Proteinuria: Wikis

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Proteinuria
ICD-10 R80.
ICD-9 791.0
DiseasesDB 25320
eMedicine med/94
MeSH D011507

Proteinuria (pronounced /proʊtiːˈnʊəriə/ or /proʊtiːˈnjʊəriə/, from protein and urine) means the presence of an excess of serum proteins in the urine. The protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria),[1] retrograde ejaculation,[2] pneumaturia (air bubbles in the urine) due to a fistula,[3] or drugs such as pyridium.[1]

Contents

Causes

There are three main mechanisms to cause proteinuria:
1. Due to disease in glomerulus
2. Because of increased quantity of proteins in serum (overflow proteinuria)
3. Due to low reabsorbtion at proximal tubule (fanconi)

Measurement

Proteinuria is often diagnosed by a simple dipstick test although it is possible for the test to give a false negative even with nephrotic range proteinuria if the urine is dilute. False negatives may also occur if the protein in the urine is composed mainly of globulins or Bence-Jones Proteins because the reagent on the test strips, Bromphenol blue, is highly specific for albumin. [4][5] Traditionally dipstick protein tests would be quantified by measuring the total quantity of protein in a 24-hour urine collection test, and abnormal globulins by specific requests for Protein electrophoresis.[1][6]

Alternatively the concentration of protein in the urine may be compared to the creatinine level in a spot urine sample. This is termed Protein/Creatinine Ratio (PCR). The 2005 UK Chronic Kidney Disease guidelines states that PCR is a better test than 24 hour urinary protein measurement. Proteinuria is defined as a Protein:creatinine ratio >45 mg/mmol (which is equivalent to Albumin:creatinine ratio of >30 mg/mmol) with very high levels of nephrotic syndrome being for PCR > 100 mg/mmol.[7]

Associated conditions

Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. Diabetics may suffer from damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes and in any person with proteinuria and diabetes the etiology of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field.

With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema, and hydrothorax.

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Conditions with proteinuria as a sign

Proteinuria may be a feature of the following conditions:[5]

Conditions with proteinuria consisting mainly of Bence-Jones proteins as a sign

See also

Footnotes

  1. ^ a b c URINALYSIS Ed Friedlander, M.D., Pathologist - Retrieved 2007-01-20
  2. ^ foamy urine - Urology - MedHelpRetrieved 2007-01-20
  3. ^ Pneumaturia at GPnotebook Retrieved 2007-01-20
  4. ^ http://medlib.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html Retrieved 2007-01-20
  5. ^ a b Simerville JA, Maxted WC, Pahira JJ (2005). "Urinalysis: a comprehensive review". American family physician 71 (6): 1153–62. PMID 15791892. http://www.aafp.org/afp/20050315/1153.html. 
  6. ^ http://www.answers.com/topic/protein-electrophoresis Retrieved 2007-01-20
  7. ^ "Identification, management and referral of adults with chronic kidney disease: concise guidelines" (PDF). UK Renal Association. 2005-09-27. http://www.renal.org/CKDguide/full/Conciseguid141205.pdf.  - see Guideline 4 Confirmation of proteinuria, on page 9
  8. ^ Dettmeyer RB, Preuss J, Wollersen H, Madea B (2005). "Heroin-associated nephropathy". Expert opinion on drug safety 4 (1): 19–28. doi:10.1517/14740338.4.1.19. PMID 15709895. 
  9. ^ Hermann G, Zühlke V, Faul P (1970). "Gamma globulin fragments in urine of kidney transplant patients in relation to rejection crisis". European surgical research. Europäische chirurgische Forschung. Recherches chirurgicales européennes 2 (1): 55–63. PMID 4131420. 
  10. ^ Janice Yang Chou, Dietrich Matern, Brian C. Mansfield, Yuan-Tsong Chen (2002). "Type 1 Glycogen Storage Diseases: Disorders of the Glucose-6-Phosphatase Complex". Current Molecular Medicine 2: 121–143. doi:10.2174/1566524024605798. PMID 11949931. 

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