Objectives-Hepatic venous pressure gradient (HVPG) is considered the standard in quantifying portal hypertension, but can be unreliable in dialysis patients. A noninvasive ultrasound technique, subharmonic-aided pressure estimation (SHAPE), may be a valuable surrogate of these pressure estimates. This study compared SHAPE and HVPG with pathology findings for fibrosis in dialysis patients.Methods-This was a subgroup study from an IRB-approved trial that included 20 patients on dialysis undergoing SHAPE examinations of portal and hepatic veins using a modified Logiq 9 scanner (GE, Waukesha, WI), during infusion of Sonazoid (GE Healthcare, Oslo, Norway). SHAPE was compared to HVPG and pathology findings using the Ludwig-Batts scoring system for fibrosis. Logistic regression, ROC analysis, and t-tests were used to compare HVPG and SHAPE with pathological findings of fibrosis.Results-Of 20 cases, 5 had HVPG values corresponding to subclinical and clinical portal hypertension (≥6 and ≥10 mmHg, respectively) while 15 had normal HVPG values (≤5 mmHg). SHAPE and HVPG correlated moderately (r = 0.45; P = .047). SHAPE showed a trend toward correlating with fibrosis (r = 0.42; P = .068), while HVPG did not (r = 0.18; P = .45). SHAPE could differentiate between mild (stage 0-1) and moderate to severe (stage 2-4) fibrosis (À10.4 AE 4.9 dB versus À5.4 AE 3.2 dB; P = .035), HVPG could not (3.0 AE 0.6 mmHg versus 4.8 AE 0.7 mmHg; P = .30). ROC curves showed a diagnostic accuracy for SHAPE of 80%, while HVPG reached 76%.Conclusion-Liver fibrosis staging in dialysis patients evaluated for portal hypertension appears to be more accurately predicted by SHAPE than by HVPG; albeit in a small sample size.Key Words-chronic kidney disease; contrast-enhanced ultrasound; dialysis; portal hypertension; subharmonic imaging; subharmonic pressure estimation L iver cirrhosis is the final common pathological pathway of liver damage arising from a wide variety of chronic liver diseases. [1][2][3][4][5][6][7][8][9] Histologically, it is characterized by diffuse nodular regeneration and dense fibrotic septa evolving to parenchymal extinction and collapse of liver structures. [1][2][3][4][5][6][7][8][9] Distortion of hepatic vascular architecture and increased resistance to portal blood flow leads to portal hypertension and hepatic synthetic dysfunction. [1][2][3][4][6][7][8][9][10]