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1 Core Proteomics Laboratory, Kidney Disease Program, Department of Medicine, and Departments of 2 Biochemistry and Molecular Biology and 4 Pharmacology and Toxicology, University of Louisville, 3 Veterans Affairs Medical Center, and 5 Pathology Department, Jewish Hospital, Louisville, Kentucky 40202; and 6 Division of Nephrology, Department of Medicine, Medical University of South Carolina, and 7 Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29425
Plasma sodium concentration is
maintained even when sodium intake is altered. Sodium homeostasis may
involve changes in renal tubular protein expression that are reflected
in the urine. We used proteomic analysis to investigate changes in
urinary protein excretion in response to acute sodium loading. Rats
were given deionized water followed by hypertonic (2.7%) saline for
28 h each. Urinary protein expression was determined during the
final 4 h of each treatment. Acute sodium loading increased
urinary sodium excretion (4.53 ± 1.74 vs. 1.70 ± 0.27 mmol/day, P = 0.029). Urinary proteins were separated
by two-dimensional PAGE and visualized by Sypro ruby staining.
Differentially expressed proteins were identified by matrix-assisted
laser desorption ionization-time-of-flight mass spectrometry followed
by peptide mass fingerprinting. The abundance of a total of 45 protein
components was changed after acute sodium loading. Neutral
endopeptidase, solute carrier family 3, meprin 1
, diphor-1,
chaperone heat shock protein 72, vacuolar H+-ATPase, ezrin,
ezrin/radixin/moesin-binding protein, glutamine synthetase, guanine
nucleotide-binding protein, Rho GDI-1, and chloride intracellular
channel protein 1 were decreased, whereas albumin and
-2u globulin
were increased. Some of these proteins have previously been shown to be
associated with tubular transport. These data indicate that alterations
in the excretion of several urinary proteins occur during acute sodium loading.
urine; tubular transport
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