Comparison of Urinary Enzyme Pattern in Renal Transplant Recipients Receiving Two Different Immunosuppressive Regimens: Azathioprine versus Ciclosporin

Coratelli, P; Giannattasio, Michele; Schena, Antonio; Marzolla, Rocco; Buongiorno, Erasmo

doi:10.1159/000416514

Cited by 3 publications

(2 citation statements)

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“…47, 52] (table 3). Especially m-platinum therapy causes transient or persistent increase in urinary kidney marker proteins, whereas total protein excretion and increase in serum creatinine usually achieved peak concentrations 3-8 days later [33,44,64] (fig. 7).…”

Section: Tubular Proteins In the Urine Of Patients Under Defined Clinmentioning

confidence: 99%

Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Scherberich¹

1990

Am J Nephrol

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A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal β-N-acetyl-glucosaminidase (β-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, γ-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein ‘SGP-240’ and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cz’s-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both ‘soluble’ and high-molecular-weight membrane particles (vacuolar blebs, > 10⁶ dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular ‘histuria’ which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.

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Section: Tubular Proteins In the Urine Of Patients Under Defined Clinmentioning

confidence: 99%

Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Scherberich¹

1990

Am J Nephrol

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“…Alterations in urine and serum levels of lysozyme were detected in acute renal failure [74]. Up to 1988 several publications discussed the occurrence and role of lysozyme in context of renal (transplant) damage and failure, also in view of suitability as diagnostic marker [75][76][77][78][79][80][81][82][83]. First report, that lysozyme, intravenously infused into male rats, induced functional as well as structural alterations and finally caused acute renal failure was presented by Cojocel et al [84].…”

Section: Plos Onementioning

confidence: 99%

Transcriptome analysis of renal ischemia/reperfusion (I/R) injury in BAFF and BAFF-R deficient mice

Möckel,

Boegel,

Schwarting

2023

PLoS ONE

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Acute kidney injury (AKI) accompanies with high morbidity and mortality. Incomplete renal recovery can lead to chronic and finally end-stage kidney disease, which results in the requirement of lifelong dialysis or kidney transplantation. Consequently, finding predictive biomarker and therefore developing preventive therapeutic approaches is an urgent need. For this purpose, a better understanding of the mechanism underlying AKI is necessary. The cytokine BAFF (B cell activating factor) is related to AKI by supporting B cells, which in turn play an important role in inflammatory processes and the production of antibodies. In our study, we investigated the role of BAFF and its receptor BAFF-R in the early phase of AKI. Therefore, we performed the well-established ischemia/reperfusion (I/R) model in BAFF (B6.129S2-Tnfsf13btm1Msc/J) and BAFF-R (B6(Cg)-Tnfrsf13ctm1Mass/J) deficient mice. Transcriptome of ischemic and contralateral control kidneys was analyzed and compared to wildtype littermates. We detected the upregulation of Lcn2, Lyz2, Cd44, Fn1 and Il1rn in ischemic kidneys as well as the downregulation of Kl. Furthermore, we revealed different expression patterns in BAFF and BAFF-R knockout mice. Compared to wildtype littermates, up- and downregulation of each investigated gene were higher in BAFF-R knockout and lower in BAFF knockout. Our findings indicate a positive impact of BAFF knockout in early phase of AKI, while BAFF-R knockout seems to worsen I/R injury. In addition, our study shows for the first time a remarkable renal upregulation of Lyz2 in a murine I/R model. Therefore, we consider Lyz2 as conceivable predictive or early biomarker in case of I/R and AKI.

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Urinary Enzymes in Kidney Transplantation

Jung¹,

Kotanko²

1992

Urinary Enzymes

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Comparison of Urinary Enzyme Pattern in Renal Transplant Recipients Receiving Two Different Immunosuppressive Regimens: Azathioprine versus Ciclosporin

Cited by 3 publications

References 0 publications

Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Urinary Proteins of Tubular Origin: Basic Immunochemical and Clinical Aspects

Transcriptome analysis of renal ischemia/reperfusion (I/R) injury in BAFF and BAFF-R deficient mice

Urinary Enzymes in Kidney Transplantation

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