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Chapter: Clinical Anesthesiology: Anesthetic Management: Anesthesia for Patients with Kidney Disease

Anesthesia for Evaluating Renal Function

Renal impairment can be due to glomerular dys-function, tubular dysfunction, or obstruction of the urinary tract.

Evaluating Renal Function

Renal impairment can be due to glomerular dys-function, tubular dysfunction, or obstruction of the urinary tract. Because abnormalities of glomerular function cause the greatest derangements and are most readily detectable, the most useful laboratory tests utilized currently are those related to assess-ment of glomerular filtration rate (GFR). Accurate clinical assessment of renal function is often difficult and relies heavily on laboratory determinations such as the creatinine clearance (Table 30–1). Two sys-tems for classification of AKI are helpful in defining and staging the degree of renal dysfunction; these are the Acute Dialysis Quality Initiative RIFLE cri-teria (Figure 30–2) and the Acute Kidney Injury Network (AKIN) staging system (Table 30–2). A great deal of research is currently evaluating plasma and urine biomarkers associated with AKI, such as cystatin C, neutrophil gelatinase–associated lipo-calin, interleukin-18, and kidney injury molecule-1. It is likely that biomarkers will play a prominent role in the near future for diagnosis, staging, and prog-nostic assessment of AKI.


The primary source of urea in the body is the liver. During protein catabolism, ammonia is produced from the deamination of amino acids. Hepatic con-version of ammonia to urea prevents the buildup of toxic ammonia levels:

Blood urea nitrogen (BUN) is therefore directly related to protein catabolism and inversely related to glomerular filtration. As a result, BUN is not a reli-able indicator of the GFR unless protein catabolism is normal and constant. Moreover, 40–50% of the urea filtrate is normally reabsorbed passively by the renal tubules; hypovolemia increases this fraction.

The normal BUN concentration is 10–20 mg/dL. Lower values can be seen with starvation or liver disease; elevations usually result from decreases in GFR or increases in protein catabolism. The latter may be due to a high catabolic state (trauma or sep-sis), degradation of blood either in the gastrointesti-nal tract or in a large hematoma, or a high-protein diet. BUN concentrations greater than 50 mg/dL are generally associated with impairment of renal function.


Creatine is a product of muscle metabolism that is nonenzymatically converted to creatinine. Creati-nine production in most people is relatively constant and related to muscle mass, averaging 20–25 mg/kg in men and 15–20 mg/kg in women. Creatinine is then filtered (and to a minor extent secreted) but not reabsorbed in the kidneys. Serum creatinine con-centration is therefore directly related to body mus-cle mass but inversely related to glomerular filtration (Figure 30–3). Because body muscle mass is usually relatively constant, serum creatinine measurements are generally reliable indices of GFR in the healthy patient. However, the utility of a single serum creatinine measurement as an indicator of GFR is limited in critical illness: the rate of creati-nine production, and its volume of distribution, may be abnormal in the critically ill patient, and a single serum creatinine measurement often will not accu-rately reflect GFR in the physiological disequilib-rium of AKI.


The normal serum creatinine concentration is 0.8–1.3 mg/dL in men and 0.6–1 mg/dL in women. Note from Figure 30–3 that each doubling of the serum creatinine represents a 50% reduction in GFR. Large meat meals, cimetidine therapy, and increases in acetoacetate (as during ketoacido-sis) can increase serum creatinine measurements without a change in GFR. Meat meals increase the creatinine load, and high acetoacetate concentra-tions interfere with the most common laboratory method for measuring creatinine. Cimetidine

appears to inhibit creatinine secretion by the renal tubules.


GFR declines with increasing age in most indi-viduals (5% per decade after age 20), but because muscle mass also declines, the serum creatinine remains relatively normal; creatinine production may decrease to 10 mg/kg. Thus, in elderly patients, small increases in serum creatinine may represent large changes in GFR. Using age and lean body weight (in kilograms), GFR can be estimated by the following formula for men:

For women, this equation must be multiplied by 0.85 to compensate for a smaller muscle mass. The serum creatinine concentration requires 48–72 h to equilibrate at a new level following acute changes in GFR.


Creatinine clearance measurement is the most accurate method available for clinically assessing overall renal function (actually, GFR). Although measurements are usually performed over 24 h, 2-h creatinine clearance determinations are reasonably accurate and easier to perform. Mild impairment of renal function generally results in creatinine clear-ances of 40–60 mL/min. Clearances between 25 and 40 mL/min produce moderate renal dysfunction and nearly always cause symptoms. Creatinine clear-ances less than 25 mL/min are indicative of overt kidney failure.

Progressive kidney disease enhances creati-nine secretion in the proximal tubule. As a result, with declining renal function the creatinine clear-ance progressively overestimates the true GFR. Moreover, relative preservation of GFR may occur early in the course of progressive kidney disease due to compensatory hyperfiltration in the remain-ing nephrons and increases in glomerular filtra-tion pressure. It is therefore important to look for other signs of deteriorating renal function such as hypertension, proteinuria, or other abnormalities in urine sediment.


Low renal tubular flow rates enhance urea reab-sorption but do not affect creatinine handling. As a result, the BUN to serum creatinine ratio increases above 10:1. Decreases in tubular flow can be caused by decreased renal perfusion or obstruction of the urinary tract. BUN: creatinine ratios greater than 15:1 are therefore seen in volume depletion and in edematous disorders associated with decreased tubular flow (eg, congestive heart failure, cirrho-sis, nephrotic syndrome) as well as in obstructive uropathies. Increases in protein catabolism can also increase this ratio.


Urinalysis continues to be routinely performed for evaluating renal function. Although its utility for that purpose is justifiably questionable, urinaly-sis can be helpful in identifying some disorders of renal tubular dysfunction as well as some nonrenal disturbances. A routine urinalysis typically includes pH; specific gravity; detection and quantification of glucose, protein, and bilirubin content; and micro-scopic examination of the urinary sediment. Urinary pH is helpful only when arterial pH is also known. A urinary pH greater than 7.0 in the presence of systemic acidosis is suggestive of renal tubular aci-dosis . Specific gravity is related to urinary osmolality; 1.010 usually corresponds to 290 mOsm/kg. A specific gravity greater than 1.018 after an overnight fast is indicative of adequate renal concentrating ability. A lower specific gravity in the presence of hyperosmolality in plasma is con-sistent with diabetes insipidus.Glycosuria is the result of either a low tubu-lar threshold for glucose (normally 180 mg/dL) or hyperglycemia. Proteinuria detected by routine uri-nalysis should be evaluated by means of 24-h urine collection. Urinary protein excretions greater than 150 mg/d are significant. Elevated levels of bilirubin in the urine are seen with biliary obstruction.Microscopic analysis of the urinary sedi-ment detects the presence of red or white blood cells, bacteria, casts, and crystals. Red cells may be indicative of bleeding due to tumor, stones, infec-tion, coagulopathy, or trauma. White cells and bacteria are generally associated with infection. Disease processes at the level of the nephron pro-duce tubular casts. Crystals may be indicative of abnormalities in oxalic acid, uric acid, or cystine metabolism.

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