Introduction: Ascites indicates a pathological accumulation of fluid in the abdominal cavity and it is the most common complication of liver cirrhosis. The appearance of fluid in the abdominal cavity can be established by physical examination, ultrasound and CT of the abdomen, followed by paracentesis and biochemical and microbiological analysis of ascites fluid. The appearance of ascites in the form of exudate is due to an inflammatory process in the peritoneum (peritonitis), or due to increased transudation with increased pressure (in hypoproteinemia, Nephrotic syndrome). Ascites occurs when the amount of lymph formed in the abdominal cavity transcend the resorptive capacity of the lymphatic system. Nephrogenic or Dialysis ascites is a clinical diagnosis defined as refractory ascites in patients with end-stage renal disease, and presents a complex diagnostic problem with poorly understood pathophysiology and etiology. Morbidity and potential mortality of this complex problem are significant. Diagnosis of nephrogenic ascites should be determined by excluding other causes. Patients often have moderate to massive ascites, associated with cachexia. Only continuous ambulatory peritoneal dialysis and kidney transplantation imposed as successful in controlling the mechanisms of ascites formation. Aim of the study: Evaluation of three cases of patients on hemodialysis with other signs of dialysis ascites. Cases report: We presents two men and one woman, average age 50.6 years and the length of dialysis 7.3 years, who are on chronic hemodialysis program three times a week and with verified ascites. Results: The study included three patients, two men (66.6%) and one female (33.4%) who are on chronic hemodialysis therapy at the Department of Hemodialysis in Clinical Center University of Sarajevo and whom has been clinically verified ascites. All patients had chronic glomerulonephritis of unknown etiology as a primary renal disease, and two patients had congestive cardiac failure comorbidity. Two patients developed signs of umbilical hernias. One patient had hepatitis C infection and clinically verified compensated liver cirrhosis. None of the patients had signs of peripheral edema. All patients were subjected to paracentesis of ascites on several occasions, where ascites fluid was analyzed biochemically and microbiologically in order to found the primary cause of ascites. Also, patients had intensified hemodialysis therapy, with albumin and plasma compensation, together with reduced intake of fluid and salt, while one patient did not adhered to recommendations. One of the three patients involved in the study, but 26 months has no clinical signs of ascites. Conclusion: 5% of dialysis patients has dialysis ascites unknown etiology, which is shown in our case.