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The American Journal of Case Reports Sep 2022BACKGROUND Milk-alkali syndrome is caused by excessive consumption of calcium and absorbable alkali and typically presents as a triad of hypercalcemia, acute renal...
BACKGROUND Milk-alkali syndrome is caused by excessive consumption of calcium and absorbable alkali and typically presents as a triad of hypercalcemia, acute renal failure, and metabolic alkalosis. In the era of histamine receptor blockers and proton pump inhibitors, the incidence of milk-alkali syndrome has decreased. However, the disease has not been eliminated, due to existing calcium-containing therapies. Here, we present a case of severe milk-alkali syndrome with a challenging initial diagnosis. CASE REPORT We present the case of a 64-year-old man who came to the hospital with encephalopathy. Serologic evaluation revealed acute renal failure, severe hypercalcemia, and metabolic alkalosis. He underwent volume resuscitation, with the initiation of calcitonin. Despite our efforts, the patient developed anuria and proceeded to intermittent hemodialysis. His workup was unrevealing, including an appropriately suppressed parathyroid hormone level, low vitamin D, and normal serum protein electrophoresis and angiotensin converting enzyme levels. Considering his persistent encephalopathy, the team was unable to obtain information from the patient regarding his calcium intake. However, at home, the patient's significant other read his progress notes in the electronic medical record and reported that he consumed at least 1 bottle of calcium carbonate (Tums) every week. Once the encephalopathy resolved, the patient confirmed this information. CONCLUSIONS The search for malignancy in the setting of hypercalcemia was ceased because of the family's at-home electronic medical record use and reporting of Tums overuse. Milk-alkali syndrome, although a rarity, should not be forgotten as a cause of hypercalcemia.
Topics: Acute Kidney Injury; Alkalosis; Brain Diseases; Calcium; Calcium Carbonate; Electronic Health Records; Humans; Hypercalcemia; Male; Middle Aged; Neoplasms
PubMed: 36056538
DOI: 10.12659/AJCR.936969 -
Journal of the American Society of... Feb 2012Maintenance of metabolic alkalosis generated by chloride depletion is often attributed to volume contraction. In balance and clearance studies in rats and humans, we...
Maintenance of metabolic alkalosis generated by chloride depletion is often attributed to volume contraction. In balance and clearance studies in rats and humans, we showed that chloride repletion in the face of persisting alkali loading, volume contraction, and potassium and sodium depletion completely corrects alkalosis by a renal mechanism. Nephron segment studies strongly suggest the corrective response is orchestrated in the collecting duct, which has several transporters integral to acid-base regulation, the most important of which is pendrin, a luminal Cl/HCO(3)(-) exchanger. Chloride depletion alkalosis should replace the notion of contraction alkalosis.
Topics: Aldosterone; Alkalosis; Animals; Bicarbonates; Chlorides; Extracellular Fluid; Humans; Hydrogen-Ion Concentration; Kidney; Rats
PubMed: 22223876
DOI: 10.1681/ASN.2011070720 -
Kidney International Feb 1984
Review
Topics: Absorption; Alkalosis; Animals; Bicarbonates; Chlorides; Humans; Kidney; Mineralocorticoids; Potassium
PubMed: 6374253
DOI: 10.1038/ki.1984.24 -
Archives of Disease in Childhood. Fetal... Sep 1994One hundred sixty seven survivors among very low birthweight infants with a gestational age of less than 35 weeks have been studied prospectively. The purpose of this...
One hundred sixty seven survivors among very low birthweight infants with a gestational age of less than 35 weeks have been studied prospectively. The purpose of this study was to clarify the relationship of severe prenatal and perinatal complications and hypocarbic alkalosis, defined as a carbon dioxide tension (PaCO2) of less than or equal to 2.67 kPa and a pH of 7.50 or greater during the first 24 hours of life, to cystic periventricular leukomalacia (PVL) depicted by serial cranial ultrasonographic examinations. Complications occurred in 16 infants, five of whom presented with PVL, while eight of 151 infants without complications had PVL. Twenty six of the infants had hypocarbic alkalosis, six with evidence of PVL, and seven of the 136 infants without hypocarbic alkalosis had PVL. These results suggest a significant relationship of complications and hypocarbic alkalosis to PVL. Mechanical ventilation should be managed carefully in premature infants to avoid PaCO2 of lower than 2.67 kPa.
Topics: Alkalosis; Carbon Dioxide; Echoencephalography; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Leukomalacia, Periventricular; Prospective Studies; Respiration, Artificial
PubMed: 7979462
DOI: 10.1136/fn.71.2.f107 -
Journal of the American Veterinary... Nov 2021An 11-year-old sexually intact male Shih Tzu diagnosed with acute kidney injury and left-sided congestive heart failure that had nonelective mitral valve surgery.
CASE DESCRIPTION
An 11-year-old sexually intact male Shih Tzu diagnosed with acute kidney injury and left-sided congestive heart failure that had nonelective mitral valve surgery.
CLINICAL FINDINGS
Metabolic alkalosis developed postoperatively, and plasma bicarbonate concentration peaked 2 days after surgery (40.2 mmol/L; pH, 7.550).
TREATMENT AND OUTCOME
Acetazolamide administration increased the urinary excretion of bicarbonate and contributed to the improvement of the dog's acid-base status and oxygenation capacity. Metabolic alkalosis persisted for 4 days after surgery, and no treatment was required after resolution. Plasma urea nitrogen and creatinine concentrations normalized 2 days after surgery.
CLINICAL RELEVANCE
Severe metabolic alkalosis can occur as a complication following mitral valve surgery. Acetazolamide may be suitable for the treatment of severe metabolic alkalosis.
Topics: Acetazolamide; Acute Kidney Injury; Alkalosis; Animals; Bicarbonates; Dog Diseases; Dogs; Hydrogen-Ion Concentration; Male
PubMed: 34727063
DOI: 10.2460/javma.20.09.0519 -
The Journal of Clinical Investigation Feb 1971Metabolic acidosis and alkalosis were produced in adult dogs over 5- to 10-day periods. Midtibial cortical bone was analyzed for calcium, sodium, phosphorus, and...
Metabolic acidosis and alkalosis were produced in adult dogs over 5- to 10-day periods. Midtibial cortical bone was analyzed for calcium, sodium, phosphorus, and carbonate. In acidosis bone CO(3)/Ca decreased 9.5% and bone Na/Ca decreased 6.3%. In alkalosis bone CO(3)/Ca increased 3.1% and bone Na/Ca increased 3.0%. Previous attempts to account for changes in net acid balance by summation of extra- and intracellular acid-base changes have uniformly resulted in about 40-60% of acid gained or lost being "unaccounted for." If it is assumed that changes in tibial cortex reflect changes in the entire skeletal system, changes in bone CO(3) (=) are sufficiently large to account for the "unaccounted for" acid change without postulating changes in cellular metabolic acid production.
Topics: Acidosis; Activation Analysis; Alkalosis; Animals; Blood; Bone and Bones; Calcium; Carbon Dioxide; Carbonates; Dogs; Hydrogen-Ion Concentration; Phosphorus; Sodium; Tibia
PubMed: 5540172
DOI: 10.1172/JCI106499 -
Advances in Physiology Education Dec 2010Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are...
Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied.
Topics: Acid-Base Equilibrium; Acid-Base Imbalance; Acidosis; Alkalosis, Respiratory; Education, Medical, Undergraduate; Female; Humans; Hydrogen-Ion Concentration; Laboratories; Male; Physiology
PubMed: 21098393
DOI: 10.1152/advan.90197.2008 -
Wiener Klinische Wochenschrift Apr 2014The development of metabolic alkalosis was described recently in patients with hypernatremia. However, the causes for this remain unknown. The current study serves to...
BACKGROUND
The development of metabolic alkalosis was described recently in patients with hypernatremia. However, the causes for this remain unknown. The current study serves to clarify whether metabolic alkalosis develops in vitro after removal of free water from plasma and whether this can be predicted by a mathematical model.
MATERIALS AND METHODS
Ten serum samples of healthy humans were dehydrated by 29 % by vacuum centrifugation corresponding to an increase of the contained concentrations by 41 %. Constant partial pressure of carbon dioxide at 40 mmHg was simulated by mathematical correction of pH [pH(40)]. Metabolic acid-base state was assessed by Gilfix' base excess subsets. Changes of acid-base state were predicted by the physical-chemical model according to Watson.
RESULTS
Evaporation increased serum sodium from 141 (140-142) to 200 (197-203) mmol/L, i.e., severe hypernatremia developed. Acid-base analyses before and after serum concentration showed metabolic alkalosis with alkalemia: pH(40): 7.43 (7.41 to 7.45) vs 7.53 (7.51 to 7.55), p = 0.0051; base excess: 1.9 (0.7 to 3.6) vs 10.0 (8.2 to 11.8), p = 0.0051; base excess of free water: 0.0 (- 0.2 to 0.3) vs 17.7 (16.8 to 18.6), p = 0.0051. The acidifying effects of evaporation, including hyperalbuminemic acidosis, were beneath the alkalinizing ones. Measured and predicted acid-base changes due to serum evaporation agreed well.
CONCLUSIONS
Evaporation of water from serum causes concentrational alkalosis in vitro, with good agreement between measured and predicted acid-base values. At least part of the metabolic alkalosis accompanying hypernatremia is independent of renal function.
Topics: Acid-Base Equilibrium; Alkalosis; Blood; Body Water; Desiccation; Humans; Hydrogen-Ion Concentration; Hypernatremia; In Vitro Techniques; Sodium
PubMed: 24343045
DOI: 10.1007/s00508-013-0486-0 -
Clinical Journal of the American... Feb 2016Low serum bicarbonate associates with mortality in CKD. This study investigated the associations of bicarbonate and acid-base status with mortality in healthy older...
BACKGROUND AND OBJECTIVES
Low serum bicarbonate associates with mortality in CKD. This study investigated the associations of bicarbonate and acid-base status with mortality in healthy older individuals.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS
We analyzed data from the Health, Aging, and Body Composition Study, a prospective study of well functioning black and white adults ages 70-79 years old from 1997. Participants with arterialized venous blood gas measurements (n=2287) were grouped into <23.0 mEq/L (low), 23.0-27.9 mEq/L (reference group), and ≥28.0 mEq/L (high) bicarbonate categories and according to acid-base status. Survival data were collected through February of 2014. Mortality hazard ratios (HRs; 95% confidence intervals [95% CIs]) in the low and high bicarbonate groups compared with the reference group were determined using Cox models adjusted for demographics, eGFR, albuminuria, chronic obstructive pulmonary disease, smoking, and systemic pH. Similarly adjusted Cox models were performed according to acid-base status.
RESULTS
The mean age was 76 years, 51% were women, and 38% were black. Mean pH was 7.41, mean bicarbonate was 25.1 mEq/L, 11% had low bicarbonate, and 10% had high bicarbonate. Mean eGFR was 82.1 ml/min per 1.73 m(2), and 12% had CKD. Over a mean follow-up of 10.3 years, 1326 (58%) participants died. Compared with the reference group, the mortality HRs were 1.24 (95% CI, 1.02 to 1.49) in the low bicarbonate and 1.03 (95% CI, 0.84 to 1.26) in the high bicarbonate categories. Compared with the normal acid-base group, the mortality HRs were 1.17 (95% CI, 0.94 to 1.47) for metabolic acidosis, 1.21 (95% CI, 1.01 to 1.46) for respiratory alkalosis, and 1.35 (95% CI, 1.08 to 1.69) for metabolic alkalosis categories. Respiratory acidosis did not associate with mortality.
CONCLUSIONS
In generally healthy older individuals, low serum bicarbonate associated with higher mortality independent of systemic pH and potential confounders. This association seemed to be present regardless of whether the cause of low bicarbonate was metabolic acidosis or respiratory alkalosis. Metabolic alkalosis also associated with higher mortality.
Topics: Acid-Base Equilibrium; Acidosis; Black or African American; Age Factors; Aged; Aging; Alkalosis; Bicarbonates; Biomarkers; Cause of Death; Down-Regulation; Female; Geriatric Assessment; Humans; Hydrogen-Ion Concentration; Male; Risk Factors; United States; White People
PubMed: 26769766
DOI: 10.2215/CJN.06200615 -
Critical Care (London, England) May 2023
Topics: Humans; Alkalosis; Lactic Acid; Critical Care; Intensive Care Units
PubMed: 37173749
DOI: 10.1186/s13054-023-04464-z