Mechanisms of Enzyme Release and Causes of Altered Enzyme Excretion

Burchardt, U; Scherberich, Jürgen E.

doi:10.1007/978-3-642-84313-6_3

Cited by 2 publications

(3 citation statements)

References 49 publications

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“…Fractionated collection of urines indicating that GGT and ALP were released first then LDH, GLD and DNA is consistent with histopathological findings: mercuric chloride first destroys brush bor ders, then causes swelling of tubule cells and subsequent necrosis [10]. Thus, membranebound enzymes ALP and GGT are early markers of membrane damage as previously assessed in the rat [6], while LDH and GLD are more indicative of cell disruption [22]; finally, DNA output is the ultimate demon stration of cell death.…”

Section: Urine Enzyme Reference Values In Guinea Pigssupporting

confidence: 58%

Kidney Tubule Enzymes and Extracellular DNA in Urine as Markers for Nephrotoxicity in the Guinea Pig

Bret

Hasim²,

Lefebvre³

et al. 1993

Enzyme Protein

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Guinea pigs were given a single intraperitoneal injection of 1.35 mg/kg body weight of mercuric chloride; then various kidney enzymes and extracellular DNA were assayed in urine. Dramatic increases of all studied markers were observed on the first day following treatment. Sequential collection of urines allowed for kinetic studies: membrane markers alkaline phosphatase and γ-glutamyltransferase were first released, then cytosolic lactate dehydrogenase and mitochondrial glutamate dehydrogenase, finally extracellular DNA; DNA release is equated with cell death. The features of kidney damage revealed by comparative and quantitative studies of these noninvasive markers suggest that brush border erasure was more extensive than cell necrosis.

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Section: Urine Enzyme Reference Values In Guinea Pigssupporting

confidence: 58%

Kidney Tubule Enzymes and Extracellular DNA in Urine as Markers for Nephrotoxicity in the Guinea Pig

Bret

Hasim²,

Lefebvre³

et al. 1993

Enzyme Protein

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“…These diverse functions are reflected in complex structurally and biochemically polarized cells expressing distinct membrane domains on apical and basolateral sites, which, in the case of the microvillous pole, are integrated into a specialized cytoskeletal matrix (Fig. 1) [12][13][14]. Various cell surface antigens, initially clustered as part of haemopoietic systems, recently identified as cell-surface peptidases of tubule epithelia, are also involved in the modulation of growth and differentiation [15,16], amongst them endopeptidase-24.11 (CD10, CALLA), aminopeptidase N (CD13), dipeptidylpeptidaseIV (CD26), and aminopeptidaseA, which is identical to an angiotensin-II splitting enzyme [17,18].…”

Section: Structural Architecture Of Tubular Cell Membranes Sensitive mentioning

confidence: 99%

“…The excretion of kidney tissue proteins in urine is markedly increased e.g. after injection of X-ray contrast media, aminoglycosides, during cis-platin cytostasis, and cyclosporin A nephrotoxicity [10,12,20,[26][27][28][29][30][31]. Mild toxic injury, usually not apparent at the light microscopic level, may cause early ultrastructural transformation of the tubule cell brush border and release of peripheral membrane surface components into urine, including the SGP240 antigen, aminopeptidase M, dipeptidylaminopeptidase IV, and gamma-glutamyl transpeptidase [27].…”

Section: Trans-modulatorsmentioning

confidence: 99%

Shedding and repair of renal cell membranes following drug-induced nephrotoxicity in humans

Scherberich

Wolf²,

Schoeppe³

1993

Eur J Clin Pharmacol

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Nephrotoxic drugs may account for approximately at least 20% of clinically observed cases of acute renal failure in whom tubular lethal or sublethal damage is a predominant finding. Acute toxic tubular cell injury is characterized by loss of cellular polarization, intrinsic energy deficiency, calcium overload, release of toxic proteases and free oxygen radicals, derangement of the cytoskeleton, and vacuolar transformation of brush border microvilli. These events may finally lead to irreversible cell death. Shedding of membrane enzymes and cytoskeletal components in urine (kidney tissue proteinuria) may serve as a noninvasive early marker for assessing tubular cell injury. Successful recovery of renal function depends on early repair of lethally or sublethally damaged nephrons, in which intrinsic nephrogenic adaptive and proliferative responses cooperate in concert with auto/para/-juxtacrine growth promoting factors and cytokines. Exogenously administered growth factors may enhance renal cell recovery, as shown in animal models. Increased expression of immediate early genes in tubular cells after renal injury reflects the ongoing mitogenic activity necessary for reepithelialization and remodeling (new, polarized, differentiated cells). Further progress in understanding the molecular mechanisms of renal tubular injury will probably influence the diagnostic modalities and therapeutic approaches to acute drug induced renal failure.

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Mechanisms of Enzyme Release and Causes of Altered Enzyme Excretion

Cited by 2 publications

References 49 publications

Kidney Tubule Enzymes and Extracellular DNA in Urine as Markers for Nephrotoxicity in the Guinea Pig

Kidney Tubule Enzymes and Extracellular DNA in Urine as Markers for Nephrotoxicity in the Guinea Pig

Shedding and repair of renal cell membranes following drug-induced nephrotoxicity in humans

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