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Unusual elevations of serum creatinine (S-CR) out proportion to increases in serum urea nitrogen (S-UN) are frequently observed in patients with diabetic ketoacidosis when S-CR is measured by the Jaffe end-point reaction. This has been ascribed to interference from acetoacetate but this is not however observed with kinetic DuPont ACA methodology. Eighteen patients with diabetic ketoacidosis were studied: SCR measurements were done using the end point Technicon SMA 6/60 method (Group a, 10 patients) or the kinetic DuPont ACA method (Group B, 8 patients). The values for S-CR in Group A patients (mean value and S-D were 3.3 +/- 1.1 mg/dl) were significantly different from Group B patients (1.6 +/- 0.24 mg/dl) (P less than 0.01). A significant positive correlation was obtained between the "excess anion gap" and S-CR in Group A patients (r = + 0.81, p less than 0.01). The results from two patients in whom serial measurements of S-UN, S-CR and the anion gap were carried out further demonstrate the analytical interference. The study demonstrates that in diabetic ketoacidosis elevated creatinine values measured by an end-point method should not necessarily be interpreted as evidence of significant renal impairment and if possible should be verified by a kinetic method which is free of "ketone" interference.

Congestive heart failure usually features a mild to moderate increase in aspartate aminotransferase (AST) activity. A marked increase in AST may occur rarely and is usually preceded by prolonged shock or hypotensive episodes and is accompanied by hyperbilirubinemia. I report two patients with congestive heart failure in whom the AST activity was greater than 8000 U/L. No prior episodes of shock or hypotension occurred in these patients and the accompanying increase in bilirubin was slight. In both cases, the enzyme activity decreased sharply with improvement in the patients' circulatory status. Recognition of this entity is important to distinguish it from viral or drug-induced hepatitis.

We evaluated the presence and degree of hypokalemia associated with ticarcillin disodium (ticarcillin) therapy in 16 patients. Four of these patients who received less than 10 grams of ticarcillin did not develop significant hypokalemia, but this condition developed in 6 of 9 patients receiving a daily dose of greater than 18 grams of this drug, and the mean urinary potassium was elevated in this group (mean = 78 mEq/24 hrs). The degree of hypokalemia was correlated with the volume status of the patient as judged by the serum urea nitrogen: creatinine ratio. A positive correlation (r = 0.66, p less than 0.05) was obtained between the two parameters. Hypokalemia did not develop in three patients with the syndrome of inappropriate secretion of anti-diuretic hormone who were receiving more than 18 grams of ticarcillin daily, indicating the absence of a stimulus for sodium conservation. Aggressive potassium and fluid replacement should be considered in patients with hypokalemia associated with ticarcillin therapy.

We found total protein estimates in patients with monoclonal gammopathies to be erroneously low when using the Cobas-BioR centrifugal analyzer. This problem occurred only when a serum-water blank was used. This probably results from the precipitation of these proteins under conditions of low ionic strength resulting in high blank readings. The problem can be avoided if a serum-saline blank is used.

Antibody interference with routine biochemical tests is becoming increasingly recognized as a cause of spurious results. It is important to recognize these interferences because inappropriate investigation may be instituted in response to the abnormal test result. The present review deals with the various biochemical tests in which antibody interference occurs. The tests include measurement of enzymes, hormones, immunoglobulins, vitamin B12, and a variety of other molecules and ions.

We evaluated whether urine beta 2-microglobulin (beta 2M) excretion as a function of nephrotoxicity correlated with plasma and urine platinum levels in patients receiving cisplatin. Thirty-one patients had urine platinum measurements in urine samples collected at 0 to 6 and 6 to 24 h after cisplatin administration, 25 of these patients had serial plasma platinum measurements. Sixteen of the 31 patients had an increase in urine beta 2M. A significant correlation was obtained between urine platinum and beta 2M in the 6- to 24-h samples (r = 0.61, p less than 0.02). The mean plasma platinum levels were higher (12.6 +/- 6.1 mumol/L) in the patients with an increase in urine beta 2M compared to those patients with no change in beta 2M (6.8 +/- 4.1 mumol/L) (p less than 0.02). Our study indicates that tubular damage occurs within 24 h after cisplatin administration and that the damage correlates with urine platinum levels.

Acetoacetate is known to spuriously raise serum creatinine concentration in patients with diabetic ketoacidosis. Its effect on urinary creatinine has not been studied. Since the renal threshold for ketoacids is low, large amounts of acetoacetate may be present in the urine of uncontrolled diabetics. We investigated this interference using three different automated analysers. We found that +3 or +4 reactions with Ketostix, equivalent to greater than 10 - 15 mmol/L of acetoacetate caused significant interference with the Abbott VP and Beckman Astra instruments. This could cause errors in the calculation of creatinine clearance especially when serum creatinine is close to a normal level. We recommend that measurement of creatinine clearance be delayed until better diabetic control is achieved or the creatinine be measured by a method which is free from ketone interference, e.g., by the Dupont aca.