Submitted on August 8, 2007
Accepted on August 1, 2008
Increased mast cell number in human hypertensive nephropathy
Pia Welker1, Stephanie Kramer2, David A. Groneberg3, Hans Hellmut Neumayer2, Sebastian Bachmann1, Kerstin Amann4, and Harm Peters2*
1 Institute for Cardiorenal Anatomy, Charite Berlin, Berlin, Germany
2 Nephrology, Charite Campus Mitte, Berlin, Germany
3 Dept. of Pediatrics, Charite Biomedical Research Center, 13353 Berlin, Germany
4 Pathology, University of Erlangen-Nurnberg, Erlangen, Germany
* To whom correspondence should be addressed. E-mail: harm.peters{at}charite.de.
Mast cells have recently been related to non-allergic chronic organ damage and fibrosis. In the present study we analyzed mast cell number, localisation and maturation in the kidney of a relatively unique group of middle-aged accident victims with primary essential hypertension and in normotensive controls. Hypertensive kidneys showed a significantly higher degree of arteriolosclerosis. However, glomerular and tubulointerstitial matrix accumulation did not differ significantly to normotensive controls indicating a relatively early stage of hypertensive nephropathy. Using toluidine blue staining, renal mast cell number was found to be 5-fold higher in hypertensive subjects as compared to normotensive controls. Mast cells were primarily located in the peritubular interstitial spaces, some perivascular but not in glomeruli. In a series of immunohistological staning studies, mast cell maturation grading showed that expression of early haematopoietic precursor cell marker anti-CD34 did not differ between both groups. In contrast, mast cells were mostly positive for IgE receptor, tryptase and chymase indicating a mature, differentiated cell phenotype in hypertensive nephropathy. Renal expression of stem cell factor was markedly up-regulated in primary hypertension. Kidney macrophage and lymphocytes numbers were similar in both groups. In conclusion, human hypertensive kidney disease shows an early and conspicuous up-regulation of stem cell factor along with an increased number of mature mast cells. The results suggest that renal mast cell accumulation may play a role in the pathogenesis of human hypertensive nephropathy.
