Potassium “wasting

P o tassi um - sp ari ng Diminishing potassium wasting from other diuretics... 

Aldosterone stimulates the rates of Na+ reabsorption and K+ secretion. This is relevant to the action of spironolactone, a diuretic that is a competitive inhibitor of aldosterone (discussed later). It is also pertinent because administration of diuretics can cause secondary hyperaldosteronism, which may exaggerate the potassium wasting that is a consequence of the increased delivery of Na+ and enhanced flow through distal convoluted tubules and collecting ducts. 

Glucocorticoids with mineralocorticoid activity potentiate potassium loss when they are given with potassium-wasting diuretics (491). 

Potassium wasting can occur because NaHC03 presented to the collecting tubule increases the lumen-negative electrical potential in that segment and enhances K+ secretion. This effect can be counteracted by simultaneous administration of KC1. 

An altered response of one drug on its target organ may be affected by the action of a concurrently administered drug on another organ. The hypokalemia produced by potassium-wasting diuretics, for example, may potentiate the action of digitalis on the heart to the point of toxicity. 

As a potassium-sparing diuretic, amiloride can cause hyperkalemia (3), even in patients who are taking a potassium-wasting diuretic (4). This effect can be enhanced by concomitant therapy with ACE inhibitors or angioten-sin-II receptor antagonists. In five patients with diabetes melUtus over 50 years of age who were taking an ACE inhibitor the serum potassium rose markedly 8-18 days after the addition of amiloride (5). AH but one had some degree of renal impairment In four cases potassium concentrations were between 9.4 and 11 mmol/1. 

Potassium-wasting diuretics can cause sodium and potassium depletion with hyponatremia and hypokalemia. Potassium-retaining diuretics can cause hyperkalemia. 

However, in 85 patients enoxaparin therapy was associated with an increase in mean potassium concentration from 4.26 mmol/1 at baseline to 4.43 mmol/1 on the third day potassium concentrations exceeded 5.0 mmol/1 in 9% (15). There was no life-threatening or sjmptomatic hjrperkalemia. Neither plasma renin activity nor aldosterone concentrations changed significantly and there was no correlation between the increase in potassium concentrations and the presence of diabetes mellitus or treatment with angiotensin converting enzjmes inhibitors, angiotensin receptor blockers, beta-blockers, or potassium-wasting diuretics. 

Prolongation of the QT interval by ketanserin is more pronounced when it used in combination with potassium-wasting diuretics (4). This combination must therefore be avoided. 

The most restrictive adverse effect associated with AmB therapy is its potential to induce nephrotoxicity, manifested as disturbances in both glomerular and tubular function. The clinical manifestations usually include azotemia, renal tubular acidosis, decreased concentrating ability of the kidney, and electrolyte disturbances such as urinary potassium wasting leading to hypokalemia, and magnesium wasting to result in hypomagnesemia [17]. 

Because of digoxin s narrow therapeutic range, toxicity can often occur, especially in those who have predisposing factors, such as hypokalemia, concurrent therapy with potassium wasting diuretics, age (elderly and pediatrics), small body size, and drug interactions. Common signs of toxicity include Gl complaints (nausea, vomiting, and anorexia), arrhythmias, and CNS effects (i.e., confusion, hallucinations, and visual disturbances). 

Drug interactions Amphotericin B or potassium-wasting diuretics may contribute to digoxin toxicity ACE-I, amiodarone, bepridii, diltiazem.guinidine, and verapamil may increase digoxin levels. 

Filtered sodium is reabsorbed at the proximal tubules, the Loop of Henle, distal tubules, or in the collecting tubules. Diuretics influence tubules closest to the glomeruli, causing natriuresis (sodium loss in the urine). Diuretics cause loss of other electrolytes (potassium, magnesium, chloride, bicarbonate). Diuretics that promote potassium excretion are called potassium-wasting diuretics or potassium-sparing diuretics. 

Potassium-sparing diuretics excrete sodium and water and retain potassium by interfering with the sodium-potassium pump in the collecting distal duct renal tubules. Potassium-sparing diuretics do not require potassium supplements, which are needed with potassium-wasting diuretics. The diuretic effect is intensified with the combined use of potassium-sparing diuretics and potassium-wasting diuretic. 

Potassium-wasting diuretics are diuretics that promote the excretion of potassium. 

Some patients acidify urine at a submaximal rate, but at a rate that is generally sufficient to maintain acid-base balance. Potassium wasting, hypokalemia, and hyperchloremia are generally not present. However, when patients are stressed or are given an acid load, their ability to excrete acid and to lower urine pH is suboptimal and urinary pH may exceed 5.5. 

Other unusual conditions that suggest aldosterone excess or deficiency but are not connected to the renin-angiotensin-aldosterone system include Liddle s syndrome (pseudo hyper aldosteronism),which resembles primary aldosteronism clinically, but aldosterone production is low and hypertension is absent and Barttefs syndrome,which involves a prostaglandin-mediated renal potassium wasting and renal chloride handling defect, in which both aldosterone concentrations and renin activities are elevated. In renal tubular acidosis and pseudohypoaldosteronism, the clinical picture of hypoaldosteronism is seen concurrent with greater-than-normal concentrations of aldosterone. 

Major functions of the distal nephron include the regeneration of bicarbonate, the excretion of acid (hydrogen ion), the secretion of potassium, and the reabsorption of water. Damage to this portion of the nephron may present as significant acidemia and either hypo-or hyperkalemia, depending on the mechanism of injury. For example, amphotericin B produces small pores in the luminal membrane of distal tubular cells. These pores allow small molecules such as potassium to leak out the molecules are then wasted in the urine. Consequently, amphotericin B nephrotoxicity is characterized by hypokalemia secondary to renal potassium wasting. ATN is associated with urinary sediment characterized by the presence of tubular cells, coarse granular casts, and rarely, RBC casts. 

Potassium supplementation is always necessary for patients with chronic metabolic acidosis, as the bicarbonaturia resulting from alkali therapy increases the renal potassium wasting. 

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