Abstract

Objective:To evaluate the clinical effects of continuous intravenous infusion with high-dose furosemide on early acute kidney injury (AKI) complicated with acute lung edema.Methods:Ninety patients who had been treated by furosemide at routine dose for 12 hour but with unsatisfactory outcomes were selected and subjected to continuous intravenous infusion with high-dose furosemide. The dose was adjusted according to hourly urine output. Serum levels of urea nitrogen, creatinine and potassium, pH, oxygenation index and mechanical ventilation time before and 6, 12, 24, 48 and 72 hour after treatment were compared.Results:The urine outputs before and 6, 12, 24, 48 and 72 hour after treatment were (10.71 ± 1.81), (164.52 ± 21.42), (189.71 ± 29.61), (181.33 ± 23.52), (176.82 ± 24.80) and (164.52 ± 18.91) ml/h respectively. Compared with data before treatment, the serum levels of urea nitrogen, creatinine and potassium significantly decreased while pH and oxygenation index significantly increased after six hour of treatment (P<0.05). After treatment, the kidney functions of 80 patients (88.9%) were completely recovered, without obvious adverse reactions.Conclusion:For patients with early AKI complicated with acute pulmonary edema who cannot be cured by diuretic agent at routine dose, high-dose furosemide increases urine output and improves success rate.

Highlights

  • Acute kidney injury (AKI) is a common clinical syndrome endangering human health and leading to inpatient death

  • Ninety patients with early AKI complicated with acute pulmonary edema, who had been treated by furosemide at routine dose for 12 hour but with unsatisfactory outcomes in our hospital from June 2012 to June 2016, were selected

  • Inclusion criteria: 1. In accordance with the diagnostic criteria of RIFLE grading for early AKI:[6] Obvious renal function decline within seven day, urine output of

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Summary

Introduction

Acute kidney injury (AKI) is a common clinical syndrome endangering human health and leading to inpatient death. Until 2013, about 13 million people suffered from AKI each year globally, of whom 1.7 million people died.[1] AKI is pathologically typified by proximal tubular injury, edema, necrosis and formation as well as epithelial cell apoptosis, accompanied by severe disorders of the internal environment due to rapidly damaged kidney function. Its clinical manifestations mainly include oliguria or anuria, azotemia, hyperkalemia and metabolic acidosis, seriously endangering human life in case of ineffective rescue.[2] Owing to the lack of effective therapies, over 50% of AKI patients cannot recover,[3] and progress to chronic kidney disease instead. End-stage renal disease occurs, which heavily burdens their families and the society.[4]

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