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*Sheffield Kidney Institute, Sheffield, and Nottingham Trent University, Nottingham, United Kingdom; and University of Alexandria, Alexandria, Egypt.
Correspondence to Dr. Tim Johnson, Sheffield Kidney Institute, Northern General Hospital Trust, Herries Road, Sheffield, S5 7AU, UK. Phone: +44 (0)114-2715322; Fax: +44(0) 114-2714410;
ABSTRACT. Experimental renal scarring indicates that tissue transglutaminase (tTg) may be associated with the accumulation of extracellular matrix (ECM), both indirectly via TGF-
1 activation and directly by the formation of 
(
-glutamyl) lysine dipeptide bonds within the ECM. The latter potentially accelerates deposition and confers the ECM with resistance to proteolytic digestion. Studied were 136 human renal biopsy samples from a range of chronic renal diseases (CRD) to determine changes in tTg and (-glutamyl) lysine crosslinking. Immunofluorescence for insoluble tTg showed a 14-fold increase in the kidneys of CRD patients (5.3 ± 0.5 versus 76 ± 54 mV/cm2), which was shown to be active by a similar 11-fold increase in the (-glutamyl) lysine crosslink (1.8 ± 0.2 versus 19.3 ± 14.2 mV/cm2). Correlations were obtained with renal function for tTg and crosslink. In situ hybridization for tTg mRNA showed that tubular epithelial cells were the major source of tTg; however, both mesangial and interstitial cells also contributed to elevated levels in CRD. This mRNA pattern was consistent with immunohistochemistry for soluble tTg. Changes in renal tTg and its product, the (-glutamyl) lysine crosslink, occur in progressive renal scarring in humans independently of the original etiology and in a similar manner to experimental models. tTg may therefore play a role in the pathogenesis of renal scarring and fibrosis in patients with CRD and can therefore be considered a potential therapeutic target. E-mail: T.Johnson@sheffield.ac.uk
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