Diuretics
Review of Renal Physiology

Recall that the functional unit of the kidney is the nephron, which is divided into several distinct sections.

Also, recall that the body in general and the kidney specifically exerts an endogenous control of its own function.  The release of renin will cause the formation of angiotensin II, which prompts the release of aldosterone, which causes the release of ADH, where these hormones may produce the effects described above.  Atrial natriuretic peptide (ANP, atriopeptin) is secreted from the atrium of the heart in response to stretch receptors stimulated by overfilling of the chamber.  This is interpreted as too great a blood volume.  ANP then prompts the kidney to stop the conservation of Na (increase Na excretion) so that water will follow osmotically, thus reducing blood volume.

Diuretics

Thiazide and thiazide-type diuretics -- This class includes the true thiazide diuretics (chlorothiazide, hydrochlorothiazide, hydroflumethiazide, methyclothiazide, bendroflumethiazide, benzthiazide, cyclothiazide, polythiazide, and trichlormethiazide) and the thiazide-like diuretics, that are structurally dissimilar but possess the same mechanisms and pharmacodynamics (chlorthalidone, indapamide, metolazone, and quinethazone).

Loop Diuretics -- Furosemide, Torsemide, Ethacrynic Acid, Bumetanide Potassium Sparing Diuretics Carbonic Anhydrase Inhibitors (CAI) -- Acetazolamide, Methazolamide, Dichlorphenamide, Dorzolamide (ophthalmic only) Osmotic Diuretics -- Glycerin (Oral), Mannitol (Parenteral), Urea (Parenteral), Isosorbide (Oral)
An Overview of Diuretic Therapy

Diuretics are useful in a number of conditions that may be related to total body water volume, peripheral resistance, or production of fluids within the body.  General uses for diuretics include hypertension, congestive heart failure, and oedema not associated with cardiac disease.  Additional uses include hyperaldosteronism (spironolactone as noted above), glaucoma (CAI and osmotics), acute mountain sickness (CAI), centrencephalic epilepsy (CAI, as noted above), cerebral oedema (osmotics), and increased intracranial pressure (osmotics).  They may also be useful in early nephrotic syndrome, when urine output is low.  However, as noted above, the use of diuretics is contraindicated in anuria (early total renal failure with no urine output) except for the thiazides indapamide and metolazone and the loop bumetanide, which may be used cautiously.  Loop diuretics are useful in the treatment of hyperkalaemia, as discussed below.  Thiazide diuretics may provide some usefulness in the treatment of nephrogenic diabetes insipidus, as described below.

Diabetes Insipidous

Diabetes insipidous is characterised by copious amounts of urine output.  It may originate from one of two sources, and results in massive fluid loss.

Treatment There also exists a condition referred to as syndrome of inappropriate of ADH (SIADH).  In this condition, the reverse of diabetes insipidous, too much ADH is secreted and acts upon the kidney, resulting in decreased urine output and increases in total body water volume.  This may be treated with non-specific ADH antagonists lithium and demeclocyline (noted above).

Hyperkalaemia

As noted above, both hypo- and hyper-kalaemia may result from specific diuretic agents, either of which may lead to life-threatening cardiac abnormalities.  Therefore in both instances, intervention should be made to correct the metabolic imbalance.

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