Abstract

Simple SummaryConcern about the use of hydroxyethyl starch (HES) and the development of kidney injury has emerged in human medicine. In veterinary medicine, some retrospective and prospective studies were conducted to investigate the presence of renal damage in dogs using different types and dosages of hydroxyethyl starch. The present study aimed to evaluate the effects of the constant rate infusion of HES 130/0.4 at a dose of 2 mL/kg/h for 24 h on the renal biomarkers of tubular damage and dysfunction. Ten adult dogs with hypoalbuminemia were enrolled, and serum creatinine, fractional excretion of electrolytes, urinary protein to creatinine ratio, urinary albumin to creatinine ratio, qualitative proteinuria, and urinary neutrophil gelatinase-associated lipocalin were measured at the baseline before HES infusion and after 24 and 48 h from the baseline. No significant change in the selected renal biomarkers was observed across time, ruling out the possibility of significant tubular damage after HES 130/0.4 infusion at the dose and rate applied. Further prospective studies are needed to assess the renal safety profile of low-molecular-weight HES administration in more severely affected dogs.In veterinary medicine, investigations relating the effects of hydroxyethyl starch (HES) on renal function report contrasting results. This study aimed to assess the changes in the selected biomarkers of kidney injury in dogs after the administration of HES 130/0.4 as a constant rate infusion (CRI) for 24 h. Ten adult client-owned dogs with hypoalbuminemia (albumin < 2 g/dL) and ongoing fluid losses were included. Enrolled dogs received intravenous fluid therapy with crystalloids and a CRI of HES 130/0.4 at a dose of 2 mL/kg/h for 24 h. Serum creatinine (sCr), fractional excretion (FE) of electrolytes, urinary protein to creatinine ratio (UPC), urinary albumin to creatinine ratio (UAC), SDS-page, and urinary neutrophil gelatinase-associated lipocalin (uNGAL) were measured at the baseline before HES infusion, and after 24 h (T24) and 48 h (T48) from the baseline. No statistically significant difference was found between the baseline value vs. T24 and the baseline vs. T48 for sCr, UAC, UPC, FE of sodium, chloride and calcium, and uNGAL. A significant increase in FEK (p = 0.04) was noticed between the baseline and T48. In this study sample of hypoalbuminemic dogs, HES 130/0.4 at the dose and rate of infusion applied did not cause any significant changes in the investigated biomarkers of kidney injury.

Highlights

  • Synthetic colloids are a kind of fluid characterized by a large molecular size and are administered for intravascular volume expansion

  • The highest hydroxyethyl starch (HES) concentrations have been identified in the proximal renal tubular cells; biomarkers of proximal tubular damage and dysfunction would be ideal to assess the occurrence of HES-induced acute kidney injury (AKI) [4]

  • The study population was composed of two intact males, six intact females and two spayed females, with a median age of 7 years

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Summary

Introduction

Synthetic colloids are a kind of fluid characterized by a large molecular size and are administered for intravascular volume expansion. [1] The theoretical benefits of HESs include prolonged intravascular effects, smaller volume requirements, and the reduced risk of tissue edema development compared with crystalloids [1]. Several large-scale human trials have linked HES use with dose-dependent side effects including coagulopathy, nephrotoxicity up to the development of acute kidney injury (AKI), and tissue storage [2,3,4,5,6,7,8]. There are several suggestions for the mechanisms of HES-induced AKI: a decrease in tubular flow, secondary to the activation of tubuloglomerular feedback, as well as colloid accumulation in the lysosomes of tubular cells that creates an oncotic gradient, leading to the accumulation of intracellular water, cytoplasmic swelling, lysosomal vacuolization, and disruption of cellular integrity [1,4]. The highest HES concentrations have been identified in the proximal renal tubular cells; biomarkers of proximal tubular damage and dysfunction would be ideal to assess the occurrence of HES-induced AKI [4]

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