A 52-year-old man with 6 years’ history of human immunodeficiency virus infection who was receiving highly active antiretroviral therapy presented with acute renal failure and nephrotic syndrome. Renal biopsy revealed features consistent with nephropathy associated with human immunodeficiency virus infection. Treatment consisted of intravenous methylprednisolone followed by oral prednisolone. The patient’s renal function improved, although proteinuria persisted. Human immunodeficiency virus–associated nephropathy is very rare in Asian populations and is more common among blacks. To the best of our knowledge, this is the first documented case of nephropathy associated with human immunodeficiency virus infection occurring in Hong Kong.

A 69-year-old woman with end-stage renal failure discontinued continuous ambulatory peritoneal dialysis and commenced temporary haemodialysis because of resistant peritonitis. Right internal jugular vein haemodialysis catheter placement was performed. The cuffed, tunnelled haemodialysis catheter was inserted using the modified Seldinger technique. When haemodialysis was initiated the following day, blood could not be aspirated from the catheter and the patient complained of central chest pain during the aspiration. Subsequent venography and computed tomography scan of the thorax showed that the catheter was placed extraluminally into the posterior mediastinum. The importance of a chest radiograph after placement of a central venous catheter is highlighted by this case report. Subtle deviations in catheter position from normal should alert the physician to the possibility of catheter misplacement and lead to further investigation.

Paracetamol has always been regarded as a useful and safe drug. The risk of toxicity with repeated supratherapeutic paracetamol is an underrecognised condition. We report on a 12-month-old boy who presented with hepatotoxicity, disseminated intravascular coagulation and persistent renal insufficiency 4 days after repeated ingestion of a supratherapeutic dosage of paracetamol. To the best of our knowledge, this is the first reported case of paediatric chronic paracetamol poisoning among the Chinese population. In addition, persistent renal insufficiency has not been a previously reported feature of chronic paracetamol poisoning. We propose that renal damage is the result of the synergistic effect of hypoperfusion and paracetamol overdose.

We report on two Hong Kong Chinese families with dentatorubral-pallidoluysian atrophy. Two children in one family presented with progressive myoclonic epilepsy syndrome, and two children in the other family presented with ataxochoreo-athetoid symptoms. Early-onset childhood dentatorubral-pallidoluysian atrophy involved mental retardation, whereas myoclonic epilepsy was the predominant complaint in later-onset childhood version of the disease. Aspiration pneumonia was common in the late stage of disease. Dentatorubral-pallidoluysian atrophy is an autosomal dominant condition attributed to CAG trinucleotide repeats in the dentatorubral-pallidoluysian atrophy gene. The four children in this series had 63 to 79 CAG repeats. The expanded allele was inherited from the father in both families. One father had 54 CAG repeats and was asymptomatic; the other had 66 repeats and had an unsteady gait. Because the radiological, electroencephalographic, and electrophysiological findings were non-specific, we suggest that DRPLA gene testing should be performed in any child presenting with a variable combination of myoclonic epilepsy, mental retardation or developmental regression, and ataxochoreo-athetosis.

We report the results of biochemical and genetic studies in a Chinese family with familial dysalbuminaemic hyperthyroxinaemia. Total thyroxine levels were 1.2 to 1.7 times the upper limit of the reference range and free thyroxine levels were 1.2 to 1.6 times the upper reference limit. Concentrations of thyroid-stimulating hormone (thyrotropin) and free tri-iodothyronine were normal in all family members tested. Overall, thyroid function tests showed high total thyroxine levels in five males and two females over two generations in the family. The diagnosis of familial dysalbuminaemic hyperthyroxinaemia was confirmed by the detection of a guanine to adenine missense mutation in the second nucleotide of codon 218 of the gene encoding human serum albumin, showing that the mutation in this family is the same as that previously found in Caucasian populations.