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    How Uric Acid Crystals Form

    Uric acid, also known as Uric deposit, is the end product of purine metabolism; the excretion of uric acid is the result of the process which results in the breakdown of a purine base (amines). Uric acid, which is formed from urea, urease, and free monohydrate, is a very weak acid, which combines with sodium ions to form MSU, the monosodium urate. In this process, the acid is bound with the sodium ions and purified by further precipitation with an alkali. When the crystal reaches the laboratory, its color changes to yellow-brown since the hydroxyl group of the molecule is now higher. Uric crystals can be formed in the renal tubule, where they settle in the follicles and are excreted in feces.

    How Uric Acid Crystals Form How Uric Acid Crystals Form

    The crystal usually settles in the renal tubule’s outer layer (renal pelvis) and can be found there after the passing of a kidney stone; however, the process of their formation and appearance depend on many factors such as urinary physiology, anatomy, and kidney function. Uric crystals form in response to two different stimuli. First, during urine secretion, they act as shock absorbers and increase clearance rates. Second, they accumulate in the narrow part of the urethra (renal canal) and cause obstruction and blockage. They form during periods of low urine flow or when a person is suffering from urinary blockage, thus affecting his urge to void and decrease his volume of urine.

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    Uric crystals can also be precipitated by the presence of serum factors such as albumin and interferon, which are secreted through the pores of the uppermost layer of the epidermis. These substances can promote the occurrence of the first crystals, especially in individuals predisposed to gout. The crystals eventually reach the junction between the dermis and the skin. The formation of the first crystals provides a base for new ones to grow on and transform into uric acids.

    how uric acid is formed 1 How Uric Acid Crystals Form

    Both the processes that initiate the formation of the crystals and the nucleation of the same occur in both gouty and non gouty forms. In patients affected with gout, a drastic physiologic condition is necessary to reverse the crystallization process to prevent them from growing even more. As mentioned earlier, the precipitating agents involved in both processes are protein-based antigens that are transported into the human body by the bloodstream. Serum antigens that stimulate the nucleation of the crystals in patients with both types of arthritis are based on purified proteins.

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    The role of fluid movement in crystallization is still unknown, but studies have revealed that the movement of fluid towards the area where crystals have formed helps stimulate their growth and development. The pH-dependent nature of crystallization, on the other hand, may have something to do with the mechanism through which fluid moves towards the crystals. The higher the alkalinity or acidity of the solution, the more rapid and more intense crystal nucleation occurs. In a study on the role of pH in the pathogenesis of gout, it was found that high alkalinity in the blood caused the same visual effects as the use of the acid solvents in the precipitating agent-alkaline pH.

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    Uric acid crystals are formed by the action of certain antibodies. These antibodies act on cells and antibodies by stimulating the synthesis of nucleic acids in the reaction chamber. As discussed above, amino acids that stimulate crystallization (such as arginine, glutamine, etc.) are present in the body; therefore, one can conclude that the antibodies synthesize these amino acids on their own, in a process called polysomnogenesis. Some polysomnogenic antibodies are characterized by their ability to generate antibodies against specific G proteins.

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