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Current Opinion in Nephrology and... Mar 2013Most patients with chronic kidney disease (CKD) have progressive decline in glomerular filtration rate (GFR), despite current treatment practices. Recent studies support... (Review)
Review
PURPOSE OF REVIEW
Most patients with chronic kidney disease (CKD) have progressive decline in glomerular filtration rate (GFR), despite current treatment practices. Recent studies support that dietary acid reduction with oral sodium based alkali or base-inducing food types add kidney protection to that provided by current kidney-protective interventions. Related studies also support that correction of metabolic acidosis with dietary acid reduction slows CKD progression. We reviewed these recent studies that show improvement in CKD parameters and slower CKD progression in response to improvement of CKD-associated metabolic acidosis with these interventions.
RECENT FINDINGS
Animal as well as human models of CKD show that alkali treatment ameliorates indices of kidney injury and also might slow GFR decline in patients with or without metabolic acidosis. These benefits have been similar with oral sodium-based alkali and base-inducing fruits and vegetables, supporting dietary acid reduction as an effective adjunct to conventional kidney-protective interventions.
SUMMARY
Recent studies suggest that metabolic acidosis mediates nephropathy progression, and its treatment with the comparatively inexpensive and well tolerated intervention of dietary acid reduction holds promise to be an additional kidney-protective strategy in CKD management.
Topics: Acid-Base Equilibrium; Acidosis; Animals; Diet; Disease Progression; Fruit; Glomerular Filtration Rate; Humans; Kidney; Renal Insufficiency, Chronic; Sodium Bicarbonate; Time Factors; Treatment Outcome; Vegetables
PubMed: 23380803
DOI: 10.1097/MNH.0b013e32835dcbbe -
The Medical Clinics of North America Nov 2005Metabolic acidosis may arise from several drugs and toxins through a variety of mechanisms. Differentiating the causes of metabolic acidosis in the poisoned patient is... (Review)
Review
Metabolic acidosis may arise from several drugs and toxins through a variety of mechanisms. Differentiating the causes of metabolic acidosis in the poisoned patient is an indispensable skill in clinical practice. Comprehension of toxin-induced metabolic acidosis, combined with a thorough history, physical examination, appropriate use of laboratory tests, and a stepwise approach, should aid the clinician in determining the cause of metabolic acidosis in the poisoned patient. When confronted with such a patient, it is imperative that one administer appropriate antidotal therapy, when necessary, and provide the patient with exceptional supportive care.
Topics: Acidosis; Antidotes; Buffers; Drug-Related Side Effects and Adverse Reactions; Humans; Poisoning
PubMed: 16227056
DOI: 10.1016/j.mcna.2005.06.011 -
American Journal of Kidney Diseases :... Dec 2020Sodium bicarbonate is the mainstay treatment of the metabolic acidosis of chronic kidney disease but associated concerns center on administering sodium to patients with... (Review)
Review
Sodium bicarbonate is the mainstay treatment of the metabolic acidosis of chronic kidney disease but associated concerns center on administering sodium to patients with hypertension and sodium-retentive states. Veverimer (formerly referred to as TRC101), a drug candidate for which Tricida, Inc is seeking approval from the US Food and Drug Administration, is a novel nonabsorbable polymer that binds hydrogen cations and chloride anions in the gastrointestinal tract and then is excreted fecally, thereby increasing serum bicarbonate concentration without administering sodium. We examine the published evidence on the investigational use of veverimer in patients with chronic kidney disease and metabolic acidosis. We highlight the achieved increase in serum bicarbonate concentration without coadministering sodium, effects on physical functioning, and the safety record of the drug. We also scrutinize certain unanticipated findings: a lack of dose dependency in the increase in serum bicarbonate concentration observed and that despite the presumed large hydrogen chloride losses in feces, veverimer induces an isochloremic increase in serum bicarbonate concentration that is accompanied by a decrease in serum anion gap. We propose likely explanations for these puzzling findings and raise questions about veverimer's mode of action and its potential interaction with colonic bacterial flora. Additional work is required to fill these knowledge gaps that could have important clinical implications.
Topics: Acid-Base Imbalance; Acidosis; Disease Management; Humans; Polymers; Renal Insufficiency, Chronic
PubMed: 32920151
DOI: 10.1053/j.ajkd.2020.07.019 -
European Journal of Clinical Nutrition Aug 2020Not all metabolic acidosis is associated with an elevated chloride replacing the low bicarbonate concentration. When other acids, usually non-Cl organic acids are... (Review)
Review
Not all metabolic acidosis is associated with an elevated chloride replacing the low bicarbonate concentration. When other acids, usually non-Cl organic acids are introduced into the blood an "Anion Gap" metabolic acidosis exists. The serum anion gap is calculated as [Na+] - ([Cl] + [HCO]) = Unmeasured anions - Unmeasured cations. The normal gap is mostly due to negatively charged albumin: (Normal range: 8-12 meq/l) as the unmeasured anions, since albumin is usually reported in grams per liter (not meq/l). For diagnostic purposes, calculating the serum anion gap allows determination of coexisting acid-base processes in a patient. Assuming a 1:1 fall in bicarbonate compared with rise in anion gap in a usual gap acidosis, one can compare the Δ anion Gap/ΔHCO: Δ gap = observed anion gap - normal anion gap and the Δ HCO = normal HCO - observed HCO. A ratio of 1 suggests a simple anion gap acidosis; if <1 a superimposed non-gap acidosis is lowering HCO and if >1 a superimposed metabolic alkalosis is raising HCO. Comparing the anion gap and osmolar gap can narrow the differential diagnosis to include toxic alcohol ingestions with acidic metabolites such as ethylene glycol and methanol. Not all metabolic acidosis is associated with an elevated chloride replacing the low bicarbonate concentration. When other acids, usually non-Cl organic acids are introduced into the blood an "Anion Gap" metabolic acidosis exists. This review will consider the generation of anion-gap acidoses through case discussions.
Topics: Acid-Base Equilibrium; Acidosis; Anions; Humans
PubMed: 32873962
DOI: 10.1038/s41430-020-0685-5 -
Journal of Clinical Pharmacology Jun 1992Cholestyramine is a nonabsorbable anion exchange resin that is used predominantly for the treatment of hypercholesterolemia in adults and the management of acute... (Review)
Review
Cholestyramine is a nonabsorbable anion exchange resin that is used predominantly for the treatment of hypercholesterolemia in adults and the management of acute diarrhea in children. The authors report two cases of severe hyperchloremic nonanion gap metabolic acidosis associated with the use of cholestyramine therapy. The authors recommend that patients taking cholestyramine who have concomitant renal insufficiency or who are volume depleted or who are taking spironolactone be monitored carefully for the emergence of a hyperchloremic metabolic acidosis.
Topics: Acidosis; Chlorides; Cholestyramine Resin; Female; Humans; Male; Middle Aged
PubMed: 1634640
DOI: 10.1177/009127009203200608 -
Kidney International Jan 2021
Topics: Acidosis; Humans
PubMed: 33390235
DOI: 10.1016/j.kint.2020.07.051 -
The Veterinary Clinics of North... Mar 1990Metabolic acidosis is one of the prime factors responsible for the death of many diarrheic calves. This article begins with a general discussion about the recognition of... (Review)
Review
Metabolic acidosis is one of the prime factors responsible for the death of many diarrheic calves. This article begins with a general discussion about the recognition of metabolic acidosis. The remaining sections detail the utilization of certain subjective and objective methods to assess the severity of acidosis as well as the approach to treatment of this metabolic condition.
Topics: Acetates; Acidosis; Animals; Bicarbonates; Cattle; Cattle Diseases; Diarrhea; Fluid Therapy; Gluconates; Hydrogen-Ion Concentration; Lactates
PubMed: 2178740
DOI: 10.1016/s0749-0720(15)30892-6 -
The Canadian Veterinary Journal = La... Nov 2023Metabolic acidosis (MA) is the most common acid-base disorder reported in horses with colitis but its association with survival is yet to be determined.
BACKGROUND
Metabolic acidosis (MA) is the most common acid-base disorder reported in horses with colitis but its association with survival is yet to be determined.
OBJECTIVE
Investigate the types of MA in horses with colitis to determine effects of various anions on fatality rates.
ANIMALS AND PROCEDURES
We studied 158 horses with colitis. Horses were classified into 4 groups depending on the anion contributing to MA: i) no MA, ii) lactic acidosis (LA), iii) unmeasured strong ion (USI) acidosis, and iv) hyperchloremic acidosis (HA).
RESULTS
Sixty percent (95/158) of horses had no MA, 22% (34/158) had LA, 12% (19/158) had HA, and 6% (10/158) had USI acidosis. The fatality rate of horses without MA was 20% (20/95), whereas the rates for those with LA, USI, and HA were 53% (18/34), 30% (3/10), and 16% (3/19), respectively. Horses with LA were more likely to die or be euthanized than horses without MA (OR: 4.2, 95% CI: 1.83 to 9.72, < 0.001) and HA (OR: 5.9, 95% CI: 1.47 to 24.4, < 0.01).
CONCLUSION AND CLINICAL RELEVANCE
Lactic acidosis was the most common type of MA in horses with colitis, and it was associated with non-survival.
Topics: Animals; Horses; Acidosis, Lactic; Acidosis; Colitis; Horse Diseases
PubMed: 37915775
DOI: No ID Found -
Pediatric Nephrology (Berlin, Germany) Aug 2023
Topics: Infant, Newborn; Humans; Acidosis; Weight Loss
PubMed: 36598596
DOI: 10.1007/s00467-022-05845-2 -
Pediatric Nephrology (Berlin, Germany) Aug 2023
Topics: Infant, Newborn; Humans; Acidosis; Weight Loss
PubMed: 36598597
DOI: 10.1007/s00467-022-05847-0