GLYCOSURIA by STELLA INSTONE, M.D., M.R.C.P

Total Page:16

File Type:pdf, Size:1020Kb

GLYCOSURIA by STELLA INSTONE, M.D., M.R.C.P Postgrad Med J: first published as 10.1136/pgmj.23.258.185 on 1 April 1947. Downloaded from THE DIAGNOSIS AND TREATMENT OF GLYCOSURIA By STELLA INSTONE, M.D., M.R.C.P. Assistant Physician, New Sussex Hospital for Women, Brighton Part I. The Diagnosis of Glycosuria I. Diabetic Glycosuria When a young adult complains of thirst, Introduction excessive hunger, polyuria, exhaustion and Since glycosuria is often found only on loss of weight, the discovery of glycosuria routine examination of the urine, the impor- usually confirms an obvious diagnosis of tance of this simple procedure in every case is Diabetes Mellitus. Milder cases, especially in obvious. Unless this symptom is severe or patients over middle age, may have less marked long-standing, many of these patients make no symptoms. Minor degrees of wasting and suggestive complaint when first seen. lassitude should not be dismissed without When .a reducing substance is found in the examination of the urine, together with a glucose tolerance test, or at least a urine, it is necessary to prove that it is glucose. fasting by copyright. Fehling's solution should not be used, since blood-sugar estimation, if glycosuria is found. this reagent is reduced not only by sugar, but Sometimes one of the complications of also by uric acid, glycuronic acid and diabetes may first suggest the need to test the creatinine; the degree of reduction is slight, urine. Thus the patient may present with usually only a change in colour to green or recurrent boils, carbuncles or other septic vellowish-green. The more delicate Benedict's infection. It is important in such cases not to test may detect such sugars as lactose, laevulose miss a diabetic origin, so that the patient may be or pentose, which need more elaborate tests for properly prepared for any operative treat- http://pmj.bmj.com/ their identification. ment needed. Lactosuria is suggested by the presence of Pulmonary tuberculosis *is common in sugar in the urine during pregnancy or lacta- diabetics, and its symptoms may be few and tion, or when breast-feeding is suddenly undetected unless the chest be X-rayed in stopped. Lactose is identified by the yeast- every case. Less often, the pulmonary lesion fermentation test (glucose being the only sugar may cause symptoms before diabetes is which ferments yeast), and by the characteristic suspected; in these cases a urine test is most on September 29, 2021 by guest. Protected 'hedgehog' crystals of lactosazone. Laevulo- important. suria may occur during the course of liver Nervous symptoms may have a diabetic disease. Pentosuria is extremely rare. basis. In addition to peripheral neuritis, pains The usual type of glycosuria is due to the in the legs resembling sciatica may be associated presence ofglucose in the urine. Four varieties with diabetes, without other suggestive will be considered. symptoms. I. Diabetic Glycosuria. In severe diabetes the tendon reflexes may II. Renal Glycosuria. be absent, and paraesthesia and signs of posterior column involvement may lead to a III. Glycosuria of Cerebral Origin. suspicion of tabes unless their origin is IV. Glycosuria of Endocrine (non- appreciated. In cases of failing vision, the pancreatic) origin. urine should always be tested; diabetic Postgrad Med J: first published as 10.1136/pgmj.23.258.185 on 1 April 1947. Downloaded from i86 POST-GRADUATE MEDICAL JOURNAL APril, I 947 cataract and retinitis can be improved, or at Alimentary Glycosuria least 'arrested in their progress, by early In this condition, after a large meal of treatment. carbohydrate, the patient passes sugar in the urine. There may be no diabetic symptoms, Coma and renal glycosuria may be suspected, but a In every unconscious patient, whatever the glucose tolerance test will show that the blood history, the urine must be examined for sugar, sugar rises abnormally high and takes unduly acetone bodies and albumen. The finding of long to return to its fasting value, which may glycosuria and ketosis strongly suggests be above the normal. These cases are diabetic coma,' but some cerebral lesions may essentially mild diabetics, with lowered carbo- produce these signs (q.v.). If there is a history hydrate tolerance, in which the insulin of previous diabetes the diagnosis is simple. produced is enough to deal with average, but Useful confirmatory signs are' the low ocular not heavy, carbohydrate meals. The transient tension (rarely found except in conditjons of glycosuria sometimes found in fat, hypertensive dehydration leading to coma), dry skin, lips women after middle age, is probably of this and tongue, a smell of acetone in the breath nature. and, if available, laboratory findings showing hypeiglycaemia and a lowered alkali reserve. II. Renal Glycosuria If blood sugar estimations are not available, The normal renal threshold for sugar, is the distinction of hypoglycaemia from diabetic about i8o mgm. per cent. and above this leval coma may be difficult. In the former, the onset the storage mechanisms prevent a further rise is more sudden, the skin moist and sweating of blood sugar. In cases of renal glycosuria, and the ocular tension -normal. Sugar and the renal threshold is lower than normal, and acetone are usually absent from the urine, at these patients pass sugar in the urine when the by copyright. least, in the second specimen obtained. The blood sugar is only I40-I50 mgm. per cent., immediate response to the giving of sugar in' or less. The patient is usually a healthy young hypoglycaemia is also diagnostic. adult without diabetic symptoms. He may Glycosuria may be an incident in coma due complain of recurrent boils, or of local pruritus, to poisoning, uraemia or a cerebral vascular but the glycosuria is often found only on lesion; in such cases there will be charac- routine examination. A glucose tolerance test teristic physical signs. Even when glycosuria shows that' the fasting blood sugar is rather is found, every comatose patient should, be low and that the blood sugar never, rises above http://pmj.bmj.com/ thoroughly examined to make sure that no i8o mgm. per cent.-usually'not above I50 lesion other than diabetes is present. In mgm. per cent.-but that sugar appears in the particular, one should note the state of the urine each time its blood level exceeds I40-150 reflexes, cranial nerves and pupil reactions, mgm. per cent. This test is the only certain also, the presence of any needle marks or signs method of diagnosing renal glycosuria. of poisoning. The breath may smell of acetone and so lead to the detection of III. Glycosuria of Cerebral Origin on September 29, 2021 by guest. Protected glycosuria. Since Claude Bernard first described glyco- When the cause of coma is in doubt, lumbar suria following puncture of the floor of the puncture should be done to exclude the fourth ventricle, the condition has been noted presence of a subarachnoid haemorrhage. In in many basal cerebral lesions. When neuro- some cases of severe diabetic coma, the logical signs predominate the case, and presence of albumen and casts in the urine glycosuria is incidentally found, there is no may suggest uraemia and may cause neglect of difficulty in diagnosis. Some difficulty may the essential treatment with insulin and arise from lesions near the fourth ventricle in glucose. In every case of coma the urine which glycosuria precedes other signs. should be examined for albumen and sugar In some cases of cerebral haemorrhage, and, if possible, the blood urea should be glycosuria and even acetonuria may occur- estimated. the latter following starvation and vomiting. Apl I947 DIAGNOSIS AND TREATMENT OF GLYCOSURIA I87 Postgrad Med J: first published as 10.1136/pgmj.23.258.185 on 1 April 1947. Downloaded from Subarachnoid haemorrhage is suggested by adrenalin upon the blood sugar. Great the sudden onset of intense headache, coma emotional disturbances may possibly produce and signs of meningeal irritation, often with glycosuria by means of an outpouring of glycosuria. The cerebrospinal fluid, first adrenalin. Such an effect would be transient, bloodstained and later stained yellow, is under but it is possible that prolonged mental strain greatly increased pressure, and is diagnostic. might, by the same mechanism, cause diabetes. Internal capsular haemorrhage may track This would explain the common development into the ventricle; but in this coma the onset of diabetes in times of stress. Any disturbance is more rapid than in diabetic coma, and there of function of the ductless glands which are some localizing signs, e.g., hemiplegia and antagonize the pancreas may, if sustained, conjugate deviation of the eyes. cause true diabetes. Glycosuria occurring, for Tuberculous meningitis occurs especially in example, in hyperthyroidism, cannot therefore childhood, in which diabetes is uncommon. be dismissed as unimportant. Even through glycosuria may coexist, the presence of meningeal irritation, ocular pareses Summary of Differential Diagnosis of and raised intracranial pressure should Glycosuria establish the diagnosis. i. The importance of routine examination of the urine is stressed. IV. Endocrine Glycosuria 2. If sugar is found, it must first be identified Sometimes diabetes is part of a generalized as glucose. pancreatic insufficiency; these cases show 3. If glycosuria is accompanied by hunger, other signs such as chronic dyspepsia, steator- thirst, polyuria, loss of weight and lassitude, rhoea, raised blood and urinary diastase, and the diagnosis is diabetes mellitus. a positive Loewi's adrenalin test. The signs Recurrent 4. septic infections, cataract or by copyright. may be due to pancreatitis, neoplasm or retinitis, pulmonary tuberculosis or other syphilitic infection. well-known complications of diabetes, should Glycosuria is not uncommon in thyroid and always call for an examination of the urine. pituitary diseases; the thyroid, pituitary and 5. Inconstant glycosuria in a healthy young suprarenal hormones antagonize insulin, so adult is probably due to a low renal threshold that their hypersecretion may cause a state of for sugar.
Recommended publications
  • Leading Article the Molecular and Genetic Base of Congenital Transport
    Gut 2000;46:585–587 585 Gut: first published as 10.1136/gut.46.5.585 on 1 May 2000. Downloaded from Leading article The molecular and genetic base of congenital transport defects In the past 10 years, several monogenetic abnormalities Given the size of SGLT1 mRNA (2.3 kb), the gene is large, have been identified in families with congenital intestinal with 15 exons, and the introns range between 3 and 2.2 kb. transport defects. Wright and colleagues12 described the A single base change was identified in the entire coding first, which concerns congenital glucose and galactose region of one child, a finding that was confirmed in the malabsorption. Subsequently, altered genes were identified other aZicted sister. This was a homozygous guanine to in partial or total loss of nutrient absorption, including adenine base change at position 92. The patient’s parents cystinuria, lysinuric protein intolerance, Menkes’ disease were heterozygotes for this mutation. In addition, it was (copper malabsorption), bile salt malabsorption, certain found that the 92 mutation was associated with inhibition forms of lipid malabsorption, and congenital chloride diar- of sugar transport by the protein. Since the first familial rhoea. Altered genes may also result in decreased secretion study, genomic DNA has been screened in 31 symptomatic (for chloride in cystic fibrosis) or increased absorption (for GGM patients in 27 kindred from diVerent parts of the sodium in Liddle’s syndrome or copper in Wilson’s world. In all 33 cases the mutation produced truncated or disease)—for general review see Scriver and colleagues,3 mutant proteins.
    [Show full text]
  • Surgeons, Columbia University, New York City) (Received for Publication August 9, 1932)
    THE ADDIS SEDIMENT COUNT IN NORMAL CHILDREN By JOHN D. LYTTLE (From the Babies Hospit and the Department of Pediatrics, Colege of Physicians and Surgeons, Columbia University, New York City) (Received for publication August 9, 1932) THE METHOD In 1925 Addis (1) described a method by which, in a concentrated acid urine, the rate of excretion of protein, casts and red and white cells could be determined. His method, with certain modifications, has been followed here. All of the counts were made on the 12 hour night specimen from 7 or 8 P.M. to 7 or 8 A.M. Addis recommended that fluids be restricted during, and for 12 hours preceding the collection, since in dilute and alkaline urine hyaline casts dissolve and red cells may be completely lysed. With children this rigid restriction of fluid proved impossible. Withholding fluid during the afternoon and night except for 200 cc. at the evening meal, gave urines of such concentration and acidity that they were suitable for a count. Most children had an early supper and col- lections were started at 7 or 8 P.M. Under these conditions, the urinary pH was between 5.0 and 6.0 and the specific gravity usually well above 1.020. The specimens were treated as described by Addis: "the con- centrated night urine is thoroughly mixed by repeated inversion of the rubber-stoppered bottle and a 10 cc. sample is transferred to a special graduated tube, and centrifugalized for five minutes at 1,800 revolutions per minute. The supernatant urine is decanted and pipetted down to a known volume which varies with the amount of sediment as judged by direct observation.
    [Show full text]
  • Inherited Renal Tubulopathies—Challenges and Controversies
    G C A T T A C G G C A T genes Review Inherited Renal Tubulopathies—Challenges and Controversies Daniela Iancu 1,* and Emma Ashton 2 1 UCL-Centre for Nephrology, Royal Free Campus, University College London, Rowland Hill Street, London NW3 2PF, UK 2 Rare & Inherited Disease Laboratory, London North Genomic Laboratory Hub, Great Ormond Street Hospital for Children National Health Service Foundation Trust, Levels 4-6 Barclay House 37, Queen Square, London WC1N 3BH, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-2381204172; Fax: +44-020-74726476 Received: 11 February 2020; Accepted: 29 February 2020; Published: 5 March 2020 Abstract: Electrolyte homeostasis is maintained by the kidney through a complex transport function mostly performed by specialized proteins distributed along the renal tubules. Pathogenic variants in the genes encoding these proteins impair this function and have consequences on the whole organism. Establishing a genetic diagnosis in patients with renal tubular dysfunction is a challenging task given the genetic and phenotypic heterogeneity, functional characteristics of the genes involved and the number of yet unknown causes. Part of these difficulties can be overcome by gathering large patient cohorts and applying high-throughput sequencing techniques combined with experimental work to prove functional impact. This approach has led to the identification of a number of genes but also generated controversies about proper interpretation of variants. In this article, we will highlight these challenges and controversies. Keywords: inherited tubulopathies; next generation sequencing; genetic heterogeneity; variant classification. 1. Introduction Mutations in genes that encode transporter proteins in the renal tubule alter kidney capacity to maintain homeostasis and cause diseases recognized under the generic name of inherited tubulopathies.
    [Show full text]
  • Distribution of Glucose Transporters in Renal Diseases Leszek Szablewski
    Szablewski Journal of Biomedical Science (2017) 24:64 DOI 10.1186/s12929-017-0371-7 REVIEW Open Access Distribution of glucose transporters in renal diseases Leszek Szablewski Abstract Kidneys play an important role in glucose homeostasis. Renal gluconeogenesis prevents hypoglycemia by releasing glucose into the blood stream. Glucose homeostasis is also due, in part, to reabsorption and excretion of hexose in the kidney. Lipid bilayer of plasma membrane is impermeable for glucose, which is hydrophilic and soluble in water. Therefore, transport of glucose across the plasma membrane depends on carrier proteins expressed in the plasma membrane. In humans, there are three families of glucose transporters: GLUT proteins, sodium-dependent glucose transporters (SGLTs) and SWEET. In kidney, only GLUTs and SGLTs protein are expressed. Mutations within genes that code these proteins lead to different renal disorders and diseases. However, diseases, not only renal, such as diabetes, may damage expression and function of renal glucose transporters. Keywords: Kidney, GLUT proteins, SGLT proteins, Diabetes, Familial renal glucosuria, Fanconi-Bickel syndrome, Renal cancers Background Because glucose is hydrophilic and soluble in water, lipid Maintenance of glucose homeostasis prevents pathological bilayer of plasma membrane is impermeable for it. There- consequences due to prolonged hyperglycemia or fore, transport of glucose into cells depends on carrier pro- hypoglycemia. Hyperglycemia leads to a high risk of vascu- teins that are present in the plasma membrane. In humans, lar complications, nephropathy, neuropathy and retinop- there are three families of glucose transporters: GLUT pro- athy. Hypoglycemia may damage the central nervous teins, encoded by SLC2 genes; sodium-dependent glucose system and lead to a higher risk of death.
    [Show full text]
  • Albuminuria Versus Egfr
    Albuminuria versus GFR as markers of diabetic CKD progression KDIGO Controversies Conference: “Diabetic Kidney Disease” New Delhi, March 2012 Richard J MacIsaac PhD FRACP Director of Endocrinology & Diabetes, St Vincent's Hospital Professorial Fellow, University of Melbourne Evolution of Diabetic CKD Incipient Overt Nephropathy Nephropathy GFR 100 Log AER (ml/min) GFR 10 15 20 yrs Normoalbuminuria Microalbuminuria Macroalbuminuria (AER < 20 µµµg/min) (AER 20-200 µµµg/min) (AER > 200 µµµg/min) Stages of CKD Stage eGFR Description Predominant (ml/min/1.73 m2) AER status 1 > 90 Kidney damage with normal/high GFR Normo- Micro- 2 60-89 Kidney damage with mild reduction in GFR Micro- 3 30-59 Kidney damage with moderate reduction in Micro/Macro- GFR 4 15-29 Kidney damage with severe reduction in Macro- GFR 5 < 15 Kidney failure Albuminuria versus GFR as markers of diabetic CKD progression 1. Albuminuria as a predictor of diabetic CKD 2. GFR as a predictor of diabetic CKD 3. Albuminuria & GFR uncoupling/coupling 4. Summary Albuminuria as a marker of diabetic CKD progression • High Variability M N • Low Specificity • Spontaneous Regression µ • Δ AER ≠ Δ GFR Higher levels of urinary albumin excretion within the normal range predict faster decline in glomerular filtration rate in diabetic patients Babazono T et al. Diabetes Care 2009;32:1518-1520 Albuminuria versus GFR as markers of diabetic CKD progression 1. Albuminuria as a predictor of diabetic CKD 2. GFR as a predictor of diabetic CKD 3. ALbuminuria & GFR uncoupling/coupling 4. Summary GFR as
    [Show full text]
  • Biochemical Profiling of Renal Diseases
    INTRODUCTION TO LABORATORY PROFILING Alan H. Rebar, DVM, Ph.D., Diplomate ACVP Purdue University, Discovery Park 610 Purdue Mall, West Lafayette, IN 47907-2040 Biochemical profiling may be defined as the use of multiple blood chemistry determinations to assess the health status of various organ systems simultaneously. Biochemical profiling rapidly has become a major diagnostic aid for the practicing veterinarian for several reasons. First, a more educated clientele has come to expect increased diagnostic sophistication. Secondly, the advent of high-volume clinical pathology laboratories has resulted in low prices that make profiling in veterinary practice feasible and convenient. In addition, improved technology has resulted in the development of procedures that can be used to obtain accurate analyses on microsamples of serum. Such procedures offer obvious advantages to veterinarians, who in the past were hindered by requirements for large sample size. Although biochemical profiling offers exciting potential, it is not a panacea. Since standard chemical screens provide 12 to 30 test results, interpretation of data may be extremely complex. Interpretation is often clouded by the fact that perfectly normal animals may have, indeed, are expected to have, an occasional abnormal test result. It is estimated that in a panel of 12 chemistry tests, approximately 46% of all normal subjects will have at least one abnormal test result. Such abnormalities do not reflect inaccuracies in laboratory test procedures but rather the way in which reference (or normal) values are determined. In order to establish the "normal range" for a given test, the procedure is performed on samples from a large population of clinically normal individuals.
    [Show full text]
  • Cartilage-Hair Hypoplasia
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1969 Cartilage-hair hypoplasia Kenneth A. Vogel University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Vogel, Kenneth A., "Cartilage-hair hypoplasia" (1969). MD Theses. 133. https://digitalcommons.unmc.edu/mdtheses/133 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. CARTILAGE-HAIR HYPOPLASIA By Kenneth Allen Vogele A THESIS Presented to the Faculty of The College of Medicine :in the University of Nebraska In Partial FUlfillment of Requirements For the Degree of I'bctor of Medicine Under the SUperviSion of Carol Angle, 14.D. <halla, Nebraska .April 18, 1969 _____"_U lii"~_"'7l(111W$_"""'---'---_________________________ TABLE OF CONTENTS mTRorocTIOl~ • • ••.•••••••••••••••••••••••••••••••••••••••••••••••••• 1 CI..INICAL FEA.'I'tJRES •••••••••••••••••••••• , ••••••••••••••••••••••••••• 1 The skeleton ••••••••••.•••••••••••••.•••••••••••••..•••••••••• 1 The hair •••••••••••••••••••••••••••••••••••••••••••••••••••••• :3 Motor development •••••••••••••••••••••••••••••••••••••••••••••
    [Show full text]
  • Genetic Disorder
    Genetic disorder Single gene disorder Prevalence of some single gene disorders[citation needed] A single gene disorder is the result of a single mutated gene. Disorder Prevalence (approximate) There are estimated to be over 4000 human diseases caused Autosomal dominant by single gene defects. Single gene disorders can be passed Familial hypercholesterolemia 1 in 500 on to subsequent generations in several ways. Genomic Polycystic kidney disease 1 in 1250 imprinting and uniparental disomy, however, may affect Hereditary spherocytosis 1 in 5,000 inheritance patterns. The divisions between recessive [2] Marfan syndrome 1 in 4,000 and dominant types are not "hard and fast" although the [3] Huntington disease 1 in 15,000 divisions between autosomal and X-linked types are (since Autosomal recessive the latter types are distinguished purely based on 1 in 625 the chromosomal location of Sickle cell anemia the gene). For example, (African Americans) achondroplasia is typically 1 in 2,000 considered a dominant Cystic fibrosis disorder, but children with two (Caucasians) genes for achondroplasia have a severe skeletal disorder that 1 in 3,000 Tay-Sachs disease achondroplasics could be (American Jews) viewed as carriers of. Sickle- cell anemia is also considered a Phenylketonuria 1 in 12,000 recessive condition, but heterozygous carriers have Mucopolysaccharidoses 1 in 25,000 increased immunity to malaria in early childhood, which could Glycogen storage diseases 1 in 50,000 be described as a related [citation needed] dominant condition. Galactosemia
    [Show full text]
  • Guidelines for Approach to a Child with Metabolic Acidosis (Including RTA)
    Guidelines for approach to a child with Metabolic acidosis (including RTA) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the authors reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Sept 2007 Metabolic acidosis ormal acid base balance Maintaining normal PH is essential for cellular enzymatic and other metabolic functions and normal growth and development. Although it is the intracellular PH that matter for cell function, we measure extra cellular PH as 1. It is easier to measure 2. It parallels changes in intracellular PH 3. Subject to more variation because of lesser number of buffers extra cellularly. Normal PH is maintained by intra and extra cellular buffers, lungs and kidneys. Buffers attenuate changes in PH when acid or alkali is added to the body and they act by either accepting or donating Hydrogen ions. Buffers function as base when acid is added or as acid when base is added to body. Main buffers include either bicarbonate or non-bicarbonate (proteins, phosphates and bone). Source of acid load: 1. CO2- Weak acid produced from normal metabolism, dealt with by lungs pretty rapidly(within hours) 2.
    [Show full text]
  • Proteinuria and Albuminuria: What’S the Difference? Cynthia A
    EXPERTQ&A Proteinuria and Albuminuria: What’s the Difference? Cynthia A. Smith, DNP, CNN-NP, FNP-BC, APRN, FNKF What exactly is the difference between TABLE Q the protein-to-creatinine ratio and the Persistent Albuminuria Categories microalbumin in the lab report? How do they compare? Category Description UACR For the non-nephrology provider, the options for A1 Normal to mildly < 30 mg/g evaluating urine protein or albumin can seem con- increased (< 3 mg/mmol) fusing. The first thing to understand is the impor- tance of assessing for proteinuria, an established A2 Moderately 30-300 mg/g marker for chronic kidney disease (CKD). Higher increased (3-30 mg/mmol) protein levels are associated with more rapid pro- A3 Severely > 300 mg/g gression of CKD to end-stage renal disease and in- increased (> 30 mg/mmol) creased risk for cardiovascular events and mortality in both the nondiabetic and diabetic populations. Abbreviation: UACR, urine albumin-to-creatinine ratio. Monitoring proteinuria levels can also aid in evaluat- Source: KDIGO. Kidney Int. 2012.1 ing response to treatment.1 Proteinuria and albuminuria are not the same low-up testing. While the UACR is typically reported thing. Proteinuria indicates an elevated presence as mg/g, it can also be reported in mg/mmol.1 Other of protein in the urine (normal excretion should be options include the spot urine protein-to-creatinine < 150 mg/d), while albuminuria is defined as an “ab- ratio (UPCR) and a manual reading of a reagent strip normal loss of albumin in the urine.”1 Albumin is a (urine dipstick test) for total protein.
    [Show full text]
  • Understanding What It Means to Have Protein in Your Urine Understanding What It Means to Have Protein in Your Urine
    UNDERSTANDINGUnderstanding WHAT ITYour MEANS TO HAVE Hemodialysis PROTEINAccess Options IN YOUR URINE 2 AAKP: Understanding What It Means to Have Protein in Your Urine Understanding What It Means to Have Protein in Your Urine The kidneys are best known for making urine. This rather simple description does not tell the whole story. This brochure describes other important functions of the kidneys; including keeping protein in the blood and not letting any of the protein in the liquid (plasma) part of blood escape into the urine. Proteinuria is when “Proteinuria” is when kidneys allow proteins to kidneys appear in the urine and be lost from the body. allow Proteinuria is almost never normal, but it can proteins to be normal - rarely - in some healthy, active appear in the urine children or young adults. and be The kidneys are paired organs located on either lost from the body. side of the backbone. They are located at the Proteinuria level of the lowest part of the rib cage. They are is almost the size of an adult fist (4.5 – 5 inches in length). never Together the two kidneys receive a quarter of normal, but it can the blood that is pumped from the heart every be normal minute. This large blood flow is needed in order - rarely - for the kidneys to do one of the kidneys’ main in some jobs: healthy, active • remove waste products in the blood every children day or young adults. • keep the body in balance by eliminating the extra fluids and salts we consume on a regular basis.
    [Show full text]
  • Tests for Abnormal Constituents in Urine
    By Sandipkumar Kanazariya Tuesday, December 11, 2018 1 Under pathological conditions urine excreted by patient shows the presence of abnormal constituents along with normal constituents. Abnormal constituents of urine are sugar, proteins, blood, bile salts, bile pigments and ketone bodies. Tuesday, December 11, 2018 2 A. Physical Characteristics 1. Volume : a. Polyuria: Volume more than 3000 ml / 24 hours It is observed in Diabetes mellitus, Diabetes insipidus, Addison’s disease, Chronic progressive renal failure, excess water intake, intake of diuretics like caffeine, alcohol etc. b. Oliguria: Volume less than 400 ml / 24 hours. It is observed in fluid deprivation, excess fluid loss as in hemorrhage and neurogenic shock, dehydration, acute glomerulonephritis, obstruction in the urinary tract, disease of heart and lungs & strenuous muscular exercise. Tuesday, December 11, 2018 3 c. Anuria: Less than 150ml / 24hrs Complete absence of urine output. It is observed in shock and renal failure. Tuesday, December 11, 2018 4 2. Colour:- The colour of urine is variable in following disease conditions as given following table Sr. No Colour possible causes/ disorder 1 Colour less Fatty disease, diabetes mellitus, Polyuria 2 Yellowish brown Bile pigment, fever 3 Reddish brown Hemoglobin in urine, hemorrhage, menstrual contamination 4 Milky Presence of Fat 5 Dark Yellow Fever 6 Dark green typhoid and cholera 7 Black Due to Melanin (Melanoma) or Homogentisic acid in Tuesday, December 11, 2018 Alkaptonuria 5 3. Odour:- Normal urine has faint aromatic odour. On standing it has ammoniacal odour due to bacterial contamination. Odour of urine is variable in certain diseased condition. Sr. No Odour diseases 1 Fruity odour ketosis 2 Cabbage type odour methionine Malabsorption 3 Maple sugar odour maple sugar urine disease(MSUD) 4 Mousy phenylketonuria 5 Rancid odour tyrosine 6 Foul Urinary Tract Infection, Tuesday, December 11, 2018 Vaginitis 6 Tuesday, December 11, 2018 7 4.
    [Show full text]