oxalates and Acidosis

A variety of genetic, mechano-response-related, endocrine-metabolic, and nutritional determinants impact bone health. Among the nutritional influences, protein intake and dietary acid load are two of the factors most controversially discussed. Although in the past high protein intake was often assumed to exert a primarily detrimental impact on bone mass and skeletal health, the majority of recent studies indicates the opposite and suggests a bone-anabolic influence. Studies examining the influence of alkalizing diets or alkalizing supplement provision on skeletal outcomes are less consistent, which raises doubts about the role of acid-base status in bone health. The present review critically evaluates relevant key issues such as acid-base terminology, influencing factors of intestinal calcium absorption, calcium balance, the endocrine-metabolic milieu related to metabolic acidosis, and some methodological aspects of dietary exposure and bone outcome examinations. It becomes apparent that for an adequate identification and characterization of either dietary acid load's or protein's impact on bone, the combined assessment of both nutritional influences is necessary.

Topics: Acid-Base Equilibrium; Acidosis; Bone and Bones; Bone Density; Calcium; Calcium, Dietary; Diet; Dietary Fiber; Dietary Proteins; Humans; Hydrogen-Ion Concentration; Intestinal Absorption; Nutritional Physiological Phenomena; Oxalates

Topics: Acidosis; Case Management; Comorbidity; Diet Therapy; Drug-Related Side Effects and Adverse Reactions; Environment; Humans; Kidney Calculi; Oxalates; Pain Management; Risk Factors; Secondary Prevention; Tomography, X-Ray Computed; Uric Acid; Urologic Surgical Procedures

Whereas the etiology of urinary calculi and their metabolic exploration should be known, it appears unreasonable to conduct exhaustive metabolic explorations in all patients, therapy being usually symptomatic and based on advice on hygiene and diet. However, etiologic diagnosis is essential in a small number of cases: those which could benefit from effective preventive and curative measures and for which morbidity is elevated: cystinuria, hyperparathyroidism, uric acid calculi, patients at high developmental risks. It is possible, by simple, low cost means to select 95% of these patients. After a theoretical study of the distribution and lithiasic etiology, a practical conduct is proposed which takes into account the cost-effective ratio.

Topics: Acidosis; Calcium; Citrates; Cystinuria; Humans; Hypercalcemia; Hyperparathyroidism; Intestinal Absorption; Kidney Calices; Osteoporosis; Oxalates; Sarcoidosis; Uric Acid; Urinary Calculi

Although acute poisoning with ethylene glycol (EG) used in antifreeze mixtures is well known in man, only a few reports have described acute intoxication with diethylene glycol (DEG) and only one has mentioned oxaluria. Furthermore, there is no experimental evidence that DEG is metabolized into oxalate. The ability of ethanol infusions to prevent hepatic oxidation of DEG has not been proved. Moreover, failure of this treatment has been reported by some authors. In order to resolve such questions, Wistar male adult rats possessing a hepatic alcohol deshydrogenase were given a single oral dose of 15 ml/kg-1 DEG. Rats were either untreated or treated with hydration alone or associated with bicarbonate or ethanol. Urinary output, urinary oxalate excretion, acid-base balance in peripheral blood and renal histology were studied. Acute poisoning induced metabolic acidosis, polyuria, hyperoxaluria with renal tubular necrosis and a 66% mortality. Massive hydration improved acidosis and prognosis, but mortality and renal lesions were avoided only when bicarbonate or ethanol were added. Only ethanol significantly decreased oxaluria. In acute DEG poisoning, both the mechanism and the treatment appear to be the same as in acute EG intoxication.

Topics: Acidosis; Acute Kidney Injury; Animals; Ethylene Glycols; Humans; Kidney; Lethal Dose 50; Male; Oxalates; Prognosis; Rats; Rats, Inbred Strains

Anion gap metabolic acidosis (AGMA) is common in patients presenting for emergency care. While some disease processes and ingestions are easily excluded, diagnosing toxic alcohol (TA) ingestion can be challenging. This is especially true if drug concentrations are not readily available, which forces clinicians to rely on surrogate markers. Like TA ingestion, alcoholic ketoacidosis (AKA) produces an elevated osmol gap and an AGMA. The aim of this study was to identify risk factors suggestive of AKA when TA ingestion was the primary alternative differential diagnosis. We hypothesized that the odds of an AKA diagnosis would increase as ethanol concentration increased.. This was a retrospective analysis of data from 2000 through 2019 from a single US Poison Control Center. Records were reviewed to identify cases coded as "methanol" or "ethylene glycol"; or coded as "alcohol" or "ethanol with acidosis." The case definition for AKA required: (1) documented alcohol use disorder; (2) urine or serum ketones or elevated blood beta-hydroxybutyrate concentration; (3) anion gap ≥ 14 mmol/L. The inclusion criterion for TAs was a detectable methanol or ethylene glycol concentration.. In this retrospective analysis, the odds of diagnosing AKA instead of TA ingestion increased as ethanol concentration increased. The limited ability of common clinical factors to differentiate these diagnoses highlights the need to obtain quantitative TA concentrations in real time. Until prospective validation, interpretation of ketone concentrations and toxic alcohol concentrations (when available) will continue to guide decision making.

Topics: Acidosis; Adolescent; Adult; Aged; Alcoholic Intoxication; Child; Child, Preschool; Ethanol; Ethylene Glycol; Female; Humans; Infant; Ketosis; Lactic Acid; Male; Methanol; Middle Aged; New York City; Oxalates; Retrospective Studies; Risk Factors; Young Adult

In rats, we recently showed how a chronic metabolic acidosis simultaneously reduced urinary oxalate excretion and promoted oxalate secretion by the distal colon leading to the proposition that acid-base disturbances may trigger changes to renal and intestinal oxalate handling. The present study sought to reproduce and extend these observations using the mouse model, where the availability of targeted gene knockouts (KOs) would offer future opportunities to reveal some of the underlying transporters and mechanisms involved. Mice were provided with a sustained load of acid (NH

Topics: Acetazolamide; Acidosis; Ammonium Chloride; Animals; Carbonic Anhydrase Inhibitors; Carbonic Anhydrases; Disease Models, Animal; Female; Homeostasis; Humans; Intestinal Mucosa; Kidney; Kidney Calculi; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Oxalates; Rats; Renal Elimination; Species Specificity

Urinary oxalate excretion is reduced in rats during a chronic metabolic acidosis, but how this is achieved is not clear. In this report, we re-examine our prior work on the effects of a metabolic acidosis on urinary oxalate handling [Green et al., Am J Physiol Ren Physiol 289(3):F536-F543, 2005], offering a more detailed analysis and interpretation of the data, together with new, previously unpublished observations revealing a marked impact on intestinal oxalate transport. Sprague-Dawley rats were provided with 0.28 M ammonium chloride in their drinking water for either 4 or 14 days followed by 24 h urine collections, blood-gas and serum ion analysis, and measurements of (14)C-oxalate fluxes across isolated segments of the distal colon. Urinary oxalate excretion was significantly reduced by 75% after just 4 days compared to control rats, and this was similarly sustained at 14 days. Oxalate:creatinine clearance ratios indicated enhanced net re-absorption of oxalate by the kidney during a metabolic acidosis, but this was not associated with any substantive changes to serum oxalate levels. In the distal colon, oxalate transport was dramatically altered from net absorption in controls (6.20 ± 0.63 pmol cm(-2) h(-1)), to net secretion in rats with a metabolic acidosis (-5.19 ± 1.18 and -2.07 ± 1.05 pmol cm(-2) h(-1) at 4 and 14 days, respectively). Although we cannot rule out modifications to bi-directional oxalate movements along the proximal tubule, these findings support a gut-kidney axis in the management of oxalate homeostasis, where this shift in renal handling during a metabolic acidosis is associated with compensatory adaptations by the intestine.

Topics: Acidosis; Animals; Calcium; Chlorides; Colon; Creatinine; Male; Oxalates; Random Allocation; Rats, Sprague-Dawley

We have adapted automated assays for quantification of pyruvate (PYR), acetoacetate (AA), and betahydroxybutyrate (BOHB) in plasma, total acid phosphatase (TAP), angiotensin converting enzyme (ACE) and fructosamine (FRUCT) in serum, and oxalate (OXAL) and citrate (CIT) in urine that can be performed on the ABX Pentra 400. The aim of this study was to evaluate the analytical performances of these parameters and to compare data obtained in patient samples with those obtained with the Cobas Mira. Within-run and between-run imprecisions ranged from 0.55 to 14.2 and 0.37 to 11.8%, respectively. Correlations with the Cobas Mira showed r2 coefficients ranging from 0.816 to 0.983 and linear regression slopes from 0.706 to 1.087. The ABX Pentra 400 provides precise and accurate measurement for a wide variety of analytes including PYR, AA, BOHB, TAP, ACE, FRUCT in blood samples and OXAL, CIT in urine.

Topics: Acid Phosphatase; Acidosis; Blood Chemical Analysis; Citrates; Fructosamine; Humans; Oxalates; Peptidyl-Dipeptidase A

Ethylene glycol (EG) consumption is commonly employed as an experimental regimen to induce hyperoxaluria in animal models of calcium oxalate nephrolithiasis. This approach has, however, been criticized because EG overdose induces metabolic acidosis in humans. We tested the hypothesis that EG consumption (0.75% in drinking water for 4 wk) induces metabolic acidosis by comparing arterial blood gases, serum electrolytes, and urinary chemistries in five groups of Sprague-Dawley rats: normal controls (CON), those made hyperoxaluric (HYP) with EG administration, unilaterally nephrectomized controls (UNI), unilaterally nephrectomized rats fed EG (HRF), and a metabolic acidosis (MA) reference group imbibing sweetened drinking water (5% sucrose) containing 0.28 M NH4Cl. Arterial pH, plasma bicarbonate concentrations, anion gap, urinary pH, and the excretion of titratable acid, ammonium, phosphate, citrate, and calcium in HYP rats were not significantly different from CON rats, indicating that metabolic acidosis did not develop in HYP rats with two kidneys. Unilateral nephrectomy alone (UNI group) did not significantly affect arterial pH, plasma bicarbonate, anion gap, or urinary pH compared with CON rats; however, HRF rats exhibited some signs of a nascent acidosis in having an elevated anion gap, higher phosphate excretion, lower urinary pH, and an increase in titratable acid. Frank metabolic acidosis was observed in the MA rats: decreased arterial pH and plasma HCO3(-) concentration with lower urinary pH and citrate excretion with elevated excretion of ammonium, phosphate and, hence, titratable acid. We conclude that metabolic acidosis does not develop in conventional EG treatments but may ensue with renal insufficiency resulting from an oxalate load.

Topics: Acidosis; Animals; Carbon Dioxide; Disease Models, Animal; Electrolytes; Ethylene Glycol; Hyperoxaluria; Kidney Calculi; Kidney Failure, Chronic; Kidney Function Tests; Male; Oxalates; Oxygen; Rats; Rats, Sprague-Dawley

Topics: Acidosis; Bicarbonates; Coma; Ethylene Glycol; Ethylene Glycols; Humans; Male; Middle Aged; Osmolar Concentration; Oxalates; Renal Dialysis; Sodium; Sodium Bicarbonate

The role of the vitamins of the B group in the therapy of metabolic diseases has been the theme of a recent symposium. All these vitamins exert essential functions in the balance of the intermediary metabolism and consequently in the treatment of their disorders. As far as metabolic diseases and the use of vitamins, i.e. of biological substances, are concerned, the boundaries between the fields of therapy and prophylaxis are difficult to settle strictly. The recent literature concerning these points is reviewed and some concepts discussed.

Topics: Acidosis; Homocystinuria; Humans; Hyperglycemia; Ketosis; Metabolic Diseases; Oxalates; Vitamin B Complex

Topics: Acidosis; Amino Acids; Anthraquinones; Child; Female; Humans; Male; Oxalates; Plants, Medicinal; Rheum; Seasons

The causes of, and physiopathological factors underlying the most common metabolic disorders implicated in the formation of renal stones are reviewed. These include hypercalciuria, hyperoxaluria, renal tubular acidosis, cystinuria and disturbances of purine metabolism. Apart from metabolic disorders the risk of stone formation is also influenced by a low inhibitor activity in urine. Though some aspects in the pathogenesis of urolithiasis remain uncertain, the exact knowlege of important aetiological factors of stone formation is the basis of correct treatment and the prevention of recurrence of urinary calculi.

Topics: Acidosis; Adult; Calcium; Cystinuria; Humans; Kidney Tubules; Male; Oxalates; Purine-Pyrimidine Metabolism, Inborn Errors; Uric Acid; Urinary Calculi; Urography

The definition of lactate acidosis (lactic acidosis) is discussed. The metabolism of lactate and pyruvate are described. An increase in lactate concentration should be called lactic acidemia (lactate emia). This increase in lactate concentration can be caused either by an increased production (primarily by the so-called peripheral tissues) or by a decreased utilization (by the liver or by the kidneys). Therefore, various metabolic alterations can cause lactate acidosis.

Topics: Acidosis; Gluconeogenesis; Humans; Lactates; Liver; Malate Dehydrogenase; Oxalates; Oxidative Phosphorylation; Pyruvates

A case of massive ingestion of ethylene glycol is described. The clinical characteristics of this disorder such as persistent metabolic acidosis and oxaluria as well as changes in serum osmolality that may accompany ingestion of certain toxins are emphasized. The rapid clearance of ethylene glycol from the blood during hemodialysis is noted and the use of ethyl alcohol to block metabolic conversion of ethylene glycol to oxalic acid, which is also a toxin, is described. The importance of early diagnosis and therapy is stressed.

Topics: Acidosis; Bicarbonates; Ethylene Glycols; Humans; Kidney Tubules; Male; Middle Aged; Oxalates

Topics: Acidosis; Ascorbic Acid; Blood; Cholesterol; Gastrointestinal Diseases; Glycosuria; Humans; Hydrogen-Ion Concentration; Hyperglycemia; Kidney Calculi; Oxalates; Prothrombin; Vitamin B 12

Topics: Acidosis; Acute Kidney Injury; Adult; Aldehydes; Blood Urea Nitrogen; Brain; Brain Diseases; Ethylenes; Glycols; Glyoxylates; Heart Failure; Humans; Lung Diseases; Male; Oxalates; Poisoning

Topics: Acidosis; Adult; Aged; Alcoholism; Bicarbonates; Coma; Dialysis; Ethylenes; Female; Glycols; Humans; Intubation; Male; Mental Disorders; Oxalates; Poisoning; Respiration, Artificial; Tromethamine

Topics: Acidosis; Animals; Chemical and Drug Induced Liver Injury; Fructose; Humans; Lactates; Oxalates; Parenteral Nutrition; Pyruvates; Rats; Sorbitol; Uric Acid; Xylitol

Topics: Acidosis; Adolescent; Adult; Aged; Anuria; Bicarbonates; Calcium; Carbon Dioxide; Chemical and Drug Induced Liver Injury; Chemical Phenomena; Chemistry; Female; Humans; Hydrogen-Ion Concentration; Liver; Male; Middle Aged; Neurologic Manifestations; Nitrogen; Oxalates; Parenteral Nutrition; Solutions; Uremia; Uric Acid; Water-Electrolyte Balance; Xylitol

Topics: Acidosis; Amino Acid Metabolism, Inborn Errors; Amino Acids; Child; Child, Preschool; Glutamates; Glycine; Glyoxylates; Humans; Infant; Intelligence; Leucine; Male; Osteoporosis; Oxalates; Psychomotor Disorders; Serine

Topics: Acidosis; Alkalosis; Animals; Bicarbonates; Calcium; Citrates; Diuresis; Dogs; Female; Hydrochloric Acid; Male; Oxalates; Parathyroid Glands; Sodium; Sodium Chloride

Topics: Acidosis; Amino Acid Metabolism, Inborn Errors; Carbon Dioxide; Carbon Isotopes; Child; Child, Preschool; Female; Glycine; Glyoxylates; Humans; Male; Oxalates; Serine

Topics: Acidosis; Brain Edema; Child; Child, Preschool; Ethanol; Female; Glycols; Humans; Injections, Intravenous; Male; Oxalates; Peritoneal Dialysis

Topics: Acidosis; Amino Acid Metabolism, Inborn Errors; Body Weight; Creatinine; Female; Glycine; Glyoxylates; Humans; Infant; Male; Oxalates

Topics: Acidosis; Alkalosis; Animals; Bicarbonates; Dogs; Endocrinology; Hypocalcemia; Oxalates; Parathyroid Glands; Pharmacology; Research; Toxicology

Topics: Acidosis; Alkalies; Humans; Hyperparathyroidism; Kidney Calculi; Lithiasis; Milk; Nephrolithiasis; Osteoporosis; Oxalates; Sarcoidosis; Urinary Tract Infections; Vitamin D

Topics: Acidosis; Chlorides; Humans; Hyperoxaluria; Oxalates

Topics: Acidosis; Alkalosis; Diagnostic Techniques, Urological; Humans; Kidney; Kidney Diseases; Oxalates