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Oliguria Medication

  • Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
 
Updated: Jun 10, 2014
 

Medication Summary

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.

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Diuretics, Loop

Class Summary

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 (Lasix)

 

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.

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Electrolytes

Class Summary

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 (Neut)

 

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 (Cal-Glu)

 

Calcium gluconate is indicated if hyperkalemia is accompanied by peaked T waves or if peaked T waves persist after bicarbonate therapy.

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Antidotes

Class Summary

Hyperkalemia in oliguric acute kidney injury is a medical emergency that may be managed by agents that shift potassium into cells.

Insulin regular human (Novolin, Humulin)

 

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.

Sodium polystyrene sulfonate (Kayexalate, Kalexate, Kionex)

 

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.

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Calcium Salts

Class Summary

Oliguric acute kidney injury is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders.

Calcium carbonate (Nephro-Calci, Caltrate)

 

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.

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Alkalinizing Agents

Class Summary

Mild metabolic acidosis is treated with oral sodium citrate. Severe acidosis requires IV bicarbonate, as previously discussed.

Citrate and citric acid (Bicitra, Oracit)

 

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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Contributor Information and Disclosures
Author

Prasad Devarajan, MD, FAAP Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of the Nephrology Fellowship Program, Medical Director of the Kidney Stone Center, Co-Director of the Institutional Office of Pediatric Clinical Fellowships, Director of Clinical Nephrology Laboratory, CEO of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

Prasad Devarajan, MD, FAAP is a member of the following medical societies: American Heart Association, American Society of Nephrology, American Society of Pediatric Nephrology, National Kidney Foundation, Society for Pediatric Research

Disclosure: Received none from Coinventor on patents submitted for the use of NGAL as a biomarker of kidney injury for none.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Acknowledgements

Laurence Finberg, MD Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine and Stanford University School of Medicine

Laurence Finberg, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Luther Travis, MD Professor Emeritus, Departments of Pediatrics, Nephrology and Diabetes, University of Texas Medical Branch School of Medicine

Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Pathogenesis of prerenal failure
Compensatory mechanisms for preventing a fall in glomerular filtration rate (GFR) in the presence of prerenal failure
Mechanisms of intrinsic acute renal failure.
 
 
 
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