Biomedical subjects

J Goldinger

Publications and source records attributed to J Goldinger.

3 recordsLinked to original sources

PubMed1990

Persistent proximal tubule dysfunction late in Heymann nephritis.

To determine whether proximal tubule function returned to normal after cessation of active immunological injury in Heymann nephritis, we compared kidney function in an acute stage of the disease, when antibodies were being deposited on the brush border, to a later, chronic stage. Renal blood flow measurements via a flow probe, along with clearance and micropuncture techniques, were used to measure renal plasma flow, glomerular filtration rate, protein and albumin excretion, organic ion (PAH and TEA) extraction and tubule fluid inulin concentration. Proximal tubule fluid reabsorption, which was depressed in the acute stage of injury, returned to normal in chronic Heymann nephritis, but both PAH and TEA extraction continued to be depressed. PAH extraction was also decreased in isolated perfused kidneys from rats with Heymann nephritis. A three fold increase in PAH content of these perfused kidneys indicated that there was a defect in luminal PAH transport. Reconstitution of the proximal tubule brush border in chronic Heymann nephritis was not accompanied by functional recovery of secretory processes.

Animals↗

PubMed1985

Anion carrier in the human erythrocyte exists as a dimer.

The in situ state of assembly of the human erythrocyte anion carrier (band 3) has been investigated by applying target size analysis on the radiation-induced inactivation of anion flux and degradation of polypeptide band 3. Irradiation with a high energy electron beam resulted in inactivation of carrier-mediated anion flux in intact cells, in inside-out vesicles devoid of cytoskeletal and cytoplasmic proteins, and in inside-out vesicles whose band 3 protein has been partially proteolyzed, with little change in leak pathway. The inactivation showed a single exponential function of radiation dose from which the target size of the anion carrier was estimated to be 210,000, 220,000, and 98,000 daltons in intact cells, in the inside-out vesicles, and in the vesicles after a limited proteolysis, respectively. Irradiation also resulted in degradation of the band 3 of the inside-out vesicles, as detected on sodium dodecyl sulfate-gel electrophoresis, with a dose dependence characteristic of a target size of 220,000 daltons. It is suggested that the human erythrocyte anion carrier exists in situ as a dimer of band 3.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1985

Impaired organic ion transport in proximal tubules of rats with Heymann nephritis.

Organic ion transport across the basolateral membrane of proximal tubules was measured by means of the tissue slice technique in each of the four different stages of Heymann nephritis. Impairment of both organic anion and cation transport was detected early in Stage 2, and became more severe in Stage 3 of Heymann nephritis. The decreased transport function was associated with extensive damage to proximal tubule cells, including loss of brush border microvilli and basal infoldings. Despite these abnormalities of structure and function, oxygen consumption of proximal tubule cells remained essentially normal. Partial recovery of organic cation transport was noted late in Heymann nephritis (Stage 4). Recovery of the cation transport function was associated with a partial restoration of brush border microvilli and basal infoldings to proximal tubule cells. However, organic anion transport remained depressed throughout the entire course of disease. Impairment of organic ion transport in rats with Heymann nephritis appeared to result from damage to basolateral membrane transport elements rather than general deterioration of the metabolic machinery of proximal tubule cells. Decreased organic cation transport appeared to be the consequence of a reduction in the number of carrier sites, a phenomenon that could have resulted from decreased membrane surface area. However, the depression of organic anion transport was associated with decreased substrate affinity of the anion carrier, indicating that qualitative, rather than quantitative changes, were primarily responsible for that defect. Specific antibody-mediated damage to the anion transport elements in basolateral membranes of proximal tubules is postulated to occur in Heymann nephritis.

Adjuvants, Immunologic↗