No abstract

No abstract

The relative roles of hepatic lipase and lipoprotein lipase in the pathogenesis of uremic lipid abnormalities were studied in 92 hemodialysis patients. Fasting serum cholesterol, triglyceride, and HDL-cholesterol concentrations were measured. Plasma lipoprotein electrophoretic patterns were determined in all patients. Hepatic lipase and lipoprotein lipase activities were selectively measured in post-heparin plasma in 59 patients. Hemodialysis patients had higher serum triglyceride and lower HDL-cholesterol concentrations than did their age and sex-matched control subjects. Both hepatic and lipoprotein lipase activities were reduced in hemodialysis patients. An inverse relation between lipoprotein lipase activities and serum triglyceride concentrations emerged. Lipoprotein lipase activities correlated with in vivo post-heparin fractional clearance rates of Intralipid. A positive correlation between lipoprotein lipase activities and HDL-cholesterol concentrations probably reflected impaired catabolism of triglyceride-rich lipoproteins being responsible for the low HDL-cholesterol concentrations. Hemodialysis patients (41.3%) had an abnormal lipoprotein (the 'mid-band'). While hepatic lipase activities did not correlate with any parameters of lipid metabolism, patients with 'low' hepatic lipase activities had a significantly higher prevalence of 'mid-bands' than did those with 'normal' activities. No evidence was developed to prove that the 'mid-band' lipoproteins were remnant particles.

The characteristics of 5 patients who developed tuberculous peritonitis while receiving long-term peritoneal dialysis (PD) are presented. There were 2 males and 3 females. 3 patients were on intermittent and 2 were on continuous ambulatory peritoneal dialysis when tuberculous peritonitis was first diagnosed. None of the patients had recently received immunosuppression therapy or were diabetics. The clinical presentations were similar to other forms of peritonitis complicating PD except for a more insidious onset. As extraperitoneal involvement and peritoneal lymphocytosis were rarely present, the diagnosis was mainly dependent on the direct demonstration of Mycobacterium tuberculosis with smear (1 patient) and culture (4 patients). In 1 patient with a pleuroperitoneal communication, the diagnosis was made by pleural biopsy and a positive response to antituberculous therapy. All patients responded to treatment with a combination of three antituberculous drugs which included streptomycin, isoniazid, rifampicin and pyrazinamide. Two patients were transferred to hemodialysis. In 3 patients, peritoneal dialysis was continued. Peritoneal clearance and ultrafiltration capacity were unchanged for up to 16 months after treatment in 2 patients who continued peritoneal dialysis but was reduced by 30 and 50%, respectively, in the remaining patient. Only 1 patient died, but her death was not directly related to tuberculous peritonitis. It was concluded that with a high index of suspicion and early institution of treatment, tuberculous peritonitis complicating PD can be successfully treated with low mortality and without compromising the dialysis capacity of the peritoneal membrane.