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Development of an “In Situ” renal perfusion system to study the origin of urinary biomarkers in a nephrotoxicity model induced by gentamicin

Authors:

Francisco J. López-Hernández ,

Instituto de Estudios de Ciencias de la Salud (IECSCYL), Unidad de Investigación, Hospital Universitario de Salamanca, Salamanca, Spain; Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, Spain; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo, Madrid, Spain, ES
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Blanco-Gozalo V.,

Instituto de Estudios de Ciencias de la Salud (IECSCYL), Unidad de Investigación, Hospital Universitario de Salamanca, Salamanca, Spain; Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, Spain; Bio-inRen, S.L., Salamanca, Spain, ES
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L. Prieto-García,

Instituto de Estudios de Ciencias de la Salud (IECSCYL), Unidad de Investigación, Hospital Universitario de Salamanca, Salamanca, Spain; Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, Spain, ES
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S.M. Sancho-Martínez,

Instituto de Estudios de Ciencias de la Salud (IECSCYL), Unidad de Investigación, Hospital Universitario de Salamanca, Salamanca, Spain; Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, Spain; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo, Madrid, Spain, ES
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J.M López-Novoa

Instituto de Estudios de Ciencias de la Salud (IECSCYL), Unidad de Investigación, Hospital Universitario de Salamanca, Salamanca, Spain; Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, Spain; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo, Madrid, Spain, ES
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Abstract

Background and Aims

Gentamicin is an aminoglycoside antibiotic widely used for the treatment of many infectious diseases. Its main side effect is its nephrotoxicity, which occurs in 10-25% of therapeutic courses, despite proper monitoring and hydration of patients, can lead to acute kidney injury (AKI). We have previously demonstrated that urinary damage markers like albuminuria increased as a consequence of the addition of gentamicin. In the present work we aimed at specifically studying the renal handling of albuminuria in a nephrotoxicity model, through in situ renal perfusion experiments.

Methods

Male Wistar rats were administrated by a single dose of gentamicin (150 mg/kg), or not. After 5 days, rats were anesthetized and an extracorporeal circuit for kidney perfusion was set up. The renal artery, vein and ureter of the right kidney were ligated. The renal artery of the left kidney and the urinary bladder were canulated. A catheter was placed in the right carotid artery and connected directly to the renal artery. Urine was continuously collected from a catheter placed in the urinary bladder at 10 min intervals. After 1 h of renal perfusion with blood from the carotid artery, oxygenated and warm (37 °C) Krebs-dextran (40 g/L of dextran) was perfused through the renal artery at 3 mL/min, and was discarded through the renal vein. Albuminuria was measured in the different urine fractions.

Results

From the second day after gentamicin administration, albuminuria was significantly increased, as compared to control rats, in which urinary markers were undetectable. When exogenous Krebs solution prefunding the kidney, neither gentamicin rats nor control rats excreted albuminuria. As a control of the perfusion experiments, urinary markers still appeared in the urine in gentamicin rats whose kidney was perfused with its own blood. However, albuminuria was undetectable in control rats.

Conclusions

Our results support the idea that excess albumin found in the urine (albuminuria) as a consequence of treatment with gentamicin comes from the blood ultrafiltrate reaching Bowman’s capsule and not from the renal parenchyma. More interestingly, our results provide and in situ method to test the origin of urinary biomarkers in different conditions.

How to Cite: J. López-Hernández, F., V., B.-G., Prieto-García, L., Sancho-Martínez, S.M. and López-Novoa, J.M., 2015. Development of an “In Situ” renal perfusion system to study the origin of urinary biomarkers in a nephrotoxicity model induced by gentamicin. European Journal of Molecular & Clinical Medicine, 2(2), p.71. DOI: http://doi.org/10.1016/j.nhtm.2014.11.055
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Published on 07 Feb 2015.
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