• Acute kidney injury (AKI) is a frequently encountered postoperative complication with significant short-term and long-term consequences.
• The Acute Kidney Injury Network classifies AKI as:
  • Stage 1: Increase in SrCr >0.3 mg/dL or 1.5–2-fold increase from baseline, or urine output (UOP) <0.5 mL/kg/hr × 6 hours
  • Stage 2: 2–3-fold increase in SrCr, or UOP <0.5 mL/kg/hr × 12 hours
  • Stage 3: >3-fold increase in SrCr or an acute increase of >0.5 mg/dL in patients with a baseline SrCr >4 mg/dL, or UOP <0.3 mL/kg/hr × 24 hours or anuria × 12 hours; or patients requiring renal replacement therapy (RRT)
• Despite being the basis of the AKI definition, SrCr is not a very sensitive marker of the condition:
  • Changes in GFR are reflected by SrCr levels 2–3 days after an insult.
  • Levels vary with the patient's age, body habitus, and volume status.
• Newer biomarkers of AKI are being developed:
  • Neutrophil gelatinase-associated lipocalin (NGAL). A protein is upregulated by tubular endothelial cell after an ischemic injury. Urinary and plasma levels are being studied.
  • KIM-1: Transmembrane protein that is highly expressed by de-differentiated tubular cells following injury.
  • Cystatin C: Produced by all nucleated cells. It is freely filtered and completely reabsorbed and degraded by the tubules. Reflects glomerular filtration, not tubular injury. Value not yet certain but could identify AKI before elevations of creatinine occur.
  • IL-18: Tubular epithelial pro-inflammatory cytokine that gets activated in proximal tubules following injury. May be a predictor of mortality in critically ill patients.

• High risk surgical procedures include: Cardiac and vascular surgery, heart and liver transplant, hepatobiliary surgery, and procedures utilizing radiocontrast
• High risk patients include:
  • Renal insufficiency, both mild and moderate
  • Ascites
  • Active congestive heart failure
  • Emergency surgery
  • Age >56 years
  • Diabetes mellitus
  • Hypertension
  • Male sex

• Total renal blood flow (TRBF) is about 20% of the cardiac output with an oxygen delivery of 80 mL/min/100 g of tissue.
• The renal cortex receives most of the TRBF and has a low oxygen extraction ratio (~20%).
• The renal medulla has a smaller blood flow and a high oxygen extraction ratio (~80%), consequent to the high metabolic demand of tubular reabsorptive function. Thus, the renal medulla is susceptible to ischemic insults.
• In acute tubular necrosis (ATN), ischemia and/or direct toxicity result in apoptosis and shedding of tubular cells as well as recruitment of vasoactive and inflammatory mediators that worsen ischemic injury. Loss of tubular cells allows leakage of glomerular filtrate into the interstitium which results in edema that may progress to chronic inflammation and fibrosis, ultimately leading to chronic kidney disease.
• Perioperatively, a combination of factors contribute to renal dysfunction:
  • Preoperatively: Hypovolemia due to preoperative fasting, bowel preparation
  • Intraoperatively: Effect of anesthetics on hemodynamics and renal perfusion, effect of surgical technique on renal blood flow (e.g., laparoscopic procedures), blood loss, neuroendocrine response to anesthesia and surgery, excessive fluid resuscitation
  • Use of nephrotoxins such as contrast media, antibiotics, NSAIDs, etc.

• The cornerstone of treatment is prevention.
• Pharmacologic interventions have been controversial, and as of yet, no pharmacologic interventions have definitively been beneficial in the prevention of renal failure in the perioperative period with the exception of mannitol administration prior to renal transplant reperfusion.
• Maintain adequate blood pressure.
  • Autoregulation maintains a constant renal blood flow between mean arterial pressures (MAPs) of 80–160 mm Hg.
  • Improved renal hemodynamics has been shown with MAPs around 75 mm Hg.
  • The autoregulation curve may be shifted to the right in chronic hypertensives, so higher pressures may be needed.
• Ensure euvolemia.
  • Oxygen delivery to the kidneys may be reduced in hypovolemia, resulting in ischemic ATN.
  • Excessive fluid resuscitation may lead to abdominal compartment syndrome (intra-abdominal hypertension [IAH]) and impaired renal perfusion.
  • Normal saline given in volumes >30 mL/kg can cause a non-gap hyperchloremic metabolic acidosis and hyperkalemia. Hyperchloremia may result in a decrease in renal blood flow, glomerular filtration rate, and urine output.
  • Albumin may not be more beneficial than crystalloids except in specific situations such as in cirrhotic patients with spontaneous bacterial peritonitis.
  • There is conflicting evidence on the renal safety of hydroxyethyl starch.
• Optimize the oxygen delivery to the kidneys by maintaining an adequate hemoglobin level and cardiac output.
• Avoid nephrotoxins.
  • Iodinated contrast agents are being used with increasing frequency and can cause contrast induced-acute kidney injury (CI-AKI). In addition to being directly toxic to tubular cells, they can cause renal vasoconstriction. Unfortunately at this time, no definitive technique has been shown to consistently decrease or eliminate this risk. The following may be considered: Adequate hydration to a goal of 100–150 mL/hr of UOP to potentially "wash off" the agent and minimize contact time with tubular cells; antioxidants such as N-acetyl cysteine, statins, and urine alkalinizers such as sodium bicarbonate may reduce free radical-related tubular cell apoptosis; the use of low osmolar agents (approximately twice the osmolarity of plasma) in normal patients and iso-osmolar agents in patients at risk of CI-AKI; avoid concomitant use of other nephrotoxins as well as repeat exposure (within 72 hours) of receiving a contrast medium load.
  • NSAIDs inhibit vasodilatory prostaglandins and can result in decreased glomerular filtration pressure by vasoconstricting afferent arterioles. Consider avoiding in high-risk patients. However, in one study, no long-term impairment in renal function was found when given postoperatively to kidney donors.
  • ACEI and ARBs: Decrease glomerular filtration pressure by vasodilating efferent arterioles. Avoid in hypovolemia.
  • Antibiotics such as aminoglycosides can cause ATN by accumulating in the proximal tubules.
  • Other nephrotoxins include antifibrinolytics such as aprotinin, immunosuppressants such as cyclosporine and tacrolimus, and chemotherapeutic agents such as cisplatin.

• Prerenal AKI results as a consequence of true hypovolemia or decreased effective circulating blood volume (as in cirrhosis, CHF).
• Intrinsic AKI can be due to tubular, interstitial, or glomerular injury.
  • ATN is the most common cause of intrinsic AKI. It occurs as a result of ischemia (prolonged absolute or relative hypotension), exposure to nephrotoxins, and/or the endotoxins and inflammatory mediators released in septic patients.
  • Acute interstitial nephritis is infiltration of the interstitium by lymphocytes secondary to the use of NSAIDs or antibiotics.
  • Acute glomerulonephritis is characterized by rapid progression and may be seen in post-streptococcal infection or in the setting of endocarditis.
• Postrenal AKI: Urinary tract obstruction can be seen perioperatively in pelvic surgery following inadvertent injury to the bladder or ureter(s). Intraoperative identification may include the use of intravenous methylene blue or indigo carmine.

Perioperative renal failure Closed Claims Data. There were 75 claims from 1978 to 2006:

• Male: 53%
• Age >53 years: 50%
• ASA 3–5: 45%
• Intraoperative oliguria or anuria: 31%
• Emergency surgery (ASA classification): 29%
• Vascular surgery: 16%
• Cardiac surgery: 3%
• Perioperative events leading to renal dysfunction/failure:
  • Patient condition or surgical cause: 17%
  • Wrong blood administered: 15%
  • Electrolyte imbalance or inappropriate fluid therapy: 13%
  • Medication error: 12%
  • Excessive blood loss: 8%
• Outcome and liability:
  • Mortality: 47%
  • Substandard anesthesia care: 48%
  • Payments/settlement to patient: 56%
  • Median payment: $255,000 (range: $4,000–$3,625,000)

• 584.9 Acute kidney failure, unspecified
• 997.5 Urinary complications, not elsewhere classified

• N17.8 Other acute kidney failure
• N99.89 Oth postprocedural complications and disorders of GU sys

Patrick Kim , MD

Selma Ishag , MB, BS, MD