Evaluation of urinary neutrophil gelatinase‐associated lipocalin to detect renal tubular damage in dogs with stable myxomatous mitral valve disease

cardiorenal syndrome Settore MVET-04/B - Clinica medica veterinaria renal biomarker Veterinary medicine Heart Valve Diseases 610 heart failure 04 agricultural and veterinary sciences Acute Kidney Injury 630 tubular damage 3. Good health 0403 veterinary science Dogs acute kidney injury Lipocalin-2 SF600-1100 Animals Mitral Valve SMALL ANIMAL Dog Diseases acute kidney injury; cardiorenal syndrome; heart failure; renal biomarker; tubular damage
DOI: 10.1111/jvim.16503 Publication Date: 2022-10-05T07:40:56Z
ABSTRACT
AbstractBackgroundDogs with myxomatous mitral valve disease (MMVD) can experience progressive renal tubular damage and dysfunction. The prevalence of renal tubular damage is not known in dogs with stable MMVD.ObjectiveTo evaluate renal tubular damage in dogs with stable MMVD by evaluation of urinary neutrophil gelatinase‐associated lipocalin (NGAL).AnimalsNinety‐eight MMVD dogs grouped according to the American College of Veterinary Internal Medicine (ACVIM) staging (group B1, n = 23; group B2, n = 27; group C + D, n = 48) and 46 healthy dogs.MethodsMulticenter prospective observational study. Serum and urine chemistry including NGAL reported as uNGAL concentration (uNGAL) and normalized with urinary creatinine (uNGALC) were compared between MMVD dogs and healthy controls, and among different MMVD ACVIM stages.ResultsThe MMVD dogs had significantly higher uNGAL and uNGALC (1204 pg/mL; range, 30‐39 732 and 1816 pg/mg; range, 22‐127 693, respectively) compared to healthy dogs (584 pg/mL; range, 56‐4072 and 231 pg/mg; range, 15‐2407, respectively; P = .002 and P < .0001, respectively). Both uNGAL and uNGALC increased with the increasing ACVIM stage (P = .001 and P < .001, respectively).Conclusions and Clinical ImportanceRenal tubular damage is present in dogs with stable MMVD, as measured by increased uNGAL. This tubular damage is subclinical, occurs in all stages of MMVD even in the absence of azotemia, and increases with the severity of MMVD. Reno‐protective approaches to manage MMVD dogs should be explored to slow the progression of renal tubular damage in these patients.
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