Does this patient have acute kidney injury (AKI)?
Acute kidney injury (AKI), formerly acute renal failure, refers to an abrupt (within 48 hours) reduction in kidney function leading to azotemia. Traditional markers–blood urea nitrogen (BUN) and serum creatinine (SCr) remain the gold standard for the assessment of kidney function. The use of creatinine is complicated by the following:
There is no consensus on the magnitude of rise of serum creatinine to indicate AKI. Many studies refer to a rise in creatinine of 0.5 mg/dl but there is evidence that even a smaller rise in SCr may be significant.
SCr does not reflect GFR. Early AKI may not be reflected in a rise in creatinine as not enough time has elapsed to demonstrate a rise in SCr.
Drugs such as cimetidine and trimethoprim may result in a rise in SCr without any evidence of kidney injury, since they use same transport mechanism as creatinine for secretion in the proximal renal tubule.
Other drugs or intervention may interfere with production and release of creatinine from the muscle tissue without changing renal function.
Measuring urea nitrogen may also be misleading. High protein load with tube feeding or total parenteral nutrition (TPN), use of corticosteroids and gastrointestinal bleeding may result in elevation of BUN without any evidence of kidney injury.
Therefore, despite their widespread use, BUN and creatinine are poor biomarkers of GFR.
For this reason the Acute Dialysis Quality Initiative (ADQI) composed of intensivists and nephrologists developed a criteria for AKI: RIFLE (Risk, Injury, Failure, Loss and ESRD). Based on this classification a 50% rise in baseline serum creatinine or a urine output of <0.5 mL/mg for at least 6 hours are the minimum requirements for a diagnosis of AKI.
A modification of the RIFLE criteria was proposed by the Acute Kidney Injury Network (AKIN). AKIN stage I includes the same parameters included stage R of the RIFLE criteria but expands the definition to include a rise of >0.3 mg/dL in baseline serum creatinine
More recently urinary and serum biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), interleukin 18(IL-18) and kidney injury molecule 1 (KIM-1), Liver fatty acid binding protein (LFABP) and others have been shown to be more sensitive than SCr in detecting early kidney injury. Commercial kits to detect these biomarkers have or are being developed but currently used for research purpose only. They are not used clinically at present.
How severe is this patient's AKI?
Two recent classification systems–RIFLE and AKIN–have categorized AKI based on the rises in SCr and urine output. These stages of AKI correlate with its outcomes; ie, the higher the stage, the higher the mortality and the lower the likelihood of renal recovery
AKIN Stage I: increase in SCr >0.3 (26 μmol/L) OR >50% – 100% from baseline, urine putput <0.5 mL/kg/hr for >6 hours
AKIN Stage II: Increase in SCr >100% – 200% from baseline, urine output <0.5 mL/kg/hr for >12 hours
AKIN Stage III: Increase in SCr >200 from baseline OR SCr >4 after a rise of at least 0.5 mg/dL OR on renal replacement therapy, urine putput <0.3 mL/kg/hr for >24 hours or anuric >12 hours
RIFLE criteria are very similar to AKIN criteria with R in the RIFLE being equivalent of stage I in AKIN, I being equivalent to stage II, and F being equivalent to stage III. The main difference is the addition of a rise >0.3 mg/dL (26 μmol/L) in SCr to define stage I in AKIN, which is not included in RIFLE R definition.
Does this patient have AKI or is this chronic kidney disease (CKD)?
The best way to differentiate between AKI and CKD is to look at the baseline SCr or GFR. AKI refers to an abrupt increase in SCr or drop in GFR from baseline. It is possible to have AKI on CKD. If previous laboratory values are not available history, physical examination and clinical investigations may be helpful.
Recent history of major surgery, especially cardiovascular surgery, hypotension, septicemia, severe volume loss, use of nephrotoxic agents such as intravenous contrast dye or aminoglycosides suggest AKI. A history of longstanding diabetes mellitus with other microvascular complications or longstanding history of hypertension raise the possibility of CKD, but does not eliminate the possibility of AKI.
Ultrasound (US) examination of the kidey could be very helpful. Small and echogenic kidneys are highly suggestive of CKD. US may assist in the diagnosis of obstructive uropathy. The lack of evidence of urinary obstruction (eg, hydronephrosis or dilated calices) rules out the possibility of obstructive uropathy as the cause of AKI unless the ultrasound is done very early in the course of AKI. In this case, there may not have been enough time to develop dilated calices and a repeat ultrasound 1-2 days later should be done.
Evidence of CKD complications on laboratory examinations, such as elevated parathyroid hormone levels, can be helpful.
What is the cause of this patient's AKI?
The causes of AKI can be divided into three major categories: prerenal, intrinsic renal or post renal. Prerenal AKI is probable the most common type and is caused by hemodynamic changes resulting in reduced perfusion of kidneys.
Intrinsic renal AKI could be due to glomerular, tubular, interstitial or vascular diseases Acute tubular necrosis (ATN) is the most common cause of AKI in hospitalized patients ATN can result from either ischemic injury to the tubules (prolonged and severe reduction in renal perfusion) or direct tubular toxicity (aminoglycosides, iodinated contrast dye, hemoglobin and myoglobin).
Urine sodium and FENa are expcted to be high in ATN (FENa>2). Urine microscopy may have dense granular (muddy brown) or tubular cells casts and high number of renal tubular epithelial cells. A finding of blood on the dipstick urine examination with no red blood cells (RBCs) on urine microscopy should raise the possibility of intravascular hemolysis or rhabdomyolysis
Acute interstitial nephritis (AIN) can occur as a result of exposure to certain drugs, penicillins and cephalosporins as examples, or during infections. Urine sodium and FENa are expected to be high in AIN (FENa>2). Urine microscopy usually shows white blood cells (WBCs), eosinophils and WBC casts. Peripheral eosinophilia is also possible.
Glomerular causes of AKI may be associated with systemic symptoms suggestive of the underlying cause (systemic lupus erythematosus [SLE], vasculitis, etc). In presence of hemoptysis or diffuse alveolar hemorrhage, pulmonary-renal syndromes such as Goodpasture syndrome, small vessel vasculitis, and SLE should be considered.
Glomerular AKI is usually associated with proteinuria and dysmorphic red blood cells and RBC casts in the urine. Early glomerular AKI may be associated with a low FENa.
Vascular diseases involving large vessels (eg, renal artery stenosis or thrombosis) or small vessels (eg, malignant hypertension, thrombotic microangiopathies) have different presentations. A history and physical examination looking at evidence of these diseases is most useful.
Atheroemboli (cholesterol emboli) can occur during invasive arterial procedures such as angioplasties. Levido reticularis on the skin and finding of eosinophils in the urine are highly suggestive in the setting of AKI after invasive vascular procedures.
Postrenal AKI is not common (5 – 10% of cases) but might be easy to treat. A careful history can be very helpful. A history of symptoms suggesting prostate enlargement, exposure to abdominal radiation or certain drugs that can result in retroperitoneal fibrosis, malignancy with potential mass effect due to tumor itself or enlarged lymph nodes provide information that might lead the clinical to consider postobstructive AKI.
The physical exam should include prostate exam in cases suspected of having prostate enlargement and examination of lower abdominal compartments looking for evidence of distended bladder. A simple bladder scan or a complete renal ultrasound examination would be very helpful in ruling out obstructive uropathy as the cause of AKI. Alternatively, placement of urinary catheter in the bladder can be both diagnostic and therapeutic
What tests to perform?
What tests should I perform for diagnosis and differential diagnosis of acute kidney injury?
Measurement of SCr and BUN and urine output assist in establishing the diagnosis of AKI. Formulae such as Modification of Diet in Renal Disease (MDRD) and Cockroft and Gault formua developed to estimate GFR at steady state should not be used to estimate renal function during the course of AKI.
Monitoring the rate of rise in SCr is the best way to assess renal function (GFR) In general a rise of between 1-2 mg/dL in a 24-hour period suggest minimal GFR (almost zero).
The most useful tests in the differential diagnosis of AKI are urine sodium and FENa, urine microscopy and renal ultrasound. Low urine sodium (<20 mmol/L) and low FENa (<1%) suggest reduced renal perfusion without tubular damage (prerenal AKI), while high levels (>40 mmol/L and >2%, respectively) are suggestive of intrinsic AKI.
If a patient is being treated with a diuretic, fractional excretion of urea (FEUrea) should be used instead of FENa to differentiate between causes of AKI. FEUrea <30 – 35% is consistent with prerenal and a level >35% with intrinsic AKI. Urine sodium and FENa may not be as accurate in presence of metabolic alkalosis and patients with advanced CKD (due to severe tubular atrophy) and need to be interpreted carefully. Certain cases of intrinsic AKI such as contrast nephropathy and glomerulonephritis (GN) may be associated with a low FENa
Urine osmolality may be of some help when used in conjunction with other evidence. Prerenal AKI is expected to be associated with a high urine osmolality (>500 mosm/kg water).
Urinalysis with microscopy is probably the most useful tool in differential diagnosis of AKI. High urine specific gravity may indicate reduced renal perfusion (prerenal AKI). Presence of iodinated contrast agent in the urine can also result in higher than expected SG (>1.030).
Proteinuria raises the possibility of GN. Hematuria associated with dysmorphic RBC and RBC casts suggests GN. Hematuria with normal-appearing red blood cells could be seen in a variety of conditions. in this setting imaging of the urinary tract is critical to rule out malignancies, stones and infections.
Hematuria with no RBCs on microscopy suggests intravascular hemolysis or rhabdomyolysis. In these situations, tests such serum creatinine kinase, myoglobin, haptoglobin or lactate dehydrogenase may be helpful depending on presenting symptoms and history. Muddy brown casts are diagnostic for ATN. WBC casts are seen in AIN, pyelonephritis and possibly in atheroembloic disease
Ultrasound examination is useful in
diagnosis of obstructive uropathy
assisting in differentiating AKI and CKD
detecting large stones and masses in most cases
Duplex US examination can be used in some cases to diagnose renal artery stenosis
A kidney biopsy should be considered if glomerular AKI is suspected or if prerenal and postrenal causes are excluded and ATN is unlikely. Kidney biopsy is a critical component of management of patients presenting with rapidly progressive GN.
How should patients with risk for acute kidney injury be managed?
What is my patient's risk for developing acute kidney injury?
Prevention of AKI can best be accomplished by identifying those patients at high risk for AKI (Table 1). In this manner one can then determine the risk/benefit of any procedures (surgery, contrast study). The most important risk factor for AKI is chronic kidney disease. Therefore, assessing renal function and estimating the GFR is the first step in assessing the risk of AKI
|Chronic Kidney Disease|
|Congestive heart failure|
|Severe valcular heart disease|
|Insulin requiring diabetes|
|Advanced liver disease|
|Renal artery stenosis|
|Procedure Related Factors|
|Coronary artery bypass surgery plus valve|
|Coronary artery bypass surgery|
|Abdominal aortic aneurysm surgery|
|Surgery for obstructive jaundice|
|Angiography using iodinated contrast agent|
|Contrast enhanced CT|
|Significant blood loss|
|Acute Conditions and Medications|
|Critical illness (ICU admission)|
|Low effective circulating volume|
|Arrhythmia associated hemodynamic instability|
|Treatment with NSAIDs|
|Treatment with ACE inhibitors/ARB|
|Treatment with tacrolimus or cyclosporin|
|Exposure to nephrotoxins|
In a study to develop a scoring model for the risk factors to predict AKI after cardiac surgery, while all other risk factors received a score of 1 or 2, serum creatinine >2.1 received a score of 5 for prediction of AKI.
While risk factors such as patients’ age or comorbidities cannot be altered, there may be opportunities to alter the risk of AKI by modifying some other risk factors, such as the nature of the procedure, patients’ hemodynamics status, and medications.
How can I prevent acute kidney injury in high risk patients?
Preventive strategies should be considered when an individual at high risk for AKI is undergoing a procedure or being exposed to a drug associated with risk of AKI. The first step would be to alter or consider alternatives to interventions or treatments that could potentially cause kidney injury.
Use MRI or ultrasound or noncontrast computed tomography (CT) examinations instead of CT with contrast, if possible
Consider CO2 angiogram instead of standard angiography using iodinated contrast agent when possible
Consider using other analgesics or antiinflammatory agents than NSAIDs
Consider other antibiotics than aminoglycosides
Avoid cardiac or aortic surgery immediately after coronary angiogram, if possible
Minimize the duration of cardiopulmonary bypass
Advanced planning for high-risk interventions in high-risk populations is critical. Since hemodynamic instability is a major risk factor for AKI during interventions the following should be considered
Medications such as ACE inhibitors, ARB, NSAIDs may need to be held before an intervention using iodinated contrast agent
Volume status needs to optimized. In some caes adjustment in the dose of diuretics might be necessary
Optimization of renal blood flow and renal tissue perfusion is critical in preventing acute kidney injury, especially ischemic ATN. Factors such as cardiac output, peripheral vascular resistance, renal vascular resistance and renal tissue oxygen demand determine tissue perfusion.
Within the kidney, the main site of ischemic injury is the outer medulla.
The partial pressure of oxygen is usually lower in this region than in the cortical tissue, while oygen demand is higher due to high activity of tubular cells in this region.
Delivery of blood to the medulla is dependent on cortical blood flow as the efferent arterioles from glomeruli located in the corticomedullary junction give rise to vasa recta that deliver blood to the renal medulla. As a result, the renal medulla receives only 10 – 15% of total renal blood flow.
Medullary blood flow is, at least partially, controlled separately from cortical blood flow. While autoregulation maintains cortical blood flow constant with changes in mean arterial pressure (MAP), medullary flow is not autoregulated as well and changes in the same direction as the MAP.
Interestingly, in shock states there is a shift of blood from the cortex toward renal medulla
Although in theory the reduction of sodium absorption in the thick ascending limb of the Henle’s loop with the use of loop diuretics could reduce oxygen consumption and reduce the risk of ischemic damage, solid clinical evidence to support routine use of loop diuretics to prevent AKI is lacking.
Intraoperative fluid management can affect outcomes following elective surgery. In some instances even patients at low risk may suffer from AKI if suboptimal fluid management. The goal of optimizing fluid status is to maintain tissue perfusion and oxygenation.
Patients’ heart rate, blood pressure, central venous pressure, tissue oxygenation and urine output have been monitored during surgical procedure to assess the systemic hemodynamic state and to guide fluid management. However, none of these parameters appear to be sensitive or specific for determining the volume status or to predict AKI.
Recently, dynamic monitoring techniques have been shown to be superior in guiding fluid management during surgery. Assessing stroke volume by transesophageal Doppler or by analysis of arterial wave form has been shown to be associated with lower rates of complications and reduced length of hospital stay, but not mortality, in patients undergoing major abdominal surgeries.
In patients on positive pressure ventilation, high degree of variation in stroke volume (>10%) and pulse pressure during the respiratory cycle indicate the need for fluid resuscitation. This information can be obtained using certain new commercial monitoring systems.
In a systematic review of 29 studies including 685 ICU or surgical patients the AUC for variation in pulse pressure (PPV), systolic pressure (SPV) and stroke volume (SVP) to predict an increase of about 15% in cardiac index, stroke volume or cardiac output in response to fluid therapy were 0.94, 0.86 and 0.84. The AUC for CVP was 0.55.
In summary, at least for for critically ill patients or those undergoing surgical procedures, dynamic monitoring techniques should be used to assess the need for fluid resuscitation and to optimize tissue perfusion.
In septicemia, volume expansion combined with the use of vasopressor agents might be needed to optimize renal perfusion.
Increasing mean arterial pressure from 65 to 75 (but not higher) using norepinephrine in patients with septic shock was associated with increase in urine output and lowered the resistive index by Doppler ultrasound in a small human study.
Use of norepinephrine in AKI associated with vasodilatory shock with a target MAP of 75 mm Hg (from 60 mm Hg) was associated with higher GFR and urine output in another small human study. Further increases in MAP did not have any beneficial effect on renal parameters.
A recent randomized controlled trial in patients with shock did not show any difference in mortality rates comparing patients treated with norepinephrine and dopamine. However, compared to norepinephrine treatment with dopamine was associated with more arrhythmia and higher mortality among the subgroup of patients with cardiogenic shcok.
In a randomized control study of patients with septic shock treatment with fenoldopam, selective dopamine-1 receptor agonist, at a rate of 0.09 μg/kg/min was associated with 53% reduction in the risk of AKI (absolute risk reduction of almost 15%) with no significant side effects. However, similar beneficial effects have not been observed in all studies using fenoldopam and larger RCTs are needed to clarify its role in prevention of AKI in different settings.
Fluid management can be achieved with the use of crystalloids or colloid solutions. Crystalloids include saline and Ringer’s lactate. Colloids include human albumin, dextrans and hydroxyethyl starch.
Hydroxy ethyl starch solutions are nephrotoxic and should be avoided in high risk patients and those with established AKI
Use of balanced electrolyte solutions is preferred by most surgeons and anesthesiologists since fluid challenge with saline solutions results in non anion gap metabolic acidosis
Transfusion with pack red blood cells should be considered in cases with acute blood loss and those with low hemoglobin concentrations and evidence of volume depletion. Due to the evidence from some studies suggesting increased mortality rates associated with blood transfusion, its use has become limited to lower hemoglobin concentrations.
In contrast-induced AKI (CI-AKI) a number of studies have been performed to evaluate the effectiveness of interventions in the prevention of CI- AKI, however there continues to be uncertainties in many of the results of these interventions as these studies have been hampered by study design. Many of these studies have been small and underpowered. There have been attempts to classify these interventions into definitive, possible and doubtful.
High, low and isosmolar contrast agents. Most centers no longer use high osmolar agents as the risk of AKI is greater in moderate to high risk patients exposed to high osmolar agents compared to low osmolar agents. In comparing isosmolar vs low osmolar contrast agents, there is no conclusive evidence to recommend one over the other.
Intravenous isotonic saline should be started at least 1 hr before and continued for 4-6 hrs following contrast administration. This may need to be varied to achieve a urine output of 150 ml/h, a urine flow associated with reduced AKI. There is evidence that isotonic may be more effective than hypotonic solutions.
Intravenous isotonic sodium bicarbonate solutions may prevent CI-AKI. Various studies have been performed that preclude definitive statement however the potential to scavenge free radicals is thought to provide additional benefit.
N-acetyl cysteine may be used to prevent CI-AKI however the studies thus far are numerous, heterogenous and not consistent. Never the less because of the low risk and cost it maybe considered along with intravenous hydration.
Fenoldopam, theophylline, and “low dose” dopamine should not be used.
What happens to patients with acute kidney injury?
The renal prognosis of AKI depends on the baseline renal function, comorbidities, type and severity of kidney injury and duration of renal replacement therapy. A normal baseline renal function is associated with good prognosis for recovery from AK. More than 85% of patients with severe ATN with a normal renal function at baseline will have full or partial recovery of renal function 6-12 months later. Severe renal paranchymal disease has the worst rate of recovery in renal function.
The presence of multiple comorbid conditions, especially poor cardiac function is also associated with lower rates of renal function recovery. In general, nonoliguric AKI are associated with better renal outcomes compared to oliguric AKI. The longer the duration of renal replacement therapy, the lower the likelihood of recovery.
AKI is an independent risk factor for mortality. Survival of patients with AKI is significantly worse than those without AKI even after adjustments for other risk factors. The association between AKI and higher mortality is proportional to the severity of AKI. This association is observed both during the intensive care unit (ICU) or hospital stay and also in long term studies with several years of follow-up.
AKI can lead to partial recovery of kidney function and development of progressive CKD and end-stage renal disease. It appears that the rate of CKD and ESRD due to AKI has been steadily increasing.
Are there clinical practice guidelines to inform decision making?
Kidney Disease: Improving Global Outcomes (KDIGO) is in the final phases of developing practice guidelines for diagnosis and management of acute kidney injury.
Acute Kidney Injury 584.9
What is the evidence?
Bagshaw, SM. “Acute kidney injury: diagnosis and classification of AKI: AKIN or RIFLE?”. Nat Rev Nephrol. vol. 6. 2010. pp. 71-3.
Bellomo, R, Cass, A, Cole, L, Finfer, S, Gallagher, M, Lo, S, McArthur, C, McGuinness, S, Myburgh, J, Norton, R, Scheinkestel, C, Su, S. “Intensity of continuous renal-replacement therapy in critically ill patients”. N Engl J Med. vol. 361. 2009. pp. 1627-38.
Hobson, CE, Yavas, S, Segal, MS, Schold, JD, Tribble, CG, Layon, AJ, Bihorac, A. “Acute kidney injury is associated with increased long-term mortality after cardiothoracic surgery”. Circulation. vol. 119. 2009. pp. 2444-53.
Thakar, CV, Yared, JP, Worley, S, Cotman, K, Paganini, EP. “Renal dysfunction and serious infections after open-heart surgery”. Kidney Int. vol. 64. 2003. pp. 239-46.
De Backer, D, Biston, P, Devriendt, J, Madl, C, Chochrad, D, Aldecoa, C, Brasseur, A, Defrance, P, Gottignies, P, Vincent, JL. “Comparison of dopamine and norepinephrine in the treatment of shock”. N Engl J Med. vol. 362. 2010. pp. 779-89.
Cahill, CJ. “Prevention of postoperative renal failure in patients with obstructive jaundice–the role of bile salts”. Br J Surg. vol. 70. 1983. pp. 590-5.
Abbas, SM, Hill, AG. “Systematic review of the literature for the use of oesophageal Doppler monitor for fluid replacement in major abdominal surgery”. Anaesthesia. vol. 63. 2008. pp. 44-51.
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Marik, PE, Cavallazzi, R, Vasu, T, Hirani, A. “Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature”. Crit Care Med. vol. 37. 2009. pp. 2642-7.
Redfors, B, Bragadottir, G, Sellgren, J, Sward, K, Ricksten, SE. “Effects of norepinephrine on renal perfusion, filtration and oxygenation in vasodilatory shock and acute kidney injury”. Intensive Care Med. vol. 37. 2011. pp. 60-7.
Payen, D, de Pont, AC, Sakr, Y, Spies, C, Reinhart, K, Vincent, JL. “A positive fluid balance is associated with a worse outcome in patients with acute renal failure”. Crit Care. vol. 12. 2008. pp. R74
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Morelli, A, Ricci, Z, Bellomo, R, Ronco, C, Rocco, M, Conti, G, De Gaetano, A, Picchini, U, Orecchioni, A, Portieri, M, Coluzzi, F, Porzi, P, Serio, P, Bruno, A, Pietropaoli, P. “Prophylactic fenoldopam for renal protection in sepsis: a randomized, double-blind, placebo-controlled pilot trial”. Crit Care Med. vol. 33. 2005. pp. 2451-6.
Vincent, JL, Sakr, Y, Sprung, C, Harboe, S, Damas, P. “Are blood transfusions associated with greater mortality rates? Results of the Sepsis Occurrence in Acutely Ill Patients study”. Anesthesiology. vol. 108. 2008. pp. 31-9.
Sterling, KA, Tehrani, T, Rudnick, MR. “Clinical significance and preventive strategies for contrast-induced nephropathy”. Curr Opin Nephrol Hypertens. vol. 17. 2008. pp. 616-623.
Kelly, AM, Dwamena, B, Cronin, P, Bernstein, SJ, Carlos, RC. “Meta-analysis: effectiveness of drugs for preventing contrast-induced nephropathy”. Ann Intern Med. vol. 148. 2008. pp. 284-294.
Goldfarb, S, Spinler, S, Berns, JS, Rudnick, MR. “Low-osmolality contrast media and the risk of contrast-associated nephrotoxicity”. Invest Radiol. vol. 28. 1993. pp. S7-10.
Aspelin, P, Aubry, P, Fransson, SG, Strasser, R, Willenbrock, R, Berg, KJ. “Nephrotoxic effects in high-risk patients undergoing angiography”. N Engl J Med. vol. 348. 2003. pp. 491-499.
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- Does this patient have acute kidney injury (AKI)?
- How severe is this patient's AKI?
- Does this patient have AKI or is this chronic kidney disease (CKD)?
- What is the cause of this patient's AKI?
- What tests to perform?
- How should patients with risk for acute kidney injury be managed?
- What happens to patients with acute kidney injury?
- Are there clinical practice guidelines to inform decision making?
- Other considerations
- What is the evidence?