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Articles in PresS, published online ahead of print April 23, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00001.2002
Submitted on January 3, 2002
Accepted on April 8, 2002
1 Department of Nephrology, Leicester General Hospital, Leicester, Leics, United Kingdom
2 Department of Pathology, University of Leicester, Leicester, Leics, United Kingdom
3 Department of Nephrology, Leicester General Hospital, Leicester, Leics, United Kingdom; Department of Cell Physiology and Pharmacology, University of Leicester, Leicester, Leics, United Kingdom
* To whom correspondence should be addressed. E-mail: njb18{at}le.ac.uk.
The role of the albumin carried fatty acids in the induction of tubulo-interstitial injury was studied in protein-overload proteinuria. Rats were injected with fatty acid carrying bovine serum albumin, fatty acid depleted BSA, or saline. Macrophage infiltration was measured by immunohistochemical staining, apoptotic cells were detected by in situ end labelling, and proliferating cells identified by in situ hybridisation for histone mRNA. Macrophage infiltration was significantly greater in the FA(+)BSA group, compared with the FA(-)BSA and saline groups. The infiltrate was largely restricted to the outer cortex. Apoptosis was greater in FA(+)BSA animals compared to both the FA(-)BSA and saline groups. Apoptosis was significantly increased in the FA(+)BSA group (vs. saline) but not in the FA(-)BSA group. Compared to controls cortical cells proliferated significantly more in both the FA(+)BSA and FA(-)BSA groups. FA(+)BSA is therefore a more potent inducer of macrophage infiltration and cell death than FA(-)BSA. The fatty acids carried on albumin may be the chief instigators of tubulo-interstitial injury in protein-overload proteinuria.
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