Differences in serum chloride measurements by direct potentiometry and indirect potentiometry may affect anion gap calculation

Pathology ◽  
2019 ◽  
Vol 51 ◽  
pp. S111-S112
Author(s):  
C.S.M. Lau ◽  
S.K. Phua ◽  
T.C. Aw
Keyword(s):  
Anion Gap ◽  
Direct Potentiometry ◽  
Serum Chloride

WHEN TO ADJUST SERUM CHLORIDE FOR ANION GAP CALCULATION?

2011 ◽  
Vol 22 ◽  
pp. S70
Author(s):  
Mustafa Gezer ◽  
Fatih Bulucu ◽  
Kadir Ozturk ◽  
Orhan Demir
Keyword(s):  
Anion Gap ◽  
Serum Chloride

scholarly journals False-negative diagnosis of high anion gap in patients with end-stage kidney disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
You Komatsuzaki ◽  
Masato Ikeda ◽  
Akihiro Shimizu ◽  
Nanae Matsuo ◽  
Yukio Maruyama ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Leukocyte Count ◽  
False Negative ◽  
Anion Gap ◽  
End Stage Kidney Disease ◽  
Frequent Use ◽  
Serum Chloride ◽  
Blood Leukocyte ◽  
End Stage ◽  
Sensitivity Specificity

AbstractThe traditional anion gap (AG) equation is widely used, but its misdiagnosis in end-stage kidney disease (ESKD) patients has not been investigated fully. Diagnostic accuracy to detect high AG was cross-sectionally evaluated using 3 AG equations in 1733 ESKD patients with an eGFR less than 15 mL/min/1.73 m2. The prevalence of high AG was 67.9%, 92.1% and 97.4% by the traditional, albumin-adjusted AG (aAG) and full AG equations, respectively. The sensitivity, specificity, accuracy and Kappa coefficient obtained with the traditional AG vs aAG equation were 0.70 vs 0.94, 0.98 vs 0.93, 0.7 vs 0.94, and 0.103 vs 0.44, respectively. Next, we created a subcohort comprising only patients with high full AG and investigated how the traditional AG equation leads to misdiagnoses. Multivariable-adjusted regression analysis in 1688 patients revealed that independent factors associated with a false-negative AG diagnosis were ARB use, eGFR, blood leukocyte count, serum chloride, bicarbonate, ionized calcium, potassium, albumin and phosphate. 93.2% of our subcohort prescribed any of RAAS inhibitors, Loop diuretics or Alkali which could increase either serum chloride or bicarbonate. Frequent use of these possible AG-reducing medications may conceal high AG state in patients with ESKD unless they have incidental inflammation which may increase AG value.

An Unusual Case of Severe Anion Gap Metabolic Acidosis in a 3-year-old Girl

2021 ◽  
Vol 42 (Supplement 1) ◽  
pp. S46-S51
Author(s):  
Ryan M. Fredericks ◽  
George Sam Wang ◽  
Christine U. Vohwinkel ◽  
Jessica Kraynik Graham
Keyword(s):  
Metabolic Acidosis ◽  
Unusual Case ◽  
Anion Gap

scholarly journals A218 A CASE REPORT OF PSEUDOHYPONATREMIA IN CHOLESTATIC LIVER DISEASE

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 250-252
Author(s):  
M Shpoliansky ◽  
B Kamath
Keyword(s):  
Liver Disease ◽  
Liver Transplant ◽  
Measurement Techniques ◽  
Growth Failure ◽  
Urine Osmolality ◽  
Normal Serum ◽  
Plasma Sodium ◽  
Cholestatic Liver Disease ◽  
Aqueous Fraction ◽  
Direct Potentiometry

Abstract Background True hyponatremia in the setting of cholestatic liver disease may signify cirrhosis with fluid overload, and is therefore an ominous sign of deteriorating liver function. In pediatric liver transplant candidates, it is associated with increased waitlist mortality. Pseudohyponatremia however, is a falsely low measurement of plasma sodium when measured by indirect potentiometry. Pseudohyponatremia secondary to hypercholesterolemia is a phenomenon that occurs due to a reduced aqueous fraction of the plasma when levels of cholesterol or triglycerides are greatly elevated. Severe hypercholesterolemia due to Lipoprotein X accumulation may be the cause of pseudohyponatremia in biliary obstruction or cholestasis. Aims To describe a case of pseudohyponatremia secondary to hypercholesterolemia in an infant with Alagille syndrome (ALGS) and cholestatic liver disease. Methods This 7 month-old male with ALGS (confirmed JAGGED1 mutation) and severe cholestasis, failure to thrive, and pruritus, developed new-onset progressive hyponatremia as low as 121 mmol/L at an outside institution. He was therefore transferred to our center for liver transplant assessment due to concerns of progressive liver dysfunction and for management of the hyponatremia. Results Upon admission, the patient was jaundiced but euvolemic, with no evidence of ascites or peripheral edema. Laboratory work drawn at our institution showed conjugated bilirubin of 180 mmol/L, ALT 300 U/L, AST 250 U/L, and GGT 1200 U/L. INR was 1.1 and albumin of 35 g/L. The cholesterol was elevated above 16.8 mmol/L, with high triglycerides 2.68 mmol/L, and the serum appeared visibly lipemic. The sodium level was 138 mmol/L as measured by direct potentiometry due to the visible lipemia. The osmolality of 288 mmol/kg was normal with a normal osmolar gap. Urine osmolality and sodium were also normal. He underwent routine evaluation and was listed for a liver transplant due to the profound cholestasis and growth failure. Conclusions Pseudohyponatremia is an important entity to recognize when caring for patients with cholestatic liver disease and hyponatremia. Both direct potentiometry and indirect potentiometry are currently used for sodium testing in blood in biochemistry laboratories. These measurement techniques show good agreement as long as protein and lipid concentrations in blood are normal, however, hyperlipidemia is a well-recognized cause for error in sodium estimation. It is therefore imperative to evaluate apparent hyponatremia correctly, especially when the patient appears euvolemic clinically and by normal serum osmolality. In this clinical setting, pseudohyponatremia is the likely cause and a workup should be carried out to identify possible underlying etiologies, the most probable being hypercholesterolemia. Failure to recognize this phenomenon may lead to unnecessary and potentially harmful treatments and interventions. Funding Agencies None

scholarly journals Outcome of the use of 0.9% saline versus 0.45% saline for fluid rehydration in moderate and severe diabetic ketoacidosis in children

2021 ◽  
Vol 69 (1) ◽  
Author(s):  
Nora El Said Badawi ◽  
Mona Hafez ◽  
Heba Sharaf Eldin ◽  
Hend Mehawed Abdelatif ◽  
Shimaa Atef ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Normal Saline ◽  
Sodium Concentration ◽  
Saline Group ◽  
Serum Electrolytes ◽  
Serum Chloride ◽  
Significant Difference ◽  
Rehydration Solution ◽  
The Moment

Abstract Background The debate for the optimum sodium concentration in the rehydration solution in diabetic ketoacidosis (DKA) persists till the moment. The aim was to compare the outcome of 0.9% saline versus 0.45% saline in children with moderate and severe (DKA) regarding the effect on serum electrolytes, duration of DKA resolution and the incidence of hyperchloremia. Results A retrospective analysis of 121 children with moderate or severe DKA was done. After the initial 4 h in which both groups received normal saline, patients were divided into two groups continuing on 0.9% (N=72) or switched to 0.45% saline (N=49). Serum chloride and Cl/Na ratios were significantly higher in 0.9% saline group at 4 and 8 h. The 0.9% saline group had significantly higher proportion of hyperchloremia at 4 and 8 h (P value: 0.002, 0.02). The median duration of correction of DKA (14 h among 0.9% saline versus 10 h among 0.45% saline) without significant difference (P value= 0.43). The change in plasma glucose, effective osmolarity, corrected Na levels were comparable between groups. Conclusion There is an unavoidable iatrogenically induced rise in serum chloride with higher incidence of hyperchloremia with the use of normal saline in rehydration of children presenting in DKA and shock. The use of 0.45% saline as post-bolus rehydration fluid is not associated with a decline in the corrected serum sodium concentration and does not affect the rate of correction of acidosis or rate of drop in blood glucose or duration of DKA resolution when compared to normal saline.

scholarly journals The Role of Serum Chloride in Acute and Chronic Heart Failure: A Narrative Review

2021 ◽  
Vol 11 (2) ◽  
pp. 87-98
Author(s):  
Frederick Berro Rivera ◽  
Pia Alfonso ◽  
Jem Marie Golbin ◽  
Kevin Lo ◽  
Edgar Lerma ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chloride Channel ◽  
Chloride Channels ◽  
Prognostic Value ◽  
Diuretic Therapy ◽  
Juxtaglomerular Apparatus ◽  
Sodium Chloride Cotransporter ◽  
Serum Chloride ◽  
And Function

Clinical guidelines include diuretics for the treatment of heart failure (HF), not to decrease mortality but to decrease symptoms and hospitalizations. More attention has been paid to the worse outcomes, including mortality, associated with continual diuretic therapy due to hypochloremia. Studies have revealed a pivotal role for serum chloride in the pathophysiology of HF and is now a target of treatment to decrease mortality. The prognostic value of serum chloride in HF has been the subject of much attention. Mechanistically, the macula densa, a region in the renal juxtaglomerular apparatus, relies on chloride levels to sense salt and volume status. The recent discovery of with-no-lysine (K) (WNK) protein kinase as an intracellular chloride sensor sheds light on the possible reason of diuretic resistance in HF. The action of chloride on WNKs results in the upregulation of the sodium-potassium-chloride cotransporter and sodium-chloride cotransporter receptors, which could lead to increased electrolyte and fluid reabsorption. Genetic studies have revealed that a variant of a voltage-sensitive chloride channel (CLCNKA) gene leads to almost a 50% decrease in current amplitude and function of the renal chloride channel. This variant increases the risk of HF. Several trials exploring the prognostic value of chloride in both acute and chronic HF have shown mostly positive results, some even suggesting a stronger role than sodium. However, so far, interventional trials exploring serum chloride as a therapeutic target have been largely inconclusive. This study is a review of the pathophysiologic effects of hypochloremia in HF, the genetics of chloride channels, and clinical trials that are underway to investigate novel approaches to HF management.

scholarly journals Acetazolamide and SGLT2 inhibitor as potent drugs for a patient with diabetes mellitus and worsening chronic lymphedema: A case report

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Hajime Kataoka
Keyword(s):  
Body Weight ◽  
Fluid Collection ◽  
Sglt2 Inhibitor ◽  
Chloride Concentration ◽  
Tissue Fluid ◽  
Fat Deposits ◽  
Serum Chloride ◽  
The Right ◽  
Chronic Lymphedema

Treatment of lymphedema using a pharmacologic approach is reported to have limited efficacy. Here, I report a patient with type 2 diabetes (T2DM) and acute worsening of her chronic lymphedema, in whom treatment with acetazolamide and a sodiumglucose cotransporter-2 inhibitor (SGLT2i) effectively improved the lymphedema. A 94-year-old woman, who was treated for T2DM, hyperlipidemia, and hypertension for 17 years at my hospital presented to the emergency room because of acute worsening of her chronic right leg lymphedema with increased swelling, tightness, and dull aching. A pharmacologic approach was used to treat her worsening lymphedema. Acetazolamide 500 mg/d was administered to treat the acute tissue fluid collection in the right lymphedematous leg. Ten days later, the patient’s body weight was markedly reduced by 3.2 kg, pitting in the right leg was markedly improved, and the circumference of right limb was decreased. On day 11, the glucose-lowering agent vildagliptin was switched to the SGLT2i empagliflozin 10 mg/d. On day 70, her body weight had decreased further by 2.8 kg, and the circumference of her right limb was greatly reduced compared with that under treatment with acetazolamide. Her serum chloride concentration was increased after treatment, but her hemoglobin and hematocrit values did not change during the study period. In conclusion, acetazolamide and an SGLT2i have acute diuretic effects for draining the excess tissue fluid in the lymphedematous limb without vascular contraction by enhancing vascular tonicity. Additionally, an SGLT2i may have chronic effects for reducing fat deposits in the lymphedematous limb.

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