Bovine glomerular basement membrane (GBM) was isolated and purified according to a modification of Spiro’s method. Rat and bovine tubular basement membranes (TBM) were isolated and purified by sonic disruption or by the method of Carlson et al. Electron microscopic studies on the ultrastructure of GBM and TBM were performed after negative staining with 1% phosphotungstic acid solution, pH 7.3. When negatively stained, GBM and TBM were seen as fragments varying in size. The surface of the membranes showed a characteristic felt-like or spongy appearance. At higher magnification, GBM and TBM showed a fine meshwork composed of strands and pores which three-dimensionally resembled a crystal lattice. Pores were fairly uniform in size and shape. They were round, oval or polygonal in shape. Some of the pores were elongated to form short straight or bent channels. Strands were also uniform in diameter and surrounded a pore or channel. For an average of 50 pores, the long dimension was 3.1 ± 0.6 nm and the short dimension 2.5 ± 0.3 nm in bovine GBM, 3.8 ± 1.2 and 2.5 + 0.7 nm in bovine TBM, and 4.9 ± 1.5 and 2.8 ± 0.6 nm in rat TBM, respectively. The strand was 1.8 ± 0.3 nm in diameter in bovine GBM, 2.5 ± 0.6 nm in bovine TBM and 3.7 ± 0.7 nm in rat TBM for an average of 50 strands. The diameters of the pores were less than or close to the short axis of an albumin molecule. It was concluded that renal GBM and TBM were molecular sieves composed of pores and strands.

Rat tubuli were isolated both by the method of Krisko and by a modified method of Cook and Pickering; renal tubular basement membrane (TBM) was isolated by sonic disruption and by the method of Carlson. Using electron microscopy after negative staining, TBM of rat kidney isolated under these different conditions was shown to be a fine meshwork. Strands of the meshwork were interwoven, apparently enclosing pores to make up whole basement membrane. These findings are compared with our previous observation that glomerular and alveolar basement membranes were made up of a similarly fine meshwork.

A 58-yr-old woman had frequent hypoglycemic attacks, undetectable levels of plasma cortisol, ACTH, and beta-lipotropin, and deficient responses of these hormones after insulin induced-hypoglycemia and metyrapone. Her GH responses to arginine infusion were normal as were her gonadotropin responses to LRH. Her TSH and PRL responses to TRH were abnormally high. Anaphylactic shock occurred after the injection of either synthetic ACTH-Z-(1-24) (Cortrosin-Z) or ACTH-(1-18) (Acthormone). She had received two prior injections of synthetic ACTH-Z-(1-24) 2 months earlier. Circulating anti-ACTH antibody was found in her plasma by radioimmunological methods, but this antibody did not prevent corticosterone production by ACTH in an in vitro ACTH bioassay system. The pathogenic significance of this antibody in the ACTH deficiency is doubtful, and the etiology of the isolated ACTH and beta-LPH deficiency is not clear.