Urine chemistry

Chemical analysis of urine

Currently, chemical analysis of urine is carried out on automatic analyzers using test strips, which provide information on 8-12 urine parameters.

PH. Normally, urine pH is usually slightly acidic, but can have a different reaction (4.5-8).

Diseases and conditions that may alter urine pH

Increased pH (more than 7)	Lowering pH (approximately 5)
When eating plant foods After profuse acidic vomiting For hyperkalemia During the resorption of edema Primary and secondary hyperparathyroidism Taking carbonic anhydrase inhibitors Metabolic and respiratory alkalosis	Metabolic and respiratory acidosis Hypokalemia Dehydration Fever Diabetes mellitus Chronic renal failure Urolithiasis

Protein. In healthy people, there is no protein in the urine or its concentration is less than 0.002 g/l. The presence of protein in the urine is called proteinuria. The methods for determining proteinuria using test strips and sulfosalicylic acid give similar results, but they correlate poorly with the results of more accurate and complex analytical methods. Test strips are more sensitive to albumin, but do not detect Ig light chains (Bence Jones protein), so this method cannot be used in patients with myeloma. The sulfosalicylic acid method determines all proteins, including paraproteins. In this regard, the detection of protein in urine using the sulfosalicylic acid method in combination with a negative urine test result using test strips most likely indicates the presence of Ig light chains in the urine. There are two main groups of proteinuria.

• Physiological proteinuria includes cases of temporary appearance of protein in urine not associated with diseases. Such proteinuria is possible in healthy people after eating large amounts of food rich in proteins, after strong physical exertion, emotional experiences, epileptic seizures. Orthostatic, or juvenile, proteinuria is considered functional, often observed in children and adolescents and passing with age. However, it should be borne in mind that orthostatic albuminuria often occurs during the recovery period from acute glomerulonephritis. Functional proteinuria associated with hemodynamic stress is possible in children against the background of fever, emotional stress, congestive heart failure or arterial hypertension, as well as after cooling. This proteinuria is not associated with primary kidney damage and, by definition, disappears after the elimination of the cause. It is generally accepted that these types of transient proteinuria are benign and do not require in-depth examination. However, modern research methods have revealed histological changes in the kidneys in some types of so-called physiological proteinuria, which casts doubt on the functional nature of such disorders. Proteinuria accompanied by hematuria and/or other symptoms of kidney damage has a particularly serious prognosis.
• Pathological proteinuria is divided into renal and extrarenal (prerenal and postrenal).
  • Extrarenal proteinuria is caused by an admixture of protein excreted by the urinary tract and genitals; it is observed in cystitis, pyelitis, prostatitis, urethritis, vulvovaginitis. Such proteinuria rarely exceeds 1 g/l (except in cases of pronounced pyuria). The detection of casts in the urine indicates that the detected proteinuria, at least partially, is of renal origin.
  • In renal proteinuria, protein enters the urine in the renal parenchyma. Renal proteinuria is in most cases associated with increased permeability of the glomeruli. Renal proteinuria is most often associated with acute and chronic glomerulonephritis and pyelonephritis, nephropathy of pregnancy, febrile conditions, severe chronic heart failure, renal amyloidosis, lipoid nephrosis, renal tuberculosis, hemorrhagic fevers, hemorrhagic vasculitis, hypertension.

False-positive results when using test strips may be due to severe hematuria, increased density (more than 1.025) and pH (above 8.0) of urine, as well as the use of aseptics to preserve it. The sulfosalicylic acid method gives false-positive results when radiocontrast agents enter the urine, or when treated with tolbutamide, penicillin, or cephalosporins.

Glucose. Normally, there is no glucose in urine (for a clinical assessment of glucose detection in urine, see the section “Glucosuric profile”).

Bilirubin. Normally, bilirubin is absent in urine. Determination of bilirubin in urine is used as an express method for differential diagnostics of hemolytic jaundice and jaundice of other origins (parenchymatous and mechanical). Bilirubinuria is observed mainly in case of liver parenchyma damage (parenchymatous jaundice) and bile outflow obstruction (obstructive jaundice). Bilirubinuria is not typical for hemolytic jaundice, since indirect bilirubin does not pass through the renal filter.

Urobilinogen. The upper limit of the reference value of urobilinogen in urine is 17 μmol/l (10 mg/l). In clinical practice, the definition of urobilinuria is used:

• to detect lesions of the liver parenchyma, especially in cases occurring without jaundice;
• for differential diagnosis of jaundice (in mechanical jaundice, urobilinuria is absent).

The reasons for increased excretion of urobilinogen in urine are as follows.

• Increased hemoglobin catabolism: hemolytic anemia, intravascular hemolysis (transfusion of incompatible blood, infections, sepsis), pernicious anemia, polycythemia, resorption of massive hematomas.
• Increased formation of urobilinogen in the gastrointestinal tract (GIT): enterocolitis, ileitis.
• Increased formation and reabsorption of urobilinogen during infection of the biliary system (cholangitis).
• Liver dysfunction: viral hepatitis (excluding severe forms), chronic hepatitis and liver cirrhosis, toxic liver damage (alcoholic, organic compounds, toxins in infections and sepsis), secondary liver failure (after myocardial infarction, cardiac and circulatory failure, liver tumors).
• Liver bypass: liver cirrhosis with portal hypertension, thrombosis, renal vein obstruction.

Ketone bodies. Normally, ketone bodies are absent from urine. The most common cause of ketonuria is severe decompensation of type I diabetes mellitus, as well as long-term type II diabetes with depletion of pancreatic β-cells and development of absolute insulin deficiency. Severe ketonuria is observed in hyperketonemic diabetic coma.

In patients with diabetes, ketonuria monitoring is used to control the correctness of the dietary regimen: if the amount of fats introduced does not correspond to the amount of carbohydrates absorbed, then ketonuria increases. With a decrease in the introduction of carbohydrates (treatment without insulin) and the usual amount of fats, acetone begins to be released; with insulin treatment, a decrease in glucosuria is achieved by better absorption of carbohydrates and is not accompanied by ketonuria.

In addition to diabetes mellitus, ketonuria can be detected in pre-comatose conditions, cerebral coma, prolonged starvation, severe fevers, alcohol intoxication, hyperinsulinism, hypercatecholemia, and in the postoperative period.

Nitrites. Normally, nitrites are absent from urine. Escherichia coli, Proteus, Klebsiella, Citrobacter, Salmonella, some enterococci, staphylococci and other pathogenic bacteria reduce nitrates present in urine to nitrites. Therefore, detection of nitrites in urine indicates urinary tract infection. The test may be false negative if the bacteria (Staphylococcus, Enterococcus and Pseudomonas spp.) do not produce the enzyme nitrate reductase.

The infection rate according to the nitrite test results is 3-8% among women and 0.5-2% among men. The following categories of the population have a high risk of asymptomatic urinary tract infections and chronic pyelonephritis: girls and women, elderly people (over 70 years old), patients with prostate adenoma, diabetes, gout, after urological operations or instrumental procedures on the urinary tract.

Leukocytes. Normally, leukocytes are absent from urine when tested with test strips. The leukocyte esterase test is positive if the leukocyte content in urine exceeds 10-20 cells/μl. Leukocyturia is a sign of inflammation of the kidneys and/or lower urinary tract. Leukocyturia is the most characteristic sign of acute and chronic pyelonephritis, cystitis, urethritis, and ureteral stones.

Red blood cells. Physiological microhematuria when examined with test strips is up to 3 red blood cells/µl of urine (1-3 red blood cells in the field of view during microscopy). Hematuria - the content of red blood cells over 5 in 1 µl of urine - is considered a pathological sign. The main causes of hematuria are renal or urological diseases (urolithiasis, tumors, glomerulonephritis, pyelonephritis, urinary tract infections, kidney injury, kidney damage in systemic diseases, etc.) and hemorrhagic diathesis. False positive results of urine testing for blood using test strips may occur when eating beets, food colorings, large amounts of vitamin C, taking medications (ibuprofen, sulfamethoxazole, nitrofurantoin, rifampicin, quinine, etc.), when there are bile pigments, myoglobin, porphyrins in the urine, or when blood gets in during menstruation.

According to the "Recommendations of the European Association of Urology for the treatment of urinary tract infections and reproductive system infections in men", the determination of leukocyturia (leukocyte esterase), erythrocyturia (Hb) and bacteriuria (nitrate reductase) using test strips are acceptable methods for clinical practice in diagnosing and assessing the treatment of acute cystitis and pyelonephritis.

Hemoglobin. Normally absent when tested with test strips. Hemoglobinuria and myoglobinuria may occur in severe hemolytic anemia, severe poisoning, sepsis, burns, myocardial infarction, muscle damage (crush syndrome) and heavy physical exertion.

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