Assessment of renal congestion in a rat model with congestive heart failure using superb microvascular imaging.

PURPOSE: Renal congestion is a therapeutic target in congestive heart failure. However, its detailed evaluation in a clinical setting is challenging. This study sought to assess renal congestion impairment using superb microvascular imaging (SMI), a simple and accessible method. METHODS: Dahl salt-sensitive rats, used as a model for congestive heart failure, underwent central venous pressure (CVP) measurements. Renal congestion was evaluated through measurements of renal medullary pressure (RMP) and assessment of renal perfusion using contrast-enhanced ultrasonography at both the early (control group) and heart failure phases (HF group). All rats were assessed with SMI. The region of interest (ROI) was set in interlobular vessels, interlobar vessels, and a combination of these areas. The area ratio was calculated from the color pixel count in the ROI divided by the total pixel count in the ROI. Intrarenal perfusion index (IRPI) was defined as (maximum area ratio-minimum area ratio) / maximum area ratio. RESULTS: There were no significant differences in renal function and left ventricular ejection fraction between the two groups. CVP, time-to-peak (TTP) in the medulla, and RMP were higher in the HF group than in the control group. In the HF group, IRPI, evaluated in the interlobular vessels, was significantly higher than in the control group. IRPI was positively correlated with TTP in the medulla (p = 0.028, R = 0.60) and RMP (p < 0.001, R = 0.84), indicating that IRPI reflected renal congestion. CONCLUSIONS: IRPI is a useful tool for assessing renal congestion in rats with congestive heart failure.

Sodium Glucose Co-Transporter 2 Inhibitors Improve Renal Congestion and Left Ventricular Fibrosis in Rats With Hypertensive Heart Failure.

BACKGROUND: Elevated central venous pressure (CVP) in heart failure causes renal congestion, which deteriorates prognosis. Sodium glucose co-transporter 2 inhibitor (SGLT2-i) improves kidney function and heart failure prognosis; however, it is unknown whether they affect renal congestion. This study investigated the effect of SGLT2-i on the kidney and left ventricle using model rats with hypertensive heart failure.Methods and Results: Eight rats were fed a 0.3% low-salt diet (n=7), and 24 rats were fed an 8% high-salt diet, and they were divided into 3 groups of untreated (n=6), SGLT2-i (canagliflozin; n=6), and loop diuretic (furosemide; n=5) groups after 11 weeks of age. At 18 weeks of age, CVP and renal intramedullary pressure (RMP) were monitored directly by catheterization. We performed contrast-enhanced ultrasonography to evaluate intrarenal perfusion. In all high-salt fed groups, systolic blood pressure was elevated (P=0.287). The left ventricular ejection fraction did not differ among high-salt groups. Although CVP decreased in both the furosemide (P=0.032) and the canagliflozin groups (P=0.030), RMP reduction (P=0.003) and preserved renal medulla perfusion were only observed in the canagliflozin group (P=0.001). Histological analysis showed less cast formation in the intrarenal tubule (P=0.032), left ventricle fibrosis (P<0.001), and myocyte thickness (P<0.001) in the canagliflozin group than in the control group. CONCLUSIONS: These results suggest that SGLT2-i causes renal decongestion and prevents left ventricular hypertrophy, fibrosis, and dysfunction.