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The Veterinary Clinics of North... Mar 2017Metabolic acidosis results from an increase in the concentration of a strong anion. Metabolic acidosis is divided into hyperchloremic metabolic acidosis and high anion... (Review)
Review
Metabolic acidosis results from an increase in the concentration of a strong anion. Metabolic acidosis is divided into hyperchloremic metabolic acidosis and high anion gap acidosis based on the changes in the anion gap. Hyperchloremic metabolic acidosis is the result of chloride retention, excessive loss of sodium relative to chloride, or excessive gain of chloride relative to sodium. Clinical signs are related to the underlying disease that accompanies the metabolic acidosis. Treatment of hyperchloremic acidosis is based on addressing the underlying disease process.
Topics: Acid-Base Equilibrium; Acidosis; Animals; Chlorides; Renal Insufficiency, Chronic
PubMed: 28017409
DOI: 10.1016/j.cvsm.2016.11.001 -
Nephron 2018The metabolism of a typical Western diet generates 50-100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance.... (Review)
Review
The metabolism of a typical Western diet generates 50-100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH4+) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH4+ excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studies suggest that the progressive decline in renal ammonium excretion in CKD is an important determinant of the ensuing systemic metabolic acidosis and is an independent factor for predicting the worsening of kidney function. While these studies have been primarily performed in hypertensive individuals with CKD, a closer look at renal NH4+ excretion in non-hypertensive individuals with CKD is warranted to ascertain its role in the progression of kidney disease.
Topics: Acid-Base Imbalance; Acidosis; Ammonium Compounds; Disease Progression; Humans; Renal Insufficiency, Chronic
PubMed: 29050011
DOI: 10.1159/000481892 -
Journal of Cachexia, Sarcopenia and... Dec 2023Metabolic acidosis unfavourably influences the nutritional status of patients with non-dialysis dependent chronic kidney disease (CKD) including the loss of muscle mass... (Meta-Analysis)
Meta-Analysis Review
Metabolic acidosis unfavourably influences the nutritional status of patients with non-dialysis dependent chronic kidney disease (CKD) including the loss of muscle mass and functionality, but the benefits of correction are uncertain. We investigated the effects of correcting metabolic acidosis on nutritional status in patients with CKD in a systematic review and meta-analysis. A search was conducted in MEDLINE and the Cochrane Library from inception to June 2023. Study selection, bias assessment, and data extraction were independently performed by two reviewers. The Cochrane risk of bias tool was used to assess the quality of individual studies. We applied random effects meta-analysis to obtain pooled standardized mean difference (SMD) and 95% confidence intervals (CIs). We retrieved data from 12 intervention studies including 1995 patients, with a mean age of 63.7 ± 11.7 years, a mean estimated glomerular filtration rate of 29.8 ± 8.8 mL/min per 1.73 m , and 58% were male. Eleven studies performed an intervention with oral sodium bicarbonate compared with either placebo or with standard care and one study compared veverimer, an oral HCl-binding polymer, with placebo. The mean change in serum bicarbonate was +3.6 mEq/L in the intervention group and +0.4 mEq/L in the control group. Correcting metabolic acidosis significantly improved muscle mass assessed by mid-arm muscle circumference (SMD 0.35 [95% CI 0.16 to 0.54], P < 0.001) and functionality assessed with the sit-to-stand test (SMD -0.31 [95% CI -0.52 to 0.11], P = 0.003). We found no statistically significant effects on dietary protein intake, handgrip strength, serum albumin and prealbumin concentrations, and blood urea nitrogen. Correcting metabolic acidosis in patients with CKD improves muscle mass and physical function. Correction of metabolic acidosis should be considered as part of the nutritional care for patients with CKD.
Topics: Humans; Male; Middle Aged; Aged; Female; Dietary Proteins; Hand Strength; Renal Insufficiency, Chronic; Acidosis; Muscles
PubMed: 37728018
DOI: 10.1002/jcsm.13330 -
Emergency Medicine Clinics of North... May 2022Numerous drugs and toxins can cause metabolic acidosis. The treating clinician should be aware of the many compounds that can produce metabolic acidosis following an... (Review)
Review
Numerous drugs and toxins can cause metabolic acidosis. The treating clinician should be aware of the many compounds that can produce metabolic acidosis following an accidental exposure, an overdose, or with therapeutic use. Awareness and comprehension of those substances associated with metabolic acidosis will facilitate the diagnosis and treatment of poisoned patients.
Topics: Acidosis; Causality; Drug Overdose; Humans; Poisons
PubMed: 35461622
DOI: 10.1016/j.emc.2022.01.002 -
Pediatric Nephrology (Berlin, Germany) Dec 2023Metabolic acidosis is a risk factor for faster kidney function decline in chronic kidney disease (CKD) and in adult kidney transplant recipients (KTRs). We hypothesized...
BACKGROUND
Metabolic acidosis is a risk factor for faster kidney function decline in chronic kidney disease (CKD) and in adult kidney transplant recipients (KTRs). We hypothesized that metabolic acidosis would be highly prevalent and associated with worse allograft function in pediatric KTRs.
METHODS
Pediatric KTRs at Montefiore Medical Center from 2010 to 2018 were included. Metabolic acidosis was defined as serum bicarbonate < 22 mEq/L or receiving alkali therapy. Regression models were adjusted for demographic factors and donor/recipient characteristics.
RESULTS
Sixty-three patients were identified with a median age at transplant of 10.5 (interquartile range (IQR) 4.4-15.2) years and post-transplant follow-up of 3 (IQR 1-5) years. Baseline serum bicarbonate was 21.7 ± 2.4 mEq/L, serum bicarbonate < 22 mEq/L was present in 28 (44%), and 44% of all patients were receiving alkali therapy. The prevalence of acidosis ranged from 58 to 70% during the first year of follow-up. At baseline, each 1-year higher age at transplant and every 10 ml/min/1.73 m higher eGFR were associated with 0.16 mEq/L (95% CI: 0.03-0.3) and 0.24 mEq/L (95% CI: 0.01-0.5) higher serum bicarbonate, respectively. Older age at transplant was associated with lower odds of acidosis (OR: 0.84; 95% CI: 0.72-0.97). During follow-up, metabolic acidosis was independently associated with 8.2 ml/min/1.73 m (95% CI 4.4-12) lower eGFR compared to not having acidosis; furthermore, eGFR was significantly lower among KTRs with unresolved acidosis compared with resolved acidosis.
CONCLUSIONS
Among pediatric KTRs, metabolic acidosis was highly prevalent in the first year post-transplantation and was associated with lower eGFR during follow-up. A higher resolution version of the Graphical abstract is available as Supplementary information.
Topics: Adult; Humans; Child; Child, Preschool; Adolescent; Kidney Transplantation; Bicarbonates; Acidosis; Renal Insufficiency, Chronic; Transplant Recipients; Alkalies
PubMed: 37422606
DOI: 10.1007/s00467-023-06072-z -
Reviews in Endocrine & Metabolic... Aug 2023Interpretation of existing data revealed that chronic metabolic acidosis is a pathognomic feature for type 2 diabetes (T2D), which is described here as "chronic... (Review)
Review
Interpretation of existing data revealed that chronic metabolic acidosis is a pathognomic feature for type 2 diabetes (T2D), which is described here as "chronic metabolic acidosis of T2D (CMAD)" for the first time. The biochemical clues for the CMAD are summarised in the following; low blood bicarbonate (high anionic gap), low pH of interstitial fluid and urine, and response to acid neutralization, while the causes of extra protons are worked out to be; mitochondrial dysfunction, systemic inflammation, gut microbiota (GM), and diabetic lung. Although, the intracellular pH is largely preserved by the buffer system and ion transporters, a persistent systemic mild acidosis leaves molecular signature in cellular metabolism in diabetics. Reciprocally, there are evidences that CMAD contributes to the initiation and progression of T2D by; reducing insulin production, triggering insulin resistance directly or via altered GM, and inclined oxidative stress. The details about the above clues, causes and consequences of CMAD are obtained by searching literature spanning between 1955 and 2022. Finally, the molecular bases of CMAD are discussed in details by interpretation of an up-to-date data and aid of well constructed diagrams, with a conclusion unravelling that CMAD is a major player in T2D pathophysiology. To this end, the CMAD disclosure offers several therapeutic potentials for prevention, delay or attenuation of T2D and its complications.
Topics: Humans; Chronic Disease; Diabetes Mellitus, Type 2; Acidosis; Hydrogen-Ion Concentration; Extracellular Space; Ion Transport; Gastrointestinal Microbiome
PubMed: 37380824
DOI: 10.1007/s11154-023-09816-2 -
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 -
Advances in Chronic Kidney Disease Jul 2022Human kidneys are well adapted to excrete the daily acid load from diet and metabolism in order to maintain homeostasis. In approximately 30% of patients with more... (Review)
Review
Human kidneys are well adapted to excrete the daily acid load from diet and metabolism in order to maintain homeostasis. In approximately 30% of patients with more advanced stages of CKD, these homeostatic processes are no longer adequate, resulting in metabolic acidosis. Potential deleterious effects of chronic metabolic acidosis in CKD, including muscle wasting, bone demineralization, hyperkalemia, and more rapid progression of CKD, have been well cataloged. Based primarily upon concerns related to nutrition and bone disease, early Kidney Disease Outcomes Quality Initiative guidelines recommended treating metabolic acidosis with alkali therapy targeting a serum bicarbonate ≥22 mEq/L. More recent guidelines have suggested similar targets based upon potential slowing of CKD progression. However, appropriately powered, long-term, randomized controlled trials to study efficacy and safety of alkali therapy for these outcomes are largely lacking. As a result, practice among physicians varies, underscoring the complexity of treatment of chronic metabolic acidosis in real-world CKD practice. Novel treatment approaches and rigorous phase 3 trials may resolve some of this controversy in the coming years. Metabolic acidosis is an important complication of CKD, and where it "falls" in the priority schema of CKD care will depend upon the generation of strong clinical evidence.
Topics: Acidosis; Alkalies; Bicarbonates; Humans; Kidney; Renal Insufficiency, Chronic
PubMed: 36175070
DOI: 10.1053/j.ackd.2022.05.002 -
The Journal of Surgical Research Oct 2023Very low-calorie diets (VLCDs) are used preoperatively in bariatric-metabolic surgery; however, this can lead to physiological ketosis. Euglycemic ketoacidosis is an... (Clinical Trial)
Clinical Trial
INTRODUCTION
Very low-calorie diets (VLCDs) are used preoperatively in bariatric-metabolic surgery; however, this can lead to physiological ketosis. Euglycemic ketoacidosis is an increasingly recognized complication in diabetic patients on sodium-glucose-cotransporter-2 inhibitors (SGLT2i) undergoing surgery and requires assessment of ketones for diagnosis and monitoring. VLCD induced ketosis may confound monitoring in this group. We aimed to evaluate the influence of VLCD, compared to standard fasting, on perioperative ketone levels and acid-base balance.
MATERIALS AND METHODS
Twenty-seven patients were prospectively recruited to the intervention group and 26 to the control group from two tertiary referral centres in Melbourne, Australia. Intervention group patients were severely obese (body mass index) (BMI) (≥35), undergoing bariatric-metabolic surgery, and prescribed 2 wk of VLCD preoperatively. Control group patients underwent general surgical procedures and prescribed standard procedural fasting only. Patients were excluded if diabetic or prescribed SGLT2i. Ketone and acid-base measurements were taken at regular intervals. Univariate and multivariate regression was utilised with significance defined as P < 0.005.
CLINICALTRIALS
gov ID: NCT05442918.
RESULTS
Patients on VLCD, compared to standard fasting, had an increased median preoperative (0.60 versus 0.21 mmol/L), immediate postoperative (0.99 versus 0.34 mmol/L) and day 1 postoperative (0.69 versus 0.21 mmol/L) ketone level (P < 0.001). Preoperative acid-base balance was normal in both groups, however VLCD patients were found to have a metabolic acidosis immediately postoperatively (pH 7.29 versus pH 7.35) (P = 0.019). Acid-base balance had normalized in VLCD patients on postoperative day 1.
CONCLUSIONS
Preoperative VLCD resulted in increased pre- and postoperative ketone levels with immediate postoperative values consistent with metabolic ketoacidosis. This should be considered particularly when monitoring diabetic patients prescribed SGLT2i.
Topics: Humans; Acidosis; Caloric Restriction; Diabetes Mellitus, Type 2; Ketones; Ketosis; Obesity
PubMed: 37271067
DOI: 10.1016/j.jss.2023.05.001 -
Kidney360 Apr 2022People with sickle cell disease (SCD) have an elevated estimated glomerular filtration rate (eGFR) compared with the general population, and this may alter the usual...
BACKGROUND
People with sickle cell disease (SCD) have an elevated estimated glomerular filtration rate (eGFR) compared with the general population, and this may alter the usual creatinine-based eGFR cutoffs for which physiologic evidence of kidney dysfunction is apparent. This study aimed to identify eGFR thresholds for hyperkalemia and metabolic acidosis in patients with SCD.
METHODS
This was a cross-sectional analysis of 733 patients with severe (hemoglobin SS or S-thalassemia) SCD genotype, 238 patients with moderate (hemoglobin SC or S-thalassemia) SCD genotype, and 1333 age- and sex-matched African Americans from the National Health and Nutrition Examination Survey (NHANES). The prevalence rates of hyperkalemia and metabolic acidosis were compared by eGFR category. Cutoffs for hyperkalemia and metabolic acidosis were determined using generalized additive models.
RESULTS
Hyperkalemia and metabolic acidosis were more common in those with severe SCD genotype (13% and 21%, respectively) compared with the NHANES (0.3% and 5%, respectively); the prevalence rates in the moderate SCD genotype were intermediate for hyperkalemia (3%) and metabolic acidosis (11%). The proportion of patients with hyperkalemia and metabolic acidosis progressively increased with lower eGFR category in both SCD genotype groups. The eGFR thresholds for hyperkalemia and metabolic acidosis were higher in the severe (85 and 91 ml/min per 1.73 m, respectively) and moderate (52 and 102 ml/min per 1.73 m, respectively) SCD genotypes compared with the NHANES (34 and 46 ml/min per 1.73 m).
CONCLUSIONS
We demonstrate that hyperkalemia and metabolic acidosis are more common and occur at higher eGFR values in patients with SCD compared with age- and sex-matched African Americans, including in eGFR ranges considered to be normal. Future studies using redefined creatinine-based eGFR thresholds for abnormal kidney function may identify high-risk patients for earlier intervention strategies and referral for specialized renal care in SCD.
Topics: Acidosis; Anemia, Sickle Cell; Creatinine; Cross-Sectional Studies; Glomerular Filtration Rate; Humans; Hyperkalemia; Nutrition Surveys
PubMed: 35721605
DOI: 10.34067/KID.0006802021