PREOPERATIVE EVALUATION OF RENAL FUNCTION

The greater the magnitude and duration of the surgical insult and the number of acute and chronic risk factors, the greater is the likelihood of perioperative renal compromise and the need for preoperative identification of renal function (see Chapter 25 and Chapter 27 ). In patients with inadequate blood flow, injury is commonly caused by the added risk of drugs, by abnormal hemodynamics, or by preexisting disease.^[20] Studies have shown that 12% to 14% of patients who develop acute renal insufficiency disease during hospitalization do so after radiographic procedures with contrast. If preexisting renal insufficiency exists, progressive deterioration in renal function occurs 42% of cases, with a poor prognosis if dialysis is required.^[78] Acute risk factors, such as volume depletion, aminoglycoside use, radiocontrast dye exposure, use of nonsteroidal anti-inflammatory drugs, septic shock, and pigmenturia, augment the risk of ARF rather than induce it. It appears that the combined interaction of these multiple acute risk factors is central in the pathogenesis of ARF ( Table 37-2 ).^[15] Patients with preexisting renal insufficiency, for example, are especially prone to develop ARF as a result of cardiovascular surgery. Patients with diabetes mellitus and renal insufficiency are especially vulnerable to radiocontrast agents. A review of the literature suggests that the most critical determinants of postoperative renal function are preoperative renal function, maintenance of appropriate intravascular volume, and normal myocardial function.^[13] Although variables have been identified that increase the likelihood of renal dysfunction outcomes, there remains unexplained variability in prediction accuracy. Genetic polymorphism may predispose patients to acute perioperative renal dysfunction, similar to the situation that has been identified in chronic

TABLE 37-2 -- Risk factors associated with the development of acute renal failure

Acute Factors

Volume depletion

Use of aminoglycosides

Radiocontrast dye exposure

Use of nonsteroidal anti-inflammatory drugs

Septic shock

Pigmenturia

Chronic Factors

Preexisting renal disease

Hypertension

Congestive heart failure

Diabetes mellitus

Advanced age

Cirrhosis of the liver

renal disease. The apolipoprotein E4 was reported to be more associated with reduced postoperative increases in serum creatinine after cardiac surgery compared with the apolipoprotein E3 or E2 polymorphisms.^[79]

Despite substantially reduced renal function, impaired functional reserve capacity may only become evident when stress imposes severe demands on renal function; therefore, a comprehensive evaluation of renal function reserve should be sought before surgery. In addition to intrinsic renal disease, several extrinsic variables influence the outcome of renal function tests: intracellular and extracellular volume, cardiovascular function, and neuroendocrine factors.^{[80] [81]} Advanced age also markedly decreases renal function reserve. GFR, normally about 125 mL/min in a young adult, decreases to about 80 mL/min at 60 years of age and to 60 mL/min at 80 years. Although not necessarily the primary cause for end-stage renal disease, hypertension in up to 85% of patients with renal failure is a major risk factor for the high cardiovascular morbidity that occurs.^[82]

In addition to its contribution to renal failure in hypertensive nephrosclerosis, resulting from essential hypertension and hyperfiltration in diabetic nephropathy, hypertension also contributes to the loss of renal function associated with aging. Preoperative isolated systolic blood pressure (SBP) hypertension and wide pulse pressure (i.e., the difference between SBP and diastolic blood pressure [DBP]) are strong independent predictors of postoperative renal dysfunction.^{[10] [11]} It appears that an increase in conduit vessel stiffness with inadequate flow during low-pressure states contributes to increased preoperative renal dysfunction and hemodialysis-dependent renal failure. Four groups of preoperative hypertensive patients were identified in an analysis of 5065 patients undergoing coronary artery bypass surgery. Isolated SBP (SBP > 160 mm Hg, DBP < 90 mm Hg), isolated DBP (SBP < 160 mm Hg, DBP > 90 mm Hg), combined SBP and DBP, and wide pulse pressure (> 80 mm Hg). In that analysis, the rate of wide pulse pressure was 8%, and that of isolated SBP was 2.3%. Mild hypertensive disease that is associated with renal disease therefore implies that renal disease may be primary.

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Reliable evaluation requires knowledge of various renal function tests and their diagnostic limitations. For appropriate management, ischemic causes (e.g., prerenal azotemia) should ideally be distinguished from factors that maintain the intrinsic state of renal failure (e.g., acute tubular necrosis). Prerenal azotemia and acute tubular necrosis, however, may not be mutually exclusive. Unfortunately, there is no simple, inexpensive test that adequately quantifies renal function. The readily available tests fail to accurately reflect the status of the kidneys in a large percentage of patients, especially those who are elderly, malnourished, or dehydrated. Commonly obtained tests of renal function are urinalysis, BUN determination, serum creatinine determination, and creatinine clearance.

Urinalysis provides qualitative information that must be interpreted cautiously. Hematuria (i.e., more than one or two red blood cells per high-power field in a concentrated sediment) suggests glomerular disease or, in a trauma patient, injury to the kidneys or the lower urinary tract. A urine test result that is positive for blood in the absence of red blood cells suggests the presence of free hemoglobin or myoglobin in the urine. Pyuria (i.e., more than four white blood cells per high-power field) suggests urinary tract infection. Although urine may normally contain hyaline and granular casts, cellular casts represent a pathologic condition. Red blood cell casts suggest interstitial nephritis, including pyelonephritis. Urinary pH, although difficult to interpret on a spot urine sample, may assist in the diagnosis of some acid-base disturbances. The pH of urine tends to be more acidic when factors that initiate failure are prerenal rather than postrenal. The presence of proteinuria on a routine dipstick examination may be normal, or it may suggest severe renal disease. In a concentrated urine sample, trace or 1+ proteinuria is a nonspecific finding, whereas 3+ or 4+ proteinuria suggests glomerular disease. The existence of glucosuria without hyperglycemia indicates proximal tubular damage. Lysozymuria, an increase of the enzymatic protein lysozyme in urine, occurs if the serum level is elevated above the normal renal threshold (45 mg/mL) or when renal tubular function is impaired. ^[83] The normal urinary lysozyme level is less than 1.9 mg/mL, and a level greater than 5 mg/mL is regarded as evidence for significant renal tubular damage. Elevated serum levels of lysozyme may be a consequence of renal failure as well as a marker for it. Because white blood cells have a high concentration of lysozyme, urinary tract infections may also lead to elevated serum levels.

The BUN and serum creatinine levels offer rapid but inexact estimates of creatinine clearance. Acute elevations of BUN and serum creatinine levels occur in approximately 5% of all hospital admissions and in up to 20% of intensive care patients.^[16] The incidence increases directly with the severity of trauma and the degree of injury or disease. The incidence and severity of ARF usually is greater when preoperative serum creatinine level is greater than 2 mg/dL⁴ ; however, an isolated serum creatinine measurement is an unreliable indicator of GFR when renal function is changing. There is an inverse logarithmic relationship between GFR and serum creatinine concentration ( Fig. 37-7 ). Decreasing the rate by one half results in twice the serum creatinine level. For example,

Figure 37-7 The inverse logarithmic relationship between serum creatinine concentration (y axis) and glomerular filtration rate (x axis). Notice that the serum creatinine level is not markedly increased until there is a reduction in glomerular filtration rate to about one fourth of normal (120 to 30 mL/min).