Background Recent studies have demonstrated that the normal glomerular capi
llary wall (GCW) is not charge selective to albumin. This means that albumi
n flux across the GCW is high, and this has been confirmed in studies in wh
ich albumin uptake by the tubules has been inhibited. Therefore, there must
be a high-capacity postglomerular retrieval pathway in normal kidneys that
returns filtered albumin back to the blood supply.
Methods. This study identifies the presence of glomerular-filtered albumin
in the renal vein from the analysis of the decrease of radioactivity in the
venous effluent after the injection of a pulse of tritium-labeled albumin
into the renal artery in vivo and in the isolated perfused kidney.
Results. The postglomerular filtered albumin is returned to the blood suppl
y by a high-capacity pathway that transports this albumin at a rate of 1830
+/- 292 mu g/min.rat kidney (N = 14, mean +/- SEM). This pathway has been
identified under physiological conditions in vivo and in the isolated perfu
sed kidney. The pathway is specific for albumin, as it does not occur for h
orseradish peroxidase. The pathway is inhibited in a nonfiltering kidney. T
he pathway is also inhibited by ammonium chloride (an agent that inhibits t
ubular protein uptake but does not alter glomerular size selectivity) and b
y albumin peptides (which compete for the tubular albumin receptor).
Conclusions. The high-capacity retrieval pathway for albumin is most likely
associated with transtubular cell transport. It is also apparent that most
albuminuric states could be accounted for by the malfunctioning of this pa
thway without resorting to any change in glomerular permselectivity.