Biological Chemistry - Berezov T. T., Korovkin B. F. 1998

Kidneys and Urine
General Properties and Constituents of Urine
Pathological Components of Urine

The widely used concept of "pathological urine components" is somewhat conventional, since most compounds classified as pathological components are always present in normal urine, albeit in small amounts. In other words, these are substances that do not occur in normal urine in analytically detectable quantities. These primarily include Proteins, glucose, acetone (ketone) bodies, Bile pigments, and Blood pigments.

Protein. Normal human urine contains a minimal amount of protein, the presence of which cannot be detected by standard qualitative protein tests. In A number of disorders, particularly Kidney diseases, the protein content in urine can increase dramatically (proteinuria). The source of urinary protein is Serum proteins as well as, to some extent, renal tissue proteins.

Proteinurias are divided into two major groups: renal and extrarenal. In renal proteinurias, proteins (mainly Blood Plasma Proteins) enter the urine due to organic damage to the nephron, enlarged pores of the renal filter, and slowed BLOOD FLOW IN the glomeruli. Extrarenal proteinurias are caused by Disorders of the Urinary Tract or Prostate Gland.

The term "albuminuria," frequently used in clinical practice when protein is detected in the urine, is incorrect because not only albumins but also globulins are excreted in the urine. For example, in nephrosis, the total protein content in urine can reach 26 g/L, with an albumin concentration of 12 g/L and a globulin concentration of 14 g/L.

The activity of several Enzymes can be detected in human urine: lipase, Ribonuclease, LDH, aminotransferases, urokinase, Phosphatases, a-amylase, leucine aminopeptidase, etc. The main difficulties in determining urinary enzyme activity, apart from a-amylase and a few others, lie in The Need for urine concentration and the Prevention of Enzyme Inhibition during this concentration process.

Blood. Blood may be detected in the urine either in the form of red Blood Cells (Hematuria) or as dissolved blood pigment (hemoglobinuria). Hematuria is classified as renal or extrarenal. Renal hematuria is a primary symptom of acute nephritis. Extrarenal hematuria is observed in inflammatory processes or INJURIES OF THE urinary tract. Hemoglobinurias are typically associated with hemolysis and hemoglobinemia. It is generally accepted that Hemoglobin appears in the urine after its plasma concentration exceeds 1 g per 1 L. Hematuria is usually diagnosed via Cytological examination (microscopic analysis of urinary sediment), while hemoglobinuria is identified chemically.

Glucose. Normal human urine contains minimal amounts of glucose that are undetectable by standard qualitative tests. Under pathological conditions, the glucose content in urine increases (glucosuria). For example, in Diabetes Mellitus, The amount of glucose excreted in the urine can reach several tens of grams per day.

Occasionally, other CARBOHYDRATES are also detected in urine, specifically fructose, galactose, and pentose. Fructosuria is observed in congenital deficiencies of enzymes that convert fructose to glucose; congenital pentosuria and congenital galactosuria also occur.

Ketone (acetone) bodies. In normal urine, these compounds occur only in trace amounts (no more than 0.01 g per day). They are not detected by standard qualitative tests (Legal's, Lange's nitroprusside tests, etc.). When large amounts of Ketone Bodies are excreted, qualitative tests become positive. This pathological phenomenon is known as ketonuria. For example, in diabetes mellitus, up to 150 g of ketone bodies may be excreted daily.

Acetone is never excreted in the urine without acetoacetic acid, and vice versa. Standard nitroprusside tests make it possible to determine the presence of not only acetone, but also acetoacetic acid; ß-hydroxybutyric acid appears in the urine only when There is a sharp increase in the amount of ketone bodies (diabetes mellitus, etc.).

Ketone bodies are excreted in the urine not only in diabetes mellitus, but also during starvation and the exclusion of dietary carbohydrates. Ketonuria is observed in conditions associated with accelerated carbohydrate consumption: for example, thyrotoxicosis, Subarachnoid Hemorrhage, and traumatic Brain injury. In early childhood, prolonged digestive tract disorders (dysentery, toxicosis) can cause ketonemia and ketonuria As a result of starvation and wasting. Ketonuria is frequently observed in infectious diseases such as scarlet fever, Influenza, tuberculosis, and meningitis. In these cases, ketonuria has no diagnostic significance and is secondary.

Bilirubin. Normally, urine contains a minimal amount of bilirubin that cannot be detected by standard qualitative tests. Increased bilirubin excretion, where standard qualitative tests for bilirubin in urine become positive, is termed bilirubinuria. It occurs in bile duct obstruction and Liver parenchyma disease.

Bilirubin excretion in the urine is especially pronounced in obstructive jaundice. In bile stasis, bile-engorged canaliculi are injured and allow bilirubin to leak into blood capillaries. When the liver parenchyma is damaged, bilirubin enters the blood through destroyed liver cells. Bilirubinuria manifests when direct blood bilirubin levels exceed 3.4 µmol/L. Indirect bilirubin cannot pass through the renal filter. This becomes possible only in cases of significant renal damage.

Urobilin. Urobilin, or more precisely stercobilin, is always present in urine in small amounts. Its concentration rises sharply in hemolytic and hepatic jaundice. This is due to the liver's loss of ability to retain and degrade mesobilinogen (urobilinogen) absorbed from the intestine. Conversely, the absence of urobilinogen in urine in the presence of bile pigments (bilirubin) indicates the cessation of bile flow into the intestine due to bile duct obstruction (see Chapter 16).

Porphyrins. Normally, urine contains only very small amounts of type I porphyrins (up to 300 µg in a 24-hour collection). However, porphyrin excretion can increase dramatically (10-12 fold) in liver diseases and pernicious anemia. In congenital porphyria, there is an overproduction of type I porphyrins (uroporphyrin I and coproporphyrin I). In these cases, up to 10 mg of a mixture of these porphyrins is detected in the daily urine volume. In acute porphyria, elevated excretion of uroporphyrin III, coproporphyrin III, and porphobilinogen in the urine is observed.

Urinary Calculi

Urinary calculi (kidney stones) are solid formations found in the urinary tract. Urinary calculi can be located in the renal parenchyma, calyces, renal pelvis, Ureters, bladder, and Urethra. The size, shape, and consistency of urinary calculi vary. Small urinary calculi resemble grains of sand, A large number of which form so-called urinary gravel. Larger urinary calculi typically have a round, oval, or, less commonly, staghorn shape. A common feature in The Structure of urinary calculi is the presence of a so-called Nucleus, surrounded by a shell or body of varying thickness. Approximately a third or more of such stones consist of Ca₃(PO₄)₂, MgNH₄PO₄, CaC₂O₄, or mixtures thereof, meaning they are calcium oxalate (oxalate), calcium phosphate (phosphate), or mixed urinary calculi. Stone formation frequently results from chronic alkalinization of urine in the bladder and renal pelvis caused by bacterial infection. Stone formation is promoted by the excessive excretion of Ca²⁺ ions, for example, in hyperparathyroidism, Osteoporosis (particularly immobilization-induced), and an unusually high dietary content of Ca²⁺. Furthermore, stones composed of calcium oxalate are pathognomonic for oxaluria (an inherited disorder of Glycine METABOLISM in which virtually all synthesized glycine is oxidized via glyoxylic acid to oxalic acid).

In patients with Gout, stones consisting mainly of uric acid (C₅H₄N₄O₃), and less frequently of its ammonium or sodium salt, are generally found. These stones are termed uric acid or urate stones. Cystine deposition (cystine stones) is almost constantly observed in patients with cystinuria.

It should be noted that studying etiological factors and determining The chemical composition of urinary calculi are of great importance for the prevention and Treatment of urolithiasis.