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Comparative Study
. 2011;117(3):c266-9.
doi: 10.1159/000320753. Epub 2010 Sep 17.

Accelerated decline of GFR in diabetic nephropathy predicted by interferon release assay to tuberculosis antigens

Affiliations
Comparative Study

Accelerated decline of GFR in diabetic nephropathy predicted by interferon release assay to tuberculosis antigens

Catherine Lane et al. Nephron Clin Pract. 2011.

Abstract

Background: The QuantiFERON® test (QFT) is a diagnostic tool for active and latent tuberculosis (TB) infections. High rates of positivity to QuantiFERON® have been demonstrated in patients with chronic kidney disease (CKD) and diabetic patients. We performed a pilot study to investigate if QFT positivity in diabetic CKD patients predicted the rate of renal function decline.

Methods: QFT was performed in 38 diabetic patients with CKD 4-5 not on dialysis. The rate of decline in estimated glomerular filtration rate (eGFR) was calculated.

Results: 18/38 patients had a positive QFT. Patients with a positive QFT had a steeper decline in eGFR, compared with patients with a negative QFT. Ethnicity (a marker of risk of previous TB exposure), urine protein/creatinine ratio, use of ACE inhibitors/angiotensin II receptor blockers and statins, serum C-reactive protein, vitamin D levels, HbA1c concentration and presenting GFR did not differ significantly.

Conclusions: The finding in this small cohort needs to be replicated in a larger study because our study is susceptible to both type I and type II statistical error. We found that QFT positivity was associated with a more rapid rate of decline in GFR, but this association may be coincidental (with the difference in decline attributed to differences in the blood pressure or proteinuria of the two groups). Moreover, an association does not necessarily mean causality, although it would be interesting to speculate if we are identifying patients with latent TB who have an active interstitial nephritis. Another intriguing possibility is that this assay identifies patients with an immunological phenotype that predisposes to eGFR loss.

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