Acute kidney injury is the new name for Acute renal failure, defined as a Cr increase of 0.5 mg/dL if baseline < 2.5 mg/dL, a 50% decrease in GFR, or a 20% increase if baseline > 2.5 mg/dL. Anuria is defined as UOP < 100 mL/24h, and oliguria is defined as UOP 100-400 mL/24h. Normal creatinine is 0.8-1.3 for men and 0.6-1.0 for women, as it is a function of both kidney function and skeletal muscle mass. Note that creatinine values can take several days to fully reflect changes in kidney function. Patients with creatinine clearance < 25 mL/min are at risk for significant pharmacokinetic abnormalities. When indexed GFR falls below 15 mL/min/1.73m2, uremic symptoms begin to appear. BUN is a misleading marker of renal function is it is dependent on diet and volume status, and can be affected by GI bleeding, other high protein intake, and by steroids.
Prevalence of 5.7% in ICU patients, and in these patients (based on survey of 30,000 patients), the most common contributing factor to AKI was septic shock (47.5%). AKI is associated with a mortality of up to 80% in critically-ill patients, and this has not been lowered by the introduction of hemodialysis [NEJM 334: 1448, 1996; Hosp Pract 28: 61, 1993]. The extent to which this reflects the impact of AKI and its management vs the impact of the disease bringing about AKI is a subject of controversy. Novis et al. reviewed 28 studies of preoperative risk factors for postoperative AKI (10,865 total patients) and found that there was no consistent definition of AKI and that the only risk factor that consistently predicted post-operative AKI was some form of preoperative renal injury (ex. increased Cr, increased BUN, or preoperative renal dysfunction). CHF and advanced age were less consistent, with CHF more likely to be related than age [Novis et al. Anesth Analg 78: 143, 1994]. Potential (but less uniformly accepted) intraoperative risk factors include other vascular diseases, advanced age, major surgery, sepsis, and multiorgan failure.
Uremia can lead to mental status changes and even seizures. Patients with AKI may suffer from hypertension and edema (cannot waste volume), and may have significant nausea and vomiting. Prolonged severe uremia is associated with risk of pericarditis and pleural effusion, as well as uremia-induced platelet dysfunction and malnutrition. AKI is associated with hyperkalemia and metabolic acidosis which may be anion-gap or non-anion-gap in nature.
FENA and BUN/Cr are helpful. Note that 5-10% of normal adults will have proteinuria on screening exams. Renal tract ultrasound should be carried out to exclude hydronephrosis, perinephric collections, and renal size.
Types of Renal Failure
Responsible for 30-40% of cases in the ICU, but probably more than 40% in the operating room. Caused by decreased effective arterial volume which can be due to hypovolemia, cardiac dysfunction, or loss of vascular tone, but also due to renal vasoconstriction (ex. NSAIDS) or ↓ glomerular filtration pressure (ex. ACE-I/ARB) as well as renal artery stenosis. FENA < 1% and BUN/Cr > 20
Intrinsic Renal Failure
ATN alone causes 50% of AORF in the ICU, probably significantly less in the operating room. In the ICU, intrinsic renal failure is primarily due to ATN (prolonged prerenal failure, sepsis, shock, toxin), AIN, and acute glomerulonephritis.
ATN is most common, most often secondary to sepsis, circulatory shock, and/or nephrotoxins such as dye, aminoglycosides, or myoglobin [Crit Care Med 24: 192, 1996]. Often ATN is associated with multi-organ injury and thus the treatment regimen chosen should take this into account. The mortality rates from ATN in hospitalized and ICU patients are about 37.1% and 78.6%, respectively [Chest 128: 2847, 2005]. Look for FENA > 2% (kidney can no longer retain sodium) as well as muddy casts, +/- RBCs in urine.
AIN can be difficult to distinguish from ATN, thus always look at the medication list. Almost any drug can cause AIN, and unfortunately fever, rash, and/or eosinophilia may not be present. Worse, renal injury can occur months or even years after therapy [New Horiz 3: 608, 1995]. Oral prednisone at 0.5 – 1.0 mg/kg daily for 1-4 weeks may speed recovery [Crit Care Clin 22: 357, 2006] Myoglobinuric renal failure is usually mild. Diagnose with a positive urine dipstick in the absence of erythrocytes on microscopy. Rhabdomyolysis should be suspected if azotemia increases faster than possible by renal shutdown alone (ie BUN > 30 mg/dL, Cr > 2 mg/dL, K+ > 0.5 mEq/L, or HCO3- > 2 mEq/L). This can be confirmed by measuring serum CPK, LDH, or aldolase (specific for skeletal muscle)
Drugs That Commonly Cause AIN
Small Vessel Disease
Can lead to ARF, especially emboli, HUS/TTP/DIC, preeclampsia, and even malignant hyperthermia
Rare to manifest acutely in OR/ICU population, will see dysmorphic RBC and RBC casts on urinalysis
Any obstruction to kidney outflow. Rare in the OR/ICU patient unless only one kidney is present
Rule out treatable causes (ex. pre-renal, post-renal). Optimize hemodynamics and avoid nephrotoxins. Note that dopamine and diuretics have not been shown to be helpful. In fact, there are case reports of loop diuretics leading to irreversible renal failure. Mannitol has been shown to improve outcome in two settings – post-transplantation ATN, and combined with alkaline diuresis in crush injury.
Volume status. Avoid nephrotoxins. Drug dosing (we wary of morphine and most NDMBs). Fistula preservation.
Renal Disease and Anesthesia
- Preoperative renal dysfunction is the only reliable predictor for postoperative dysfunction
- Absolute laboratory values are almost meaningless outside the context of trends
- Cardiovascular disease is the most common cause of death in patients with ESRF
- SCh will increase by ~ 0.6 mEq/L regardless of renal status an can be safely given even when serum [K+] > 5 mEq/L
- Always check shunts and fistulas during surgery
- Use pancuronium and morphine with caution
- Dopamine has no practical use in renally impaired patients
Evidence Based Medicine
Risk factors for postoperative renal failure (10,865 total patients): [Novis et al. Anesth Analg 78: 143, 1994]