M. Atoba

Bio: M. Atoba is an academic researcher from Ruhr University Bochum. The author has contributed to research in topics: Alkaline phosphatase & Acid phosphatase. The author has an hindex of 1, co-authored 1 publications receiving 77 citations.

Prognostic Value of Tubular Proteinuria and Enzymuria in Nonoliguric Acute Tubular Necrosis

Abstract: Background: Acute tubular necrosis (ATN) has high mortality, especially in patients who require renal replacement therapy (RRT). We prospectively studied the diagnostic accuracy of the urinary excretion of low-molecular-weight proteins and enzymes as predictors of a need for RRT in ATN. Methods: In 73 consecutive patients with initially nonoliguric ATN, we measured urinary excretion of α1- and β2-microglobulin, cystatin C, retinol-binding protein, α-glutathione S -transferase, γ-glutamyltransferase, lactate dehydrogenase, and N -acetyl-β-d-glucosaminidase early in the course of ATN. Results: Twenty-six patients (36%) required RRT a median of 4 (interquartile range, 2–6) days after detection of proteinuria and enzymuria. Patients who required RRT had higher urinary cystatin C and α1-microglobulin [median (interquartile range), 1.7 (1.2–4.1) and 34.5 (26.6–45.1) g/mol of creatinine] than patients who did not require RRT [0.1 (0.02–0.5) and 8.0 (5.0–17.5) g/mol of creatinine]. Urinary excretion of cystatin C and α1-microglobulin had the highest diagnostic accuracies in identifying patients requiring RRT as indicated by the largest areas under the ROC curves: 0.92 (95% confidence interval, 0.86–0.96) and 0.86 (0.78–0.92), respectively. Sensitivity and specificity were 92% (95% confidence interval, 83–96%) and 83% (73–90%), respectively, for urinary cystatin C >1 g/mol of creatinine, and 88% (78–93%) and 81% (70–88%) for urinary α1-microglobulin >20 g/mol of creatinine. Conclusion: In nonoliguric ATN, increased urinary excretion of cystatin C and α1-microglobulin may predict an unfavorable outcome, as reflected by the requirement for RRT.

Study of lead exposure from automobile exhaust as a risk for nephrotoxicity among traffic policemen.

Abstract: Background: Traffic policemen are the most exposed population to lead (Pb) from automobile exhaust. There has been increasing concern about the possible harmful effects of Pb from a

Furosemide Enhancement of Experimental Gentamicin Nephrotoxicity: Comparison of Functional and Morphological Changes with Activities of Urinary Enzymes

Abstract: Dogs were given gentamicin (10 mg/kg) intramuscularly every 8 hr for 10 days. Levels of serum creatinine rose by day 6 (0.91 +/- 0.08 vs. 0.75 +/- 0.02 mg/dl for controls, P less than 0.05) and of blood urea nitrogen by day 8 (24.3 +/- 4.80 vs. 16.1 +/- 0.90 mg/dl for controls, P less than 0.05). Gentamicin nephrotoxicity occurred earlier and was more marked when furosemide (2 mg/kg) was added: the level of serum creatinine by day 6 was 1.62 +/- 0.25 mg/dl (P less than 0.05), and the level of blood urea nitrogen by day 8 was 181 +/- 23.5 mg/dl (P less than 0.01). Elevations in the activities of the urinary enzymes beta-glucuronidase, N-acetyl-beta-glucosaminidase, and muramidase preceded rises in levels of serum creatinine and blood urea nitrogen. Examination of serial percutaneous renal biopsy specimens showed that gentamicin administration was associated with hyaline droplet degeneration, lysosomal changes, and, later, cell necrosis (primarily of the proximal tubules). Changes in renal morphology were more severe and occurred earlier when furosemide was administered concomitantly. In summary, furosemide enhanced gentamicin nephrotoxicity. Enzymuria was an early sign of gentamicin nephrotoxicity.