Questions
- 1.
How is acute kidney injury defined?
- 2.
What are the incidence and outcome of acute kidney injury in the intensive care unit?
- 3.
Explain the pathophysiology of acute kidney injury.
- 4.
How is the etiology of acute kidney injury determined in the intensive care unit?
- 5.
- 6.
What is contrast-induced nephropathy?
- 7.
Describe the pathogenesis of contrast-induced nephropathy.
- 8.
Identify the risk factors for and probability of developing contrast-induced nephropathy.
- 9.
What are the options for preventing contrast-induced nephropathy?
- 10.
What are the indications for dialysis in the intensive care unit?
- 11.
What are the options for renal replacement therapy?
- 12.
Discuss problems encountered with renal replacement therapy.
- 13.
How is the most appropriate renal replacement therapy selected?
A 62-year-old man presented for emergency repair of a type A dissecting ascending aortic aneurysm. He had a history of hypertension, diabetes, and hyperlipidemia. In the emergency department, he complained of acute onset of chest pain. The work-up included a computed tomography scan with intravenous contrast agent administration. On postoperative day 1 in the cardiothoracic intensive care unit, his creatinine level increased twofold, with a decrease in urine output and a metabolic acidosis.
1
How is acute renal injury defined?
Acute renal failure (ARF) is the sudden development of renal insufficiency that results in the retention of urea and other nitrogenous waste products as well as dysregulation of extracellular volume and electrolytes. It is also known as acute kidney injury (AKI). AKI encompasses the entire range of renal dysfunction, from minor to requiring renal replacement therapy. The measurement of serum creatinine, which measures glomerular filtration rate (GFR), has been used to evaluate kidney function loss. The Acute Dialysis Quality Initiative developed criteria for different stages of renal injury. The RIFLE criteria consist of three graded levels of risk, injury, and failure, which are based on the magnitude of elevation of serum creatinine and urine output ( Table 90-1 ). There are also two outcome measures, loss of renal function and end-stage renal disease.
| Class | GFR | UO |
|---|---|---|
| R isk | Decreased by ≥25% or Baseline SCr increased × 1.5 | <0.5 mL/kg/hour ≥6 hours |
| I njury | Decreased by ≥50% or Baseline SCr increased × 2 | <0.5mL/kg/hour ≥12 hours |
| F ailure | Decreased by ≥75% or Baseline SCr × 3 or SCr >4 mg/dL with acute increase of 0.5 mg/dL | <0.3 mL/kg/hour ≥24 hours or Anuria ≥12 hours |
| L oss | Complete loss of kidney function >4 weeks | |
| E SRD | Complete loss of kidney function >3 months |
The RIFLE scoring system has some disadvantages. The RIFLE criteria do not have a time component for creatinine levels; this does not allow for analysis of renal function as a dynamic process. For example, a doubling of creatinine in 24 hours is more significant than if creatinine doubles in 3 days, but this is not reflected within the RIFLE criteria. Change in urine output is generally the most important criterion used in the intensive care unit (ICU) to determine renal dysfunction because it can more rapidly help identify risk.
The Acute Kidney Injury Network (AKIN), recognizing the importance of time course to kidney injury, modified the RIFLE criteria ( Table 90-2 ). Their diagnostic criteria for AKI include an abrupt (≤48 hours) reduction in kidney function defined as one of the following:
- •
Absolute increase in serum creatinine of ≥0.3 mg/dL
- •
Increase in serum creatinine of ≥50% (1.5-fold from baseline)
- •
Reduction in urine output (documented urine output of <0.5 mL/kg/hour for ≥6 hours)
| Stage | SCr | UO |
|---|---|---|
| 1 | Increase ≥0.3 mg/dL or Baseline increase ≥150% to 200% (1.5–2 fold) | <0.5 mL/kg/hour ≥6 hours |
| 2 | Baseline increase >200% to 300% (>2 to 3 fold) | <0.5 mL/kg/hour ≥12 hours |
| 3 | Baseline increase >300% (>3 fold) or ≥4 mg/dL with acute increase of at least 0.5 mg/dL or Initiation of renal replacement therapy | <0.3 mL/kg/hour ≥24 hours or Anuria for ≥12 hours |
Risk from the RIFLE criteria is equivalent to stage 1 of the AKIN classification system, injury is equivalent to stage 2, and failure is equivalent to stage 3. Loss of renal function and end-stage renal disease were removed from the AKIN classification. Both criteria are based on creatinine as a marker for renal injury, which is a routine blood test. However, there are limitations to the usefulness of creatinine as a marker because many factors affect creatinine levels, including body size, catabolic state, rhabdomyolysis, dilutional effects, and drugs. Blood urea nitrogen (BUN) has also been used as a marker of renal function, but it too is affected by various factors, including excessive protein intake, protein catabolism, total parenteral nutrition, acute myocardial infarction, gastrointestinal bleeding, steroid administration, and dehydration.
New markers of AKI are under investigation. Cystatin C is an endogenous cysteine-proteinase inhibitor that is produced by all cells. In contrast to creatinine, cystatin C is filtered and not secreted across the glomerulus. It has been shown to increase faster than creatinine in patients with AKI. Another marker, urinary neutrophil gelatinase, has been shown to be one of the earliest proteins induced in the kidney after ischemic or nephrotoxic insult. More studies are needed to test the specificity and sensitivity of these markers.
2
What are the incidence and outcome of acute kidney injury in the intensive care unit?
AKI occurs with significant frequency in the hospital and especially in the ICU. The incidence of AKI ranges from 1%–36% of critically ill patients. Risk factors for AKI are well established and include age, sepsis, cardiac surgery, intravenous contrast media, diabetes, rhabdomyolysis, preexisting renal disease, hypovolemia, and shock. There are a few settings that are very closely associated with ICU-acquired renal failure ( Table 90-3 ). Based on the RIFLE criteria, hospital mortality among ICU patients is as follows:
- •
5%–10% in patients without renal dysfunction
- •
9%–27% in patients at risk
- •
11%–30% in patients with renal injury
- •
26%–40% in patients with renal failure
| Condition | Incidence (%) |
|---|---|
| Multiorgan failure | 30–75 |
| Sepsis | 30–50 |
| Drugs | 20–40 |
| Postoperative state | 15–30 |
| Impaired cardiac output/hypovolemia | 15–30 |
3
Explain the pathophysiology of acute kidney injury.
Blood is delivered to the kidneys and proceeds through the glomerulus, where it is filtered. The filtrate migrates to tubules where reabsorption and secretion take place and is eliminated as formed urine through the ureters, bladder, and urethra. The first steps to diagnosing renal failure come from determining if the etiology is prerenal (reduction in renal perfusion), renal (disorder of renal vasculature, glomeruli, interstitium, or tubules), or postrenal (obstruction of urine flow). In the ICU, renal failure is 17%–36% prerenal, 63%–81% renal, and 1%–4% postrenal. Many cases of renal failure have more than one cause, especially in critically ill patients.
Prerenal AKI is caused by extracellular fluid loss, extracellular fluid sequestration, or significantly reduced cardiac output. It is readily reversible if diagnosed and treated early. Kidneys compensate for reduced GFR by reabsorption of salt and water to increase circulating blood volume. Fluid resuscitation is the treatment of choice for AKI caused by renal hypoperfusion secondary to hypovolemia. Whether crystalloids or colloids are better for fluid resuscitation is still debatable. The essential principle is intravascular volume expansion to provide adequate preload and renal perfusion. Low cardiac output and hypotensive states resulting in prerenal AKI are treated with vasopressors and inotropes that help increase mean arterial pressure and cardiac output, ensuring optimal renal perfusion. Drugs that can cause prerenal AKI are norepinephrine, angiotensin II, endothelin, and prostaglandins that cause afferent arteriolar constriction, which reduces glomerular capillary hydrostatic pressure and glomerular ultrafiltrate. Diuretics cause depletion of extracellular fluid volume. Nonsteroidal antiinflammatory drugs (NSAIDs) are cyclooxygenase inhibitors that impair renal vasodilation, resulting in increased renal vascular tone. This form of ARF is easily reversible if diagnosed and treated early. If treatment is not instituted early, NSAIDs can result in decreased renal perfusion to renal tubular epithelial cells causing acute tubular necrosis (ATN). Finally, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) reduce renal perfusion pressure and dilate efferent arterioles. This combination of effects results in reduced glomerular capillary filtration pressure and causes ARF.
Postrenal azotemia is an unusual cause, especially in the ICU, and is easy to rule out using renal ultrasound. The most common etiology in men is bladder outlet obstruction from prostate disease. Obstruction to urine flow can occur within the kidneys when distal tubules become occluded with crystals (e.g., uric acid). Bilateral ureteral obstruction is rare but can be caused from extensive intraabdominal cancer or retroperitoneal fibrosis. Occluded Foley catheters can result in postrenal AKI. Blocked urine flow increases intratubular pressure so that net glomerular filtration pressure is decreased; this results in either severely reduced or stopped glomerular filtration.
Intrarenal renal failure is the likely diagnosis when prerenal and postrenal failures have been excluded. The most common renal cause of AKI is ATN. ATN is primarily due to renal ischemia secondary to renal hypoperfusion. The degree of ischemia required to cause ATN is variable. Ischemic ATN results in depletion of adenosine triphosphate (ATP) causing renal tubular cell death. Other causes of ATN include nephrotoxins and pigmenturia (hemoglobinuria, myoglobinuria). Two of the most commonly encountered nephrotoxins are aminoglycoside antibiotics and radiocontrast media. Pigmented induced AKI is caused by tubular obstruction, direct proximal tubular cell injury, and vasoconstriction. Protection from pigment-associated AKI includes maintenance of adequate extracellular fluid volume, renal perfusion, and urinary alkalization (increases solubility of hemoglobin and myoglobin to reduce cast formation).
Other renal causes of AKI that are less prevalent in the ICU include renal vascular disorders of both large and small vessels and acute glomerulonephritis. Vascular disorders include thrombotic occlusion, emboli, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, and vasculitis. These disorders can reduce blood flow to the kidneys and their filtering unit.
4
How is the etiology of acute kidney injury determined in the intensive care unit?
Assessment of AKI and oliguria starts with placement of a urinary drainage catheter to trend hourly urine output. Cardiac hemodynamics and volume status are assessed for optimization of preload and renal perfusion. An echocardiogram may be considered to assess ventricular function. Nephrotoxic drugs (e.g., ACE inhibitors, ARBs, NSAIDs, certain antibiotics) are eliminated. Commonly administered antibiotics that can cause AKI include aminoglycosides, amphotericin B, β-lactams, penicillins, rifampin, and vancomycin. Laboratory studies including BUN, creatinine, electrolytes, and osmolality should be performed ( Table 90-4 ). If diuretics are not taken, the fractional excretion of sodium should be measured. Examination of urinary sediment could be helpful. Tubular epithelial or granular casts are indicative of tubular injury, whereas hyaline casts are seen in low perfusion states.
| Laboratory Test | Prerenal | Renal |
|---|---|---|
| BUN/Cr | >20:1 | <10:1 |
| Urine osmolality | >500 | <400 |
| Urine/plasma osmolality | >1.3 | <1.1 |
| Urine specific gravity | >1.016 | <1.010 |
| Urine Na + (mEq/L) | <20 | >40 |
| FENa | <1% | >2% |
| Urinary sediment | Hyaline casts | Tubular epithelial cells Granular casts |
5
Discuss acid-base balance regulation, and identify acid-base disturbances resulting from acute kidney injury.
The largest amount of acid within the body is carbon dioxide (CO 2 ). It is controlled by chemoreceptors within the carotid bodies, aortic arch, and medulla. Alveolar ventilation is increased when the carotid bodies and aortic arch are exposed to increased CO 2 levels or when the medulla is exposed to decreased pH of cerebrospinal fluid. CO 2 is buffered by hemoglobin, where it binds with water (H 2 O). The reaction is catalyzed by carbonic anhydrase to form carbonic acid (H 2 CO 3 ). H 2 CO 3 subsequently ionizes to hydrogen and bicarbonate.
HCO 3 + H + n H 2 CO 3 n CO 2 + H 2 O CO 2 + H 2 O ← Carbonic anhydrase H 2 CO 2
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