The cirrhotic patients with ascites present unique challenge to the renal caregiver. Hydrothorax in a cirrhotic patient treated with PD poses a diagnostic dilemma. Proposed mechanisms for the development of a pleuroperitoneal communication include congenital diaphragmatic defects, acquired weakening of diaphragmatic fibers caused by high intra-abdominal pressures during peritoneal dialysis, and impairments in lymphatic drainage. Pleural fluid analysis and diagnostic imaging assist in differentiation from other causes of pleural effusion. We report a case of hydrothorax in a compensated cirrhotic patient after recent introduction to peritoneal dialysis.

Bartter syndrome is a renal tubular defect in electrolyte transport characterized by hypokalemia, metabolic alkalosis, hyperreninemia, hyperaldosteronism, normal blood pressure, and other clinical symptoms. As a clinical and genetical heterogeneous disorder, this syndrome can be classified into two clinical variants, antenatal Bartter syndrome and classic Bartter syndrome according to the onset age. Nephrocalcinosis is common in antenatal Bartter syndrome, but is rare in classic Bartter syndrome. It can also be classified into five genetic subtypes by the underlying mutant gene, all of which are expressed in the tubular epithelial cells of the thick ascending limb of the loop of Henle. Patients with Bartter syndrome type 1, 2 and 4 present at a younger age than classic Bartter syndrome type 3. We have experienced a case of Bartter syndrome with nephrocalcinosis in a 42-year-old woman diagnosed by biochemical and radiologic studies. We had successful response with potassium chloride and spironolactone.

Peritonitis is a common and potentially serious infection in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). The most common organisms usually associated with CAPD peritonitis are Staphylococcus aureus and Staphylococcus epidermidis. Rarely, aerobic gram negative bacilli have been the causative agents of CAPD peritonitis. The treatment of CAPD peritonitis requires removal of the peritoneal catheter and treatment with parenteral antibiotics active against the causative pathogen. While hospitalized for CAPD peritonitis, a 55-year-old man on CAPD had nosocomial peritonitis secondary to infection by ESBL–producing E. coli, that was sensitive to imipenem and meropenem. He was treated successfully with a 4-week course of intraperitoneal meropenem therapy without subsequent relapse, loss of peritoneal catheter, ultrafiltration failure, or dialysis inadequacy.