Transforming growth factor-β (TGF-β) is the key player in tissue fibrosis. However, antifibrotic therapy targeting this multifunctional protein may interfere with other physiological processes to cause side effects. Thus, precise therapeutic targets need to be identified by further understanding the underlying mechanisms of TGF-β1 signalling during fibrogenesis. Equilibrium of Smad signalling is crucial for TGF-β-mediated renal fibrosis, where Smad3 is pathogenic but Smad2 and Smad7 are protective. The activation of TGF-β1/Smad signalling triggers extracellular matrix deposition, and local myofibroblast generation and activation. Mechanistic studies have shown that TGF-β/Smad3 transits the microRNA profile from antifibrotic to profibrotic and therefore promotes renal fibrosis via regulating non-coding RNAs at transcriptional levels. More importantly, disease-specific Smad3-dependent long non-coding RNAs have been recently uncovered from mouse kidney disease models and may represent novel precision therapeutic targets for chronic kidney disease. In this review, mechanisms of TGF-β-driven renal fibrosis via non-coding RNAs and their translational capacities will be discussed in detail.

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The usage of three x 2 liter daily exchanges is adopted as the standard CAPD regime in Hong Kong over the last 10 years due to budgetary constraint. This dialysis prescription is considered suboptimal in Western standard. However, the necessity of maintaining Kt/V > 1.7 for CAPD dialysis adequacy is not unanimously agreed. We performed a cross-sectional study of 117 patients on CAPD. Seventy-eight percent of our patients had 3 x 2 liter daily exchange while the rest had 4 daily exchanges. Fifteen percent of patients were diabetic. Patients with Kt/V < 1.7 were similar to those with Kt/V > 1.7 in age, duration of CAPD, BUN, plasma creatinine, albumin, peritonitis rate, and incidence of hypertension. Patients with Kt/V > or = 1.7 had higher hemoglobin, higher nPCR, more residual renal function; and more of them received 4 daily exchanges. Their peritoneal permeability did not differ. Their employment and rehabilitation status was also similar. Our 5-year survival was 79% despite a lower Kt/V. Notably, the protein catabolic rate of our patients was higher than that in Western patients. This is likely due to dietary difference. Our study suggests small-volume dialysis may be acceptable in Asian population with smaller body size given the financial constraint.

Interference of creatinine measurement in CAPD fluid is dependent on glucose and creatinine concentrations, and each centre should derive specific correction formulae for its analytical system.

There is a lack of information on the toxicodynamics and toxicokinetics of bromadiolone in humans; further studies are needed before the plasma bromadiolone level can serve as one of the logical and safe therapeutic endpoints for vitamin K1 therapy.

A retrospective study of 83 cases of tuberculous pleural effusion showed that the mean age of the patients was 44 years and 10 patients (12%) were over the age of 70. Pleural fluid was smear positive for tubercle bacilli in none but culture positive in 23% of the cases. Pleural biopsy was a more sensitive method of diagnosis with granulomatous inflammation seen in 97% of cases. Five patients developed significant pleural thickening during chemotherapy requiring decortication. Twenty-two patients with tuberculous effusion diagnosed and treated over 2 years previously were traced for reassessment. None of them had significant pleural thickening and lung function tests did not show significant impairment compared to matched control subjects

Abstract-It has been reported that in China, patients with heterozygous familial hypercholesterolemia (FH) may go unrecognized because they do not have xanthomata or premature coronary heart disease and their LDL cholesterol levels are lower than those in their Western counterparts. However, in the Chinese patients in Hong Kong, heterozygous FH appears to manifest in a way similar to that seen in Western countries or Japan. We studied sequence variations in the promoter and coding regions of the 18 exons of the LDL receptor gene in 30 Chinese FH patients. Eighteen mutations were identified in 21 patients scattered in the promoter and 10 exons. Eleven of them were first found in this study. We also found 6 polymorphisms with allelic frequencies different from those in whites but similar to the Japanese, indicating some isolation between white and Oriental populations. A total of 29 mutations in the LDL receptor gene are now known in the Chinese. There is no definite common mutation due to a founder effect. Meanwhile, there were no detectable LDL receptor gene mutations in 9 clinically diagnosed FH patients in whom the R3500Q mutation in apolipoprotein B had also been excluded.