6. Renal Drugs: Diuretics And Other Drugs Acting On The Kidneys BG Katzung and David G. Wa

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6. Renal Drugs: Diuretics And Other Drugs Acting On The Kidneys BG Katzung and David G. Warnock 旼컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴 I. Agents that increase salt and water excretion A. Thiazides Drug Table , Thiazide combinations B. Loop agents Drug Table C. Potassium-sparing diuretics Drug Table D. Carbonic anhydrase inhibitors Drug Table E. Osmotic Diuretics II. Agents acting on water excretion A. ADH and analogs B. Demeclocycline 읕컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴켸 (PgDn key for more text) Drugs that act on the kidneys are used in a variety of diseases; the greatest number of prescriptions are for hypertension and congestive fail- ure. The major classes of diuretics are the thiazides, loop agents, potassium-sparing diuretics, carbonic anhydrase inhibitors, and osmotic diuretics. Mercurial diuretics, though still available, are obsolete and should never be used. They are not discussed in this book. Carbonic an- hydrase inhibitors, though mostly used for other conditions, are also diuretics and are discussed in this chapter. Important agents that in- fluence water excretion by the kidney are antidiuretic hormone and its analog desmopressin, and a miscellaneous group of ADH antagonists. Pathophysiology And Therapeutic Rationale For The Use Of Diuretics * Salt and water retention: This condition is usually associated with in- creased levels of aldosterone, secreted in response to a decrease in "effective" circulating blood volume, eg, in congestive heart failure, cirrhosis, and nephrotic syndrome. The increase in total body sodium and water may be expressed as edema or ascites, in addition to an in- crease in total blood volume. The increased workload on the heart and the physical effects of pulmonary edema or massive ascites often re- quire that the excess salt and water be removed. (PgDn key for more text) However, over-enthusiastic use of diuretics may cause potassium wasting and impair cardiac output. Restriction of salt intake is often a more rational and effective therapy, especially in cirrhosis and nephrotic syndrome. * Hypertension: The underlying pathophysiology is fully not understood but reduction of blood volume and other effects of diuretic drugs are important aspects of therapy . In addition, other antihypertensive agents may cause salt and water retention; this effect may be reversed by diuretics. * Hypercalcemia and hypercalciuria: Hypercalcemia usually results from nonrenal causes, eg, metastatic cancer. Hypercalcemia is a potentially lethal condition: CNS depression can rapidly progress from lethargy to coma and respiratory arrest. Rapid reduction of serum calcium with loop diuretics may therefore be necessary while the un- derlying cause is treated and long-term therapies are begun. Chronic hypercalciuria is often associated with nephrolithiasis; it may result from underlying metabolic disease, eg, hyperparathyroidism or excessive ingestion of milk or vitamin D. Recurrent stone formers may benefit from treatment with thiazides. See also Chapter 15, Section VI. (PgDn key for more text) * Diabetes insipidus and inappropriate secretion of ADH: While pituitary diabetes insipidus is best treated with antidiuretic hormone, nephrogenic diabetes insipidus is, by definition, resistant to ADH. Furthermore, the nephrogenic form is a relatively common adverse effect of several drugs, eg, lithium carbonate. Drugs acting on renal salt transport mechanisms have beneficial effects on both forms of the dis- ease. The syndrome of inappropriate ADH secretion (SIADH) is associated with some tumors, eg, oat cell carcinoma of the lung and with a number of drugs, including oral hypoglycemic agents, carbamazepine, and vin- cristine. * Drug intoxication: Some drugs that are cleared by the kidney can be eliminated more rapidly by forced diuresis, especially if their reab- sorption from the tubule can be reduced by changing urine pH. Examples include amphetamine, salicylate, and phenobarbital. (PgDn key for more text) References 1. Acetazolamide for acute mountain sickness. FDA Bull 1983; 13: 27. 2. Ashraf N et al: Thiazide-induced hyponatremia associated with death or neurologic damage in outpatients. Am J Med 1981; 70: 1141. 3. Brater DC: Determinants of the overall response to furosemide: pharmacokinetics and pharmacodynamics. Fed Proc 1983; 42: 1711. 4. Beerman B, Groschinsky-Grind M: Clinical pharmacokinetics of diuretics. Clin Pharmacokinet 1980; 5: 221. 5. Chaffman M et al: Indapamide: Review of its pharmacodynamic properties and therapeutic efficacy in hypertension. Drugs 1984; 28: 189. 6. DeTroyer A: Demeclocycline: treatment for syndrome of inappropriate antidiuretic hormone secretion. JAMA 1977; 237: 589. 7. Greene MK, et al: Acetazolamide in prevention of acute mountain sick- ness: a double-blind controlled cross-over study. Br Med J 1981; 183: 811. 8. Maclean D, Tudhope GR: Modern diuretic treatment. Br Med J 1983; 286: 1419. 9. Narins RG, Chusid P: Diuretic use in critical care. Am J Cardiol 1986; 57: 26A (PgDn key for more references) 10. Schuster C-J, et al: Blood volume following diuresis induced by furosemide. Am J Med 1984; 76: 585. 11. Tiller DJ, Mudge GH: Pharmacologic agents used in management of acute renal failure. Kidney Int 1980; 18: 700. (Home key to return to top of file)

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