Ketones, Urine

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Ketones, Urine Lab Dept: Urine/Stool Test Name: KETONES, URINE General Information Lab Order Codes: UKE Synonyms: Urine Ketones; Nitroprusside Reaction for Ketones CPT Codes: 81003 – Urinalysis, by dipstick; automated, without microscopy Test Includes: Screen for urine ketones. Logistics Test Indications: Useful for evaluation of ketonuria, detection of acidosis, ketoacidosis, fasting, starvation, high protein diets, diabetes mellitus, and stress- hormone excess. Lab Testing Sections: Urinalysis Phone Numbers: MIN Lab: 612-813-6280 STP Lab: 651-220-6550 Test Availability: Daily, 24 hours Turnaround Time: 1 hour Special Instructions: Submit only one (1) of the following: Catheterized specimen or clean- catch specimen. Note: Indicate type of specimen (catheterized) on request form. Date and time of collection are required on request form for processing. Transport specimen to laboratory immediately following collection Specimen Specimen Type: Urine Container: Urine cup Draw Volume: Entire specimen collection (catheter or clean catch) Processed Volume: Minimum: 0.5 mL urine Collection: A specimen collected by catheterization is optimal; however, a clean- catch or mid-stream specimen is also acceptable. Random, voided specimens will be accepted, but are the least desirable and are not recommended if a urine culture is also being requested. Special Processing: N/A Patient Preparation: None Sample Rejection: Less than 0.5 mL urine submitted; mislabeled or unlabeled specimen Interpretive Reference Range: Negative Critical Values: N/A Limitations: Specimens containing large amounts of ascorbic acid or levodopa metabolites, valproic acid, phenozopyridine (Pyridium®), PSP dye, phenylketones or phthalein compounds may cause false-positives. Methodology: Multistix®, Nitroprusside reaction References: Strasinger SK (1989) Urinalysis and Body Fluids, FA Davis Company Ringsrud KM, et al (1995) Urinalysis and Body Fluids: A Color Text and Atlas, Mosby Brunzel N (1994) Fundamentals of Urine and Body Fluid Analysis, WB Saunders Updates: 2/23/2012: Acetest is no longer performed as a confirmation of urine ketones. .
Recommended publications
  • Different Response of Body Weight Change According to Ketonuria After Fasting in the Healthy Obese
    ORIGINAL ARTICLE Endocrinology, Nutrition & Metabolism http://dx.doi.org/10.3346/jkms.2012.27.3.250 • J Korean Med Sci 2012; 27: 250-254 Different Response of Body Weight Change According to Ketonuria after Fasting in the Healthy Obese Hyeon-Jeong Kim1, Nam-Seok Joo1, The relationship between obesity and ketonuria is not well-established. We conducted a Kwang-Min Kim1, Duck-Joo Lee1, retrospective observational study to evaluate whether their body weight reduction response and Sang-Man Kim2 differed by the presence of ketonuria after fasting in the healthy obese. We used the data of 42 subjects, who had medical records of initial urinalysis at routine health check-up and 1Department of Family Practice and Community Health, Ajou University School of Medicine, Suwon; follow-up urinalysis in the out-patient clinic, one week later. All subjects in the initial 2Department of Family Medicine, CHA Biomedical urinalysis showed no ketonuria. However, according to the follow-up urinalysis after three Center, CHA University College of Medicine, Seoul, subsequent meals fasts, the patients were divided into a non-ketonuria group and Korea ketonuria group. We compared the data of conventional low-calorie diet programs for ± Received: 20 August 2011 3 months for both groups. Significantly greater reduction of body weight (-8.6 3.6 kg vs 2 2 Accepted: 17 January 2012 -1.1 ± 2.2 kg, P < 0.001), body mass index (-3.16 ± 1.25 kg/m vs -0.43 ± 0.86 kg/m , P < 0.001) and waist circumference (-6.92 ± 1.22 vs -2.32 ± 1.01, P < 0.001) was Address for Correspondence: observed in the ketonuria group compared to the non-ketonuria group.
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  • Deficient Diabetic Mice
    Diminished Loss of Proteoglycans and Lack of Albuminuria in Protein Kinase C-␣–Deficient Diabetic Mice Jan Menne,1,2 Joon-Keun Park,2 Martin Boehne,2 Marlies Elger,2 Carsten Lindschau,2 Torsten Kirsch,2 Matthias Meier,2 Faikah Gueler,2 Annette Fiebeler,3 Ferdinand H. Bahlmann,2 Michael Leitges,4 and Hermann Haller2 Activation of protein kinase C (PKC) isoforms has been implicated in the pathogenesis of diabetic nephropathy. We showed earlier that PKC-␣ is activated in the kid- iabetes affects Ͼ300 million people worldwide; -neys of hyperglycemic animals. We now used PKC-␣؊/؊ 20–40% will develop overt nephropathy. Diabe mice to test the hypothesis that this PKC isoform tes is the most common cause of end-stage mediates streptozotocin-induced diabetic nephropathy. Drenal disease. The earliest clinical sign of ne- We observed that renal and glomerular hypertrophy was phropathy is microalbuminuria. Microalbuminuria also ؊ ؊ similar in diabetic wild-type and PKC-␣ / mice. How- heralds impending cardiovascular morbidity and mortality ever, the development of albuminuria was almost absent (1–4). Microalbuminuria predicts overt proteinuria, which ؊/؊␣ in the diabetic PKC- mice. The hyperglycemia-in- is now believed to actively promote renal insufficiency (5). duced downregulation of the negatively charged base- Therefore, successful treatment of diabetic patients ment membrane heparan sulfate proteoglycan perlecan -؊ ؊ should aim for the prevention or regression of albumin was completely prevented in the PKC-␣ / mice, com- pared with controls. We then asked whether transform- uria. Hyperglycemia seems to cause microalbuminuria in ␤ ␤ diabetic patients (6,7). However, how the metabolic dis- ing growth factor- 1 (TGF- 1) and/or vascular endothelial growth factor (VEGF) is implicated in the turbance causes cellular effects is incompletely under- PKC-␣–mediated changes in the basement membrane.
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  • Ideal Conditions for Urine Sample Handling, and Potential in Vitro Artifacts Associated with Urine Storage
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  • KETON.Zemia and KETONURIA in CHILDHOOD. by MURIEL J
    Arch Dis Child: first published as 10.1136/adc.1.5.302 on 1 January 1926. Downloaded from KETON.zEMIA AND KETONURIA IN CHILDHOOD. BY MURIEL J. BROWN, M.B., Ch.B., D.P.H., AND GRACE GRAHAMI, AM.D. From the Medical Department, The Royal Hospital for Sick Children, Glasgow. The formation of ketone bodies and their excretion in the urine in albnormall amounts have for many years been problems of much interest to both physiologist and clinician. Much of our present knowledge of the subject has been gained from the study of carbohydrate metabolism in diabetes, where ketonuria in its classical formi is frequently observed. From this it has been established that an excess of ketone bodies occurs in the blood when the fats are incompletely ' combusted ' as a result of abnormal carbohydrate metabolism, and ample justification has been provided for the well-known sta.tement myiade by Rosenfeld(l) in 1895 ' that fat burns only in the fire of carbohydrate.' A good review of our present knowledge of ketone production and its prevention is to be found in Shaffer's recent lecture entitled ' Antiketo- genesis, its Mechanism and Signifiecance. '(2) A fu-ll discussion of the stubject in all its aspects is not within the scope of the present communication, but we may quote that ' there no Shaffer's statement is to-day question that http://adc.bmj.com/ ketosis is due to carbohydrate starvation,' and make special reference also to his remninder that the inhibitory effect of carbohydrate on ketone formation depends, not on the mnere existence of sufficient glucose, as glucose, in the blood (cf.
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    Article Asymptomatic Bacteriuria and Anti-Microbial Susceptibility Patterns among Women of Reproductive Age. A Cross-Sectional Study in Primary Care, Ghana Prince Afoakwa 1, Seth Agyei Domfeh 1, Bright Oppong Afranie 2,*, Dorcas Ohui Owusu 1, Sampson Donkor 2, Kennedy Kormla Sakyi 3, Richard Akesse Adom 3, Godfred Kyeremeh 1, Bright Afranie Okyere 4, Emmanuel Acheampong 2 and Beatrice Amoah 2 1 Department of Medical Laboratory Technology, Faculty of Health and Allied Sciences, Garden City University College, P.O. Box KS 12775, Kenyasi-Kumasi, Ghana; [email protected] (P.A.); [email protected] (S.A.D.); [email protected] (D.O.O.); [email protected] (G.K.) 2 Department of Molecular Medicine, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, PMB, UPO, Kumasi, Ghana; [email protected] (S.D.); [email protected] (E.A.); [email protected] (B.A.) 3 Department of Microbiology, Tetteh Quarshie memorial hospital, Akuapem Mampong-Korforidua, P.O. Box 26, Ghana; [email protected] (K.K.S.); [email protected] (R.A.A.) 4 Department of Theoretical and Applied Biology, Faculty of Biosciences, Kwame Nkrumah University of Science and Technology, PMB, UPO, Kumasi, Ghana; [email protected] * Correspondence: [email protected]; Tel.: +233-246149286 Received: 2 November 2018; Accepted: 12 December 2018; Published: 17 December 2018 Abstract: Background: Asymptomatic bacteriuria (ASB) poses serious future clinical repercussions for reproductive women. The study determined the prevalence of asymptomatic bacteriuria along with anti-microbial susceptibility patterns among women of reproductive age in a primary care facility. Method: The study recruited a total of 300 women of reproductive age attending the Tetteh Quarshie Memorial Hospital at Akuapem-Mampong, Ghana, between January and March 2018.
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  • Prevalence of Ketosis, Ketonuria, and Ketoacidosis During Liberal Glycemic
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  • Ketonemia and Ketonuria in Gestational Diabetes Mellitus
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  • Diabetic Ketoacidosis
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  • What Tells Routine Urine Examination
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