Medication Summary
Diuretic treatment may convert oliguric acute tubular necrosis (ATN) to nonoliguric ATN, although diuretics do not appear to alter the course of acute renal failure (ARF).
Hyperkalemia in ATN is a medical emergency that may be managed by shifting potassium into cells with sodium bicarbonate, glucose/insulin infusion, or beta agonists; by increasing potassium excretion with exchange resins (sodium polystyrene) or loop diuretics (furosemide); or by dialysis. Protecting the myocardium from hyperkalemia is managed with intravenous (IV) calcium.
Hyperphosphatemia may be initially managed with oral calcium to bind dietary phosphate. Oral citrate salts may be used to manage mild metabolic acidosis, whereas IV sodium bicarbonate is needed for severe metabolic acidosis.
Loop diuretics
Class Summary
In children with recent-onset oliguria from prerenal or toxic injury who are unresponsive to hydration, a trial of furosemide may convert the oliguric ATN to a nonoliguric type, which is managed more easily. These agents have a direct vasodilatory action and additionally may prevent tubular obstruction by increasing intratubular fluid flow.
Furosemide (Lasix)
Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. It is used for ATN prevention in children with oliguria duration less than 48 hours who have not responded to adequate hydration. It may also be considered for oliguria in the presence of volume overload. Furosemide is also used for hyperkalemia to increase potassium excretion in the urine.
Alkalizing agents
Class Summary
Intravenous sodium bicarbonate and oral sodium citrate are used as buffers that break down to water and carbon dioxide after picking up free hydrogen ions, thus counteracting acidosis by raising blood pH. IV sodium bicarbonate is also used to manage hyperkalemia.
Sodium bicarbonate
Sodium bicarbonate is used to treat hyperkalemia. It causes a rapid shift of potassium into cells. The magnitude of the potassium intracellular shift varies; thus, bicarbonate is not reliable in lowering the potassium level by itself. It is also used emergently to manage severe metabolic acidosis.
Sodium citrate (Bicitra, Oracit)
Sodium citrate manages mild metabolic acidosis and is used as an alkalinizing agent when long-term maintenance of an alkaline urine is desirable.
Myocardium stabilizers
Class Summary
Intravenous calcium is primarily used to protect the myocardium from the deleterious effects of hyperkalemia (ie, arrhythmias) by antagonizing the potassium actions on the myocardial cell membrane. It does not lower serum potassium levels.
Calcium gluconate (Kalcinate)
Calcium gluconate is given intravenously to provide myocardial protection from hyperkalemia. It is indicated if hyperkalemia is accompanied by ominous electrocardiographic (ECG) changes beyond peaked T waves or if ECG changes persist after bicarbonate therapy.
Intracellular transporters
Class Summary
Insulin and glucose (dextrose) cause a transcellular shift of potassium into muscle cells, thereby lowering (temporarily) potassium serum levels.
Dextrose and insulin infusion
Dextrose and insulin infusion is used as an adjunct to bicarbonate therapy to promote intracellular shift of potassium.
Exchange resins
Class Summary
Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each 1 mEq of potassium is exchanged for 1 mEq of sodium.
Sodium polystyrene sulfonate (Kayexalate)
Sodium polystyrene sulfonate is indicated in all cases of hyperkalemia because it is the only modality (other than diuretics and dialysis) that actually removes excessive potassium from the body. It exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. Its onset of action after oral administration ranges from 2-12 hours and is longer when rectally administered.
Phosphate binders
Class Summary
ATN is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders.
Calcium carbonate (Oystercal, Caltrate)
Calcium carbonate combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces.
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Common causes of oliguric versus nonoliguric acute renal failure in children.
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Metabolic alterations in tubule cells following acute tubular necrosis.
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Compensatory mechanisms that maintain glomerular filtration rate despite a reduction in renal perfusion pressure.
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Pathogenesis of acute tubular necrosis (macrovascular changes).
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Alterations in tubule cell morphology in acute tubular necrosis.
Tables
|
ATN |
Prerenal |
Urine specific gravity |
1010 |
>1020 |
Urine sodium (mEq/L) |
>40 |
< 10 |
Urine/plasma creatinine |
< 20 |
>40 |
FENa (%) |
>2 |
< 1 |
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