ABSTRACT
Academic health centres have historically treated patients with the most complex of diseases, served as training grounds to teach the next generations of physicians and fostered an innovative environment for research and discovery. The physicians who hold faculty positions at these institutions have long understood how these key academic goals are critical to serve their patient community effectively. Recent healthcare reforms, however, have led many academic health centres to recruit physicians without these same academic expectations and to partner with non-faculty physicians at other health systems. There has been limited transparency in regard to the expertise among the physicians and the academic faculty within these larger entities. Such lack of transparency may lead to confusion among patients regarding the qualifications of who is actually treating them. This could threaten the ethical principles of patient autonomy, benevolence and non-maleficence as patients risk making uninformed decisions that might lead to poorer outcomes. Furthermore, this lack of transparency unjustly devalues the achievements of physician faculty members as well as potentially the university they represent. In this paper, it is suggested that academic health centres have an obligation to foster total transparency regarding what if any role a physician has at a university or medical school when university or other academic monikers are used at a hospital.
Subject(s)
Academic Medical Centers , Clinical Competence/standards , Faculty, Medical/standards , Physicians/standards , Beneficence , Choice Behavior , Disclosure , Health Workforce/statistics & numerical data , Humans , Patient Rights , Personal Autonomy , Physician-Patient RelationsSubject(s)
Enzyme Inhibitors/pharmacology , Fibrosis/pathology , Kidney Diseases/pathology , Transglutaminases/antagonists & inhibitors , Animals , Body Weight , Chronic Disease , Glomerulosclerosis, Focal Segmental/metabolism , Humans , Kidney/metabolism , Kidney/pathology , Kidney Tubules/metabolism , Male , Models, Biological , Organ Size , Rats , Rats, WistarABSTRACT
Experimental renal scarring indicates that tissue transglutaminase (tTg) may be associated with the accumulation of extracellular matrix (ECM), both indirectly via TGF-beta1 activation and directly by the formation of epsilon(gamma-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 epsilon(gamma-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/cm(2)), which was shown to be active by a similar 11-fold increase in the epsilon(gamma-glutamyl) lysine crosslink (1.8 +/- 0.2 versus 19.3 +/- 14.2 mV/cm(2)). 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 epsilon(gamma-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.
