Highly viscous ascites prompting reconsideration of cardiorenal syndrome in a patient with advanced CKD after TAVI.

Diagnostic paracentesis revealed highly viscous, protein-rich ascitic fluid with a low serum-ascites albumin gradient and a markedly elevated carcinoembryonic antigen level, raising suspicion of a mucinous peritoneal process.

• Ascites was initially attributed to cardiorenal syndrome or liver disease before paracentesis was performed.
• The ascitic fluid was characterized as highly viscous and protein-rich.
• The serum-ascites albumin gradient was low, inconsistent with a cardiac or hepatic etiology.
• Carcinoembryonic antigen level in the ascitic fluid was markedly elevated.
• Cytology was negative despite the suspicion of a mucinous peritoneal process.

Non-contrast MRI demonstrated multiple loculated cystic collections and fluid-fluid levels, consistent with a mucinous peritoneal process suggestive of pseudomyxoma peritonei.

• Imaging findings showed multiple loculated cystic collections in the peritoneal cavity.
• Fluid-fluid levels were identified on non-contrast magnetic resonance imaging.
• These findings, in conjunction with ascitic fluid characteristics, raised suspicion of pseudomyxoma peritonei.
• The diagnosis was suspected despite negative cytology.

Right heart catheterization showed preserved cardiac output, while echocardiography suggested right-sided pressure overload and systemic venous congestion after TAVI.

• The patient had developed refractory pleural effusion, ascites, and peripheral edema after transcatheter aortic valve implantation (TAVI).
• Right heart catheterization demonstrated preserved cardiac output.
• Echocardiography findings suggested right-sided pressure overload and systemic venous congestion.
• These hemodynamic findings initially supported cardiorenal syndrome as the primary diagnosis.

Intensified diuretic therapy led to partial body weight reduction but was accompanied by worsening renal function, and adequate volume control remained difficult.

• The patient had type 2 diabetes mellitus, stage 4 CKD, hypertension, and ischemic heart disease.
• Diuretic therapy achieved only partial body weight reduction.
• Worsening renal function accompanied the intensified diuretic therapy.
• Adequate volume control could not be achieved with standard cardiorenal management.

Recurrent deterioration of renal function was temporally associated with reaccumulation of massive ascites, while right-sided venous congestion may have acted as an aggravating hemodynamic factor.

• Episodes of renal function worsening corresponded temporally to reaccumulation of ascites.
• Right-sided venous congestion was identified as a potential aggravating hemodynamic factor.
• The combination of massive ascitic reaccumulation and venous congestion contributed to the complexity of volume management.
• The case illustrates how a non-cardiorenal etiology of ascites can confound management of CKD patients with cardiovascular disease.