Urine formation

Antidiuretic hormone (ADH), also referred to as vasopressin, has two major effects, both of which are reflected by its names (1) antidiuresis (decrease in urine formation by the kidney) and (2) vasoconstriction of arterioles. 

The major characteristics of the renal response to mannitol diuresis include a fall in urine osmolality and a decrease in the osmolality of the interstitial fluid of the renal medulla. The quantity of urine formation and Na excretion is generally proportional to the amount of mannitol excreted. Although there is a significant inhibition of proximal water reabsorption, the effects of mannitol on proximal Na+ reabsorption are not marked. 

The term shock when used in medicine relates to an acute state of general weakness and the restriction of many vital functions. Patients in shock are generally apathetic, their face is sunken and their expression is full of anxiety skin is moist, cold and gray, pulse is rapid and faint, blood pressure is normally low, musculature is lax and superficial blood vessels are empty respiration is superficial, basal metabolism is reduced and urine formation is considerably slower. Shock may be triggered by a variety of causes severe physical injury with excessive loss of blood, surgery or severe psychic trauma in predisposed persons it may also arise as a reaction to exogenous substances such as antibiotics or bee poison. 

Diuretics are the agents which increase the rate of urine formation by the kidneys, or which cause a net loss of sodium and water in urine, i.e. the diuretics increase the urine output of ions and fluids from the kidneys. 

These cells reabsorb water during urine formation, a process for which water movement across membranes is essential (Box 11-3). The plant Arabidopsis thaliana has 38 genes that encode various types of aquaporins, reflecting the critical roles of water movement in plant physiology. Changes in turgor pressure, for example, require rapid movement of water across a membrane. 

Resistance measured between two yarn electrodes implemented in a baby s nappy as a function of time, with f=0 the moment that urine formation occurs. 

The most potent type of diuretic, loop diuretics are named after the loop of Henle, a component of a nephron. The nephrons are the filtering units of the kidney, and are responsible for moving fluids and waste out of the bloodstream, resulting in urine formation. The loop of Henle is a branch within each nephron where sodium and potassium are reabsorbed back into the bloodstream instead of being filtered into the urine. Loop diuretics inhibit this action and promote excretion of the sodium and potassium instead, along with calcium and magnesium. Since excess sodium causes excess fluid build-up, this results in fluid loss. Furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), and ethacryinic acid (Edecrin) are all loop diuretics. 

Figure 12.1 illustrates the main structure of a nephron [1], The measurements to be reported in this chapter were performed on rats. A rat kidney contains approximately 30000 nephrons as compared to the one million nephrons in a human kidney. The process of urine formation starts with the filtration of plasma in the glomerulus, a system of 20-40 capillary loops. The presence of a relatively high hydrostatic pressure in this system allows water, salts and small molecules to pass out through the capillary wall and into the proximal tubule. Blood cells and proteins are retained, and the filtration process saturates when the protein osmotic pressure balances the hydrostatic pressure difference between the blood and the filtrate in the tubule. For superficial nephrons, the proximal tubule is visible in the surface of the kidney and easily accessible for pressure measurements by means of a thin glass pipette. 

Forced diuresis Induced increased urine formation. 

Dilution of the ECF reduces the thirst sensation and reduces ADH production so that normally the kidney produces diluted urine and eliminates the extra water. However, following rapid dehydration, the reduction in blood volume decreases cardiac output and BP, causing reflex vasoconstriction and reduced perfusion of tissues, including the kidney. This in turn reduces GFR and urine formation (oliguria) and the water is retained in the body. 

The essential element, hypoperfusion of vital organs, is present whatever the cause, whether pump failure (myocardial infarction), maldistribution of blood (septic shock) or loss of total intravascular volume (bleeding or increased permeability of vessels damaged by bacterial cell products, bums or anoxia). Fimction of vital organs, brain (consciousness, respiration) and kidney (urine formation) are clinical indicators of adequacy of perfusion of these organs. 

Diuretic drug preparations have promoted urine formation. They are derivatives of mercury propanol RCH2CH(OH)CH2HgX, where R is a polar hydrophilic group. The mercury diuretic preparations act as ferment inhibitors (latter containing-. They also inhibit adenosine triphosphate (ATP). These properties led to the use of mercury drug compounds in the treatment of bacterial infections. In these cases, they interacted with -SH groups of the bacteria proteins. 

Einbrodt et al. (1976) exposed students to 0.26-0.92 ppm formaldehyde vapors for 3 hours, with urine samples collected immediately after exposure and 21 hours after exposure. Urine formaldehyde and urine formic acid (formate) concentrations were found to be higher immediately after exposure compared to 21 hours later however, no baseline sample was obtained prior to exposure. If historic formaldehyde and formic acid baseline levels were assumed, then a closer examination of these data indicates that more formaldehyde (and metabolite) was excreted in the urine than could have possibly been absorbed by inhalation, indicating another route of exposure (perhaps dermal), or co-exposure to another chemical that also has formate as a metabolite (e.g., methanol), or higher personal exposures than were actually measured. There was also no indication that the urine formate levels were adjusted to compensate for urine specific gravity using urine creatinine levels, which may have markedly influenced the test results. 

Kombrust and Bus 1983 Liesivuori and Savolainen 1987). This indicates that even if blood or urine formate levels were elevated, it may be due to individual variation, formaldehyde exposure, or other chemical exposures that result in formate formation. Thus formate blood and urine levels appear to be equally unreliable as definitive biomarkers for fonnaldehyde exposure. 

Figure 19.1. Alternative processes for formation of urinary tract solids. (A) Direct formation of solids composed of chronically administered parent chemical or metabolite(s). (B) Indirect formation of urinary tract solids composed of chemicals normally present in the urine. Formation occurs because of significant alterations in urine composition secondary to altered urinary physiology, alteration of normal intermediary metabohsm, or secondary to an inherited metabolic disorder (e.g., gout, oxalosis) or surgical procedure (e.g., porta caval shunt).

The clinical features of chronic renal failure reflect the impairment of the above systems. The inability to rid the body of othertoxic metabolites may be responsible for the occurrence of many of the features of CRF which are illustrated in Figure 3. Early in chronic renal failure the normal reduetion in urine formation w hen the patient is recumbent and asleep is lost. Patients who do not experience daytime polyuria may nevertheless have nocturia... 

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