Estimation of glomerular filtration rate using serum cystatin C in overweight and obese subjects.

BACKGROUND: Obesity and overweight are strong independent risk factors for chronic kidney disease (CKD). Using serum creatinine-based estimated glomerular filtration rate (eGFR) equations in these subjects may be inaccurate. On the other hand, cystatin C-based eGFR equations may overestimate CKD prevalence as recent findings suggest an association of cystatin C with obesity. The objective of this study was to assess the accuracy of a cystatin C-based eGFR equation compared to two creatinine -based eGFR equations in overweight and obese subjects. METHODS: This was a prospective cross-sectional study which recruited healthy volunteers aged 18-55 years with a body mass index (BMI) > or = 23kg/m(2) (Asia Pacific Guidelines). Their renal profiles, serum cystatin C and 99m technetium diethylene triamine pentacetic acid (99)mTc-DTPA) scans were performed on the same day. The correlations and accuracy of the creatinine-based and cystatin C-based eGFR equations with the (99)mTc-DTPA GFR were determined. RESULTS: One hundred and one subjects with a median age of 30.0 (27.0-43.5) years and mean BMI of 28.7 +/- 4.5 kg/m(2) were recruited. The cystatin C-based eGFR equation showed the best correlation with the (99)mTc-DTPA GFR (r = 0.526, p = 0.001) and was more accurate in measuring abnormal GFR compared to the creatinine-based eGFR equations. CONCLUSION: Our study showed that the cystatin C-based eGFR equation was more accurate, sensitive and specific in overweight and obese subjects compared to the creatinine-based eGFR equations.

Subclinical acquired syphilis masquerading as membranous glomerulonephritis.

Membranous glomerulonephritis (MGN) is one of the common forms of nephrotic syndrome in the adult population. The majority of MGN are idiopathic, but the secondary forms can be seen in the setting of autoimmune disease, neoplasia, infection and following exposure to certain therapeutic agents. Histologically, MGN is an immunologically mediated disease in which immune complexes deposit in the subepithelial space. Syphilis is a venereal disease that can also be acquired by exposure to infected blood. Untreated syphilis may progress and develop renal complications such as membranous glomerulonephritis (MGN) or diffuse endocapillary glomerulonephritis with or without crescent formation. Today, with increasing awareness of sexually transmitted diseases especially HIV infection coupled by the practice of protected sexual intercourse and advancement of medicine, we have seen fewer and fewer cases of acquired syphilis. Furthermore, majority will present with typical syphilitic symptoms of such as chancre, rash, fever and lymph node enlargement in which case the diagnosis is easily obtained. We are reporting a case of acquired syphilis masquerading as membranous glomerulonephritis without typical syphilitic symptoms.

Association of the tumor necrosis factor alpha gene polymorphism with susceptibility and clinical-immunological findings of systemic lupus erythematosus.

The etiology of systemic lupus erythematosus (SLE) is unknown but genetic factors seem to play a role in the disease pathogenesis. The tumor necrosis factor alpha (TNFa) gene, encoded at the TNF locus in the MHC class III region, is now known to be an important candidate gene in SLE, due to the proinflammatory activities of the TNFa. The objectives of this study were to examine the role of the TNFa polymorphism for the susceptibility of Malaysian Chinese lupus patients to SLE and to determine its association with organ involvement. The allelic frequencies of the TNFa polymorphic variant (TNF2) of seventy lupus patients were determined during follow-up at the Medical Clinic of the National University Hospital Malaysia by PCR-RFLP technique. Sixty-four females and 6 males with a mean age of 33+/-12 years were included. Clinical data were obtained from case records. Autoantibody levels were measured by ELISA. Fifty-nine ethnically-matched blood donors were used as controls. The allelic frequency of the TNF2 variant was found to be significantly increased in the patients compared to the controls (52.8% vs 33.8%). SLE patients with the polymorphic TNF2 variant were found to be at increased risk of central nervous system involvement (p = 0.004, RR = 2.59) and to have an increased frequency of anti-La antibodies (p = 0.03). In view of these findings we suggest that TNF2 variant is playing a role in conferring susceptibility to SLE and in the disease pathogenesis.