Acute Renal Failure Medication
- Author: Biruh T Workeneh, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
Medication Summary
Pharmacologic treatment of AKI has been attempted on an empiric basis with varying success rates. Several promising experimental therapies in animal models are awaiting human trials. Experimental therapies include growth factors, vasoactive peptides, adhesion molecules, endothelin inhibitors, and bioartificial kidneys. Aminophylline has also been used experimentally for prophylaxis against renal failure.
A prophylactic strategy shown to decrease the incidence of contrast nephropathy is the IV administration of fluids. Although controversy exists regarding the ideal fluid, normal saline and isotonic NaHCO3 have proven to be effective. Normal saline solution of 1 mL/kg/h administered 12 hours before the procedure and then 12 hours after the procedure is recommended.
In patients who are at high risk for volume overload (congestive heart failure, left ventricular ejection fraction < 40%), isotonic NaHCO3 solution should be administered before and after the procedure. It can be prepared by mixing 3 ampules of NaHCO3 in a liter of D5W and can be given at a rate of 3 mL/kg/h for 1 hour prior to the procedure, decreasing the rate to 1 mL/kg/h during the procedure and for 6 hours afterward.
Another prophylactic agent, used with varying success, is N -acetylcysteine at a dosage of 1200 mg PO q12h. This is administered to high-risk patients the day before a contrast study is performed and is continued the day of the procedure. Diuretics, NSAIDs, and possibly ACEIs should be withheld near the time of the procedure.[15]
Any protective effect of N -acetylcysteine would appear to be limited to patients receiving radiocontrast. A meta-analysis of patients undergoing major surgery found no evidence that N -acetylcysteine used perioperatively can alter mortality or renal outcomes when radiocontrast is not used.[16]
Similarly, a review of randomized, controlled trials of other measures used to protect renal function perioperatively (eg, the administration of dopamine, diuretics, calcium-channel blockers, ACEIs, or hydration fluids) found no reliable evidence that these interventions are effective.[17]
Diuretics
Class Summary
Although diuretics seem to have no effect on the outcome of established acute kidney injury (AKI), they appear useful in fluid homeostasis and are used extensively. The use of isotonic sodium chloride solution in conjunction with diuretics is debatable.
The only therapeutic or preventive intervention that has an established beneficial effect in the management of AKI is the administration of isotonic sodium chloride solution to keep the patient euvolemic or even hypervolemic.
Furosemide (Lasix)
Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the thick ascending loop of Henle and the distal renal tubule. It is a potent and rapid-acting agent with peak action at 60 minutes and lasting 6-8 hours.
In renal failure, higher doses must be used for greater diuretic effects. Doses as high as 600 mg per day may be needed under monitored conditions.
Frequently, IV doses are needed in AKI to maintain urine output. IV infusions are often helpful in ICU settings, in which larger doses are necessary. This method promotes a sustained natriuresis with reduced ototoxicity compared with conventional intermittent bolus dosing.
Adrenergic Agonists
Class Summary
Dopamine in small doses (eg, 1-5 mcg/kg/min) causes selective dilatation of the renal vasculature, enhancing renal perfusion. Dopamine also reduces sodium absorption, thereby decreasing the energy requirement of the damaged tubules. This enhances urine flow, which, in turn, helps to prevent tubular cast obstruction. Most clinical studies have failed to establish this beneficial role of renal-dose dopamine infusion.
Dopamine
Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect is dose dependent. Lower doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses.
Calcium channel blockers
Class Summary
These drugs are effective in animal models, but their efficacy has not been proven in humans. The effects of calcium channel blockers are believed to be mediated through vasodilation, and they are increasingly are used to enhance the function of transplanted kidneys.
Nifedipine (Adalat, Procardia, Afeditab CR, Nifediac CC, Nifedical XL)
Nifedipine relaxes smooth muscle and produces vasodilation, which, in turn, improves blood flow and oxygen delivery.
Antidotes
Class Summary
N -acetylcysteine is used for the prevention of contrast toxicity in susceptible individuals, such as those with diabetes mellitus.
N-acetylcysteine (Acetadote)
This drug may provide substrate for conjugation with toxic metabolites.
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Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. Aug 2004;8(4):R204-12. [Medline]. [Full Text].
[Best Evidence] Kheterpal S, Tremper KK, Heung M, Rosenberg AL, Englesbe M, Shanks AM, et al. Development and validation of an acute kidney injury risk index for patients undergoing general surgery: results from a national data set. Anesthesiology. Mar 2009;110(3):505-15. [Medline].
Goldberg R, Dennen P. Long-term outcomes of acute kidney injury. Adv Chronic Kidney Dis. Jul 2008;15(3):297-307. [Medline].
Feest TG, Mistry CD, Grimes DS, Mallick NP. Incidence of advanced chronic renal failure and the need for end stage renal replacement treatment. BMJ. Oct 20 1990;301(6757):897-900. [Medline]. [Full Text].
Pannu N, James M, Hemmelgarn BR, Dong J, Tonelli M, Klarenbach S. Modification of Outcomes After Acute Kidney Injury by the Presence of CKD. Am J Kidney Dis. Aug 2011;58(2):206-13. [Medline].
Grams ME, Estrella MM, Coresh J, Brower RG, Liu KD. Fluid Balance, Diuretic Use, and Mortality in Acute Kidney Injury. Clin J Am Soc Nephrol. May 2011;6(5):966-973. [Medline]. [Full Text].
James MT, Hemmelgarn BR, Wiebe N, Pannu N, Manns BJ, Klarenbach SW, et al. Glomerular filtration rate, proteinuria, and the incidence and consequences of acute kidney injury: a cohort study. Lancet. Dec 18 2010;376(9758):2096-103. [Medline].
Molnar AO, Coca SG, Devereaux PJ, Jain AK, Kitchlu A, Luo J, et al. Statin use associates with a lower incidence of acute kidney injury after major elective surgery. J Am Soc Nephrol. May 2011;22(5):939-46. [Medline]. [Full Text].
American College of Radiology. ACR Appropriateness Criteria® renal failure. National Guideline Clearinghouse. Available at http://guideline.gov/content.aspx?id=13685. Accessed March 24, 2011.
Breidthardt T, Christ-Crain M, Stolz D, et al. A combined cardiorenal assessment for the prediction of acute kidney injury in lower respiratory tract infections. Am J Med. Feb 2012;125(2):168-75. [Medline].
Hall IE, Coca SG, Perazella MA, et al. Risk of Poor Outcomes with Novel and Traditional Biomarkers at Clinical AKI Diagnosis. Clin J Am Soc Nephrol. Dec 2011;6(12):2740-9. [Medline].
Mancini E, Caramelli F, Ranucci M, et al. Is time on cardiopulmonary bypass during cardiac surgery associated with acute kidney injury requiring dialysis?. Hemodial Int. Nov 8 2011;[Medline].
[Best Evidence] Palevsky PM, Zhang JH, O'Connor TZ, Chertow GM, Crowley ST, Choudhury D, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. Jul 3 2008;359(1):7-20. [Medline]. [Full Text].
[Best Evidence] Marenzi G, Assanelli E, Marana I, Lauri G, Campodonico J, Grazi M, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med. Jun 29 2006;354(26):2773-82. [Medline].
[Best Evidence] Ho KM, Morgan DJ. Meta-analysis of N-acetylcysteine to prevent acute renal failure after major surgery. Am J Kidney Dis. Jan 2009;53(1):33-40. [Medline].
[Best Evidence] Zacharias M, Conlon NP, Herbison GP, Sivalingam P, Walker RJ, Hovhannisyan K. Interventions for protecting renal function in the perioperative period. Cochrane Database Syst Rev. Oct 8 2008;CD003590. [Medline].
| Stage | GFR** Criteria | Urine Output Criteria | Probability |
| Risk | SCreat† increased × 1.5 or GFR decreased >25% | UO‡ < 0.5 mL/kg/h × 6 h | High sensitivity (Risk >Injury >Failure) |
| Injury | SCreat increased × 2 or GFR decreased >50% | UO < 0.5 mL/kg/h × 12 h | |
| Failure | SCreat increased × 3 or GFR decreased 75% or SCreat ≥4 mg/dL; acute rise ≥0.5 mg/dL | UO < 0.3 mL/kg/h × 24 h (oliguria) or anuria × 12 h | |
| Loss | Persistent acute renal failure: complete loss of kidney function >4 wk | High specificity | |
| ESKD* | Complete loss of kidney function >3 mo | ||
| *ESKD—end-stage kidney disease; **GFR—glomerular filtration rate; †SCreat—serum creatinine; ‡UO—urine output Note: Patients can be classified by GFR criteria and/or UO criteria. The criteria that support the most severe classification should be used. The superimposition of acute on chronic failure is indicated with the designation RIFLE-FC; failure is present in such cases even if the increase in SCreat is less than 3-fold, provided that the new SCreat is greater than 4.0 mg/dL (350 μmol/L) and results from an acute increase of at least 0.5 mg/dL (44 μmol/L). | |||
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