DOCSLIB.ORG

Misleading Biochemical Laboratorytest Results

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Misleading Biochemical Laboratorytest Results Misleading biochemical laboratory test results will examine some of the conditions bility increases with each additional AMIN A. NANJI, MB, CH B, FRCP[C] under which commonly performed test, as shown in Table I. Interpre- laboratory tests may give misleading tation of the table is subject to the results. caveat that the probability of all This article reviews the general and A few general principles may be tests giving results within the nor- specific factors that interfere with helpful. The great progress that has mal limits is slightly increased by the performance of common bio- been made in recent years in the the fact that low values for some chemical laboratory tests and the quality of laboratory tests means tests do not indicate an abnormality. interpretation of their results. The that most errors are now due to Indeed, several authors have warned clinical status of the patient, drug nonanalytic factors;' primarily these against pursuing a marginally ab- interactions, and in-vivo and in-vitro include the steps involved in request- normal test result.4-6 biochemical interactions and changes ing the test, in preparing the patient, Other factors can also alter test may alter the results obtained from and in storing and processing the results. These include the patient's biochemical analysis of blood con- specimens. Drugs can also alter lab- sex, diet, physical activity and smok- stituents. Failure to recognize invalid oratory test results, either by affect- ing habits; these factors have been laboratory test results may lead to ing a physiologic process or by inter- discussed in detail elsewhere.78 injudicious and dangerous manage- fering with the laboratory analysis.2 Table II presents a concept out- ment of patients. All laboratories publish the line of the major sources of poten- ranges of normal values for the tially misleading laboratory test re- Cet article passe en revue les fac- results of the tests they perform. sults. In the following discussion, teurs generaux et specifiques qui Limits of normal are set to include however, it will be easier for you to genent la realisation de tests de labo- the central 95% of the population, review each laboratory test com- ratoire biochimiques courants ainsi excluding the 2.5% in each tail of pletely while referring to the general que l'interpretation de leurs resul- the normal curve. In other words, by principles set out in the table. The tats. L'etat clinique du malade, les definition the probability of an ab- three categories of headings in the interactions medicamenteuses et les normal result of any given test in a following discussion represent the interactions ou changements biochi- normal individual is 0.05; the proba- main area of testing, the specific miques in vivo et in vitro peuvent fausser les resultats des analyses biochimiques des constituants san- Table I-Predicted probability that the results of at least one test will exceed guins. Le fait de ne savoir identifier laboratory limits des resultats non valables de tests de Probability* laboratoire peut conduire a un traite- ment inapproprie et dangereux pour That results of all That results of one le malade. tests will be or more tests within limits* will exceed limits Laboratory results that do not corre- No. of tests (p) (1 - p) late with the patient's clinical status 1 0.95 0.05 or with the disease process may lead 6 0.74 0.26 to an incorrect diagnosis and injudi- 8 0.66 0.34 cious management. In this paper I 12 0.54 0.46 14 0.49 0.51 From the division of clinical chemistry, Van- 17 0.42 0.58 couver General Hospital and the department 20 0.36 0.64 of pathology, University of British Columbia, 100 0.006 0.99 Vancouver = = = Reprint requests to: Dr. Amin A. Nanji, *p sw, where p the statistical probability, s the probability (usually 95%) Director of clinical biochemistry, Ottawa that a normal person will have values within the normal range for each test, and General Hospital, 501 Smyth Rd., Ottawa, n = the number of tests performed. Ont. KIG 8L5 CAN MED ASSOC J, VOL. 130, JUNE 1, 1984 1435 component being tested and the type instrument and hyperproteinemia. monoclonal protein in the plasma of error or the condition leading to In a study of 11 patients with vari- causing a decrease of 0.7 mmol/L in error. ous degrees of hyperviscosity Blank the sodium level.'8 and Ill found that the measurements Presence of cationic paraproteins Electrolytes obtained with direct potentiometry in the blood: Bloth and coworkers" were accurate, whereas those ob- described three asymptomatic pa- Serum sodium tained with flame photometry and tients with multiple myeloma whose indirect potentiometry were artifi- serum sodium levels were reported Sampling: One of the commonest cially low. No correction factor can to be around 110 mmol/L. Cationic causes of a falsely low value for the be applied to measurements ob- paraproteins may displace other cat- concentration of sodium in the tained with flame photometry; how- ions, especially sodium. serum occurs when the venous sam- ever, for the results determined by Presence of osmotically active ple is taken downstream from an indirect potentiometry each centi- particles in the blood: Glucose is ah intravenous infusion of hypotonic stoke increase in the serum viscosity osmotically active substance that fluid, such as 5% dextrose in water. accounted for a 2-mmol/L decrease can cause water to move from the I attempted to determine the cause in the serum sodium level. Serum intracellular to the extracellular of hyponatremia in 87 patients with viscosity. is temperature-dependent.'6 fluid space and thus dilute the sodi- reported serum sodium levels of less Blank and I'` found that the differ- um ions in the extracellular fluid. In than 125 mmol/L and found that in ences in the viscosity of hyperviscous patients with diabetic ketoacidosis 10 patients the blood sample had serum at 20°C and 37°C caused or with hyperglycemic, hyperosmo- been diluted by the intravenous flu- differences in the measured sodium lar, nonketotic diabetic coma the id. This type of error can usually be levels. high concentration of plasma glu- identified by the high glucose level Monoclonal gammopathy: The cose causes a dilution of sodium ions in the sample. reduced water content in the plasma in the plasma. In this case the low Hyperlipemia: With some analy- of patients with monoclonal gam- values for the serum sodium level tic techniques the reported sodium mopathy without hyperviscosity can result from renal loss of sodium and levels in serum samples from pa- result in falsely low reported serum the shift of water into the extracel- tients with hyperlipemia may be sodium levels, each gram per litre of lular fluid space. Katz20 suggested, falsely low because of the decrease in the proportion of water in the Table II-Major sources of misleading results of biochemical laboratory tests plasma secondary to the large amount of lipid present.9'0 Ladenson Use of a specimen that is not representative as a result of one of the following: and colleagues" showed that errors Biochemical change or interaction in the measurement of serum sodi- In vitro um concentrations in hyperlipemic Hemolysis/lysis of cells, with leakage of cellular constituents (e.g., lactate patients were related to the method dehydrogenase or potassium) Storage, leading to alkalinization of serum, with subsequent increase in of measurement. If the serum sam- alkaline phosphatase activity ple is diluted, as it is when analysed Evaporation-induced errors (e.g., concentration of electrolytes) by indirect potentiometry, the re- Artefactual hypoglycemia in the presence of large numbers of cells (i.e., sulting values will be falsely low; erythrocytes, leukocytes or platelets) however, with direct potentiometry In vivo the results will be valid because the Interference by endogenous metabolites or drugs (e.g., cephalosporins or concentration of sodium ions is acetoacetate, which falsely elevate the serum creatinine level) being measured in the aqueous Cell rupture, with release of cellular constituents (e.g., platelet acid phospha- phase. Frier and associates'2 des- tase, which spuriously increases the prostatic acid phosphatase level) cribed a patient with hyperlipemia, Sampling error Contamination of specimen (e.g., by residual detergent, which spuriously hemiplegia and convulsions who was increases the phosphate level) treated with normal saline because Venous stasis, which leads to increases in the lactate, potassium and calcium the serum sodium level was reported levels to be 116 mmol/L. When the level Upright posture, which leads to hemoconcentration and an increase in the total was corrected for the hyperlipemia, serum protein level however, it became 222 mmol/L. As Blood drawn downstream from an intravenous line, which leads to spurious a rule, every increase of 11.3 hyponatremia and hyperglycemia mmol/L in the serum triglyceride The patient's not being in the basal state level results in an apparent decrease After exercise, which increases the serum creatine kinase level of 1.5 mmol/L in the serum sodium During diet, which increases the serum triglyceride levels After ethanol consumption, which increases the y-glutamyl transpeptidase level level.'" Laboratory error in one of the following areas: Hyperviscosity: Serum samples Analysis from patients with hyperviscosity Interference by bilirubin, turbidity or chemicals yield falsely low values for the sodi- Poor quality control um level when analysed by flame Reporting of results with identification error photometry'4 because of problems in Normal variation sample aspiration, dilution by the 1436 CAN MED ASSOC J, VOL. 130, JUNE 1, 1984 and I have verified clinically,2' that as a cause of reported hyperkalemia decrease by an average of 4 for every 5.6-mmol/L increase in the in patients with myeloproliferative mmol/L.
Load more

Recommended publications
  • International Myeloma Working Group Guidelines for the Management Of
    Leukemia (2009) 23, 1716–1730 & 2009 Macmillan Publishers Limited All rights reserved 0887-6924/09 $32.00 www.nature.com/leu REVIEW International Myeloma Working Group guidelines for the management of multiple myeloma patients ineligible for standard high-dose chemotherapy with autologous stem cell transplantation A Palumbo1, O Sezer2, R Kyle3, JS Miguel4, RZ Orlowski5, P Moreau6, R Niesvizky7, G Morgan8, R Comenzo9, P Sonneveld10, S Kumar3, R Hajek11, S Giralt5, S Bringhen1, KC Anderson12, PG Richardson12, M Cavo13, F Davies8, J Blade´14, H Einsele15, MA Dimopoulos16, A Spencer17, A Dispenzieri3, T Reiman18, K Shimizu19, JH Lee20, M Attal21,22, M Boccadoro1, M Mateos4, W Chen23,24, H Ludwig25, D Joshua26, J Chim27, V Hungria28, I Turesson29, BGM Durie30 and S Lonial31 on behalf of the IMWGn 1Divisione di Ematologia dell’Universita` di Torino, Azienda Ospedaliera S. Giovanni Battista, Ospedale Molinette, Torino, Italy; 2Department of Hematology/Oncology, Charite´–Universitaetsmedizin Berlin, Germany; 3Division of Hematology, Mayo Clinic, Rochester, Minnesota, USA; 4Servicio de Hematologı´a, Hospital Universitario de Salamanca. CIC, IBMCC (USAL-CSIC), Salamanca, Spain; 5Department of Lymphoma/Myeloma, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA; 6Department of Clinical Hematology, University Hospital, Nantes, France; 7Center for Lymphoma and Myeloma, Weill Medical College of Cornell University, New York, New York, USA; 8Institute of Cancer Research, Royal Marsden Hospital, London, UK; 9Blood Bank and Stem Cell
    [Show full text]
  • THE EFFECT of POTASSIUM CHLORIDE on HYPONATREMIA1 by JOHN H
    THE EFFECT OF POTASSIUM CHLORIDE ON HYPONATREMIA1 By JOHN H. LARAGH2 (From the Department of Medicine, College of Physicians and Surgeons, Columbia University; and the Presbyterian Hospital in the City of New York) (Submitted for publication August 31, 1953; accepted February 10, 1954) In cardiac edema as well as in various other tration might favorably influence disturbances in states characterized by excessive retention of fluid sodium metabolism manifested by pathologic dis- there is observed frequently an abnormally low con- tribution of sodium and potassium within the body. centration of sodium in the serum and extracellular Two recent studies have served to emphasize this fluid (1, 2). Rigorous sodium restriction, mer- important relationship between sodium and potas- curial diuretics, and cation exchange resins may sium. In vivo, with potassium depletion there is exaggerate or produce this tendency to hypo- a movement of sodium ions into cells and an associ- tonicity. Sodium administration often enhances ated extracellular alkalosis. This intracellular so- accumulation of fluid, without increasing its to- dium can then be mobilized by potassium adminis- nicity, and hypertonic sodium chloride, though tration (11). In vitro it has been shown that po- effective at times, may be neither beneficial nor tassium transport is dependent upon energy of safe (3). aerobic oxidation. If the cell is injured or meta- Because of the shortcomings of these various bolically inhibited potassium fails to accumulate therapies and because hyponatremia per se may and is replaced by an influx of sodium and water play a role in the production of adverse symptoms, (12). it seemed desirable to search for another diuretic Accordingly, potassium chloride (KCl) was agent which might promote the loss of excessive given to an edematous, hyponatremic cardiac body water without aggravating disturbances in patient with the hope of effecting water diuresis.
    [Show full text]
  • A Case of Aggressive Multiple Myeloma with Cleaved, Multilobated, and Monocytoid Nuclei, and No Serum Monoclonal Gammopathy
    Annals o f Clinical & Laboratory Science, vol. 30, no. 3, 2000 283 A Case of Aggressive Multiple Myeloma with Cleaved, Multilobated, and Monocytoid Nuclei, and No Serum Monoclonal Gammopathy Y. Albert Yeh, Alex A. Pappas, James T. Flick, and Anthony W. Butch* Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas (^Current address: Department of Pathology and Laboratory Medicine, UCLA Medical Center, Los Angeles, CA) Abstract Multiple myeloma is a B-cell malignancy characterized by proliferation of neoplastic plasma cells. A few cases have been reported identifying variant forms of neoplastic plasma cells with atypical nuclei that secrete myeloma protein. We report a highly unusual case of plasma cell myeloma that presented with cleaved, multilobated, and monocytoid nuclei, without detectable myeloma protein in the serum or urine. The bone marrow contained sheets of plasma cells exhibiting pleomorphic nuclei with cleaved, multilobated, and monocytoid features that were negative for myeloperoxidase and dual esterase. Flow cytometric analysis revealed CD38hlgh/CD45low cells expressing cytoplasmic kappa light chain, without evidence of myeloid or lymphoid differentiation. Following chemotherapy, the patient developed secondary plasma cell leukemia. A high plasma cell labeling index was obtained from bone marrow and peripheral blood, indicating a poor prognosis. In addition to quantitative immunoglobulins, serum protein electrophoresis, and immunofixation electrophoresis of serum and urine, we recommend cytochemical and flow cytometric studies for evaluation of suspected plasma cell myeloma with atypical cellular features. Keywords: multiple myeloma, plasma cell, cleaved, mutilobated, monocytoid, non-secretory Introduction 11% of all myeloma cases. The other groups individually account for <10% of the remaining cases, Plasma cell myeloma constitutes approximately 1 % of with the plasmablastic type being a high-grade all malignancies and 10% of all hematologic malig­ malignancy (2% of all cases) associated with a poor nancies.
    [Show full text]
  • DKA Protocol - Insulin Deficiency - Pregnancy
    Diabetic Ketoacidosis in Pregnancy Diagnosis of DKA: Initial STAT labs include • CBC with diff • Serum electrolytes • BUN • Creatinine • Glucose • Arterial blood gases • Bicarbonate • Urinalysis • Lactate • Serum ketones • Calculation of the Anion Gap serum anion gap = serum sodium – (serum chloride + bicarbonate) • Electrocardiogram Treatment Protocol for Diabetic Ketoacidosis Reviewed 5/2/2017 1 Updated 05/02/17 DKA/HHS Pathway Phase 1 (Adult) DKA Diagnostic Criteria: Blood glucose >250 mg/dl *PREGNANCY Arterial pH <7.3 Utilize OB DKA order set Phase 1 Bicarbonate ≤18 mEq/l When glucose reaches 200mg/dL, Initiate OB Anion Gap Acidosis DKA Phase 2 Moderate ketonuria or ketonemia Glucose goals 100 -150mg/dL OB DKA Phase 2 1. Start IV fluids (1 L of 0.9% NaCl per hr initially) Look for the Cause 2. If serum K+ is <3.3 mEq/L hold insulin - Infection/Inflammation (PNA, UTI, Give 40 mEq/h until K ≥ 3.3 mEq/L pancreatitis, cholecystitis) 3. Initiate DKA Order Set Phase I ( *In PREGNANCY utilize OB DKA - Ischemia/Infarction (myocardial, cerebral, gut) order set ) - Intoxication (EtOH, drugs) 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) - Iatrogenic (drugs, lack of insulin) RN will titrate per DKA protocol - Insulin deficiency - Pregnancy IVF Insulin Potassium Bicarbonate + Determine hydration status Initiate and If initial serum K is Assess need for bicarbonate continue insulin gtt <3.3 mEq/L, hold until serum insulin and give 40 + glucose reaches mEq K per h (2/3 250 mg/dl. KCL and 1/3 KP0 ) Hypovolemic Mild Cardiogenic 4 pH <6.9 pH >7.0 shock hypotension shock RN will titrate per until K ≥ 3.3 mEq/L protocol to achieve target.
    [Show full text]
  • Acid-Base Physiology & Anesthesia
    ACID-BASE PHYSIOLOGY & ANESTHESIA Lyon Lee DVM PhD DACVA Introductions • Abnormal acid-base changes are a result of a disease process. They are not the disease. • Abnormal acid base disorder predicts the outcome of the case but often is not a direct cause of the mortality, but rather is an epiphenomenon. • Disorders of acid base balance result from disorders of primary regulating organs (lungs or kidneys etc), exogenous drugs or fluids that change the ability to maintain normal acid base balance. • An acid is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. • A base is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. • Strength of acids or bases refers to their ability to donate and accept H+ ions respectively. • When hydrochloric acid is dissolved in water all or almost all of the H in the acid is released as H+. • When lactic acid is dissolved in water a considerable quantity remains as lactic acid molecules. • Lactic acid is, therefore, said to be a weaker acid than hydrochloric acid, but the lactate ion possess a stronger conjugate base than hydrochlorate. • The stronger the acid, the weaker its conjugate base, that is, the less ability of the base to accept H+, therefore termed, ‘strong acid’ • Carbonic acid ionizes less than lactic acid and so is weaker than lactic acid, therefore termed, ‘weak acid’. • Thus lactic acid might be referred to as weak when considered in relation to hydrochloric acid but strong when compared to carbonic acid.
    [Show full text]
  • Hyperchloremia – Why and How
    Document downloaded from http://www.elsevier.es, day 23/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited. n e f r o l o g i a 2 0 1 6;3 6(4):347–353 Revista de la Sociedad Española de Nefrología www.revistanefrologia.com Brief review Hyperchloremia – Why and how Glenn T. Nagami Nephrology Section, Department of Medicine, VA Greater Los Angeles Healthcare System and David Geffen School of Medicine at UCLA, United States a r t i c l e i n f o a b s t r a c t Article history: Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of Received 5 April 2016 clinical conditions. The kidney plays an important role in the regulation of chloride concen- Accepted 11 April 2016 tration through a variety of transporters that are present along the nephron. Nevertheless, Available online 3 June 2016 hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low Keywords: with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis Hyperchloremia or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia Electrolyte disorder will, to a large extent, determine how to treat this electrolyte disturbance. Serum bicarbonate Published by Elsevier Espana,˜ S.L.U. on behalf of Sociedad Espanola˜ de Nefrologıa.´ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
    [Show full text]
  • Solitary Plasmacytoma: a Review of Diagnosis and Management
    Current Hematologic Malignancy Reports (2019) 14:63–69 https://doi.org/10.1007/s11899-019-00499-8 MULTIPLE MYELOMA (P KAPOOR, SECTION EDITOR) Solitary Plasmacytoma: a Review of Diagnosis and Management Andrew Pham1 & Anuj Mahindra1 Published online: 20 February 2019 # Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Purpose of Review Solitary plasmacytoma is a rare plasma cell dyscrasia, classified as solitary bone plasmacytoma or solitary extramedullary plasmacytoma. These entities are diagnosed by demonstrating infiltration of a monoclonal plasma cell population in a single bone lesion or presence of plasma cells involving a soft tissue mass, respectively. Both diseases represent a single localized process without significant plasma cell infiltration into the bone marrow or evidence of end organ damage. Clinically, it is important to classify plasmacytoma as having completely undetectable bone marrow involvement versus minimal marrow involvement. Here, we discuss the diagnosis, management, and prognosis of solitary plasmacytoma. Recent Findings There have been numerous therapeutic advances in the treatment of multiple myeloma over the last few years. While the treatment paradigm for solitary plasmacytoma has not changed significantly over the years, progress has been made with regard to diagnostic tools available that can risk stratify disease, offer prognostic value, and discern solitary plasmacytoma from quiescent or asymptomatic myeloma at the time of diagnosis. Summary Despite various studies investigating the use of systemic therapy or combined modality therapy for the treatment of plasmacytoma, radiation therapy remains the mainstay of therapy. Much of the recent advancement in the management of solitary plasmacytoma has been through the development of improved diagnostic techniques.
    [Show full text]
  • Laboratory Testing Requirements for Diagnosis and Follow-Up of Multiple Myeloma and Related Plasma Cell Dyscrasias
    Clin Chem Lab Med 2016; 54(6): 907–919 Review Maria A.V. Willrich* and Jerry A. Katzmann Laboratory testing requirements for diagnosis and follow-up of multiple myeloma and related plasma cell dyscrasias DOI 10.1515/cclm-2015-0580 Received June 19, 2015; accepted September 15, 2015; previously Monoclonal gammopathies published online October 28, 2015 overview and categorization Abstract: Monoclonal immunoglobulins are markers of Immunoglobulins are produced by plasma cells, and plasma cell proliferative diseases and have been described clonal plasma cell proliferative diseases usually secrete as the first (and perhaps best) serological tumor marker. a monoclonal immunoglobulin (M-protein) that can The unique structure of each monoclonal protein makes be used as a serologic “tumor” marker. Because of this them highly specific for each plasma cell clone. The dif- secreted monoclonal immunoglobulin, these diseases are ficulties of using monoclonal proteins for diagnosing and also called monoclonal gammopathies. The secreted pro- monitoring multiple myeloma, however, stem from the teins can be used as a diagnostic tool for the identifica- diverse disease presentations and broad range of serum tion of the clone of plasma cells as well as a quantitative protein concentrations and molecular weights. Because of marker to follow the course of the disease and response to these challenges, no single test can confidently diagnose therapy. Unlike most serologic tumor markers, M-proteins or monitor all patients. Panels of tests have been recom- are extremely diverse. The M-proteins each have unique mended for sensitivity and efficiency. In this review we variable region sequences and the molecules may range discuss the various disease presentations and the use of from pentameric IgM (~900,000 Daltons) to monomeric various tests such as protein electrophoresis and immuno- free light chains (~24,000 Daltons).
    [Show full text]
  • Should the Actual Or the Corrected Serum Sodium Be Used to Calculate the Anion Gap in Diabetic Ketoacidosis?
    1-MINUTE CONSULT ONEONE MINUTE CONSULT BRIEF ANSWERS TO SPECIFIC Q: Should the actual or the corrected serum CLINICAL sodium be used to calculate the anion gap QUESTIONS in diabetic ketoacidosis? LAURENCE H. BECK, MD ic effect on the normal anion gap in the case Chairman, Department of Internal Medicine, Cleveland Clinic Florida, Fort Lauderdale of a 10% gain or 10% loss of water. Since all of the components of the anion gap calculation ONE SHOULD USE the actual, measured are concentrated or diluted to the same A: sodium concentration to calculate extent, the anion gap is minimally altered— the anion gap,1 and use the corrected sodium too little to interfere with proper interpreta- concentration to estimate the severity of tion of the acid-base status. dehydration in severe hyperglycemia. Use corrected sodium to evaluate dehydration Use the anion gap to evaluate ketoacidosis On the other hand, correcting the serum sodi- The anion gap (the serum sodium concentra- um concentration in patients with severe tion minus the sum of the serum chloride and hyperglycemia is very useful in estimating the bicarbonate concentrations) is useful in esti- magnitude of water loss that has occurred dur- mating the concentration of other anions not ing the development of hyperglycemia. The usually measured—notably, ketones such as most commonly used formula for correction is beta-hydroxybutyrate and acetoacetate. to add 1.6 mmol/L to the measured serum Why use the measured sodium and not sodium concentration for every 100-mg/dL Using the the corrected sodium? The anion gap reflects increase in glucose, although other conversion corrected the balance between positively and negatively factors have been suggested.2 charged constituents of extracellular fluid.
    [Show full text]
  • Baseline Chloride Levels Are Associated with the Incidence Of
    www.nature.com/scientificreports OPEN Baseline Chloride Levels are Associated with the Incidence of Contrast-Associated Acute Kidney Received: 26 June 2017 Accepted: 30 November 2017 Injury Published: xx xx xxxx Hyung Jung Oh1,2, Sungwon Kim3, Jung Tak Park4, Sang-Joon Kim5, Seung Hyeok Han 4, Tae-Hyun Yoo4, Dong-Ryeol Ryu 1,6,7, Shin-Wook Kang4,8 & Yong Eun Chung 3,8 Although hypo- and hyperchloremia have been associated with worsening renal outcomes, there has been no study that correlates hypo- and hyperchloremia and the incidence of contrast-associated acute kidney injury (CA-AKI). A total of 13,088 patients with less than 2.0 mg/dL of serum creatinine (Cr) who underwent contrast-enhanced abdominal CT (CECT) were included. Patients were divided into 3 groups based on Cl (the hypo-, normo- and hyperchloremia groups). Patients were also classifed by baseline Cr (<1.2; the ‘Normal Cr group’ and 1.2–2.0 mg/dL; the ‘Slightly increased Cr group’). Multivariate logistic regression analysis was used to reveal the association between Cl and CA-AKI. Among patients, 2,525 (19.3%) and 241 (1.8%) patients were classifed in the hypo- and hyperchloremia group. The incidence of CA-AKI was signifcantly lower in the normochloremia group (4.0%) compared to the hypo- (5.4%) and hyperchloremia groups (9.5%). On multivariate logistic regression, hypochloremia was signifcantly associated with the incidence of CA-AKI compared with normochloremia (1.382, P = 0.002). Moreover, hypochloremia was still signifcantly associated with the incidence of CA-AKI in ‘Normal Cr group’ compared with normochloremia (1.314, P = 0.015), while hyperchloremia did not show signifcant association with CA-AKI incidence.
    [Show full text]
  • Effect of Blood Storage on Complete Biochemistry
    isord D ers od & lo T r B f a n o s l f a u n s r Journal of i o u n o J Verma et al., J Blood Disord Transfus 2015, 6:6 ISSN: 2155-9864 Blood Disorders & Transfusion DOI: 10.4172/2155-9864.1000329 Research Article Open Access Effect of Blood Storage on Complete Biochemistry Monica Verma1*, Kiran Dahiya1, Deepika Malik1, Sehgal PK1, Rama Devi2, Abhishek Soni2 and Veena Singh Ghalaut1 1Department of Biochemistry, Pt. B.D. Sharma, University of Health Sciences, Rohtak, Haryana, India 2University of Health Sciences, Rohtak, Haryana, India *Corresponding author: Monica Verma, MBBS, MD (Biochemistry), Senior Resident, Department of Biochemistry, Pt. B.D. Sharma, University of Health Sciences, 236- G, Model Town, Rohtak, Haryana-124001, India, Tel: +919813334543; E-mail: [email protected] Received date: Oct 12, 2015, Accepted date: Dec 28, 2015, Publication date: Dec 31, 2015 Copyright: © 2015 Verma M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background: Prolonged storage of blood leads to alteration in RBCs biochemistry which may lose viability with time. Aim: This study was planned to observe biochemical changes on stored blood on 19 different analytes. Material and Methods: The study was conducted on blood donated by 30 healthy volunteer donors. Effect of storage was analyzed at 0, 3, 7, 14 and 21 days interval. Biochemical parameters were measured using Randox suzuka autoanalyzer and Combiline ISE analyzer.
    [Show full text]
  • Original Article Serum Sodium, Potassium, Calcium, and Chlorine For
    Int J Clin Exp Med 2016;9(5):8264-8271 www.ijcem.com /ISSN:1940-5901/IJCEM0020913 Original Article Serum sodium, potassium, calcium, and chlorine for predicting the in-hospital mortality in cirrhotic patients with acute upper gastrointestinal bleeding: a retrospective observational study Zheng Ning1,2*, Xingshun Qi1*, Feifei Hou1,3, Jiancheng Zhao1,3, Ying Peng1,2, Hongyu Li1, Jing Li1,2, Han Deng1,2, Xintong Zhang1,4, Xiaozhong Guo1 1Liver Cirrhosis Study Group, Department of Gastroenterology, General Hospital of Shenyang Military Area, Shenyang, China; 2Postgraduate College, Dalian Medical University, Dalian, China; 3Postgraduate College, Liaon- ing University of Traditional Chinese Medicine, Shenyang, China; 4Postgraduate College, Fourth Military Medical University, Xi’an, China. *Equal contributors. Received December 1, 2015; Accepted March 29, 2016; Epub May 15, 2016; Published May 30, 2016 Abstract: Background and aims: The association of electrolytes with the outcomes of acute upper gastrointestinal bleeding (AUGIB) in liver cirrhosis remains unclear. A retrospective observational study aimed to explore whether or not serum sodium, potassium, calcium, and chlorine could predict the in-hospital mortality in such patients. Meth- ods: All consecutive patients with liver cirrhosis and AUGIB admitting to our hospital between January 2011 and June 2014 were retrospectively included in this study. Serum sodium, potassium, calcium, and chlorine concentra- tions were collected. Their prognostic values were evaluated by receiver operating
    [Show full text]