The effect of low molecular weight heparin (LMWH) on serum lipid profile in hemodialysis remains controversial and its effect on bone metabolism has not been studied. A crossover study was conducted in 40 patients on stable hemodialysis using unfractionated heparin (UFH) for more than 24 months. These patients were then treated with a LMWH (nadroparin-Ca) for 8 months during hemodialysis and subsequently switched back to UFH for 12 months. Serum lipid profile, biochemical markers for bone metabolism, and bone densitometry (BMD) were monitored at four-month intervals while all medications remained unchanged. Cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), lipoprotein(a) (Lp(a)), apolipoprotein B (Apo B) were raised in 35%, 29%, 12%, 24% and 24% of patients respectively. High-density lipoprotein-cholesterol (HDL-C) and apolipoprotein A1 (Apo A-1) were reduced in 47% and 9% of patients. Bone-specific alkaline phosphatase (BALP) and intact osteocalcin (OSC), both reflecting osteoblastic activity, were raised in 65% and 94% of patients. Tartrate-resistant acid phosphatase (TRACP) reflecting osteoclastic activity and parathyroid hormone (PTH) were elevated in 35% and 88% of patients. Following LMWH treatment, TC, Tg, Lp(a) and Apo B were reduced by 7%, 30%, 21% and 10% respectively (p<0.05 or <0.01) while Apo A-1 were raised by 7% (p<0.01). Simultaneously, TRACP was reduced by 13% (p<0.05). These biochemical changes were detected soon after 4 months of LMWH administration. Although BMD values in our patients were lower than those of age-matched normal subjects, significant changes were not observed with LMWH treatment. After switching back to UFH for hemodialysis, these biochemical indices reverted to previous values during UFH treatment with a significant higher level in TC and Apo B while serum Apo A-1 remained elevated. Our study suggests LMWH may partially alleviate hyperlipidemia and, perhaps, osteoporosis associated with UFH administration in patients on maintenance hemodialysis.

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Nocardia peritonitis is an uncommon infection complicating peritoneal dialysis (PD). Because of the rarity of data, there is no consensus on the optimal choice of antibiotics and duration of treatment. We report here a case of Nocardia nova peritonitis in a Chinese continuous ambulatory peritonitis dialysis (CAPD) patient.A 68-year-old Chinese CAPD patient was hospitalized because of a 2-day history of abdominal pain and turbid PD effluent. She suffered from end-stage renal disease of unknown etiology. Self-CAPD was commenced March 1999. She enjoyed reasonably good health with no prior episodes of peritonitis. Six months before this admission, she was hospitalized for pseudomonas pneumonia. Computerized tomogram (CT) scan of the thorax showed a 1 ∞2-cm subpleural mass with contrast enhancement. There were fibrotic changes over both right upper lobes and middle lobe. She was treated with oral ciprofloxacin and intravenous gentamicin. Subsequent CT-guided aspiration of the pleural mass was aborted because the mass had disappeared on followup thoraxCT .Concerning the current admission, a preliminary diagnosis of CAPD-related peritonitis was established due to suggestive signs and symptoms and a PD effluent polymorph-predominating cell count of > 250/mm 3 . Intraperitoneal cefazolin and netilmycin were given immediately. No response was observed after 48 hours and intraperitoneal ceftazidime was substituted for netilmycin.Four days after admission, culture of the PD fluid specimen showed scanty growth of gram-positive rods suggestive of Nocardia species. The antibiotic regimen was then changed to intraperitoneal amikacin and imipenem. There was minimal abdominal pain but the PD effluent was persistently cloudy. The patient remained afebrile.No clinical improvement was seen 5da ys after the change in antibiotics. We stopped imipenem and started intraperitoneal trimethoprim-sulfamethoxazole. Three days later, we received the formal bacteriological report: Nocardia nova was identified and it was resistant to trimethoprim-sulfamethoxazole and sensitive to imipenem, amikacin, and ceftriaxone. However, the cell

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