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Articles by F. M. M Lai
Total Records ( 3 ) for F. M. M Lai
  C. C Szeto , B. C. H Kwan , K. B Lai , F. M. M Lai , K. M Chow , G Wang , C. C. W Luk and P. K. T. Li
 

Background and objectives: The outcome of renal transplantation after an episode of acute rejection is difficult to predict, even with an allograft biopsy. We examined whether urinary expression of specific biomarker mRNA could be used as a noninvasive prognostic marker in kidney transplant recipients.

Design, setting, participants, & measurements: We studied 63 kidney transplant recipients who require graft biopsy because of progressive worsening of kidney function. The mRNA of neutrophil gelatinase-associated lipocalin, kidney injury molecule-1 (KIM-1), IL-18, surfactant protein-C, and S100 calcium-binding proteins A8 and A9 in urinary sediment were quantified.

Results: Urinary expressions of neutrophil gelatinase-associated lipocalin, KIM-1, and IL-18, but not other target genes, were significantly different between histologic groups (P < 0.0001 for all). After followed for an average of 39.7 ± 21.1 months, the rate of renal function decline significantly correlated with urinary KIM-1 expression (r = –0.434, P = 0.0004) but not other target genes. At 48 months, the graft survival rate for the high and low KIM-1 groups were 46.2 and 78.6%, respectively. After adjusting for confounding variables, each log of higher urinary KIM-1 expression conferred an ~2.9-fold higher risk of developing graft failure (95% confidence interval, 1.3- to 6.2-fold; P = 0.006). The result remained similar when only patients with no acute cellular rejection were analyzed.

Conclusions: In kidney allograft recipients, urinary KIM-1 expression provides prognostic information in relation to the rate of renal function decline, irrespective of the kidney pathology.

  J Guan , H. L Zhao , L Baum , Y Sui , L He , H Wong , F. M. M Lai , P. C. Y Tong and J. C. N. Chan
 

Background. Diabetic nephropathy represents a heterogeneous group of renal pathologies that may be associated with genetic susceptibility. There have been clinical reports on the risk association of diabetic nephropathy with an apolipoprotein E (ApoE) exon 4 polymorphism although its correlations with renal histopathological changes have not been explored.

Methods. A total of 213 adult autopsies with type 2 diabetes and 111 non-diabetic control cases were analysed. Genomic DNA samples were obtained from spleen tissues. The ApoE genotype was determined by PCR-LDR analysis. Histopathological examination of kidney sections was performed in a subset of 51 diabetic and 111 control cases. ApoE protein expression in diabetic carriers with similar clinical status was examined by immunohistochemical staining.

Results. In type 2 diabetes, 2 carriers (P = 0.04; odds ratio = 5.42; 95% CI: 1.10–26.8) and 3/4 (P = 0.04; odds ratio = 22.5; 95% CI: 1.11–454.90) genotype carriers were more likely to have glomerular hypertrophy than were 3/3 carriers. The 2 carriers showed an increase in glomerular ApoE protein expression. A correlation between ApoE genotype and nodular glomerulosclerosis was not found.

Conclusions. Our findings confirm the risk association of the ApoE polymorphism with diabetic nephropathy in clinical studies and is the first study demonstrating the correlations between ApoE genotypes, protein expression and structural changes in diabetic nephropathy.

  G Wang , F. M. M Lai , L. S Tam , E. K. M Li , B. C. H Kwan , K. M Chow , P. K. T Li and C. C. Szeto
 

Objective. Regulatory T lymphocytes (Tregs) probably play an important role in the pathogenesis of SLE.

Methods. We quantified messenger RNA (mRNA) expression of FOXP3, a critical regulator for the development and function of Tregs, in the urinary sediment of 25 subjects with active lupus nephritis (LN), 17 with inactive lupus and 7 healthy subjects.

Results. We found that the expression level of FOXP3 was significantly higher in urine from patients with active LN than from subjects with inactive lupus and healthy controls (24.5 ± 45.8 vs 0.8 ± 1.0 vs 0.6 ± 0.8 copy; P < 0.001). In the active group, urinary FOXP3 mRNA expression level was higher in patients with proliferative LN than non-proliferative nephritis (34.6 ± 56.3 vs 2.7 ± 2.1 copy; P = 0.019). Urinary FOXP3 mRNA level significantly correlated with SLEDAI (r = 0.668; P < 0.001) and proteinuria (r = 0.414; P = 0.006). In the active group, urinary FOXP3 mRNA level also significantly correlated with histological activity index (r = 0.541; P = 0.009) and marginally with intra-renal FOXP3 mRNA level (r = 0.360; P = 0.08). Urinary FOXP3 mRNA in patients with no response to therapy was higher than those with partial response or complete response (57.6 ± 69.8 vs 2.4 ± 1.9 copies; P = 0.02).

Conclusion. We concluded that urinary FOXP3 mRNA is markedly up-regulated in patients with active LN, and the level of expression is closely correlated with the clinical and histological disease activity. A high urinary FOXP3 mRNA in LN predicts a poor therapeutic response. Measurement of FOXP3 mRNA in urine sediment may be a non-invasive biomarker for assessing the severity and risk stratification in LN.

 
 
 
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