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Acute Kidney Injury Treatment & Management

  • Author: Biruh T Workeneh, MD, PhD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Oct 31, 2015
 

Approach Considerations

Measures to correct underlying causes of acute kidney injury (AKI) should begin at the earliest indication of renal dysfunction. Serum creatinine does not rise to abnormal levels until a large proportion of the renal mass is damaged, because the relationship between the glomerular filtration rate (GFR) and the serum creatinine level is not linear, especially early in disease. Indeed, the rise of serum creatinine may not be evident before 50% of the GFR is lost.

It cannot be overstated that the current treatment for AKI is mainly supportive in nature; no therapeutic modalities to date have shown efficacy in treating the condition. Therapeutic agents (eg, dopamine, nesiritide, fenoldopam, mannitol) are not indicated in the management of AKI and may be harmful for the patient.

Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment and may include the following measures:

  • Correction of fluid overload with furosemide
  • Correction of severe acidosis with bicarbonate administration, which can be important as a bridge to dialysis
  • Correction of hyperkalemia
  • Correction of hematologic abnormalities (eg, anemia, uremic platelet dysfunction) with measures such as transfusions and administration of desmopressin or estrogens

Volume overload

Furosemide can be used to correct volume overload when 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, response to furosemide can be taken as a good prognostic sign.

Hyperkalemia

Hyperkalemia in patients with AKI can be life-threatening. Approaches to lowering serum potassium include the following:

  • 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, dextrose solutions, and beta agonists
  • Instituting dialysis

Nephrotoxic agents

In AKI, the kidneys are especially vulnerable to the toxic effects of various chemicals. All nephrotoxic agents (eg, radiocontrast agents, antibiotics with nephrotoxic potential, heavy metal preparations, cancer chemotherapeutic agents, nonsteroidal anti-inflammatory drugs [NSAIDs]) should be avoided or used with extreme caution. Similarly, all medications cleared by renal excretion should be avoided, or their doses should be adjusted appropriately.

A 2013 study indicated that triple therapy using nonsteroidal anti-inflammatory drugs (NSAIDs) with 2 antihypertensive medications—a diuretic along with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin-receptor blocker (ARB)—significantly increases the risk of hospitalization for AKI, particularly in the first 30 days of treatment with these drugs.

The retrospective, case-controlled study involved a cohort of 487,372 users of antihypertensive drugs between 1997 and 2008. During a mean follow-up of almost 6 years, 2215 cases of acute kidney injury were identified (incidence rate of 7 per 10 000 person-years), and each was compared with up to 10 matched controls.[40, 41]

Consultation

Nephrology consultation should be sought early in the course of AKI. A nephrologist can help to optimize management and avoid the preventable complications of AKI.

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Vasodilators

The rationale for vasodilator therapy in AKI is that improved renal perfusion may reduce renal damage. Strong evidence in support of this approach is lacking, however.

A meta-analysis of 16 randomized studies concluded that the vasodilator fenoldopam reduces the need for renal replacement therapy and lowers the mortality rate in patients with AKI.[42] However, larger trials need to be conducted before the use of fenoldopam can be recommended.

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; this enhances urine flow, which helps to prevent tubular cast obstruction. However, most clinical studies have failed to establish this beneficial role of low-dose dopamine infusion, and one study demonstrated that low-dose dopamine may worsen renal perfusion in patients with AKI.[42]

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Dietary Modification

Dietary changes are an important facet of AKI treatment. Restriction of salt and fluid 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. Restriction of these elements in the diet may be necessary, with guidance from frequent measurements. In the polyuric phase of AKI, potassium and phosphorus may be depleted, so that patients may require dietary supplementation and IV 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/day protein but should avoid hyperalimentation, which can lead to an elevated blood urea nitrogen (BUN) level and water loss resulting in hypernatremia.

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Dialysis

Dialysis, especially hemodialysis, may delay the recovery of patients with AKI. Most authorities prefer using biocompatible membrane dialyzers for hemodialysis. Indications for dialysis (ie, renal replacement therapy) 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

Timing and intensity

Great controversy exists regarding the timing of dialysis. Older studies suggested decreased mortality with early, versus late, initiation of dialysis, but timing of dialysis initiation has not been assessed in large, randomized, controlled trials.[43] Approaches vary widely at present.

The Acute Renal Failure Trial Network (ATN) Study found that increasing the intensity of dialysis (either intermittent or continuous) did not improve clinical outcomes (morbidity/mortality).[44] The best evidence suggests that patients with dialysis-dependent AKI should receive at least 3 hemodialysis treatments per week with a delivered Kt/V value of 1.2, or continuous hemodialysis (continuous venovenous hemodialysis or hemofiltration) of 20 mg/kg/h (prescribed).

CRRT

There seems to be no difference in outcome between the use of intermittent hemodialysis and continuous renal replacement therapy (CRRT), but this question is currently under investigation. CRRT 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.

Peritoneal dialysis

Peritoneal dialysis is not frequently used in patients with AKI. Nevertheless, it can technically be used in acute cases and probably is tolerated better hemodynamically than is conventional hemodialysis.

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Prevention of Contrast-Induced Nephropathy

Saline

In patients undergoing imaging studies with contrast, prophylactic administration of IV fluid has been shown to decrease the incidence of contrast nephropathy. Although controversy exists regarding the ideal fluid, normal saline and isotonic NaHCO3 have proved to be effective. A normal saline solution of 1 mL/kg/h administered 12 hours before the procedure and then 12 hours after the procedure is recommended for most patients.

NaHCO

In patients who are at high risk for volume overload—in particular, those with chronic heart failure who have a left ventricular ejection fraction of less than 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 5% dextrose in water (D5W) and can be given at a rate of 3 mL/kg/h for 1 hour prior to the procedure, with the rate decreased to 1 mL/kg/h during the procedure and for 6 hours afterward.

N -acetylcysteine

Another prophylactic agent, used with varying success, is oral N -acetylcysteine at a dosage of 1200 mg every 12 hours. This is administered to high-risk patients the day before a contrast study is performed and is continued the day of the procedure. N -acetylcysteine appears to provide only borderline benefit.[45] Diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), and possibly angiotensin-converting enzyme (ACE) inhibitors should be withheld near the time of the procedure.[46]

Statins

A meta-analysis found that statin treatment before coronary angiography can reduce contrast-induced AKI. Risk was 3.91% in the statin group versus 6.98% in the control group. On subanalysis, benefit was highly significant benefit in patients whose GFR was ≥60 ml/min (relative risk [RR] 0.40, P <0.0001).[21]

A meta-analysis of intensive statin therapy before coronary angiography and percutaneous coronary intervention reported that in patients with acute coronary syndrome (ACS), statin treatment significantly reduced the incidence of contrast-induced AKI (RR 0.37, P<0.0001). In patients without ACS, however, only a nonsignificant positive trend was seen (RR 0.65, P=0.07).[22]

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Long-Term Monitoring

Renal recovery in most cases is not complete, with the kidneys remaining vulnerable to the 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 AKI. It is always better to check these patients periodically, because some patients may regain renal function much later.

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Prevention of Perioperative Nephropathy

Remote ischemic preconditioning (RIPC) is a novel investigative method for preventing perioperative AKI. The rationale is that producing ischemia in a patient’s extremity immediately before surgery will stimulate the release of endogenous protective molecules, thereby reducing the likelihood that the surgery will precipitate AKI.[47]

In a randomized trial in 240 patients who were undergoing on-pump coronary bypass grafting and were at moderate to high risk for perioperative AKI, 37.5% of patients who received RIPC developed AKI within 72 hours after surgery, compared with 52.5% of controls (P = 0.02). In patients who developed AKI, 5.8% who had received RIPC required renal replacement therapy versus 15.8% of those in the control arm (10% absolute risk reduction).[47]

In this study, remote ischemia was induced by inflating a blood pressure cuff to 200 mm Hg on one upper extremity for 5 minutes; this was repeated twice, for a total of three cycles. Control patients received three cycles of blood pressure cuff inflation to 20 mm Hg for 5 minutes.[47]

Pharmacologic agents

A review of randomized, controlled trials of pharmacologic measures used to protect renal function perioperatively found no reliable evidence that any of the following interventions are effective[48] :

  • Dopamine and its analogues
  • Diuretics
  • Calcium channel blockers
  • Angiotensin-converting enzyme (ACE) inhibitors
  • N-acetylcysteine [49]
  • Atrial natriuretic peptide (ANP)
  • Sodium bicarbonate
  • Antioxidants
  • Erythropoietin (EPO)
  • Specific hydration fluids
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Contributor Information and Disclosures
Author

Biruh T Workeneh, MD, PhD FASN, Assistant Professor of Nephrology, Baylor College of Medicine

Biruh T Workeneh, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation

Disclosure: Received ownership interest/medical directorship from South Shore DaVita Dialysis Center for other; Received ownership/medical directorship from Space City Dialysis /American Renal Associates for same; Received ownership interest from US Renal Care for other.

Rajiv Gupta, MD Assistant Professor, Department of Medicine, Texas A&M Health Science Center College of Medicine; Consulting Staff, Veterans Affairs Medical Center

Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

Aruna Agraharkar, MD, FACP Consulting Staff, Department of Gerontology, Space Center Clinic

Aruna Agraharkar, MD, FACP is a member of the following medical societies: American Medical Assocation

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Laura Lyngby Mulloy, DO, FACP Professor of Medicine, Chief, Section of Nephrology, Hypertension, and Transplantation Medicine, Glover/Mealing Eminent Scholar Chair in Immunology, Medical College of Georgia

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Photomicrograph of a renal biopsy specimen shows renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells with loss of brush border is observed, suggesting acute tubular necrosis as the cause of acute renal failure.
Flattening of the renal tubular cells due to tubular dilation.
Intratubular cast formation.
Intratubular obstruction due to the denuded epithelium and cellular debris. Note that the denuded tubular epithelial cells clump together because of rearrangement of intercellular adhesion molecules.
Sloughing of cells, which is responsible for the formation of granular casts, is a feature of acute tubular necrosis.
Table 1. RIFLE Classification System for Acute Kidney Injury
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).



Table 2. Acute Kidney Injury Network Classification/Staging System for AKI [3]
Stage Serum Creatinine Criteria Urine Output Criteria
1 Increase of ≥0.3 mg/dL (≥26.4 µmol/L) or 1.5- to 2-fold increase from baseline < 0.5 mL/kg/h for >6 h
2 >2-fold to 3-fold increase from baseline < 0.5 mL/kg/h for >12 h
3* >3-fold increase from baseline, or increase of ≥ 4.0 mg/dL (≥35.4 µmol/L) with an acute increase of at least 0.5 mg/dL (44 µmol/L) < 0.3 mL/kg/h for 24 h or anuria for 12 h
*Patients who receive renal replacement therapy (RRT) are considered to have met the criteria for stage 3 irrespective of the stage they are in at the time of RRT.
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