Detection of Renal Tubular Lesions after Abdominal Aortography and Selective Renal Arteriography by Quantitative Measurements of Brush-Border Enzymes in the Urine

Abstract

Quantitative determination of brush-border enzyme excretion in the 24-hour urine is a much more sensitive index of renal tubular damage after aortography and selective renal arteriography than the conventional renal function tests such as serum creatinine and clearance determinations. Among the five brush-border enzymes which we investigated, alkaline phosphatase (AP) was the most sensitive diagnostic pointer. In 90% of hypertensive patients without detectable pre-existing renal parenchymal damage, abnormal levels of AP excretion in the urine were found on the same day as or on the day after the intra-arterial injection of contrast medium. Measurement of other brush-border enzymes does not provide any further diagnostic information. Provided there is no pre-existing renal parenchymal damage, the lesion caused by the contrast medium is transient and is usually reversed within 48 h. For the early detection of tubular lesions caused by tri-iodinated benzoic acid derivatives, AP excretion in the 24-hour urine should be measured at least twice – on the day of the contrast medium injection and on the following day.

Biomarkers of Acute Renal Injury and Renal Failure

“…Especially, +-GT is a marker of proximal tubular injury and in some prospective studies (17, 32), but not in others (20,23,31); it was helpful in predicting ARF in critically ill (transplant) patients. The enzymes may be particularly sensitive for radiocontrastinduced tubular injury (30). As for NAG, prior diabetes mellitus may confound the predictive value of AF and +-GT, when diabetes is poorly controlled and complicated by tubular injury (29).…”

Hypotensive anesthesia with propofol and remifentanil: protective effect of alpha-tocopherol on renal function

“…In fact, the increase of NAG i that we assessed at time t 3 was similar in both the control and treatment patients. We are unable to explain this unexpected finding because NAG i is one of the most sensitive and specific indicators of tubular impairment [20,21].…”

Renal Toxicity Mediated by Continuous Infusion of Recombinant lnterleukin-2

“…almost at all times within the normal kidney autoregulatory range, with a stable cardiac output and intravascular vol ume status, the urea/creatinine ratio did not change, as it should in a prerenal condition, and the urinary NAG activ ity, one of the most sensitive markers of renal tubular injury [14,15], increased in all the treatment cycles from day I to day 5. Also the abnormalities found in the urinary sediment, mainly the increased numbers of epithelial cells and brown casts, are in favor of an organic acute renal failure, event ually an acute tubular necrosis.…”