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Articles by J. C Tan
Total Records ( 2 ) for J. C Tan
  S Chandar , L. S Yeo , C Leimena , J. C Tan , X. H Xiao , V Nikolova Krstevski , Y Yasuoka , M Gardiner Garden , J Wu , S Kesteven , L Karlsdotter , S Natarajan , A Carlton , S Rainer , M. P Feneley and D. Fatkin
 

Rationale: Mutations in the LMNA gene, which encodes the nuclear lamina proteins lamin A and lamin C, are the most common cause of familial dilated cardiomyopathy (DCM). Mechanical stress-induced apoptosis has been proposed as the mechanism underpinning DCM in lamin A/C–deficient hearts, but supporting in vivo evidence has been lacking.

Objective: Our aim was to study interventions to modify mechanical stress in heterozygous Lmna knockout (Lmna+/–) mice.

Methods and Results: Cardiac structure and function were evaluated before and after exercise training, thoracic aortic constriction, and carvedilol treatment. Lmna+/– mice develop adult-onset DCM with relatively more severe disease in males. Lmna+/– cardiomyocytes show altered nuclear morphology and perinuclear desmin organization, with enhanced responses to hypo-osmotic stress indicative of cytoskeletal instability. Despite these structural defects that provide a template for mechanical stress-induced damage, young Lmna+/– mice subjected to 6 weeks of moderate or strenuous exercise training did not show induction of apoptosis or accelerated DCM. In contrast, regular moderate exercise attenuated DCM development in male Lmna+/– mice. Sustained pressure overload generated by thoracic aortic constriction depressed ventricular contraction in young wild-type and Lmna+/– mice with no sex or genotype differences in the time-course or severity of response. Treatment of male Lmna+/– mice from 12 to 40 weeks with the β-blocker, carvedilol, prevented the dilatation and contractile dysfunction that was observed in placebo-treated mice.

Conclusions: These data suggest that factors other than mechanical stress-induced apoptosis contribute to DCM and provide the first demonstration that regular moderate exercise and carvedilol can modify disease progression in lamin A/C–deficient hearts.

  J. C Tan , B Ho , S Busque , K Blouch , G Derby , B Efron and B. D. Myers
 

Background and objectives: To ensure long-term safety of living kidney donors, it is now recommended that they be followed for at least 2 years after donation and that serum creatinine levels be monitored. Such levels are often subjected by clinical laboratories to estimating equations and are reported as estimated GFR (eGFR). The accuracy of such equations in uninephric living donors has yet to be validated. This is especially important in older living donors, who often have senescence-related depression of GFR.

Design, setting, participants, & measurements: We compared urinary creatinine clearance, four-variable Modification of Diet in Renal Disease estimating equation (eGFR), and the recently reported CKD-EPI GFR estimating equation with true GFR measured by the urinary iothalamate clearance (iGFR) in 64 subjects after kidney donation.

Results: Creatinine clearance overestimated iGFR. Both creatinine-based estimating equations were poorly correlated with and underestimated iGFR. More than half of kidney donors had eGFR <60 ml/min per 1.73 m2 after donation, a level that categorized them as having stage 3 chronic kidney disease by our current laboratory reporting, whereas only 25% had iGFR <60 ml/min per 1.73 m2. This misclassification disproportionately affected older donors age ≥55 years, of whom 80% had eGFR <60 ml/min per 1.73 m2. Neither significant albuminuria nor hypertension was observed.

Conclusions: The current practice of reporting eGFR after donation commonly leads to a misclassification of chronic kidney disease, particularly in older donors. To ensure long-term well-being of living kidney donors, more precise estimates of GFR are required, particularly among older potential donors.

 
 
 
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