Serotonin in experimental histidinemia

An experimental histidinemia was obtained in rats by in vivo administration of nitromethane, a histidase inhibitor. The magnitude of increase in plasma histidine in the nitromethane-treated rats was in the same range as that in the histidinemic subjects. No modifications were observed in the serotonin concentrations in blood or in various areas of brain between the nitromethane-treated rats and the control rats. No dramatic modifications of serotonin metabolism seem to be implicated in histidinemia, unlike phenylketonuria.     

Tissue lipoprotein lipase,serum, and urinary lipids and lipoproteins in experimental glomerulonephritis of rats (Heymann's nephritis)

Serum and urinary cholesterol, triglycerides, high-density lipoproteins, and tissue lipoprotein lipase levels were measured in a group of rats in which experimental glomerulonephritis (EGN) was induced by an injection of renal tubular antigen in Freund's complete adjuvant. Progressively increasing proteinuria beginning after approximately the eighth week was associated with a progressive increase in the levels of serum cholesterol, triglycerides, and high-density lipoprotein cholesterol. Significant lipiduria occurred at the ninth week. Lipoprotein electrophoresis of concentrated urine showed the presence of a band with alpha lipoprotein (high-density lipoprotein) mobility. Eleven weeks after disease induction, the rats were killed and the tissue levels of lipoprotein lipase were measured. A homogenized preparation of the heart, liver, adipose tissue, and skeletal muscle using [¹⁴C]triolein as substrate was used. Nephrotic rats had less than half the myocardial lipoprotein lipase levels of controls (2099 ± 420 and 962 ± 142 (mean ± SD) nm free fatty acids/mg tissue/hr, respectively; P < 0.05). Hepatic, skeletal muscle, and adipose tissue lipoprotein lipase levels were not significantly different in the two groups of rats.These results document the potential usefulness of the rat (EGN) model for further studies in lipoprotein metabolism in nephrotic syndrome. The significance and pathogenesis of reduced myocardial lipoprotein lipase requires further investigation.     

Participation of auto-anti-idiotypes in immune complex glomerulonephritis in rabbits

We report the presence of auto-anti-Id antibodies in the glomerular immune deposits of a rabbit with chronic serum sickness induced by daily i.v. injections of bovine serum albumin. Auto-anti-Id antibodies were also documented in the serum of the same animal during the phase of chronic serum sickness in which immune complex glomerulonephritis develops. These results suggest that auto-anti-Id may normally participate in pathologic reactions and may be one of the mechanisms of potentiation and/or progression of immunopathologic lesions.     

HBs antigenemia in glomerulonephritis in children

Altogether 194 glomerulonephritis patients were examined by three methods: countercurrent immunoelectrophoresis, passive hemagglutination test, and enzyme immunoassay. Use of the most sensitive method, viz. enzyme immunoassay, has yielded the highest HBsAg detection rate: 29.1% in acute glomerulonephritis and 21.4% in chronic glomerulonephritis. This method may be recommended for the examination of glomerulonephritis patients whose sera contain HBsAg in low titers.     

Intraglomerular fibronectin in rat experimental glomerulonephritis.

To clarify the mechanisms of glomerular pericapillary fibronectin deposition in human membranous nephropathy and mesangial proliferative glomerulonephritis, intraglomerular fibronectin distribution was examined by light and electron microscopy using the experimental rat models of Heymann and nephrotoxic serum nephritis. As previously demonstrated by immunofluorescence microscopy (Pettersson and Colvin 1978; Ikeya et al. 1985, 1986), fibronectin was distributed in the mesangial areas and occasionally on percicapillary walls of normal glomeruli, while in nephrotoxic serum nephritis and Heymann nephritis, fibronectin was diffusely located along glomerular capillary walls as well as in the mesangium. By immunoelectron microscopy using the immunogold technique, fibronectin was also noted in the mesangial areas and the lamina densa of the glomerular basement membrane (GBM) in normal glomeruli. In nephrotoxic serum nephritis, fibronectin was seen around mesangial cells situated between endothelial cells and the GBM, suggesting that pericapillary fibronectin in nephrotoxic serum nephritis reflects mesangial extension. However, in Heymann nephritis, it was found uniformly in the lamina rara interna, lamina densa and lamina rara externa of the GBM, indicating no specific relation to glomerular cells. When sections of normal and both experimental nephritis kidneys were incubated with fluorescein isothiocyanate conjugated with rat plasma fibronectin, a linear pattern of fluorescein staining along the glomerular capillary walls was observed in Heymann nephritis but not in normal or nephrotoxic serum nephritic rats. The GBM in Heymann nephritis would thus appear to have an affinity for plasma fibronectin. Based on the above findings, fibronectin in the GBM of rats with Heymann nephritis may reasonably be concluded to originate from the plasma.