| 20349428 |
Sirvent AE, Gonzalez C, Enriquez R, Fernandez J, Millan I, Barber X, Amoros F: Serum tryptase levels and markers of renal dysfunction in a population with chronic kidney disease. J Nephrol. 2010 Mar 26. pii: C0C2F712-6AAB-4CAC-BA1A-22FA73658087.
Background: Mast cells (MCs) might play a pathogenetic role in renal fibrosis. Tryptase is a marker for activated MCs. Little is known about tryptase levels in the chronic renal disease population. Methods: We examined serum MC tryptase concentrations in relation to specific laboratory abnormalities in 153 outpatients with chronic kidney disease (CKD) and in 35 hemodialysis (HD) patients. Results: Here we found that tryptase mean values were higher in men than in women (12.4 +/- 7.6 microg/L vs. 10.2 +/- 8.4 microg/L; p <0.05). Tryptase levels were increased in CKD stages 4 and 5 and in HD patients, versus CKD stages 1 and 2: 12.7 +/- 7.3 microg/L, 13.8 +/- 7.8 microg/L, 15 +/- 8.9 microg/L vs. 6.7 +/- 5.1 microg/L (p <0.01). In univariate analysis, in the conservative treatment CKD population, tryptase was positively correlated with urea, creatinine, potassium, uric acid, phosphorus, parathyroid hormone, homocysteine, fibrinogen and proteinuria (p <0.01); tryptase was negatively correlated with calcium, albumin, creatinine clearance, estimated glomerular filtration rate (by abbreviated MDRD equation) and urine creatinine (p <0.01). In HD patients, the only significative correlation found was with systolic blood pressure and diastolic blood pressure (p <0.01). No significant correlations were found between tryptase and other parameters such as albumin, glucose, hemoglobin, leukocytes, immunoglobulins or C-reactive protein. Multiple regression analysis showed estimated glomerular filtration rate and proteinuria to be independent determinants of tryptase. Conclusions: This is the first study to determine that tryptase levels increase with higher degrees of kidney dysfunction. The association with markers of diminished renal function suggests impaired metabolism or a negative effect of inflammation on glomerular filtration rate. Further studies are required to ascertain the clinical implications of these findings. |
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