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1 Department of Nephrology, Leicester General Hospital, Leicester; and Departments of 2 Pathology and 3 Cell Physiology and Pharmacology, Faculty of Medicine and Biological Sciences, University of Leicester, Leicester LE5 4PW, United Kingdom
The role of the albumin-carried
fatty acids in the induction of tubulointerstitial injury was studied
in protein-overload proteinuria. Rats were injected with fatty
acid-carrying BSA [FA(+)BSA], fatty acid-depleted BSA [FA(
)BSA],
or saline. Macrophage infiltration was measured by immunohistochemical
staining, apoptotic cells were detected by in situ end labeling,
and proliferating cells were identified by in situ hybridization for
histone mRNA. Macrophage infiltration was significantly greater in the
FA(+)BSA group than in the FA()BSA and saline groups. The infiltrate
was largely restricted to the outer cortex. Apoptosis was
greater in the FA(+)BSA group than in the FA()BSA and saline groups.
Compared with the saline group, apoptosis was significantly
increased in the FA(+)BSA group but not in the FA()BSA group.
Cortical cells proliferated significantly more in the FA(+)BSA and
FA()BSA groups than in the saline group. 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 tubulointerstitial injury in protein-overload proteinuria.
lipid; albuminuria; proximal tubule; apoptosis; macrophage; proliferation
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