Diuretics

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Final segment of the nephron is the last tubular site of sodium reabsorption and is controlled by aldosterone. The reabsorption of sodium occurs via channels and is accompanied by an equivalent loss of potassium or hydrogen ions. Thus this is also the primary site of acidification of the urine and of potassium excretion

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Cortical Collecting Tubule (CCT)

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The aldosterone receptor and sodium channels in the CCT are the sites of action of these drugs

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Potassium-sparing diuretics

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Reabsorption of water occurs in the medullary collecting tubule under the control of ______

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ADH

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Prototypical carbonic anhydrase inhibitor

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Acetazolamide

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MOA of carbonic anhydrase inhibitors

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Inhibition of carbonic anhydrase in the brush border and intracellular carbonic anhydrase in the PCT cells

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Major renal effects of carbonic anhydrase inhibitors

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Bicarb diuresis; body bicarb is depleted and metabolic acidosis results; as increased sodium is presented to the CCT, some of the excess sodium is reabsorbed and potassium is secreted, resulting in potassium wasting

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Reason diuresis from carbonic anhydrase inhibitors is self limiting w/in 2-3 days

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As a result of bicarb depletion, sodium bicarb excretion slows, even w/ continued diuretic admin

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Only time carbonic anhydrase inhibitors are used for their diuretic effects

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Edema is accompanied by significant metabolic alkalosis

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Toxicity of carbonic anhydrase inhibitors

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Drowsiness, paresthesias, cross allergenicity w/ sulfonamides, alkalinization of urine may cause precipitation of calcium salts and formation of renal stones; renal potassium wasting; hepatic encephalopathy in patients w/ liver problems b/c of increased ammonia reabsorption

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Prototypical loop diuretic

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Furosemide

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Loop diuretic that is a phenoxyacetic acid derivative; it is not a sulfonamide

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Ethacrynic acid

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MOA of loop diuretics

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Inhibit the Na+/K+/2Cl- cotransporter

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DOA of loop diuretics

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4 hour period

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Reason NSAIDs decrease the efficiency of diuretics, especially loops

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Inhibit prostaglandins which are important in maintaining glomerular filtration

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Clinical use of loop diuretics

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Treatment of edematous states (eg heart failure, ascites) Particularly valuable in acute pulmonary edema, in which the pulmonary vasodilating action plays a useful role. Also used for severe hypercalcemia

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Toxicity of loop diuretics

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Hypokalemic metabolic alkalosis, SEVERE potassium wasting, hypovolemia and CV complications, ototoxicity, and sulfonamide allergy

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Prototypical thiazide diuretic

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Hydrochlorothiazide

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DOA of thiazides

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6-12 hours, considerably longer than loops

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MOA of thiazide diuretics

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Inhibit NaCl transport in the early segment of the distal convoluted tubule

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Clinical use of thiazides

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main use is HTN for which their long DOA and moderate intensity of action are particularly useful. Chronic renal calcium stone formation can be controlled w/ thiazides b/c of their ability to reduce urine calcium concentration (opposite of loops and CAIs)

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Toxicity of Thiazides

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Massive sodium diuresis w/ hyponatremia, potassium wasting, diabetic patients may have significant hyperglycemia, and serum uric acid and lipid levels can be increased

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Potassium-sparing diuretics that are steroid derivatives and act as pharmacologic antagonists of aldosterone in the CTs

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Spironolactone and eplerenone

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MOA of spironolactone and eplerenone

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Combine w/ and block the intracellular aldosterone receptor to reduce the expression of genes controlling synthesis of epithelial sodium ion channels and Na+/K+ ATPase

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MOA of amiloride and triamterene (potassium sparing)

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blocking the epithelial sodium channels in the collecting tubules

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Important indication for spironolactone

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Aldosternism (eg the elevated serum aldosterone levels that occur in cirrhosis)

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General toxicity of potassium sparing diuretics

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Hyperkalemia and even hyperkalemic metabolic acidosis

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A shift in body electrolyte and pH balance involving elevated chloride, diminished bicarb concentration, and a decrease in pH in the blood. Typical result of bicarb diuresis

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Hyperchloremic metabolic acidosis

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Loss of urine-concentrating ability in the kidney caused by a lack of responsiveness to ADH (ADH is normal to high)

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Nephrogenic diabetes insipidus

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Loss of urine-concentrating ability of the kidney caused by lack of ADH

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Pituitary diabetes insipidus

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A diuretic that increases uric acid excretion, usually by inhibiting uric acid reabsorption in the proximal tubule. Example: ethacrynic acid

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Uricosuric diuretic

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Segment of the nephron that carries out isosmotic reabsorption of AAs, glucose and numerous cations. Also the major site of sodium chloride and sodium bicarb reabsorption (60-70% of the total reabsorption of sodium)

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Proximal convoluted tubule (PCT)

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Enzyme in the PCT required for bicarb reabsorption process on the brush border and in the cytoplasm

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carbonic anhydrase

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Segment of the nephron that has active secretion and reabsorption of weak acids and bases. Uric acid transport is especially important and is targeted by some of the drugs used in gout

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Proximal tubule

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Segment of the nephron that pumps sodium, potassium, and chloride out of the lumen into the interstitium of the kidney. Also a major site of calcium and magnesium reabsorption

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Thick ascending limb of the loop of Henle (TAL)

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Reabsorption of sodium, potassium, and chloride in the TAL is accomplished by a single carrier that is targeted by these drugs

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Loop diuretics

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Segment of the nephron that actively pumps sodium and chloride out of the lumen of the nephron. Calcium is reabsorbed under the influence of PTH

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Distal convoluted tubule (DCT)

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The co-transporter for sodium and chloride in the DCT is the target of these drugs

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thiazide diuretics

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Diuretic used for mountain sickness and glaucoma

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Acetazolamide

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SE of acetazolamide

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Parasthesias, alkalization of the urine (which may ppt Ca salts); acidosis, and encephalopathy in patients w/ hepatic impairment

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MOA of loop of diuretics

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Inhibits Na+/K+/2Cl- cotransport

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Site of action of loop diuretics

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Thick ascending limb of the loop of Henle

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SE of loop (furosemide) diuretics

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Hyperuricemia, hypokalemia, and ototoxicity

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Aminoglycosides used w/ loop diuretics potentiate this AE

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Ototoxicity

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Loops lose and thiazide diuretics retain

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calcium

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MOA of thiazide diuretics

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Inhibit Na+/Cl- cotransport

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Site of action of thiazide diuretics

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Work at early distal convoluted tubule

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Class of drugs that may cause cross-sensitivity w/ thiazide diuretics

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sulfonamides

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SE of thiazide (HCTZ) diuretics

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Hyperuricemia, hypokalemia, and hyperglycemia

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Potassium sparing diuretics inhibit

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Na+/K+ exchange

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Diuretic used to treat primary aldosteronism

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Spironolactone

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SE of spironolactone

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Gynecomastia, hyperkalemia and impotence

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Osmotic diuretic used for increased ICP

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mannitol

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Diuretics work in CHF by

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reducing preload

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Diuretic used to antagonize aldosterone receptors

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Spironolactone

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This diuretic decreases aqueous secretion due to lack of HCO3 ion. Causes drowsiness and paresthesias, alkalinization of the urine may precipitate calcium salts, hypokalemia, and acidosis

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Acetazolamide

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A segment of the nephron that removes solute w/out water; the thick ascending limb and the distal convoluted tubule are active salt-absorbing segments that are not premeant to water

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Diluting segment

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Toxicity of spironolactone (in addition to hyperkalemia)

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Endocrine abnormalities, including gynecomastia, and antiandrogenic effects

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Prototypical osmotic diuretic

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mannitol

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Major site of action of mannitol

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PCT, where the bulk of isosmotic reabsorption normally occurs

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Clinical use of mannitol

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Used to maintain high urine flow when renal blood flow is reduced in conditions of solute overload from severe hemolysis or rhabdomyolysis; reducing IOP in acute glaucoma and ICP in neurologic conditions

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Toxicity of mannitol

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Removal of water from the intracellular compartment may cause hyponatremia and pulmonary edema. As the water is excreted hypernatremia may follow. Headache, nausea, and vomiting are common

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Prototypical ADH agonists

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ADH and desmopressin

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ADH antagonists

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Demeclocycline and conivaptan

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MOA of ADH

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facilitates water reabsorption from the collecting tubule by activation of V2 receptors which stimulate adenylyl cyclase via Gs

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MOA of Conivaptan

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ADH inhibitor at V1a and V2 receptors

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MOA of Demeclocycline and lithium

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inhibit the action of ADH at some point distal to the generation of cAMP and presumably interfere w/ the insertion of water channels into the membrane

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Clinical use of ADH and desmopressing

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Pituitary D.I.

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Clincal use of demeclocycline and conivaptan

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SIADH

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Toxicity of ADH or desmopressing

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large water load may cause dangerous hyponatremia, possible HTN

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Toxicity of demeclocycline

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like other tetracyclines it causes bone and teeth abnormalities in children under 8

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Reason lithium is NEVER used to treat SIADH

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Causes nephrogenic DI