Assessment of renal perfusion impairment in a rat model of acute renal congestion using contrast-enhanced ultrasonography.

Renal congestion is caused by elevated central venous pressure (CVP), and decreases glomerular filtration in patients with congestive heart failure. Since real-time contrast-enhanced ultrasonography (CEUS) using microbubble-based contrast agents can visualize the perfused microvascular bed, we sought to evaluate the impairment of renal perfusion during acute renal congestion with CEUS. In Wister rats, CEUS of kidney was performed with the direct monitoring of CVP and intra-renal pressure (IRP). When CVP was elevated to 10 and 15 mmHg after the bolus injection of normal saline via the femoral vein, peak intensity (PI, dB) and time to PI (TTP) in the renal cortex and medulla were compared with control rats. There was a strong correlation between IRP and CVP (r = 0.95, p < 0.0001). In the congestion model, more time was required for enhancement of the parenchyma, especially in the medulla compared to control; TTP of the medulla and cortex at 15 mmHg CVP (CVP15) was significantly prolonged compared with controls (medulla, 4351 ± 98 vs. 1415 ± 267 ms, p = 0.003; cortex, 3219 ± 106 vs. 1335 ± 264 ms, p = 0.005). In addition, medullary PI at CVP15 decreased, but not significantly, compared to those of controls and at 10 mmHg CVP (20.1 ± 0.9, 22.8 ± 1.6, 21.6 ± 0.2 dB). In contrast, cortical PIs at CVP15 were significantly lower than that of control (24.6 ± 1.0 vs. 31.4 ± 1.0 dB, p = 0.007). CEUS revealed that impaired renal parenchymal flow in an acute congestion model is accompanied with increased renal interstitial pressure.

Demonstration of Improved Renal Congestion After Heart Failure Treatment on Renal Perfusion Imaging With Contrast-Enhanced Ultrasonography.

Background: Renal congestion is a critical pathophysiological component of congestive heart failure (CHF). Methods and Results: To quantify renal congestion, contrast-enhanced ultrasonography (CEUS) was performed at baseline and after treatment in 11 CHF patients and 9 normal subjects. Based on the time-contrast intensity curve, time to peak intensity (TTP), which reflects the perfusion rate of renal parenchyma, and relative contrast intensity (RCI), an index reflecting renal blood volume, were measured. In CHF patients, TTP at baseline was significantly prolonged compared with that in controls (cortex, 10.8±3.5 vs. 4.6±1.2 s, P<0.0001; medulla, 10.6±3.0 vs. 5.1±1.6 s, P<0.0001), and RCI was lower than that in controls (cortex, -16.5±5.2 vs. -8.8±1.5 dB, P<0.0001; medulla, -22.8±5.2 vs. -14.8±2.4 dB, P<0.0001). After CHF treatment, RCI was significantly increased (cortex, -16.5±5.2 to -11.8±4.5 dB, P=0.035; medulla, -22.8±5.2 to -18.7±3.7 dB, P=0.045). TTP in the cortex decreased after treatment (10.8±3.5 to 7.6±3.1 s, P=0.032), but it was unchanged in the medulla (10.6±3.0 to 8.3±3.2 s, P=0.098). Conclusions: Renal congestion can be observed using CEUS in CHF patients.

Left ventricular noncompaction with intractable heart failure responsive to empagliflozin.

Despite several reports on the mechanism of the effect of empagliflozin, which has the potential for improved prognosis in heart failure, it is still not fully understood. We experienced a case of left ventricular noncompaction that caused fluid retention in a patient who showed resistance to existing diuretics. By using empagliflozin, we successfully treated this case of acute heart failure and observed stabilized symptoms with no renal dysfunction and deterioration of patient condition. Although the potential for improved prognosis with this drug in a high-risk group for cardiovascular events has been reported, based on EMPA-REG OUTCOME trial results, there are few reports on its effect of treatment and mechanism in treating acute heart failure. The effect of this drug in treating heart failure from the acute phase to the chronic phase can be expected. .