COEXISTENCE OF NON‐COMMUNICATED CHYLOTHORAX AND CHYLOUS ASCITES IN NEPHROTIC SYNDROME

A 38-year-old man presented to our hospital with progressive oedema of 2 months duration. The patient had no history of surgery, cirrhosis, heart failure or underlying malignancy. Physically, auscultation of chest disclosed diminished breath sounds over the left thorax and the abdomen showed mild distention. Bilateral extremities showed grade III pitting oedema. No lymphoadenopathy was present. Laboratory findings showed impaired renal functions, low levels of serum albumin (1.6 g/dL) and hyperlipidaemia (serum triglyceride, 229 mg/dL; total cholesterol, 304 mg/dL) were identified. Daily urinary protein loss reached 9.94 g and a diagnosis of nephrotic syndrome was made. Simultaneously, a standing chest radiograph revealed predominant opacification of the left hemithorax and abdominal ultrasonography demonstrated moderate ascites. Diagnostic thoracentesis and aparacentesis were performed, respectively, and both removed 1000 mL of milky-coloured transudative fluids. The cytological findings were negative, as were bacterial, mycobacterial and fungal cultures. In addition, the patient underwent nuclear Technetium-99m macroaggregated albumin injection into the peritoneal cavity and, after 24 h, the scintigraphy showed no pleural radioactivity, which excluded a shunt existing between the peritoneal and pleural cavities. Minimal-change nephropathy was confirmed by renal biopsy. A series of coagulation tests revealed low levels of anti-thrombin III (58.3%) and increased levels of D-dimer (1560 ng/mL), fibrin degradation product (>40 µg/mL) and fibrinogen (801.1 mg/dL). The patient started to receive human albumin infusion coupled with diuretics for nephrotic syndrome and prednisolone was prescribed for minimal change disease. Heparin overlapping with warfarin was administered for high risk of thrombosis. After consecutive anticoagulant treatment for 2 weeks, there were no more recurrent chylothorax or ascites of this patient. Recently, the incidence of chylothorax and chylous ascites has increased because of more aggressive cardiothoracic and abdominal surgery and because of the longer survival of patients with cancer.1 Nevertheless, in a small population, the chylothorax and chylous ascites may be transudative in nature. The aetiologies are fewer and include nephrotic syndrome, cirrhosis and congestive heart failure. Collectively, there have been six cases of coexisting chylothorax and chylous ascites associated with nephrotic syndrome.2 In contrast to our case, most of them had right-side chylothorax with a transdiaphragmatic shunt. It is well known that the thoracic duct anatomically crosses to the left at the level of the fifth or sixth thoracic vertebra, and it terminates at the junction of the left subclavian and internal jugular veins. In absence of a transdiaphragmatic shunt, the occurrence of left-sided chylothorax could be reasoned when the thoracic duct was obstructed above the level of the fifth thoracic vertebra. In addition, the corresponding level of thoracic venous thrombosis due to renal loss of anti-thrombin III and initiation of coagulant cascade associated with nephrotic syndrome potentially leads to the chylothorax without an abdominal source.3 In conclusion, chylous ascites and chylothorax may be present concurrently in a nephrotic patient without a transdiaphragmatic shunt. Thoracic venous thrombosis at a higher level should be emphasized as one possible cause if the patient has evident hypercoagulability and predominant left-sided chylothorax.

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