Urine pathophysiology

Analysis of BAs in urine, serum, bile and stool is crucial for the diagnosis of inborn errors of BA metabolism. It is also helpful for understanding their pathophysiological role in acquired hepatic diseases and for monitoring the effects of therapy on metabolism. Several different inborn defects affecting BA synthetic pathway, have been described over last 20 years [7]. 

Stem et aL [149] made use of a hyaluronan-binding protein obtained from the tryptic digestion of the proteoglycan core protein of bovine nasal cartilage to detect hy alumni da sc activities in urine samples from wiles tumor patients. The pathophysiology of this tumor is associated with major alterations in the metabolism of hyaluiouan, and it is thought that urinary hyaluronidase can be used as an additional marker. 

Bikunin (Bik), a peptide excreted in the urine, is one of the primary inhibitors of the trypsin family of serine proteases. This peptide plays a key role in inflammation and innate immunity because of its two Kunitz-type binding domains [1, 2], Bik suppresses proteolytic activity in a variety of tissues and can also exert localized anti-inflammatory effect [3-5], Inflammation is an important indicator of infection, cancer, and tissue injury in acute and chronic states. In acute inflammation, fluids and plasma components accumulate in the affected tissues due to vascular dilation. Subsequent activation of platelets and increased presence of immune cells occur during repair. Long-standing inflammation may be present before the disorder is identified. Due to its inhibitory role and potential use as an early marker of inflammation, we will review the synthesis, structure, pathophysiology of Bik as well as the various approaches for its measurement in this chapter. 

The lower urinary tract consists of the bladder, urethra, urinary or urethral sphincter, and the surrounding musculofascial structures including connective tissue, nerves, and blood vessels. The urinary bladder is a hollow organ composed of smooth muscle and connective tissue located deep in the bony pelvis in men and women. The urethra is a hollow tube that acts as a conduit for urine flow out of the bladder. The interior surface of both the bladder and urethra is lined by an epithelial cell layer termed transitional epithelium, which is in constant contact with urine. Previously considered inert and inactive, transitional epithelium may actually play an active role in the pathophysiology of many lower urinary tract disorders, including interstitial cystitis and UI. The urinary or urethral sphincter is a combination of smooth and striated muscle within and surrounding the most proximal portion of the urethra adjacent to the bladder in both men and women. This is a functional but not anatomic sphincter that includes a portion of the bladder neck or outlet as well as the proximal urethra. 

The pathophysiologic approach to the evaluation of hyperuricemia requires determining whether the patient is overproducing or underexcreting uric acid. This can be accomplished by placing the patient on a purine-free diet for 3 to 5 days and then measuring the amount of uric acid excreted in the urine in 24 hours. Normal individuals produce 600 to 800 mg of uric acid daily and excrete less than 600 mg in urine. Individuals who excrete more than 600 mg on a purine-free diet may be considered overproducers. Hyperuricemic individuals who excrete less than 600 mg of uric acid per 24 hours... 

Urinary incontinence—Involuntary leakage of urine. May result from urethral underactivity (stress urinary incontinence), urethral overactivity (overflow incontinence), or mixed pathophysiologic mechanisms. 

The isoeicosanoids, a family of eicosanoid isomers, are formed nonenzymatically by direct free radical-based attack on AA and related lipid substrates. Unlike eicosanoids, these compounds are generated initially on the esterified lipid in cell membranes, from which they are cleaned, presumably by phospholipases the free isoeicosanoids circulate and are excreted in urine. Consequently, their production is not blocked in vivo by agents that suppress metabolism of free arachidonate, such as inhibitors of COX-1 or COX-2. Since several isoprostanes can activate prostanoid receptors, it has been speculated that they may contribute to the pathophysiology of inflammatory responses in a manner insensitive to COX inhibitors. 

Histamine is formed from the amino acid histidine and is stored in high concentrations in vesicles in mast cells. Histamine is metabolized by the enzymes monoamine oxidase and diamine oxidase. Excess production of histamine in the body (by. for example, systemic mastocytosis) can be detected by measurement of imidazoleacetic acid (its major metabolite) in tbe urine. Because it is released from mast cells in response to IgE-mediated (immediate) allergic reactions, this autacoid plays an important pathophysiologic role in seasonal rhinitis (hay fever), urticaria, and angioneurotic e ma. Histamine also plays an important physiologic role in the control of acid secretion in the stomach and as a neurotransmitter. 

Al-Dujaili, E. A., L. J. Mullins, M. A. Bailey, and C. J. Kenyon. 2009. Development of a highly sensitive ELISA for aldosterone in mouse urine Validation in physiological and pathophysiological states of aldosterone excess and depletion. Steroids 74 456-62. 

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