Renal Cortical Necrosis Medication

  • Author: Prasad Devarajan, MD; Chief Editor: Craig B Langman, MD   more...
 
Updated: May 26, 2011
 

Medication Summary

The restoration of hemodynamic stability may require use of intravenous (IV) crystalloids, colloids, blood products, and/or pressors to maintain blood pressure and cardiac output.

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Electrolytes

Class Summary

These agents are used to maintain blood pressure and cardiac output.

Lactated Ringer with Normal Saline

 

Lactated Ringer is essentially isotonic and has restorative properties. It restores interstitial and intravascular volume.

Normal saline

 

Normal saline is used for restoration of interstitial and intravascular volume.

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Colloids

Class Summary

These agents are used for volume expansion to treat shock. They are preferred over crystalloids because the excessive administration of fluids can lead to extravasation caused by vascular leak, especially during the febrile and hypotensive stages.

Albumin (Albuminar, AlbuRx, Albutein, Flexbumin, Plasbumin)

 

Albumin is used for certain types of shock or impending shock. It is useful for plasma volume expansion and maintenance of cardiac output. Although theoretically attractive, the benefit of colloid resuscitation over isotonic crystalloids is not proven.

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Vasopressors

Class Summary

These agents maintain blood pressure and cardiac output in patients with renal cortical necrosis.

Dopamine

 

Dopamine stimulates both adrenergic and dopaminergic receptors. The hemodynamic effect depends on the dose. Low doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. High doses produce cardiac stimulation and renal vasodilation. After initiating therapy, increase the dose by 1-4 mcg/kg/min every 10-30 minutes until an optimal response is obtained. Maintenance dosing at less than 20 mcg/kg/min is satisfactory in greater than 50% of patients.

Norepinephrine (Levophed)

 

Norepinephrine is used in protracted hypotension after adequate fluid replacement. It stimulates beta1- and alpha-adrenergic receptors, which, in turn, increases cardiac muscle contractility and the heart rate, as well as vasoconstriction. As a result, it increases systemic blood pressure and cardiac output. Adjust and maintain the infusion to stabilize blood pressure (eg, 80-100 mm Hg systolic) sufficiently to perfuse vital organs.

Vasopressin (Pitressin)

 

Vasopressin has vasopressor and antidiuretic hormone (ADH) activity. It increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). Vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

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Contributor Information and Disclosures
Author

Prasad Devarajan, MD  Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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.

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.

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, Children's Memorial Hospital

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

Disclosure: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

References
  1. Kamioka I, Nozu K, Fujita T, Kaito H, Tanaka R, Yoshiya K, et al. Prognosis and pathological characteristics of five children with non-Shiga toxin-mediated hemolytic uremic syndrome. Pediatr Int. Apr 2007;49(2):196-201. [Medline].

  2. Prakash J, Vohra R, Wani IA, Murthy AS, Srivastva PK, Tripathi K, et al. Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing countries: a single-centre experience of 22 years from Eastern India. Nephrol Dial Transplant. Apr 2007;22(4):1213-7. [Medline].

  3. Ali A, Ali MA, Ali MU, Mohammad S. Hospital outcomes of obstetrical-related acute renal failure in a tertiary care teaching hospital. Ren Fail. 2011;33(3):285-90. [Medline].

  4. Papnicolaou N, Francis IR, Casalino DD, Arellano RS, Baumgarten DA, Curry NS, et al. ACR Appropriateness Criteria renal failure. [online publication]. Reston, VA: American College of Radiology (ACR); 2008.

  5. Archer L, Kilburn-Toppin F, Sneddon K, et al. A "fussy eater" with renal failure. Lancet. Feb 20 2010;375(9715):696. [Medline].

  6. Krishna GS, Kishore KC, Sriram NP, et al. Bilateral renal cortical necrosis in acute pancreatitis. Indian J Nephrol. Jul 2009;19(3):125. [Medline]. [Full Text].

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