Renal handling of high-density lipoproteins by isolated perfused kidneys

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Recent studies show that the normal and diseased kidney is an important organ in the catabolism of high-density lipoproteins (HDL). However, little is known about the renal handling of HDL. To investigate this aspect, kidneys were isolated from normal rats and rats made nephrotic with puromycin aminonucleoside. They were perfused in a chamber at 37°C with a modified Krebs-Hensleit Bicarbonate Buffer containing 1%, 3%, 6%, and 10% Bovine Serum Albumin (BSA). Presence of 10% BSA in the perfusate prevented glomerular filtration and urine formation. Thus, the filtering and the nonfiltering kidney perfusion models distinguish the renal parenchymal function independently of luminal events that follow filtration. 125I-labeled rat HDL was injected into the perfusate and radioactivity in perfusate, urine, and kidney was examined. At the end of perfusion (30 minutes or four hours), each kidney was flushed with 125I-HDL-free perfusate and kidney radioactivity was measured. At four hours, 1.9% ± 0.5% of injected radioactivity was present in urine from kidneys perfused with 6% BSA. Kidneys with intact glomerular filtration sequestered significantly more radioactivity (1.1% ± 0.2% of injected radioactivity) than nonfiltering kidneys (0.7% ± 0.2%); P < 0.05. Radioactivity in filtering kidneys was significantly higher than in nonfiltering kidneys (33.9 ± 7.8 v 15.6 ± 2.6 cpm/mg kidney tissue protein, respectively; P < 0.001). Nephrotic kidneys (filtering and nonfiltering) sequestered two to four times more 125I-HDL than normal kidneys. These data support the hypothesis that prior to urinary excretion, partial reabsorption of filtered HDL (or subfractions) occurs in the normal kidney. In the nephrotic kidney, increased filtration (and reabsorption) may account for the enhanced uptake of HDL by the diseased kidney.