Effect of potassium citrate on cephradine residues in broilers

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Sara Ali ◽  
Waleed Khalil ◽  
Abdelfattah Abdelfattah
Keyword(s):  
Potassium Citrate

scholarly journals Recurrent noncirrhotic hyperammonemia causing acute metabolic encephalopathy in a patient with a continent ileocecal pouch: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
T. M. Skipina ◽  
S. Macbeth ◽  
E. L. Cummer ◽  
O. L. Wells ◽  
S. Kalathoor
Keyword(s):  
Emergency Department ◽  
Metabolic Acidosis ◽  
Mental Status ◽  
Rare Case ◽  
Liver Function Tests ◽  
Altered Mental Status ◽  
Potassium Citrate ◽  
Metabolic Encephalopathy ◽  
History Of ◽  
Normal Urine

Abstract Introduction Acute encephalopathy, while a common presentation in the emergency department, is typically caused by a variety of metabolic, vascular, infectious, structural, or psychiatric etiologies. Among metabolic causes, hyperammonemia is relatively common and typically occurs in the setting of cirrhosis or liver dysfunction. However, noncirrhotic hyperammonemia is a rare occurrence and poses unique challenges for clinicians. Case presentation Here we report a rare case of a 50-year-old Caucasian female with history of bladder cancer status post chemotherapy, radical cystectomy, and ileocecal diversion who presented to the emergency department with severe altered mental status, combativeness, and a 3-day history of decreased urine output. Her laboratory tests were notable for hyperammonemia up to 289 μmol/L, hypokalemia, and hyperchloremic nonanion gap metabolic acidosis; her liver function tests were normal. Urine cultures were positive for Enterococcus faecium. Computed tomography imaging showed an intact ileoceal urinary diversion with chronic ileolithiasis. Upon administration of appropriate antibiotics, lactulose, and potassium citrate, she experienced rapid resolution of her encephalopathy and a significant reduction in hyperammonemia. Her hyperchloremic metabolic acidosis persisted, but her hypokalemia had resolved. Conclusion This case is an example of one of the unique consequences of urinary diversions. Urothelial tissue is typically impermeable to urinary solutes. However, when bowel segments are used, abnormal absorption of solutes occurs, including exchange of urinary chloride for serum bicarbonate, leading to a persistent hyperchloremic nonanion gap metabolic acidosis. In addition, overproduction of ammonia from urea-producing organisms can lead to abnormal absorption into the blood and subsequent oversaturation of hepatic metabolic capacity with consequent hyperammonemic encephalopathy. Although this is a rare case, prompt identification and treatment of these metabolic abnormalities is critical to prevent severe central nervous system complications such as altered mental status, coma, and even death in patients with urinary diversions.

Maintenance of ΔpH by a butanol-tolerant mutant of Clostridium beijerinckii

Microbiology ◽  
2005 ◽  
Vol 151 (2) ◽  
pp. 607-613 ◽  
Author(s):  
Fanqiang Wang ◽  
Shelby Kashket ◽  
Eva R. Kashket
Keyword(s):  
Phosphate Buffer ◽  
Sodium Citrate ◽  
Potassium Citrate ◽  
Clostridium Beijerinckii ◽  
Wild Type ◽  
Arginine Residues ◽  
Tolerant Mutant ◽  
Mutant Cells ◽  
Citrate Phosphate ◽  
Citrate Phosphate Buffer

The isolation of Clostridium beijerinckii mutants that are more tolerant of butanol than the wild-type offered the opportunity to investigate whether the membrane activities which are required for maintaining the transmembrane ΔpH (the difference in pH between the cellular interior and exterior) are sensitive targets of butanol toxicity. The ΔpH was measured by the accumulation of [14C]benzoate using late-exponential-phase cells which were suspended in citrate/phosphate buffer at pH 5 (to maximize the ΔpH component of the protonmotive force) and supplemented with glucose and Mg2+. The ΔpH of the butanol-tolerant tolerant mutant, strain BR54, of C. beijerinckii NCIMB 8052 was found to be significantly more tolerant of added butanol than the wild-type. Thus, in potassium citrate/phosphate buffer the mutant cells maintained a ΔpH of 1·4 when butanol was added to a concentration of 1·5 % (w/v), while the wild-type ΔpH was reduced to 0·1. The ΔpH of both strains was completely dissipated with 1·75 % butanol, an effect attributed to a chaotropic effect on the membrane phospholipids. Similar results were obtained in sodium citrate/phosphate buffer. In the absence of added Mg2+, the ΔpH of the mutant decreased in both sodium and potassium citrate/phosphate buffer, but more rapidly in the former. Interestingly, the addition of butanol at low concentrations (0·8 %) prevented this ΔpH dissipation, but only in cells suspended in sodium citrate/phosphate buffer, and not in potassium citrate/phosphate buffer. In wild-type cells the decrease in ΔpH occurred more slowly than in the mutant, and sparing of the ΔpH by 0·8 % butanol was less pronounced. The authors interpret these data to mean that the ΔpH is dissipated in the absence of Mg2+ by a Na+- or K+-linked process, possibly by a Na+/H+ or a K+/H+ antiporter, and that the former is inhibited by butanol. Apparently, butanol can selectively affect a membrane-associated function at concentrations lower than required for the complete dissipation of transmembrane ion gradients. Additionally, since the butanol-tolerant mutant BR54 is deficient in the ability to detoxify methylglyoxal (MG) and contains higher levels of MG than the wild-type, the higher Na+/H+ antiporter activity of the mutant may be due to the greater degree of protein glycation by MG in the mutant cells. The mechanism of butanol tolerance may be an indirect result of the elevated glycation of cell proteins in the mutant strain. Analysis of membrane protein fractions revealed that mutant cells contained significantly lower levels of unmodified arginine residues than those of the wild-type cells, and that unmodified arginine residues of the wild-type were decreased by exposure of the growing cells to added MG.

scholarly journals Successful Management of Refractory Type 1 Renal Tubular Acidosis with Amiloride

2017 ◽  
Vol 2017 ◽  
pp. 1-3
Author(s):  
Patrick Oguejiofor ◽  
Robert Chow ◽  
Kenneth Yim ◽  
Bernard G. Jaar
Keyword(s):  
Citric Acid ◽  
Sodium Bicarbonate ◽  
Sjögren’S Syndrome ◽  
Muscle Pain ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Potassium Citrate ◽  
Sjögren‘S Syndrome

A 28-year-old female with history of hypothyroidism, Sjögren’s Syndrome, and Systemic Lupus Erythematosus (SLE) presented with complaints of severe generalized weakness, muscle pain, nausea, vomiting, and anorexia. Physical examination was unremarkable. Laboratory test showed hypokalemia at 1.6 mmol/l, nonanion metabolic acidosis with HCO3 of 11 mmol/l, random urine pH of 7.0, and urine anion gap of 8 mmol/l. CT scan of the abdomen revealed bilateral nephrocalcinosis. A diagnosis of type 1 RTA likely secondary to Sjögren’s Syndrome was made. She was started on citric acid potassium citrate with escalating dosages to a maximum dose of 60 mEq daily and potassium chloride over 5 years without significant improvement in serum K+ and HCO3 levels. She had multiple emergency room visits for persistent muscle pain, generalized weakness, and cardiac arrhythmias. Citric acid potassium citrate was then replaced with sodium bicarbonate at 15.5 mEq every 6 hours which was continued for 2 years without significant improvement in her symptoms and electrolytes. Amiloride 5 mg daily was added to her regimen as a potassium sparing treatment with dramatic improvement in her symptoms and electrolyte levels (as shown in the figures). Amiloride was increased to 10 mg daily and potassium supplementation was discontinued without affecting her electrolytes. Her sodium bicarbonate was weaned to 7.7 mEq daily.

Gitelman Syndrome in Pregnancy: A Clinical Challenge

2021 ◽  
Author(s):  
Seval Yilmaz Ergani ◽  
Gokcen Orgul ◽  
Harun Egemen Tolunay ◽  
Mustafa Arici ◽  
Aykan Yucel ◽  
...  
Keyword(s):  
Potassium Citrate ◽  
Gitelman Syndrome ◽  
Third Trimester ◽  
Case Presentation ◽  
Early Admission ◽  
Uterine Surgery ◽  
Elective Cesarean ◽  
Gestational Week ◽  
Routine Antenatal Care

Abstract Purpose Disease progress may be affected by pregnancy-related changes, and underlying conditions may also affekt pregnancy outcomes in women with Gitelman syndrome (GS). Case presentation A 35-year-old woman with GS (gravida 2 para 1) was referred to our hospital to start routine antenatal care follow-up at 6 weeks of gestation. At the age of 31, she had been diagnosed with GS after her first uneventful pregnancy. Upon early admission, her serum Mg+level was 0.51 mmol/L and her serum K+level 2.7 mmol/L with normal kidney function tests. She was already taking oral combined potassium citrate and potassium bicarbonate supplementation once a day before pregnancy. At the eighth gestational week, the medication was changed to an oral potassium color sachet of 1.5 gram per day until labor because of the insufficient dosage to maintain optimum potassium levels. She was also taking 365 milligrams of oral magnesium oxide twice a day before and during pregnancy. In the third trimester of the pregnancy, her serum Mg+level was 0.48 mmol/L and serum K+level 2.8 mmol/L. Because of the previous uterine surgery history, she underwent an elective cesarean operation at 39 weeks’ gestation under spinal anesthesia and delivered a healthy 3090-gram female infant. Conclusion Increased need for potassium and magnesium supplementation should be the critical considerations when managing pregnant patients with GS.

Myocardial energy substances in the dog heart during potassium and hypothermic arrest

1962 ◽  
Vol 17 (5) ◽  
pp. 815-818 ◽  
Author(s):  
Vincent L. Gott ◽  
Marilyn Bartlett ◽  
David M. Long ◽  
C. Walton Lillehei ◽  
John A. Johnson
Keyword(s):  
Lactic Acid ◽  
Pyruvic Acid ◽  
Inorganic Phosphate ◽  
Potassium Citrate ◽  
Atp Level ◽  
Average Value ◽  
Human Biopsy ◽  
Cold Blood ◽  
Hypothermic Arrest ◽  
Better Than

Canine hearts were arrested with potassium citrate at 37 C and with cold blood at 17 C. Biopsies were taken from the nonperfused hearts at 0, 5, 20, and 60 min and analyzed by specific microtechniques for AMP, ADP, ATP, phosphocreatine, inorganic phosphate, glycogen, lactic acid, and pyruvic acid. During potassium citrate arrest at 37 C the ATP level was reduced 4.41 mmoles/kg to an average value of .77 mmoles/kg. During hypothermic arrest the ATP level decreased only 1.88 mmoles/ kg. Arrested hearts at 37 C utilized four times as much glycogen and produced three times as much lactic acid as hearts at 17 C. Phosphocreatine fell to low values in both types of arrest within 20 min. The levels of AMP, ADP, and pyruvic acid remained fairly constant throughout the period of arrest. It appears from this data and earlier human biopsy data that selective hypothermic arrest is tolerated far better than potassium citrate arrest. Submitted on September 18, 1961

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