Critical Care / Emergency / Trauma

Stemming the rising tide of acute kidney injury

Acute kidney injury (AKI), which arises secondary to another disease or disorder, is common in medical, surgical, and critical-care hospital patients. The most common precipitating conditions are sepsis and hypo­-volemia.

In 2007, the Acute Kidney Injury Network (AKIN) introduced the term acute kidney injury to replace acute renal failure. The goal: to standardize the definition and thus promote earlier detection, better management, and improved outcomes. Unlike failure, which reflects a specific component of kidney function, injury captures the continuum from subclinical injury to frank failure or complete shutdown of kidney function. The literature defines AKI as an abrupt reduction in kidney function, leading to retention of nitrogenous and other waste products normally eliminated by the kidneys. Reduced renal filtration causes an increase in serum creatinine (SCr) or azotemia (a rise in both blood urea nitrogen [BUN] and SCr). (See Understanding kidney anatomy and physiology by clicking the PDf icon above.)

AKI commonly reduces urine output. To help detect AKI early, nurses must assess patients for conditions that may decrease renal blood flow. A blood pressure drop from any cause (for instance, congestive heart failure, blood loss, dehydration, or sepsis) can adversely affect the glomerular filtration rate (GFR) and increase the risk of AKI.

Incidence

The high incidence of hospital-acquired AKI stems in part from our increasingly aging population with its greater susceptibility and illness severity. Nephrotoxic exposure caused by common inpatient treatments and diagnostic studies plays a contributing role. AKI occurs in 5% to 7% of acute-care admissions and up to 30% of intensive-care admissions. Patients with AKI have a higher hospital mortality than other patients.

Classifying renal failure

Traditionally, AKI is classified according to the cause of renal dysfunction as prerenal, intrarenal, or postrenal failure. Although some experts question whether this classification system is useful, it remains a simple way to differentiate common causes of AKI.

Prerenal failure

The most common AKI type in hospital patients, prerenal failure can stem from any condition that decreases kidney perfusion and thus reduces GFR. Causes of absolute hypovolemia include acute blood loss (as in GI bleeding) and intraoperative blood loss. Hypovolemia is the most common cause of decreased mean arterial pressure and kidney perfusion. Relative hypovolemia can result from “third spacing,” nausea, vomiting, anorexia, and diarrhea; renal vasoconstriction can stem from inadequate cardiac output (as in acute heart failure).


Several conditions can alter the kidney’s autoregulatory capability and set the stage for prerenal azo­temia. Advanced age, atherosclerosis, and long-standing hypertension may cause narrowing of the intrarenal arterioles, impairing vaso­dilation of the afferent arterioles. In patients with chronic kidney disease, afferent arterioles already may be functioning at maximum capacity. Also, renal efferent vasoconstriction is limited by administration of angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers. Other medications that interfere with renal autoregulation include nonsteroidal anti-inflammatory drugs. Prerenal failure rarely causes permanent renal damage and usually reverses quickly if treated promptly.

Intrarenal (intrinsic) failure

Intrarenal failure, which reflects an injury to the renal tubules, can stem from the same conditions as prerenal failure. The most common cause is prerenal failure that has progressed due to late diagnosis and treatment, or that hasn’t resolved. Renal tubular ischemia may result from:

  • severe hypotension
  • hypovolemia
  • nephrotoxins, such as contrast media used for interventional diagnostic tests
  • multiple I.V. antibiotics
  • ingestion of toxic substances
  • certain antineoplastic agents.

Acute tubular necrosis may be an ischemic form of intrarenal failure caused by prolonged prerenal failure and marked by tubular debris and urinary casts. Sepsis is another common cause of intrarenal AKI.

Postrenal failure

Less common than prerenal or intrarenal failure, postrenal failure results from total or partial obstruction of urine flow in the ureters, bladder neck, or urethra. The blockage increases retrograde hydrostatic pressure and interferes with overall GFR. In a healthy person, AKI doesn’t occur unless the obstruction affects both kidneys. Common causes of postrenal failure include bladder-neck obstruction from prostatic disease, neurogenic bladder, and obstructed indwelling urinary catheters.

Assessment and diagnosis

Be sure to assess patients for factors that may impair renal blood flow. For instance, a blood pressure decrease can reduce GFR and increase the AKI risk. Carefully monitor the patient’s fluid intake and output, detect risk factors early, and evaluate the patient’s risk for adverse effects of diuretics and nephrotoxic drugs.

Traditional tests used to diagnose AKI include SCr, BUN, and urine tests (urinary casts and fractional excretion of sodium). SCr is the most commonly used renal function test. The end-product of muscle breakdown, SCr is freely filtered at the glomerulus when GFR is normal. Because the kidneys don’t metabolize or reabsorb SCr, the SCr level reflects both creatinine clearance and GFR. AKI is defined as a rise in the SCr level of at least 0.3 mg/dL, a level 50% higher than baseline within a 24- to 48-hour period, or a urine output reduction to 0.5 mL/kg/hour for more than 6 hours. While relatively small SCr increases have been linked to worsening outcomes, such changes aren’t always sensitive for early AKI diagnosis. Also, a rise in SCr commonly lags behind actual kidney injury.

Age, gender, fluid volume, and dietary protein intake can influence SCr. Because muscle mass determines creatinine production, increased muscle mass raises the baseline SCr level; men generally have a greater muscle mass and therefore higher SCr levels than women. While SCr levels usually remain stable with age, GFR decreases by 1% per year after age 40. Because muscle mass also declines with age, the SCr level tends to remain stable and becomes a less reliable indicator of renal function in older people. Consequently, GFR measurement provides the best overall assessment of kidney function. In most hospitals, estimated GFR is calculated and available as part of standard blood chemistry tests.

In 2004, a multidisciplinary international collaboration called the Acute Dialysis Quality Initiative developed criteria to provide a standard definition for the diagnosis, prognosis, and treatment of acute renal failure. (See RIFLE diagnostic criteria by clicking the PDF icon above.) Also, scientists are investigating certain biomarkers for potential use in AKI diagnosis. (See Using biomarkers to diagnose AKI by clicking the PDf icon above.)

Complications

AKI can cause and result in various fluid and electrolyte imbalances that affect virtually every organ system.

Cardiovascular complications

Heart failure, arrhythmias, and myocardial infarction have been reported in up to 35% of patients with AKI. Those with both severe AKI and acute myocardial infarction have a mortality of up to 31%. Elderly patients with little cardiac reserve are at particular risk for AKI-related fluid overload.

AKI is a common complication of heart failure and atrial fibrillation; both conditions can reduce GFR by decreasing cardiac output. What’s more, hyperkalemia, a common result of AKI, predisposes patients to life-threatening arrhythmias.

Respiratory complications

The single most important risk factor for death in AKI patients, respiratory compromise affects up to 54% of AKI patients. Mechanical ventilation contributes to AKI. Hemodialysis commonly causes hypoxemia and worsens in patients with underlying lung disease. Fluid overload can lead to pulmonary congestion and may compromise oxygenation and ventilation.

GI complications

GI complications of AKI include nausea, vomiting, and anorexia. GI bleeding occurs in up to 33% of AKI patients.

Neurologic complications

Nearly 40% of AKI patients have neurologic signs and symptoms resulting from uremia, such as lethargy, altered mental status, and cognitive deficits.

Infections

Various infections, especially of the respiratory system and urinary tract, can complicate AKI. Occurring in up to 30% of AKI patients, infections are the leading cause of illness and death in AKI patients.

Intervention

Despite advances in supportive treatment, death rates in hospital patients with AKI haven’t improved in the last 30 years. Effective treatment centers on restoring adequate renal blood flow and varies with the underlying cause of AKI. Diuretics are used mainly for fluid management, especially in patients with chronic kidney disease and heart failure.

Hypovolemia exacerbates and potentiates all AKI types. In many cases, rapid fluid infusion reverses AKI. To avoid potentially life-threatening fluid overload, however, caregivers must accurately determine the patient’s fluid status. In patients with postrenal failure, obstruction removal leads to an immediate GFR rise.

For intrarenal failure, treatment focuses on removing nephrotoxins. Contrast-induced nephropathy, one of the most common types of intrarenal failure, causes nearly 10% of hospital-acquired AKI. A history of chronic kidney disease or diabetes predisposes a patient to this nephropathy. Acetylcysteine (Mucomyst&#174) and sodium bicarbonate may be used as adjuncts in treating renal failure caused by drug toxicity. Acetylcysteine causes vasodilation of the kidney bed and has antioxidant effects.

In patients with sepsis, treatment aims to eradicate the infection. This requires a delicate balance, as sepsis treatment may require use of multiple antibiotics that are nephrotoxic when given together.

Renal replacement therapy

When renal dysfunction is severe enough to threaten the patient’s life, renal replacement therapy (RRT) may be used. Indications for RRT include hyperkalemia, volume overload, metabolic acidosis, uremia, and drug overdose.

The most common type of RRT is hemodialysis, which removes blood from the patient via a vascular access device and pumps it through a dialyzer. Continuous renal replacement therapy (CRRT) removes water and waste by continuously circulating the patient’s blood through a highly porous hemofilter for 12 hours or longer. Because CRRT is slower than hemodialysis, it’s commonly used in critically ill patients unable to tolerate hemo­dialysis and rapid fluid removal. Advantages of CRRT over intermittent hemodialysis include better hemodynamic tolerance and less variation in fluid removal. About 20% to 60% of hospital patients with AKI require dialysis; the percentage is rising as the patient population ages. Most patients who receive RRT recover, with only 25% requiring long-term RRT.

Patient outcomes

AKI carries an increased risk of both in-hospital and long-term mortality. Prerenal AKI carries a better prognosis than most cases of intrarenal AKI. While the kidneys usually recover even from severe AKI necessitating dialysis, survivors of an AKI episode who need temporary dialysis are at extremely high risk for progressive chronic kidney disease; up to 10% may develop end-stage renal disease. Risk factors associated with progression to chronic kidney disease include advanced age, diabetes mellitus, decreased baseline GFR, and severe AKI.

Nursing considerations

Becoming familiar with AKI risk factors can help you help prevent it. Review your patient’s past medical history and check for chronic diseases that can predispose a patient to AKI. Consider concurrent diagnoses, such as heart failure, anemia, and chronic lung conditions. Ensure that patients scheduled for diagnostic studies with contrast media are screened appropriately for previous contrast-related allergies; also make sure they get preprocedural hydration. When caring for patients at risk for contrast-induced nephropathy, follow the hospital’s protocol.

Accurately monitor volume and hydration status based on the patient’s weight, skin turgor, urine output, and fluid intake. Evaluate the patient’s risk of side effects from diuretics and nephrotoxic drugs. Know that diuretics, vomiting, diarrhea, and fever can cause dehydration and elevated SCr.

Finally, provide appropriate education to patients who have AKI or are at risk for it; be sure to include family members in your teaching. Teaching points to cover include the purpose of monitoring blood chemistry tests, the importance of accurate fluid intake and output records, and indications for starting or withdrawing diuretic therapy. Also explain the purpose of AKI treatments, such as antibiotics, I.V. hydration, acetylcysteine, and sodium bicarbonate.

Selected references

Broden CC. Acute renal failure and mechanical ventilation: reality or myth? Crit Care Nurse. 2009; 29(2):62-75.

Chawla LS. Acute kidney injury leading to chronic kidney disease and long-term outcomes of acute kidney injury: the best opportunity to mitigate acute kidney injury? Contrib Nephrol. 2011;174:182-90.

Dirkes S. Acute kidney injury: not just acute renal failure anymore? Crit Care Nurse. 2011;31(1):37-49.

Fox CS, Muntner P, Chen AY, Alexander KP, Roe MT, Wiviott SD. Short-term outcomes of acute myocardial infarction in patients with acute kidney injury: a report from the National Cardiovascular Data Registry. Circulation. 2012;125(3):497-504.

Gotfried J, Wiesen J, Raina R, Nally JV Jr. Finding the cause of acute kidney injury: which index of fractional excretion is better? Cleve Clin J Med. 2012;79(2):121-6.

Han WK. Biomarkers for early detection of acute kidney injury. Neph Rounds. 2008:6(4). www.nephrologyrounds.org/crus/nephus_04_08.pdf. Accessed November 13, 2012.

Hoste EA, Schurgers M. Epidemiology of acute kidney injury: how big is the problem? Crit Care Med. 2008;36(suppl 4):S146-51.

Isaac S. Contrast-induced nephropathy: nursing implications. Crit Care Nurse. 2012;32(3):41-8.

Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements. March 2012;2:1-138. doi:10.1038/kisup.2012.

Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. doi:10.1186/cc5713

Peacock PR. Management of acute complications of acute renal failure. Medscape Reference. Updated May 2, 2011. http://emedicine.medscape.com/article/777845. Accessed November 13, 2012.

Ricci Z, Ronco C. New insights in acute renal failure in the critically ill. Swiss Med
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Waikar SS, Bonventre JV. Acute kidney injury. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill Professional; 2011.

Workeneh BT. Acute renal failure. Medscape Reference. Updated February 9, 2012. http://emedicine.medscape.com/article/243492-overview. Accessed November 13, 2012.

Michelle Fournier is director of clinical consulting with J.A. Thomas & Associates in Atlanta, Georgia.

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