Urine is a typically sterile liquid by-product of the body secreted by the kidneys through a process called urination and excreted through the urethra. It is also an aqueous solution of greater than 95% water, with the remaining constituents, in order of decreasing concentration urea 9. 3 g/L, chloride 1. 87 g/L, sodium 1. 17 g/L, potassium 0. 750 g/L, creatinine 0. 670 g/L and other dissolved ions, inorganic and organic compounds. Urine is sterile until it reaches the urethra, where epithelial cells lining the urethra are colonized by facultatively anaerobic Gram negative rods and cocci.
Subsequent to elimination from the body, urine can acquire strong odors due to bacterial action and in particular the release of ammonia from the breakdown of urea. Cellular metabolism generates numerous by-products, many rich in nitrogen, that require elimination from the bloodstream. These by-products are eventually expelled from the body during urination, the primary method for excreting water-soluble chemicals from the body. These chemicals can be detected and analyzed by urinalysis.
Certain disease conditions can result in pathogen-contaminated urine. The pH of urine can vary between 4. 6 and 8, with neutral (7) being normal. In persons with hyperuricosuria, acidic urine can contribute to the formation of stones of uric acid in the kidneys, ureters, or bladder. A diet high in citrus, vegetables, or dairy can increase urine pH (more basic]. Some drugs also can increase urine pH, including acetazolamide, potassium citrate, and sodium bicarbonate while a diet high in meat can decrease urine pH (more acidic).
Cranberries, popularly thought to decrease the pH of urine, have actually been shown not to acidify urine. Drugs that can decrease urine pH include ammonium chloride, chlorothiazide diuretics, and methenamine mandelate. Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C5H4N4O3. It forms ions and salts known as urates and acid urates such as ammonium acid urate. Uric acid is a product of the metabolic breakdown of purine nucleotides. High blood concentrations of uric acid can lead to gout.
The chemical is associated with other medical conditions including diabetes and the formation of ammonium acid urate kidney stones. The enzyme xanthine oxidase makes uric acid from xanthine and hypoxanthine, which in turn are produced from other purines. Xanthine oxidase is a large enzyme whose active site consists of the metal, molybdenum, bound to sulfur and oxygen. Within cells, xanthine oxidase can exist as xanthine dehydrogenase and xanthine oxireductase, which has also been purified from bovine milk and spleen extracts.
Uric acid is released in hypoxic conditions. In humans and higher primates, uric acid is the final oxidation (breakdown) product of purine metabolism and is excreted in urine. Saturation levels of uric acid in blood may result in one form of kidney stones when the urate crystallizes in the kidney. These uric acid stones are radiolucent and so do not appear on an abdominal plain X-ray, and thus their presence must be diagnosed by ultrasound for this reason. This explains the high prevalence of uric stones and unusually acidic urine seen in patients with type 2 diabetes.
Uric acid crystals can also promote the formation of calcium oxalate stones, acting as “seed crystals” (heterogeneous nucleation). Ketone bodies are three water-soluble compounds that are produced as by-products when fatty acids are broken down for energy in the liver. Two of the three are used as a source of energy in the heart and brain while the third (acetone) is a waste product excreted from the body. In the brain, they are a vital source of energy during fasting. Although termed “bodies”, they are dissolved substances, not particles.
The three endogenous ketone bodies are acetone, acetoacetic acid, and beta-hydroxybutyric acid, although beta-hydroxybutyric acid is not technically a ketone but a carboxylic acid. Other ketone bodies such as beta-ketopentanoate and beta-hydroxypentanoate may be created as a result of the metabolism of synthetictriglycerides such as triheptanoin. Ketone bodies are produced from acetyl-CoA mainly in the mitochondrial matrix of hepatocytes when carbohydrates are so scarce that energy must be obtained from breaking down fatty acids.
Because of the high level of acetyl CoA present in the cell, the pyruvate dehydrogenase complex is inhibited, whereas pyruvate carboxylase becomes activated. High levels of ATP and NADH inhibit the enzyme isocitrate dehydrogenase in the TCA cycle and as a result cause an increase in the concentration of malate (due to the equilibrium between itself and oxaloacetate). The malate then leaves the mitochondrion and undergoes gluconeogenesis. The elevated level of NADH and ATP result from ß-oxidation of fatty acids. Unable to be used in the citric acid cycle, the excess acetyl-CoA is therefore rerouted to ketogenesis.
Acetone is produced by spontaneous decarboxylation of acetoacetate, meaning this ketone body will break down in five hours if it is not needed for energy and be removed as waste. This “use it or lose it” factor contributes to much of the weight loss found in ketogenic diets. Acetone cannot be converted back to acetyl-CoA, so it is excreted in the urine, or (as a consequence of its high vapor pressure) exhaled. Acetone is responsible for the characteristic “Sweet & fruity” odor of the breath of persons in ketoacidosis.
Both acetoacetic acid and beta-hydroxybutyric acid are acidic, and, if levels of these ketone bodies are too high, the pH of the blood drops, resulting in ketoacidosis, a complication of untreated Type I diabetes, and sometimes in Type II. Glycosuria or glucosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reclaim all of the filtered glucose back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus.
Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys themselves, a condition termed renal glycosuria. Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis. Urea serves an important role in the metabolism of nitrogen-containing compounds by animals and is the main nitrogen-containing substance in the urine of mammals. It is a colorless, odorless solid, although the ammonia that it gives off in the presence of water, including water vapor in the air, has a strong odor.
It is highly soluble in water and practically non-toxic (LD50 is 15 g/kg for rat). Dissolved in water, it is neither acidic nor alkaline.. Ammonia is smaller, more volatile and more mobile than urea. If allowed to accumulate, ammonia would raise the pH in cells to toxic levels. Therefore many organisms convert ammonia to urea, even though this synthesis has a net energy cost. Being practically neutral and highly soluble in water, urea is a safe vehicle for the body to transport and excrete excess nitrogen.
In water, the amine groups undergo slow displacement by water molecules, producing ammonia and carbonate anion. For this reason, old, stale urine has a stronger odor than fresh urine. Proteinuria means the presence of an excess of serum proteins in the urine. The excess protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia (air bubbles in the urine) due to afistula, or drugs such as pyridium. Conclusion: Therefore, the pH range of the urine ranges from 4. to 8. 0 with variation among human male and female. The test for electrolytes showed the presence of some inorganic ions such as phosphate, chloride and calcium. The test for the presence of abnormally occurring compounds can help in detecting diseases or any abnormally functioning organs inside the body.
References
- Kurzer, Frederick; Sanderson, Phyllis M. (1956). “Urea in the History of Organic Chemistry”. Journal of Chemical Education (American Chemical Society)33 (9)
- Rose, Burton; Rennke, Helmut (1994). Renal pathophysiology – the essentials (1st ed ed. . Philadelphia: Lippincott Williams & Wilkins. pp. 194. ISBN 0-683-07354-0.
- Mary K. Campbell, Shawn O. Farrell (2006). Biochemistry (5th ed. ). Cengage Learning. p. 579. ISBN 0-534-40521-5.
- McCrudden, Francis H. (2008). Uric Acid. BiblioBazaar. Ethics, also known as moral philosophy, is a branch of philosophy that involves systematizing, defending, and recommending concepts of right and wrongconduct.
