Urinary Excretion of Alanine Aminopeptidase and N-Acetyl-β-<i>D</i>-Glucosaminidase During Sequential Combination Chemotherapy

Diener, U.; Knoll, E.; Ratge, D.; Langer, Bruno; Wisser, H.

doi:10.1515/cclm.1982.20.9.615

Cited by 9 publications

(6 citation statements)

References 4 publications

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“…The measurement of high-molecular-weight enzymes in urine is a more specific indicator of renal tubular effects [Trnavsky and Rovensky, 1973;Mattenheimer, 1977;Adelman et al, 1979;Burchardt et al" 1979aBurchardt et al" , 1979bKirschbaum, 1979;Mondorf et al, 1979;Price, 1979Price, , 1982Vanderlinde, 1981;Diener et al, 1982;Meyer et al, 1984;Gotelli et al, 1985], and cadmium exposure is asso ciated with elevated urine levels of various enzymes [Nomiyama et al, 1975: Bernard et al, 1979: Taniguchi et al, 1979: Bernard. 1980: Bonner et al.…”

Section: Introductionmentioning

confidence: 99%

Chronic Renal Tubular Effects in Relation to Urine Cadmium Levels

Mueller

Sj²,

Steinberg³

et al. 1989

Nephron

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In this study the urine activities of two brush border membrane enzymes, alanine aminopeptidase (AAP) and γ-glutamyltranspeptidase (GGT), and the lysosomal enzyme N-acetyl-β-D-glucosaminidase (NAG) were measured in men exposed to cadmium to investigate chronic renal toxicity. The subjects consist of a group with urine cadmium levels < 2.0 μg/l and a group with higher cadmium levels (urine cadmium > 2.0 μg/l) with past or present occupational exposure to cadmium. The mean NAG value corrected for creatinine in the higher cadmium group (2.95 U/g creatinine) is significantly different from the mean low cadmium group value (0.92 U/g creatinine, p = 0.0083). Likewise, AAP in the higher group (13.83 U/g creatinine) is significantly different from that of the low group (6.58 U/g creatinine; p = 0.0018). NAG and AAP also give significant correlations with cadmium levels in urine (NAG: r = 0.51; p = 0.0001; AAP: r = 0.56; p = 0.0001). There is no similar statistically significant difference in GGT means in the two groups. In contrast to cadmium correlations, blood lead does not correlate with NAG, AAP, or GGT. A dose-response relationship was found between NAG and cadmium and between AAP and cadmium. The analysis of this relationship gives estimates of a 10% chance of observing an elevated NAG value at a cadmium level of 6.3 μg/g creatinine (8.0 μg/l) and a 10% chance of observing an elevated AAP at a cadmium level of 5.0 μg/g creatinine (3.4 μg/l). These data indicate elevations of NAG and AAP at urine cadmium levels below the level of 10 μg/g creatinine recommended as an upper limit by the 1980 World Health Organization Study Group. Since elevated levels of NAG and AAP in cadmium-exposed workers may reflect chronic renal tubular nephrotoxicity, these findings indicate that cadmium levels below 10 μg/g creatinine may be accompanied by subclinical tubular dysfunction, and that WHO guidelines should be interpreted cautiously, particularly with reference to workers who are no longer exposed and may have had higher cadmium body burdens in the past.

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Section: Introductionmentioning

confidence: 99%

Chronic Renal Tubular Effects in Relation to Urine Cadmium Levels

Mueller

Sj²,

Steinberg³

et al. 1989

Nephron

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“…However, creatinine determination, a reflection of glomerular filtration, is a relatively insensitive measure of druginduced renal tubular damage. Cisplatin-induced nephrotoxicity can be quantitated by monitoring urinary markers for tubular cell damage [1,5,8,9,15,17]. Two widely used markers are urinary alanine aminopeptidase (AAP) and N-acetyl-13-D-glucosaminidase (NAG), high-molecular-mass enzymes that are localized within the microvilli and lysosomes of renal tubular cells, respectively [2,18].…”

Section: Introductionmentioning

confidence: 99%

Carboplatin (CBDCA), iproplatin (CHIP), and high dose cisplatin in hypertonic saline evaluated for tubular nephrotoxicity

Goren

Forastiere

Wright

et al. 1987

Cancer Chemother. Pharmacol.

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We compared the acute tubular nephrotoxicity of three platinum compounds in children and adults with solid tumors by monitoring the urinary excretion of alanine aminopeptidase, N-acetyl-beta-D-glucosaminidase, and total protein. Cisplatin (100 mg/m2) was administered with mannitol, or at a twofold larger total dosage (50 mg/m2 per day for 4 days) in a 3% saline infusion. Carboplatin (300 mg/m2) was administered in combination with 5-fluorouracil, and iproplatin was administered in dosages ranging from 216 to 388 mg/m2. Enzymuria and proteinuria induced by cisplatin at a total dosage of 200 mg/m2 on a divided schedule did not significantly differ from that observed for the single 100 mg/m2 dose. Enzymuria and proteinuria induced by carboplatin and iproplatin were significantly less than that for cisplatin; however, one patient developed chronic tubular damage after three courses of carboplatin, and the acute tubular toxicity of iproplatin in one of 15 patients was exceptional. Our findings support the value of administering cisplatin in hypertonic saline on a divided schedule as a strategy to reduce acute tubular damage. Although carboplatin and iproplatin are less nephrotoxic than cisplatin, occasionally patients experience subclinical acute or chronic tubular damage that may lead to overt nephrotoxicity with continued therapy.

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“…[22] Numerous investigations have confirmed the informative value of enzymes and proteins for specific situations such as kidney transplant rejection, drug over-dosing or intoxications. [21,[23][24][25][26] However, only a few reports have appeared regarding the etiology of renal dysfunction in operated intensive-care patients and the frequency distribution of its possible cause. [27] According to the literature, 80% of all cases of acute renal failure are caused by circulation-induced forms.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Monitoring of Renal Function in Poly-Traumatized Intensive Care Patients

Dehne¹,

Sablotzki²,

Mühling³

et al. 2002

Renal Failure

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During treatment in the ICU, all examined patients showed at times pathological excretion rates of specialized kidney function parameters. Such transient damage was only apparent in a few of the patients when the standard parameters serum creatinine and serum urea were employed. In 90% of the surviving patients the kidney parameters had normalized until the time they were transferred, indicating that such parameters reflected the general state of health of these patients.

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Urinary Excretion of Alanine Aminopeptidase and N-Acetyl-β-D-Glucosaminidase During Sequential Combination Chemotherapy

Cited by 9 publications

References 4 publications

Chronic Renal Tubular Effects in Relation to Urine Cadmium Levels

Chronic Renal Tubular Effects in Relation to Urine Cadmium Levels

Carboplatin (CBDCA), iproplatin (CHIP), and high dose cisplatin in hypertonic saline evaluated for tubular nephrotoxicity

Long-Term Monitoring of Renal Function in Poly-Traumatized Intensive Care Patients

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