic inactivating mutations in the SLC12A3 gene. This gene encodes the... (Review)
Review
Gitelman syndrome (GS) is an autosomal recessive salt-losing tubulopathy caused by biallelic inactivating mutations in the SLC12A3 gene. This gene encodes the thiazide-sensitive sodium-chloride cotransporter (NCC) which is exclusively expressed in the distal convoluted tubules (DCT). GS patients classically present with hypokalemic metabolic alkalosis with hypocalciuria and hypomagnesemia. While hypokalemia and metabolic alkalosis are easily explained by effects of the genotypic defect in GS, the mechanisms by which hypomagnesemia and hypocalciuria develop in GS are poorly understood. In this review, we aim to achieve three major objectives. First, present a concise discussion about current understanding on physiologic calcium and magnesium handling in the DCT. Second, integrate expression data from studies on calciotropic and magnesiotropic proteins relevant to the GS disease state. Lastly, provide insights into the possible mechanisms of calcium-magnesium crosstalk relating to the co-occurrence of hypocalciuria and hypomagnesemia in GS models. Our analyses highlight specific areas of study that are valuable in elucidating possible molecular pathways of hypocalciuria and hypomagnesemia in GS.
PubMed: 35173827
DOI: No ID Found