The Urine Dipstick
March 12th, 2023
The urine dipstick is used to assess for a wide variety of renal, urinary tract and systemic pathologies. Using a paper strip containing several reagent-containing squares corresponding to blood, glucose, protein and other analytes, it is possible to gain a significant amount of insight into the cause of a patient's presentation.
There are many ways in which a urine sample can be collected. The method of collection depends on the type of test performed, and certain patient factors.
Types of Urine Collection
- Random urine - taken at any time; Used for testing of electrolytes etc.
- Morning urine - the first urine of the day is the most concentrated, increasing the yield; Used for urinalysis, microscopy and beta-HCG testing
- Clean catch / midstream urine - the first few mL are discarded and then urine is collected, removing urethral bacterial flora from the sample; Best for urine culture and sensitivity testing
- 24 hour urine - all of the urine passed over 24 hours is collected; Used to measure certain analytes, such as creatinine, protein, electrolytes, uric acid, cortisol, catecholamines / metanephrines
- Catheterised sample - e.g. from an in and out / indwelling / suprapubic catheter
- Suprapubic aspiration - a needle is used to aspirate urine; May be required if a patient cannot be catheterised, or if sterile urine absolutely must be collected
The colour and consistency of a patient's urine can provide significant information regarding the cause of their urinary complaint.
Urine is normally clear and pale yellow.
ColourDark yellow or brown urine is classically a sign of dehydration, though urine may be a variety of colours that suggest underlying pathology:
- Clear urine - high fluid intake, diabetes insipidus, diabetes mellitus, diuretic use
- Yellow / orange urine - concentrated urine (dehydration), bilirubin
- Brown urine - very concentrated urine (dehydration), haemoglobin (haemolysis), metastatic melanoma
- Black urine - iron, L-dopa, metastatic melanoma, porphyria
- Red urine - blood, haemoglobin (haemolysis), myoglobin (rhabdomyolysis), porphyria, beetroot, malingering
- White urine - lipiduria, propofol infusion, proteinuria, pyuria (UTI), minerals (calcium, oxalate, phosphate)
- Blue / green urine - amitriptyline, indomethicin, porphyria, pseudomonal infection, food dye
- Purple urine - purple urine bag syndrome (UTI causing metabolism of tryptophan to indole then indicant)
- Turbid or cloudy urine suggests pyuria, due to infection or inflammation; the turbidity may also be due to lipids (lipiduria) or lymphatic fluid (chyluria). Frothy urine suggests the presence of proteinuria.
- Urine smell has historically been useful, however is currently rarely used in clinical practice.
A strong urine smell suggests that the patient is dehydrated. Sweet urine classically suggests glycosuria in the context of diabetes, while an ammonia smell suggests urinary tract infection. Faeculant-smelling urine raises concern for a colovesical fistula.
Urine pH is a measure of the acid content in urine. This often reflects the acidity of serum, however there are certain cases (e.g. renal tubular acidosis) in which the urine pH does not match the serum pH.
The normal urine pH is 4.5 - 8.0.
A reduction in urine pH suggests an abundance of acid in the urine. This may be due to a high protein diet, ingestion of acidic foods (like cranberries), any cause of metabolic acidosis, or respiratory acidosis.
An increase in the urine pH suggests an abundance of base in the urine. This is commonly a sign of infection with a urease-producing bacteria, which convert urea into the alkaline ammonia. Alkaluria may also occur in the presence of metabolic alkalosis, respiratory alkalosis, renal tubular acidosis or a low carbohydrate diet.
The urine specific gravity is a measure of the amount of solute compared to water. Pure water has a specific gravity of 1.000, and the specific gravity of urine is normally 1.002 - 1.035.
- If the urine specific gravity is increased then this reflects an inability to produce dilute urine. As a result, the urine is excessively concentrated. This may be due to:
- Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
- Adrenal insufficiency
- Hypervolaemic hyponatraemia - liver cirrhosis, CCF or nephrotic syndrome
- Glycosurea (diabetes)
- Proteinuria (e.g. glomerulonephropathy, myeloma)
- If the urine specific gravity is reduced, this reflects an inability to concentrate urine. As a result, the urine is excessively diluted. This may be due to:
- Polydipsia (excessive fluid consumption)
- Diabetes insipidus
- Acute tubular necrosis
Leukocyte esterase (LE) is an enzyme produced by white blood cells. Its presence in urine is indicative of an increase in leukocytes in urine, also known as pyuria. This classically indicates urinary tract infection, however can also occur in the presence of renal or urinary tract inflammation, neoplasia, irradiation or foreign body.
Bacteria convert nitrates into nitrites within urine, and therefore the presence of nitrites within urine is highly suggestive of (usually gram negative) bacterial urinary tract infection.
A urine dipstick is able to detect urinary haemoglobin (free or within red cells) as a surrogate for blood. A positive dipstick for blood means one of three things: blood (haematuria), haemoglobin (haemolysis) or myoglobin (rhabdomyolysis).
Causes of Positive Dipstick for Blood
- Haematuria (true blood in urine) - glomerulonephropathy, vascular pathology, polycystic kidney disease, UTI, neoplasm, renal calculus, trauma
- Haemoglobinuria (haemolysis) - microangiopathic haemolytic anaemia, mechanical haemolysis, alloimmune haemolysis, paroxysmal nocturnal haemoglobinuria
- Myoglobinuria - immobilisation, strenuous exercise, limb ischaemia, trauma, burns, myositis, electrolyte disturbances, drugs, inherited causes
Urine does not normally contain glucose - it is filtered by the glomerulus but almost completely reabsorbed. Glucose may be present in urine in hyperglycaemia where the amount of serum glucose exceeds the kidney's ability to absorb it.
Glycosuria is classically a feature of diabetes, though may also occur with acute tubular necrosis, SGLT2 inhibitors (like empagliflozin), familial renal glycosuria or pregnancy.
Urine does not normally contain protein, as the glomerular filter is too small to allow for filtration of protein. Protein found in the urine may be albumin or globulins; the urine dipstick is more sensitive for the former rather than the latter.
- Causes of proteinuria include:
- Primary glomerulonephropathies - minimal change disease, membranous nephropathy, FSGS
- Secondary glomerulonephropathies - lupus nephritis, diabetic nephropathy, pre-eclampsia, amyloidosis, certain viral infection, NSAIDs, certain malignancies
- Tubular dysfunction - ATN, AIN, fanconi syndrome
- Overflow - multiple myeloma, rhabdomyolysis, heart failure
- Other - orthostatic proteinuria
Urine does not normally contain ketones, though a small amount may be present after vigorous exercise, vomiting or diarrhoea. Significant amounts of urinary ketone suggest the presence of ketosis, such as due to a carbohydrate-free diet, diabetic ketoacidosis, alcoholic ketoacidosis or starvation.
Bilirubin & Urobilinogen
Bilirubin is a breakdown product of the haem portion of haemoglobin. Bilirubin is converted to urobilinogen by bacteria within the intestines, reabsorbed and excreted by the kidneys.
- Urine does not normally contain bilirubin, and only conjugated bilirubin is able to be filtered into urine (it is water soluble, while unconjugated biluribin is fat soluble) and therefore only causes of conjugated hyperbilirubinaemia may result in bilirubinuria. The presence of bilirubin in urine suggests the presence of acute hepatitis, liver cirrhosis or cholestatic disease.
- Urobilinogen is normally present in small amounts in the urine, though an increase in urine urobiliogen suggests an excess of conjugated or unconjugated bilirubin. An increase in urine urobilinogen cannot occur in the context of cholestasis, as conjugated bilirubin is unable to pass into the gut and be reabsorbed.
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Aycock RD, Kass DA. Abnormal urine color. South Med J. 2012;105:43-47.Byrne C, Cove-Smith A. Clinical assessment of renal disease. Medicine (United Kingdom). 2015;43:361-367.
Carroll MF, Temte JL. Proteinuria in adults: a diagnostic approach. American family physician. 2000 Sep 15;62(6):1333-40.
Cartwright MM, Hajja W, Al-Khatib S, Hazeghazam M, Sreedhar D, Li RN, Wong-McKinstry E, Carlson RW. Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes. Critical care clinics. 2012 Oct 1;28(4):601-31.
Chute R. The significance of urea-splitting bacteria in the formation of urinary calculi. New England Journal of Medicine. 1938 Dec 29;219(26):1030-2.
Hedelin H, Bratt CG, Eckerdal G, Lincoln K. Relationship between ureaseâ€producing bacteria, urinary pH and encrustation on indwelling urinary catheters. British journal of urology. 1991 May;67(5):527-31.Kinsella G, MacNab R. Clinical assessment of renal patients. Anaesthesia and Intensive Care Medicine. 2012;13:325-327.
Kouri T, Fogazzi G, Gant V, Hallander H, Hofmann W, Guder WG. European urinalysis guidelines. Scandinavian journal of clinical and laboratory investigation. 2000 Jan 1;60(sup231):1-96.
McLean RJ, Nickel JC, Cheng KJ, Costerton JW, Banwell JG. The ecology and pathogenicity of urease-producing bacteria in the urinary tract. CRC Critical reviews in microbiology. 1988 Jan 1;16(1):37-79.
Muriithi AK, Nasr SH, Leung N. Utility of urine eosinophils in the diagnosis of acute interstitial nephritis. Clinical Journal of the American Society of Nephrology. 2013 Nov 7;8(11):1857-62.
Perazella MA, Coca SG, Kanbay M, Brewster UC, Parikh CR. Diagnostic value of urine microscopy for differential diagnosis of acute kidney injury in hospitalized patients. Clinical Journal of the American Society of Nephrology. 2008 Nov 1;3(6):1615-9.Raymond JR, Yarger WE. Abnormal urine color: Differential diagnosis. South Med J. 1988;81:837-841.
Sauret JM, Marinides G, Wang GK. Rhabdomyolysis. American family physician. 2002 Mar 1;65(5):907.
Simerville JA, Maxted WC, Pahira JJ. Urinalysis: a comprehensive review. American family physician. 2005 Mar 15;71(6):1153-62.
Tryggvason K, Pettersson E. Causes and consequences of proteinuria: the kidney filtration barrier and progressive renal failure. Journal of internal medicine. 2003 Sep;254(3):216-24.
Wise GJ, Schlegel PN. Sterile pyuria. New England Journal of Medicine. 2015 Mar 12;372(11):1048-54.