- Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD more...
As previously mentioned, oliguria with volume overload requires fluid restriction and IV furosemide. If the patient fails to respond to furosemide, acute tubular necrosis, rather than renal hypoperfusion, may be present, and fluid may have to be removed by dialysis or hemofiltration, especially if signs of pulmonary edema are evident.
In patients with hyperkalemia, a cation exchange resin, such as sodium polystyrene sulfonate (Kayexalate), is administered when serum potassium levels rise to 5.5 mEq/L or above. When potassium exceeds 6.5 mEq/L or if peaked T waves are present on electrocardiography, calcium gluconate (with continuous electrocardiographic monitoring) should be administered along with it to counteract the effects of hyperkalemia on the myocardium.
Sodium bicarbonate is also used in cases of hyperkalemia but is recommended only when severe acidosis is present concomitantly. This agent can precipitate hypocalcemia and sodium overload and should therefore be used with caution.
In patients with recent-onset oliguria from prerenal or toxic injury who do not respond to hydration, agents such as mannitol and furosemide can convert the oliguric state to a nonoliguric acute renal failure, which is more easily managed. These agents may prevent tubule obstruction by increasing intratubular fluid flow via direct renal vasodilatory action and by decreased reabsorption of sodium and chloride.
Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system. This interference inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.
Hyperkalemia in oliguric acute renal failure is a medical emergency that may be managed by shifting potassium into cells (sodium bicarbonate, glucose/insulin infusion, beta agonists), increasing the removal of potassium (exchange resins, dialysis), and protecting the myocardium (calcium).
Sodium bicarbonate is indicated for the treatment of hyperkalemia with concomitant acidosis. Sodium bicarbonate increases serum bicarbonate and reacts with hydrogen ions to form water and carbon dioxide. It acts as a buffer against acidosis by raising blood pH.
Calcium gluconate is indicated if hyperkalemia is accompanied by peaked T waves or if peaked T waves persist after bicarbonate therapy.
Hyperkalemia in oliguric acute kidney injury is a medical emergency that may be managed by agents that shift potassium into cells.
This agent is used as an adjunct to bicarbonate therapy. Insulin promotes the intracellular shift of potassium. Administer insulin with dextrose to maintain serum glucose levels.
This agent is indicated in all cases of hyperkalemia. Sodium polystyrene sulfonate exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. The onset of action after oral administration ranges from 2-12 hours.
Oliguric acute kidney injury is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders.
Calcium carbonate successfully normalizes phosphate concentrations in patients on dialysis. It combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces. Calcium carbonate is marketed in various dosage forms and is relatively inexpensive.
Mild metabolic acidosis is treated with oral sodium citrate. Severe acidosis requires IV bicarbonate, as previously discussed.
This drug combination is used to treat metabolic acidosis and is employed as an alkalinizing agent when long-term maintenance of alkaline urine is desirable.
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