1. While azotaemic sera depressed the in-vitro Na-iodohippurate transport of rat kidney slices at any concentration, normal sera excited transport at low concentrations and depressed transport at high concentrations. The depression of transport by azotaemic sera was partially overcome by neomycin feeding in contrast to the depression by normal sera, which was not altered by neomycin feeding.

2. Plotting the reciprocal of sodium-iodohippurate accumulated by slices against the reciprocal of the media concentrations of sodium iodohippurate suggested that the depression of hippurate transport produced by normal and azotaemic sera was competitive in nature.

3. Normal sera slowed the efflux of Na-iodohippurate from kidney slices while azotaemic sera affected it very little.

4. The depression produced by normal and azotaemic sera and the stimulation produced by low concentrations of normal sera were seen with serum ultrafiltrates and dialysates, and after passage through cation exchange columns, but not anion exchange columns.

5. The effects on Na-iodohippurate accumulation by normal and azotaemic sera could be reproduced with metabolizable (lactate), and nonmetabolizable (hippurate) organic anions as well as combinations of these.

6. The implications of these observations on the altered renal transport of Na-iodohippurate produced by azotaemic and normal sera are discussed.

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