Renal Effect of Triolein in a Rat Model of Fat Embolism Syndrome

Abstract

Fat embolism syndrome (FES) is a lung process following bone fracture, surgery, and liposuction, expressed by inflammation, vasculitis, and fibrosis. A rat model of FES is induced by IV injection of triolein. Besides the lung damage at 48‐96 hours post injection, fat emboli were present in renal glomeruli, with vasoconstriction, glomerular and tubular hemorrhages, and increased renin secretion. Captopril and Losartan protected both organs, suggesting a role of the renin‐angiotensin system in injury pathogenesis. The pulmonary damage worsened at six weeks post injection. A second mild injury (i.p. injection of lipopolysaccharides (LPS)) exacerbated the condition. Renin was present in the lungs at this time. 
 Reported is the renal damage following triolein at six weeks. Triolein (0.2mL IV) was given to 18 rats and saline to 18 controls. Six weeks post‐injection, each group received i.p. LPS (3mg/kg) n = 9 or saline n = 9. Two days later at necropsy, kidneys were stained for H&E and renin and damaged scored.
 Triolein caused severe glomerular damage with basal membrane thickening, crescents, hemorrhages, but no fat globules. Cortical arterial vasculitis with reduced lumen patency was seen in 59% of the triolein‐treated groups vs. 36% for saline (P = 0.003). Renin staining was seen in 32% of glomeruli of rats receiving saline, 53% of LPS‐treated, 54% of triolein‐treated, and 76% of those treated with triolein and LPS. 
 Therefore, triolein not only damages the lungs, but also the kidneys up to six weeks post‐embolization. Only lungs had fat droplets. The increased glomerular secretion of renin underlines its role in the FES pathogenesis; clinically, the renal damage should also be taken in consideration.