Skip to main content
UploadLanguage (EN)Support
BusinessMobileSocial MediaMarketingTechnologyArt & PhotosCareerDesignEducationPresentations & Public SpeakingGovernment & NonprofitHealthcareInternetLawLeadership & ManagementAutomotiveEngineeringSoftwareRecruiting & HRRetailSalesServicesScienceSmall Business & EntrepreneurshipFoodEnvironmentEconomy & FinanceData & AnalyticsInvestor RelationsSportsSpiritualNews & PoliticsTravelSelf ImprovementReal EstateEntertainment & HumorHealth & MedicineDevices & HardwareLifestyle
Sharlene Sy, profile picture
Uploaded bySharlene Sy
PPTX, PDF33,015 views

Glucosuria

Glucosuria, or glucose in the urine, can occur due to diabetes mellitus resulting in hyperglycemia that exceeds the renal threshold, or due to renal tubular disorders resulting in glycosuria without hyperglycemia. Renal glycosuria is caused by defects in glucose transporters like SGLT2 that normally reabsorb glucose from the glomerular filtrate in the proximal tubule. This leads to glucose appearing in the urine despite normal blood glucose levels. Renal glycosuria is usually benign and inherited in an autosomal recessive pattern, though it can also be caused by advanced chronic kidney disease.

Health & Medicine◦
Downloaded 361 times
Glucosuria An Overview
Glucose • Six-carbon reducing sugar • Essential for: • Production of cellular energy and ATP • Most frequently performed chemical analysis in urine • Detection and monitoring of: • Diabetes mellitus and • Renal tubular disorders
What is Glycosuria?  Appearance of glucose in urine following cessation of active transport (tubular reabsorption) as renal threshold is exceeded 160 – 180 mg/dL  What is the renal threshold?  90% filtered glucose is reabsorbed in the PCT Tubular maximum for glucose reabsorption: 260350 mg/min/1.73 m2  Remaining: proximal straight tubule, loop of Henle, collecting duct  0.05% of renal glucose load -> excreted in urine
Glucose Reagent Strip  Provides a specific test for glucose  Strip pads are impregnated with glucose oxidase and peroxidase ( double sequential enzyme reaction)  False positive: detergent, peroxide, strong oxidizing agents  False negative: ascorbic acid, ketones, high specific gravity, low temperature and improper preservation of long-standing urine
Random Blood Sugar Glucosuria Glycosylated Hemoglobin Hyperglycemia Diabetes mellitus until proven otherwise Without Hyperglycemia
Causes of glycosuria  Glycosuria with hyperglycaemia- diabetes,acromegaly, cushing’s disease, hyperthyroidism, drugs like corticosteroids.  Glycosuria without hyperglycaemia- renal tubular dysfunction
Diabetes mellitus  Diabetes mellitus (DM) is an important endocrine disorder that presents commonly in children and adolescents. Diabetes mellitus Type I   Diabetes mellitus Type II one of the most common chronic diseases in children  Characterized by insulin deficiency as a result of autoimmune destruction of pancreatic beta islet cells; Presence of high blood glucose with insulin resistance and relative insulin deficiency  Estimated 3600/100,000 cases of type 2 DM in Canadian adolescents and
Diabetes mellitus Type I  Approximately 2/3 of all new diabetes diagnoses in patients less than 19 years of age in the United States are type 1 DM.  Age of onset has a bimodal distribution,   first peak in children 4-6 years old, and the second peak in children 10-14 years old (early puberty).
Glycosuria with Hyperglycemia Diabetes mellitus Type I  autoimmune-mediated destruction of insulin-producing pancreatic beta cells that results in insulin deficiency.  It is a progressive condition  A large number of functional beta cells must be lost before clinical symptoms like hyperglycemia occurs. Classic new onset: Hyperglycemia without acidosis
Glycosuria with Hyperglycemia Diabetes mellitus Type I    Symptoms include: Polyuria – serum glucose > 10 mmol/L (exceeding renal threshold for glucose à increased urinary glucose excretion) Can present as nocturia, bedwetting, daytime incontinence in a previously continent child  Polydipsia – due to increased serum osmolality and hypovolemia  Weight loss – due to hypovolemia and increased catabolism  Impaired glucose utilization in skeletal muscle and increased fat and muscle breakdown
Glycosuria with Hyperglycemia Diabetes mellitus Type I   Clinical: polydipsia, polyuria, dehydration, hypotension, ketosis, etc. Metabolic: hyperglycemia, glycosuria, metabolic acidosis, ketonemia, etc.  Reported frequency varies between 15-67%  Young children (<6) from low socioeconomic backgrounds are more likely to present with diabetic ketoacidosis  Silent Presentation  Diagnosis before onset of clinical symptoms  Typically occurs in children with a family member with type 1 DM (close monitoring)
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction • Rare metabolic disorder; • excretion of glucose in the urine in the presence of normal plasma glucose levels. • Inherited form: involves a reduction in the glucose transport maximum (the maximum rate at which glucose can be resorbed) and subsequent escape of glucose in the urine. • Glucose transporters: • Acquired form: occurs primarily in advanced chronic kidney disease.
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  Variable amounts of glucose are excreted in the urine at normal concentrations of blood glucose  Renal defect is specific for glucose only  A benign condition  The metabolism, storage and use of carbohydrates and insulin secretions are normal
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  The disorder is typically initially noted on routine urinalysis.  Diagnosis is based on finding glucose in a 24-h urine collection (when the diet contains 50% carbohydrate) in the absence of hyperglycemia (serum glucose < 140 mg/dL).  To confirm that the excreted sugar is glucose and to exclude pentosuria, fructosuria, sucrosuria, maltosuria, galactosuria, and lactosuria, the glucose oxidase  Method should be used for all laboratory measurements. Some experts require a normal result on an oral glucose tolerance test for the diagnosis.
How to Differentiate Renal Glucosuria VS. Fasting Blood Sugar OGTT Diabetes mellitus
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  Autosomal recessive, some autosomal dominant  Mechanism: isolated, selective defect in the proximal tubular glucose trasnport  Two Types:  Type A or Classic Renal Glycosuria:  Minimal glucose threshold and maximum rate of glucose reabsorption are reduced  Reflects reduction in the capacity of the glucose transport system which might arise from a uniform defect in all nephrons  Type B  Minimal glucose threshold is reduced  Decrease in the affinity of the transport system
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  As of 2000: SGLT2 gene (SLC5A2) -> established to be the mutated gene in hereditary renal glycosuria  To date, close to 30 mutations have been identified in patients with hereditary renal glycosuria  Type O  Rare  Tubular reabsorption of glucose is virtually absent and all glucose filtered is excreted in the urine
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction Defect in glucose cotransporter (SGLT2/SLC5A2) • Defect in the early proximal tubule, • Reabsorbs most renal tubular glucose, • Produce type A or type O, classic renal glycosuria • Has no effect on glucose absorption in the intestine. Defect in SGLT1/SLC5A1, glucose cotransporter • Defect in the late proximal tubule (which also carries galactose) • Mediates residual glucose reabsorption in the renal tubule and, • when defective as in glucose-galactose malabsorption, • causes only mild type B renal glycosuria.
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  As of 2000: SGLT2 gene (SLC5A2) -> established to be the mutated gene in hereditary renal glycosuria  Other mutations of SLC5A2  Renal glycosuria + generalized aminoaciduria  a feature of MODY 3 (maturity-onset diabetes of the young type 3)
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  Glucose-Galactose Malabsorption  Potentially lethal disease  Autosomal recessive disease  Missense mutation in the intestinal brush-border SGLT1 N+-glucose cotransporter  HOMOZYGOTES: neonatal onset of severe atry diarrhea that results in death unless glucose and galactose are removed
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  Glucose-Galactose Malabsorption  Jejunal biopsy: defect in intestinal Na+- dependent glucose transport  Mild defect in renal tubular reabsorption of glucose with decreased renal threshold for glucose  Renal glycosuria: mutation in SGLT2  No defect in intestinal D-gluose absorption
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction Defect in glucose cotransporter (SGLT2/SLC5A2) • Defect in the early proximal tubule, • Reabsorbs most renal tubular glucose, • Produce type A or type O, classic renal glycosuria • Has no effect on glucose absorption in the intestine. Defect in SGLT1/SLC5A1, glucose cotransporter • Defect in the late proximal tubule (which also carries galactose) • Mediates residual glucose reabsorption in the renal tubule and, • when defective as in glucose-galactose malabsorption, • causes only mild type B renal glycosuria.
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  Mutations on the gene GLUT2 (SLC2A2) - - the glucose transported on the basolateral membranebound  Associated with glycosuria in the Fanconi-Bickel Syndrome  Fanconi-Bickel Syndrome  Autosomal recessive  Hepatorenal glycogen accumulation  Fasting hypoglycemia  Impaired utilization of glucose and galactose
Glycosuria without Hyperglycemia Renal Glycosuria Dysfunction  Rickets, stunted growth, fanconi syndrome  Renal loss of glucose  Due to the transport defect for monosaccharides across the basolateral membrane
Glucosuria