Figure 628

A and B, Potential defects and causes of hyperkalemic distal renal tubular acidosis (RTA) (type 4). This syndrome represents the most common type of RTA encountered in adults. The characteristic hyperchloremic metabolic acidosis in the company of hyperkalemia emerges as a consequence of generalized dysfunction of the collecting tubule, including diminished sodium reabsorption and impaired hydrogen ion and potassium secretion. The resultant hyperkalemia causes impaired ammonium excretion that is an important contribution to the generation of the metabolic acidosis. The causes of this syndrome are broadly classified into disorders resulting in aldosterone deficiency and those that impose resistance to the action of aldosterone. Aldosterone deficiency can arise from hyporeninemia, impaired conversion of angiotensin I to angiotensin II, or abnormal aldosterone synthesis. Aldosterone resistance can reflect the following: blockade of the mineralocorticoid receptor; destruction of the target cells in the collecting tubule (tubulointer-stitial nephropathies); interference with the sodium channel of the principal cell, thereby decreasing the lumen-negative potential difference and thus the secretion of potassium and hydrogen ions (voltage-mediated defect); inhibition of the basolateral sodium ion, potassium ion-adenosine triphosphatase; and enhanced chloride ion permeability in the collecting tubule, with consequent shunting of the transepithelial potential difference. Some disorders cause combined aldosterone deficiency and resistance [20].

Benefits

• Prevents or reverses acidemia-related hemodynamic compromise.

• Reinstates cardiovascular responsiveness to catecholamines.

• "Buys time," thus allowing cause-specific measures and endogenous reparatory processes to take effect.

• Provides a measure of safety against additional acidifying stresses.

Benefits

• Prevents or reverses acidemia-related hemodynamic compromise.

• Reinstates cardiovascular responsiveness to catecholamines.

• "Buys time," thus allowing cause-specific measures and endogenous reparatory processes to take effect.

• Provides a measure of safety against additional acidifying stresses.

Risks

• Hypernatremia/ hyperosmolality

• Volume overload

• "Overshoot" alkalosis

• Hypokalemia

• Decreased plasma ionized calcium concentration

• Stimulation of organic acid production

• Hypercapnia

Treatment of acute metabolic acidosis. Whenever possible, cause-specific measures should be at the center of treatment of metabolic acidosis. In the presence of severe acidemia, such measures should be supplemented by judicious administration of sodium bicarbonate. The goal of alkali therapy is to return the blood pH to a safer level of about 7.20. Anticipated benefits and potential risks of alkali therapy are depicted here [1].

0 0

Post a comment