Osmotic diuresis is the increase ofurination rate caused by the presence of certain substances in theproximal tubule (PCT) of thekidneys.[2] The excretion occurs when substances such as glucose enter thekidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance). The substances cause an increase in theosmotic pressure within the tubule, causing retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (i.e., diuresis). The same effect can be seen in therapeutics such asmannitol, which is used to increase urine output and decrease extracellular fluid volume.[citation needed]
Substances in the circulation can also increase the amount of circulating fluid by increasing the osmolarity of the blood. This has the effect of pulling water from theinterstitial space, making more water available in the blood, and causing the kidney to compensate by removing it as urine. Inhypotension,colloids are used often intravenously to increase circulating volume in themselves, but as they exert a certain amount of osmotic pressure, water is therefore also moved, further increasing circulating volume. As blood pressure increases, the kidney removes the excess fluid as urine.Sodium,chloride andpotassium are excreted in osmotic diuresis, originating fromdiabetes mellitus (DM). Osmotic diuresis results indehydration frompolyuria and the classicpolydipsia (excessive thirst) associated with DM.[3][4]
Most diuretic drugs are eitherweak acids orweak bases. When urine is madealkaline, elimination of acidic drugs in the urine is increased. The converse applies for alkaline drugs. This method is only of therapeutic significance where the drug is excreted in active form in urine and where thepH of urine can be adjusted to levels above or below thepK value of the active form of drug. For acidic drugs, urine pH should be above thepK value of that drug, and converse for the basic drugs. It is because theionization of acidic drug is increased in alkaline urine and ionized drugs cannot easily cross aplasma membrane so cannot re-enter blood fromkidney tubules. This method is ineffective for drugs that are strongly protein bound (e.g.,tricyclic antidepressants) or which have a large apparentvolume of distribution (e.g.paracetamol, tricyclic antidepressants).[6]
Forforced alkaline diuresis,sodium bicarbonate is added to the infusion fluid to make blood and, in turn, urine alkaline.Potassium replacement becomes of utmost importance in this setting because potassium is usually lost in urine. If blood levels of potassium are depleted below normal levels, thenhypokalemia occurs, which promotes bicarbonate ion retention and prevents bicarbonate excretion, thus interfering with alkalinization of the urine. Forced alkaline diuresis has been used to increase the excretion of acidic drugs likesalicylates andphenobarbitone, and is recommended forrhabdomyolysis.[medical citation needed]
An example of the pattern of urine flow and plasma creatinine levels following acute tubular necrosis
Rebound diuresis refers to the sudden resurgence of urine flow that occurs during recovery fromacute kidney injury.[8] In acute kidney injury, particularlyacute tubular necrosis, the tubules become blocked with cellular matter, particularlynecrotic sloughing of dead cells. This debris obstructs the flow of filtrate, which results in reduced output of urine. The arterial supply of thenephron is linked to the filtration apparatus (glomerulus), and reduced perfusion leads to reduced blood flow; usually this is the result ofpre-renal pathology.[9]
Thekidney's resorptive mechanisms are particularly energetic, using nearly 100% of the O2 supplied. Thus, the kidney is particularly sensitive to reduction in blood supply.This phenomenon occurs because renal flow is restored prior to the normal resorption function of the renaltubule. As shown by the graph, urine flow recovers rapidly and subsequently overshoots the typical daily output (between 800 mL and 2L in most people). Since the kidney's resorption capacity takes longer to re-establish, there is a minor lag in function that follows recovery of flow. A goodreference range for plasmacreatinine is between 0.07 - 0.12 mmol/L.[10]
Immersion diuresis is caused by immersion of the body in water (or equivalent liquid). It is mainly caused by lower temperature and by pressure.[11]
Thetemperature component is caused by water drawing heat away from the body and causingvasoconstriction of the cutaneousblood vessels within the body to conserve heat.[12][13][14] The body detects an increase in theblood pressure and inhibits the release ofvasopressin (also known as antidiuretic hormone (ADH)), causing an increase in the production ofurine. Thepressure component is caused by thehydrostatic pressure of the water directly increasing blood pressure. Its significance is indicated by the fact that the temperature of the water does not substantially affect the rate of diuresis.[15] Partial immersion of only the limbs does not cause increased urination. Thus, thehand in warm water trick (immersing the hand of a sleeping person in water to make them urinate) has no support from the mechanism of immersion diuresis. On the other hand, sitting up to the neck in a pool for a few hours clearly increases the excretion of water, salts, and urea.[15]
Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderatehypothermia.[16] It is currently thought to be caused by the redirection of blood from the extremities to the core due toperipheral vasoconstriction, which increases the fluid volume in the core. Overall, acute exposure to cold is thought to induce a diuretic response due to an increasemean arterial pressure.[17]
The arterial cells of the kidneys sense the increase in blood pressure and signal the kidneys to excrete superfluous fluid in an attempt to stabilize the pressure. The kidneys increase urine production and fill the bladder; when the bladder fills, the individual may then feel the urge to urinate. This phenomenon usually occurs after mental function has decreased to a level significantly below normal. Cold diuresis has been observed in cases of accidental hypothermia as well as a side effect oftherapeutic hypothermia, specifically during the induction phase.[18][19]
^Dibartola, Stephen P. (2006). "Disorders of Sodium and Water: Hypernatremia and Hyponatremia".Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. pp. 47–79.doi:10.1016/B0-72-163949-6/50006-0.ISBN978-0-7216-3949-9.
^Brown, Karen A. (2001).Chemotherapy and Biotherapy: Guidelines and Recommendations for Practice. Oncology Nursing Society.ISBN978-1-890504-26-7.[page needed]
^Györke, Z. S.; Sulyok, E.; Guignard, J. -P. (June 1991). "Ammonium chloride metabolic acidosis and the activity of renin-angiotensin-aldosterone system in children".European Journal of Pediatrics.150 (8):547–549.doi:10.1007/BF02072203.PMID1954957.
^Helms, Richard A.; Quan, David J. (2006).Textbook of Therapeutics: Drug and Disease Management. Lippincott Williams & Wilkins.ISBN978-0-7817-5734-8.[page needed]
^Epstein M (June 1984). "Water immersion and the kidney: implications for volume regulation".Undersea Biomedical Research.11 (2):113–21.PMID6567431.
^Knight, D. R.; Horvath, S. M. (May 1990). "Immersion diuresis occurs independently of water temperatures in the range 25 degrees-35 degrees C".Undersea Biomedical Research.17 (3):255–256.PMID2356595.
^Hynynen, M.; Ilmarinen, R.; Tikkanen, I.; Fyhrquist, F. (1993). "Plasma atrial natriuretic factor during cold-induced diuresis".European Journal of Applied Physiology and Occupational Physiology.67 (3):286–289.doi:10.1007/BF00864230.PMID8223545.
^Polderman, Kees H. (July 2009). "Mechanisms of action, physiological effects, and complications of hypothermia".Critical Care Medicine.37 (Supplement):S186 –S202.doi:10.1097/CCM.0b013e3181aa5241.PMID19535947.
