Acute Renal Failure Treatment & Management
- Author: Biruh T Workeneh, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
Approach Considerations
Measures to correct underlying causes of acute kidney injury (AKI) should begin at the earliest indication of renal dysfunction. A large proportion of the renal mass is damaged before any biochemical evidence of renal dysfunction is appreciated, because the relationship between the GFR and the serum creatinine level is not linear, especially early in disease; the rise of serum creatinine may not be evident before 50% of the GFR is lost.
The Acute Renal Failure Trial Network (ATN) Study, completed in 2008, was designed to compare clinical outcomes between patients allocated to an intensive dose versus a less-intensive dose of renal replacement therapy.[14] No additional benefit (morbidity/mortality) was conferred to patients who received more intensive dialysis (either intermittent or continuous dialysis). The best evidence suggests that patients with dialysis-dependent AKI should receive at least 3 hemodialysis treatments per week with delivered Kt/V value of 1.2 or continuous hemodialysis (continuous venovenous hemodialysis or hemofiltration) of 20 mg/kg/h (prescribed).
Timing of dialysis
Great controversy exists regarding the timing of dialysis. Dialysis, especially hemodialysis, may delay the recovery of patients with AKI. Most authorities prefer using biocompatible membrane dialyzers for hemodialysis.
There seems to be no difference in outcome between the use of intermittent hemodialysis and continuous renal replacement therapy (CRRT), but this is currently under investigation. However, CCRT may have a role in patients who are hemodynamically unstable and who have had prolonged renal failure after a stroke or liver failure. Such patients may not tolerate the rapid shift of fluid and electrolytes caused during conventional hemodialysis. Although not frequently used, peritoneal dialysis can also technically be used in acute cases and probably is tolerated better hemodynamically than conventional hemodialysis.
Indications for dialysis in patients with AKI are as follows:
- Volume expansion that cannot be managed with diuretics
- Hyperkalemia refractory to medical therapy
- Correction of severe acid-base disturbances that are refractory to medical therapy
- Severe azotemia (BUN >80-100)
- Uremia
Maintenance of Volume Homeostasis and Correction of Biochemical Abnormalities
Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment. Furosemide can be used to correct volume overload when the patients are still responsive; this often requires high intravenous (IV) doses.
Furosemide plays no role in converting an oliguric AKI to a nonoliguric AKI or in increasing urine output when a patient is not hypervolemic.
However, the response to furosemide can be taken as a good prognostic sign. At this stage, the kidneys remain vulnerable to the toxic effects of various chemicals. All nephrotoxic agents (eg, radiocontrast agents, antibiotics with nephrotoxic potential, heavy metal preparations, cancer chemotherapeutic agents, NSAIDs) are either avoided or used with extreme caution. Similarly, all medications cleared by renal excretion should be avoided or their doses should be adjusted appropriately.
Correcting Severe Acidosis
Correcting severe acidosis with bicarbonate administration can be important as a bridge to dialysis. It cannot be overstated that the current treatment of acute kidney injury (AKI) is mainly supportive in nature and no therapeutic modalities to date have shown efficacy in treating the condition. Therapeutic agents, such as dopamine, nesiritide, fenoldopam, and mannitol, are not indicated in the management of AKI and may be harmful for the patient.
Treatment of Hyperkalemia
Hyperkalemia, which can be life-threatening, should be treated by decreasing the intake of potassium in diet or tube feeds, exchanging potassium across the gut lumen using potassium-binding resins, promoting intracellular shifts in potassium with insulin and dextrose solutions, and instituting dialysis.
Correcting Hematologic Abnormalities
Correcting hematologic abnormalities (eg, anemia, uremic platelet dysfunction) warrants appropriate measures, including transfusions and administration of desmopressin or estrogens.
Dietary Modification
Dietary modulation is an important facet of the treatment of acute kidney injury (AKI). Salt and fluid restriction becomes crucial in the management of oliguric renal failure, wherein the kidneys do not adequately excrete either toxins or fluids.
Because potassium and phosphorus are not excreted optimally in patients with AKI, blood levels of these electrolytes tend to be high. Frequent measurements are mandatory to initiate early treatment and avoid complications.
In the polyuric phase of AKI, potassium and phosphorus may be depleted, and patients require dietary supplementation and intravenous replacement.
Calculation of the nitrogen balance can be challenging, especially in the presence of volume contraction, hypercatabolic states, GI bleeding, and diarrheal disease. Critically ill patients should receive at least 1 g/kg/d protein intake but should avoid hyperalimentation, which can lead to an elevated BUN level and water loss resulting in hypernatremia.
Consultations
Nephrology consultation should be sought early in the course of acute kidney injury (AKI) so that management can be optimized and preventable complications of AKI can be avoided.
Long-Term Monitoring
Always keep in mind that renal recovery in most cases is not complete and that the kidneys remain vulnerable to nephrotoxic effects of all therapeutic agents. Therefore, agents with nephrotoxic potential are best avoided.
Renal recovery is usually observed within the first 2 weeks, and many nephrologists tend to diagnose patients with end-stage (ie, irreversible) renal failure 6-8 weeks after the onset of acute kidney injury (AKI). It is always better to check these patients periodically, because some patients may regain renal function much later.
Schrier RW, Wang W, Poole B, Mitra A. Acute renal failure: definitions, diagnosis, pathogenesis, and therapy. J Clin Invest. Jul 2004;114(1):5-14. [Medline]. [Full Text].
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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