Ketones, Urine

Copy Link

Lab Dept:
Urine/Stool

Test Name:
KETONES, URINE

General Information

Lab Order Codes: Synonyms:

UKE Urine Ketones; Nitroprusside Reaction for Ketones 81003 – Urinalysis, by dipstick; automated, without microscopy Screen for urine ketones.

CPT Codes: Test Includes:

Logistics

Test Indications:

Useful for evaluation of ketonuria, detection of acidosis, ketoacidosis, fasting, starvation, high protein diets, diabetes mellitus, and stresshormone excess.

Lab Testing Sections: Phone Numbers:

Urinalysis MIN Lab: 612-813-6280 STP Lab: 651-220-6550 Daily, 24 hours 1 hour

Test Availability: Turnaround Time: Special Instructions:

Submit only one (1) of the following: Catheterized specimen or cleancatch 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: Container:

Urine Urine cup

Draw Volume: Processed Volume:

Entire specimen collection (catheter or clean catch) Minimum: 0.5 mL urine

Collection:

A specimen collected by catheterization is optimal; however, a cleancatch 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: Patient Preparation: Sample Rejection:

N/A None Less than 0.5 mL urine submitted; mislabeled or unlabeled specimen

Interpretive

Reference Range: Critical Values: Limitations:

Negative N/A 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: References:

Multistix®, Nitroprusside reaction 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.
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.
Ideal Conditions for Urine Sample Handling, and Potential in Vitro Artifacts Associated with Urine Storage

Urinalysis Made Easy: The Complete Urinalysis with Images from a Fully Automated Analyzer A. Rick Alleman, DVM, PhD, DABVP, DACVP Lighthouse Veterinary Consultants, LLC Gainesville, FL Ideal conditions for urine sample handling, and potential in vitro artifacts associated with urine storage 1) Potential artifacts associated with refrigeration: a) In vitro crystal formation (especially, calcium oxalate dihydrate) that increases with the duration of storage i) When clinically significant crystalluria is suspected, it is best to confirm the finding with a freshly collected urine sample that has not been refrigerated and which is analyzed within 60 minutes of collection b) A cold urine sample may inhibit enzymatic reactions in the dipstick (e.g. glucose), leading to falsely decreased results. c) The specific gravity of cold urine may be falsely increased, because cold urine is denser than room temperature urine. 2) Potential artifacts associated with prolonged storage at room temperature, and their effects: a) Bacterial overgrowth can cause: i) Increased urine turbidity ii) Altered pH (1) Increased pH, if urease-producing bacteria are present (2) Decreased pH, if bacteria use glucose to form acidic metabolites iii) Decreased concentration of chemicals that may be metabolized by bacteria (e.g. glucose, ketones) iv) Increased number of bacteria in urine sediment v) Altered urine culture results b) Increased urine pH, which may occur due to loss of carbon dioxide or bacterial overgrowth, can cause: i) False positive dipstick protein reaction ii) Degeneration of cells and casts iii) Alter the type and amount of crystals present 3) Other potential artifacts: a) Evaporative loss of volatile substances (e.g.
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.
Asymptomatic Bacteriuria and Anti-Microbial Susceptibility Patterns Among Women of Reproductive Age

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.
Plasma 'Ketone' Levelin the Diagnosis and Treatment of Diabetic Acidosis

Postgrad. med. J. (October 1968) 44, 799-802. Postgrad Med J: first published as 10.1136/pgmj.44.516.799 on 1 October 1968. Downloaded from Plasma 'ketone' level in the diagnosis and treatment of diabetic acidosis M. S. KNAPP MARGARET E. HORN M.D., M.R.C.P. M.B., M.R.C.P. Lecturer in Medicine, University ofBristol Medical Registrar, Bristol Royal Hospital All patients in possible diabetic acidosis admit- Summary ted to one of the medical firms at the Bristol A simple method of estimating the plasma Royal Infirmary over a 3-year period had an 'ketone' level with 'Acetest' tablets has been used estimation of the plasma 'ketone' level performed in the diagnosis and treatment of diabetic acid- by the clinical staff in the ward side-room. In osis. The method is valuable when used in those patients treated for a moderate or severe association with full biochemical facilities, but it diabetic keto-acidosis the estimation was is especially useful in situations where these can- repeated, usually every four hours. The second not be easily obtained. and subsequent doses of insulin were based to a considerable extent on the plasma 'ketone' titre. Introduction If the titre had not fallen or had risen, an in- In a patient suspected of having diabetic keto- creased dose of insulin was given. A fall in titre acidosis it is useful to be able to rapidly confirm indicated a satisfactory response and either a Protected by copyright. the diagnosis. In this situation we have used a similar dose or a smaller one was used, depending simple side-room method for the detection of on previous blood sugar results.
Medical Assessment of Drug Induced Rhabdomyolysis and Metabolic Disorders

ISoP Training Course- Zagreb, 3-4 April 2014 Medical assessment of drug induced rhabdomyolysis and metabolic disorders Marco Tuccori, ISoP EC member Unit of Adverse Drug Reacon Monitoring University Hospital of Pisa, Pisa, Italy At the forefront of pharmacovigilance around the world 1 ISoP training course Zagreb 3-4 April 2014 Proacve Pharmacovigilance, Risk Management and Pharmacovigilance in the Era of Personalised Medicine All presentaons provided as PDF files are protected by copyright. Prinng and storage is for scholarly research, educaonal and personal use only. Any copyright or other noces or disclaimers must not be removed, obscured or modified. If used for training the original source must be properly credited. Copying and make copies of the PDF presentaons (including through e-mail) are not permied. The PDF files must not be posted on an open- access website. At the forefront of pharmacovigilance around the world 2 Summary • Metabolic adverse reactions • Muscular adverse reactions • Definitions and classifications • Signs and symptoms • Main (alternative) causes • Drugs most frequently involved • Biological plausibility • Drug-induced lipids metabolism alterations • Drug-induced glucose metabolism alterations At the forefront of pharmacovigilance around the world 3 Metabolic Adverse Reacons Metabolism is the set of life-sustain- ing chemical transformations within the cells of living organisms. These enzyme-catalyzed reactions allow organisms to grow and reproduce, maintain their structures, ? and respond to their environments. DRUGS Lipids Myopathies Carbohydrates At the forefront of pharmacovigilance around the world 4 Muscular adverse events Definions and Classificaons Term ACC/AHA/NHLBI NLA FDA Myopathy Any disease of the Symptoms of myalgia (muscle CK > 10 ULN muscle pain or soreness), weakness.
Urinary Albumin Excretion Rate Is Associated with Increased Ambulatory Blood Pressure in Normoalbuminuric Type 2 Diabetic Patients

Pathophysiology/Complications ORIGINAL ARTICLE Urinary Albumin Excretion Rate Is Associated With Increased Ambulatory Blood Pressure in Normoalbuminuric Type 2 Diabetic Patients 1 1 CRISTIANE B. LEITAO˜ , MD MARCEL P. MOLON emerging evidence that patients with dia- 1 2 LUÍS H. CANANI, MD ANTONIOˆ F. PINOTTI, MD betes in the high-normal range of UAER 1 1 PATRÍCIA B. POLSON JORGE L. GROSS, MD are already at high risk for progressing to microalbuminuria or even more ad- vanced stages of renal disease (6–9). Arterial hypertension follows the es- tablishment of microalbuminuria in pa- OBJECTIVE — To evaluate the 24-h blood pressure profile in normoalbuminuric type 2 tients with type 1 diabetes (10). In type 2 diabetic patients. diabetes, this relationship is not that clear because hypertension is a common fea- RESEARCH DESIGN AND METHODS — A cross-sectional study was conducted in 90 type 2 diabetic patients with a urinary albumin excretion rate (UAER) Ͻ20 ␮g/min on two ture in these patients, regardless of renal occasions, 6 months apart (immunoturbidimetry). Patients underwent clinical and laboratory status (11). Ambulatory 24-h blood pres- evaluations. Ambulatory blood pressure monitoring and echocardiograms were also performed. sure monitoring has a better correlation with target organ damage than doctor’s RESULTS — UAER was found to correlate positively with systolic doctor’s office blood pres- office blood pressure measurements (12) sure measurements (r ϭ 0.243, P ϭ 0.021) and ambulatory blood pressure (24 h: r ϭ 0.280, P ϭ and allows the evaluation of blood pres- 0.008) and left ventricular posterior wall thickness (r ϭ 0.359, P ϭ 0.010).
Prevalence of Ketosis, Ketonuria, and Ketoacidosis During Liberal Glycemic

Luethi et al. Critical Care (2016) 20:297 DOI 10.1186/s13054-016-1462-7 RESEARCH Open Access Prevalence of ketosis, ketonuria, and ketoacidosis during liberal glycemic control in critically ill patients with diabetes: an observational study Nora Luethi1, Luca Cioccari1,2, Marco Crisman1,3, Rinaldo Bellomo1,4, Glenn M. Eastwood1 and Johan Mårtensson1,5* Abstract Background: It is uncertain whether liberal glucose control in critically ill diabetic patients leads to increased ketone production and ketoacidosis. Therefore, we aimed to assess the prevalence of ketosis, ketonuria and ketoacidosis in critically ill diabetic patients treated in accordance with a liberal glycemic control protocol. Methods: We performed a prospective observational cohort study of 60 critically ill diabetic patients with blood and/or urine ketone bodies tested in ICU. All patients were treated according to a liberal glucose protocol targeting a blood glucose level (BGL) between 10 and 14 mmol/l in a single tertiary intensive care unit in Australia. We measured quantitative bedside blood 3-beta-hydroxybutyrate (β-OHB) and semi-quantitative urine ketones on ICU admission and daily during ICU stay, for a maximum of 10 consecutive days. Results: Median blood β-OHB level on admission was 0.3 (0.1, 0.8) mmol/l. Ketoacidosis was rare (3 %), but some level of ketosis (β-OHB ≥0.6 mmol/l) was found in 38 patients (63 %) early during their ICU stay. However, there was no significant difference in prevalence or severity of ketonemia and ketonuria among patients with BGL above (permissive hyperglycemia) or below 10 mmol/l. On multivariable linear regression analysis there was no association between blood ketone levels and BGL, HbA1c, lactate levels, hematocrit, catecholamine infusion or APACHE III score.
Ketonemia and Ketonuria in Gestational Diabetes Mellitus

HORMONES 2015, 14(4):644-650 Research paper Ketonemia and ketonuria in gestational diabetes mellitus Loukia Spanou,1 Kalliopi Dalakleidi,2 Konstantia Zarkogianni,2 Anastasia Papadimitriou,1 Konstantina Nikita,2 Vasiliki Vasileiou,1 Maria Alevizaki,1 Eleni Anastasiou1 1Diabetes Center, 1st Endocrine Section, Alexandra General Hospital, Athens; 2Faculty of Electrical and Computer Engineering, National Technical University of Athens, Athens; Greece ABSTRACT %$&.*5281'7KHXVHRIFDSLOODU\EORRGȕK\GUR[\EXW\UDWH +% LVDPRUHSUHFLVH method than urine ketones measurement for the diagnosis of diabetic ketoacidosis. Fasting ketonuria is common during normal pregnancy, while there is evidence that it is increased among pregnant women with Gestational Diabetes Mellitus (GDM) who are on a diet. 3HB levels have been related to impaired offspring psychomotor development. Reports with concomitant measurement of blood and urine ketones in women with GDM who followed a balanced diet are lacking. OBJECTIVE: To compare the prevalence of fasting ketonemia and ketonuria in women with GDM following the Institute of Medicine diet instructions and assess their possible relation with metabolic parameters and therapeutic interventions. RESEARCH DESIGN AND METHODS: 180 women with GDM were studied. In each patient, in successive visits, capillary blood and urine ketones were simultaneously measured. The total measurements were 378, while the average number of measurements per patient was 2.1. RESULTS: The prevalence of ketonuria was significantly higher than that of ketonemia (x2=21.33, p <0.001). Significantly higher mean 3HB levels were observed with respect to ketonuria severity (p=0.001). Bedtime carbohydrate intake was associated with significantly lower 3HB levels (p=0.035). Insulin treatment was associated with significant 3HB levels reduction (p=0.032).
Diabetic Ketoacidosis

Diabetic ketoacidosis Diabetic Ketoacidosis Dr. Christiane Stengel Dipl. ECVIM-CA (IM) FTÄ für Kleintiere High blood glucose with the presence of ketones in the urine and bloodstream, often caused by having/giving too little insulin or during illness. Dr. Christiane Stengel Diabetic ketoacidosis v Diabetes mellitus not diagnosed so far (common) v Or „derailed“ Diabetes (possible) & a “triggering condition” lead to increased „counter- regulatory“ hormones: o Glucagon ↑ o Cortisol ↑ o Adrenalin ↑ o GH ↑ v Low insulin and high glucagon increased glucagon:insulin-ratio medpets.de v Bacterial infections v Endocrine disease o Urinary tract o Hypercortisolism o Pneumonia o Hypothyroidism o Pyometra /prostatitis o Hyperthyroidism o Pyoderma o Acromegaly v Inflammatory v Physiological condition endocrine change o Pancreatitis o Dioestrus v Iatrogenic v Miscellaneous o Steroid administration o Chronic kidney disease o Neoplasia Dr. Christiane Stengel Diabetic ketoacidosis v Vomiting, lethargy, anorexia, weakness, (PU/PD), triggering effect signs v Severe dehydration (hypovolaemic shock) o Glukosuria osmotic diuresis o Ketonuria osmotic diuresis o Fluid loss from vomiting o Decreased fluid intake from anorexia and lethargy A. Kussmaul v Tachycardia, change in pulse quality, colour and capillary refill time v Increased breathing effort (often with normal frequency) due to metabolic acidosis (Kussmaul breathing) , ketone smell v Haematology v Biochemistry profile ± ketones in plasma v Urinalysis and urine culture v Blood gas analysis v ± abdominal
What Tells Routine Urine Examination

What tells Routine Urine Examination Specific gravity Animals producing large volume of urine have low specific gravity where as very small volume of urine has high specific gravity (animal with oliguric acute intrarenal failure that has a low urine volume and low specific gravity). Fluid therapy, diuretics, glucocorticoids and diet affect urine specific gravity. Sp. gr. is higher in morning samples and was observed to decrease as the age of the animal increased. Urine pH Acidic urine: - ingestion of meat, respiratory and metabolic acidosis, severe vomition, severe diarrhea, starvation, pyrexia, other protein catabolic states and administration of urinary acidifiers. Alkaline urine:- recent meal, ingestion of alkali, UTI with urease-producing bacteria, renal tubular acidosis, diets rich in vegetables and cereals, and metabolic and respiratory alkalosis, urine allowed to stand open to air at room temperature. Proteinuria Trace or 1+ protein level is considered normal with a specific gravity greater than 1.035. Highly alkaline urine (>8) can produce a false positive result. The most common cause of inflammatory proteinuria is urinary tract infection (UTI). If hematuria and pyouria is ruled out, then another urinalysis should be performed to determine the persistent proteinuria. Transient proteinuria is due to strenuous exercise, fever, seizures, and venous congestion of the kidneys and it is insignificant. Persistent proteinuria is usually due to glomerulonephritis or amyloidosis. The urine protein: creatinine ratio helps to determine the magnitude and significance of proteinuria. Glucosuria False negative results come due to large quantity of ascorbic acid, contaminated with H2O2, Cl, hypochlorite, formaldehyde or fluorides in urine. Cats with cystitis may give a false positive reaction.