Urinary lysosomal glycosidases after renal allotransplantation: Correlation of enzyme excretion with allograft rejection and ischemia

Sandman, Robert; Margules, Richard; Kountz, Samuel L.

doi:10.1016/0009-8981(73)90035-1

Cited by 57 publications

(23 citation statements)

References 17 publications

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“…NAG activity was measured fluorometrically by the method of Sandman et al (38). GGT was measured by an automated method on an Hitachi 737 apparatus (Boehringer, Meylan, France).…”

Section: Methodsmentioning

confidence: 99%

Effects of diltiazem on netilmicin-induced nephrotoxicity in rabbits

Lortholary

Blanchet

Nochy

et al. 1993

Antimicrob Agents Chemother

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Aminoglycoside nephrotoxicity remains a common clinical problem and is the major cause of acute toxic renal failure in hospitalized patients. In recent studies, calcium channel blockers gave controversial results in the prevention of acute ischemic or toxic renal failure. The aims of the study were (i) to describe a rabbit model of mild renal failure (50%o reduction in glomerular filtration rate with a mean value of 1.78 0.46 ml/kg/min) induced by netilmicin given intramuscularly at 20 mg/kg of body weight every 8 h for 5 days, (ii) to investigate the protective effect of diltiazem given at a therapeutic dose (1 mg/kg given intramuscularly every 8 h for 5 days), and (iii) to investigate the mechanisms of this protection through evaluation of function tests, optic histology, and glomerular morphometry. Animals treated with netilmicin and diltiazem exhibited an unchanged glomerular filtration rate compared with controls (3.39 + 0.58 versus 3.68 -0.78 ml/kg/min, respectively). This protective effect was not associated with any change in systemic or renal hemodynamics (i.e., no change in renal plasma flow) or changes in the pharmacokinetics of netilmicin, as assessed by fractional excretion and cortical uptake. Netilmicin-induced tubular toxicity was unchanged by diltiazem. Our results suggest that (i) netilmicin exhibits a toxic effect at both the glomerular and the tubular levels, (ii) diltiazem, a calcium channel blocker, when given at low therapeutic doses, is able to prevent the aminoglycoside-induced renal failure through a potential glomerular mechanism. The precise mechanisms of the protection remain to be elucidated. These results deserve clinical evaluation in high-risk patients. (5,21,24). In models of aminoglycoside toxicity, contradictory results have been published. Calcium channel blockers have been reported to be of no use (9,18,43), to exhibit a deleterious effect (17), or again, to be efficient (25, 35) in * Corresponding author. preventing renal failure. In those studies in rats, aminoglycoside and calcium channel blocker doses were high and gentamicin, one of the most nephrotoxic aminoglycosides, was frequently used.We have observed, in human volunteers, that diltiazem (60 mg given three times a day for 7 days) could prevent the increase in urinary N-acetylglucosaminidase (NAG) levels and the loss of dilution ability induced by netilmicin (4.5 mg/kg of body weight given once daily for 7 days) (30). However, in studies performed in humans, it is difficult to investigate the precise mechanisms of such protective effects (37).The aims of the present study were (i) to describe a rabbit model of moderate renal failure induced by netilmicin at the lowest dose that induced a toxic effect (a regimen of three injections per day was chosen to increase the toxic potential over a short period of time [5 days]), (ii) to investigate the protective effect of diltiazem given at therapeutic doses, and (iii) to elucidate at which level protection could occur.Both drugs were chosen because they have previously bee...

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“…NAG activity was measured fluorometrically by the method of Sandman et al (38). GGT was measured by an automated method on an Hitachi 737 apparatus (Boehringer, Meylan, France).…”

Section: Methodsmentioning

confidence: 99%

Effects of diltiazem on netilmicin-induced nephrotoxicity in rabbits

Lortholary

Blanchet

Nochy

et al. 1993

Antimicrob Agents Chemother

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“…The combinations HEX/PK/GST and HEX/GST sufficed to detect all 12 rejections in the CON group, but only one in the CyA group (Kotanko et al, 1986). Daily monitoring of urinary HEX excretion is a helpful adjunct method in diagnosis of renal damage caused by rejection and ischemia (Sandman et al, 1973), as determination of urinary HEX excretion is a reliable, rapid, sensitive and simple method. Excretion of urinary HEX may be a sign of impending rejection of kidney transplant, and daily measurement of HEX output may be useful in the early diagnosis of rejection (Koivula et al, 1978).…”

Section: Hex In Renal Transplantationmentioning

confidence: 99%

“…HEX activity in crude urine conserved with 30% glycerol or ethylene glycol, was maintained for over 1 year in -20°C; in gel filtrate or dialyzate for 3 months in 4°C or -20°C (Jung et al, 1992). It was shown that using albumin solution for urine dilution is essential for stability of HEX in diluted urine (Sandman et al, 1973).…”

Section: Stabilization Of Fbp-16 and Hex Activities In Human Urinementioning

confidence: 99%

Urinary Fructose-1,6-Bisphosphatase (FBP-1,6) and N-Acetyl-β-Hexosaminidase (HEX) in Monitoring Kidney Transplantation - Literature Review

Kępka¹,

Szajda²,

Waszkiewicz³

et al. 2011

Kidney Transplantation - New Perspectives

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“…Urine NAG content was determined using a fluorimetrie method and 4-methyl umbelliferi ß-D-N-acetylglucosamidc as a substrate [Sandman et al, 1973], NAGB deter mination required previous extraction according to Bourbouze …”

Section: Methodsmentioning

confidence: 99%

Urinary Excretion of N-Acetyl-Glucosaminidase and Beta-2-Microglobulin as Early Markers of Gentamicin Nephrotoxicity in Neonates

Jb¹,

Aujard²,

Abisror³

et al. 1987

Dev Pharmacol Ther

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A prospective study in 16 healthy and 16 gentamicin-treated neonates was undertaken to compare the urinary excretion of proximal tubular markers such as β(2)- microglobulin (β(2)-m) and total N-acetyl-β-D-glucosammidase (NAG) and its isoenzymatic form NAGB. β(2)-m excretion was not related to postnatal age in control full-term neonates; it was significantly increased in gentamicin-treated full-term neonates. The urinary excretion of the lysosomal markers, total NAG and NAGB, rose significantly with postnatal age in control group. fMean values for total NAG and NAGB were significantly higher in the treated group but the isoenzymatic profile (NAGB/total NAG × 100) was not modified by gentamicin treatment.

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Urinary lysosomal glycosidases after renal allotransplantation: Correlation of enzyme excretion with allograft rejection and ischemia

Cited by 57 publications

References 17 publications

Effects of diltiazem on netilmicin-induced nephrotoxicity in rabbits

Effects of diltiazem on netilmicin-induced nephrotoxicity in rabbits

Urinary Fructose-1,6-Bisphosphatase (FBP-1,6) and N-Acetyl-β-Hexosaminidase (HEX) in Monitoring Kidney Transplantation - Literature Review

Urinary Excretion of N-Acetyl-Glucosaminidase and Beta-2-Microglobulin as Early Markers of Gentamicin Nephrotoxicity in Neonates

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