Serum tryptase levels and markers of renal dysfunction in a population with chronic kidney disease

  • Sirvent, Ana Esther
  • González, César
  • Enríquez, Ricardo
  • Fernández, Javier
  • Millán, Isabel
  • Barber, Xavier
  • Amorós, Francisco
Journal of Nephrology 23(3):p 282-290, May-June 2010.

Abstract

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 μg/L vs. 10.2 ± 8.4 μg/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 μg/L, 13.8 ± 7.8 μg/L, 15 ± 8.9 μg/L vs. 6.7 ± 5.1 μg/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.

Copyright © 2010Wichtig Editore
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