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Biomedical subjects

G C Groggel

Publications and source records attributed to G C Groggel.

24 records · Page 2Linked to original sources
PubMed1986

Hypocomplementemic urticarial vasculitis syndrome responsive to dapsone.

A 45-year-old woman with cutaneous urticaria-like lesions subsequently developed polyarthritis, glomerulonephritis, and chronic obstructive pulmonary disease. Biopsy of skin showed leukocytoclastic vasculitis of superficial capillaries. Biopsy of the kidney revealed mesangioproliferative glomerulonephritis, and lung biopsy revealed severe emphysema and thick-walled blood vessels with immunoglobulin deposition. Therapy with dapsone produced dramatic improvement of the patient's cutaneous vasculitis and arthritis. This case uniquely demonstrates the efficacy of dapsone for both the urticarial vasculitic and the arthritic components of this syndrome and reemphasizes the potentially severe pulmonary and renal complications.

Arthritis↗
PubMed1986

Anterior ischemic optic neuropathy as a complication of hemodialysis.

Hypotension is a common and sometimes difficult to manage occurrence during hemodialysis. The consequences of dialysis-induced hypotension are unpredictable. Anterior ischemic optic neuropathy is an entity associated with many systemic processes, including shock. Anterior ischemic optic neuropathy presents as sudden painless loss of vision. This is the first report of anterior ischemic optic neuropathy as a result of hemodialysis-associated hypotension.

Adult↗
PubMed1985

Influence of antigen distribution on the mediation of immunological glomerular injury.

To determine if the site of immune reaction could influence the mediation and morphological expression of glomerular injury in experimental anti-glomerular basement membrane (anti-GBM) nephritis and membranous nephropathy, we studied the events that followed the in situ reaction of rat antibody with antigen planted in either the GBM (especially the lamina rara interna) or in the subepithelial space (SE). Non-nephritogenic amounts of noncomplement-fixing sheep anti-GBM or anti-tubular brushborder antibody were injected into separate groups of rats to plant sheep IgG in the GBM and SE, respectively. Kidneys containing sheep IgG were then transplanted into naive recipients that were passively immunized with rat anti-sheep IgG. There was marked proteinuria after 2 days (antigen in GBM: 226 +/- 50.7; antigen in SE: 69 +/- 50.7 mg/24 hr) that was abrogated by prior depletion of complement in both groups (antigen in GBM: 10.2 +/- 1.7; antigen in SE: 14.3 +/- 8.7 mg/24 hr). When antigen was planted in SE, inflammatory-cell depletion with either anti-neutrophil (PMN) serum or lethal irradiation had no effect on proteinuria. In contrast, anti-PMN abolished proteinuria (12.0 +/- 5.6 mg/24 hr) and irradiation reduced it by 60% when antigen was in GBM. Glomeruli of kidneys with antigen in GBM were significantly larger and more hypercellular than those with antigen in SE after transplantation into immunized recipients. Endothelial cell injury and adherence of inflammatory cells to denuded GBM were prominent in the former (antigen in GBM), while glomeruli with antigen in SE showed only subepithelial deposits, adjacent slit-diaphragm displacement, and epithelial cell foot-process effacement. Thus, the reaction of antigen and antibody in glomeruli produced complement-mediated injury which was cell-independent when complex formation occurred on the outer aspect of the GBM but was cell-dependent when the same reagents reacted more proximally to the circulation. We therefore conclude that antigen distribution can critically influence the mediation and morphologic expression of immune glomerular injury and may, in part, account for variations in the clinical and histological manifestations of antibody-induced glomerular disease in humans.

Animals↗
PubMed1985

Role of terminal complement pathway in the heterologous phase of antiglomerular basement membrane nephritis.

Terminal complement components, including the membrane attack complex, have been demonstrated in glomeruli of patients with immune complex and anti-GBM nephritis. We recently demonstrated the functional significance of C6 in the mediation of experimental membranous nephropathy in rabbits. In the present study, the role of C6 was examined in the heterologous phase of rabbit anti-GBM nephritis by studying normal and C6-deficient (C6D) rabbits. In C6D rabbits, C6 hemolytic activity was less than 0.01% of control. All control rabbits became heavily proteinuric in the first 24 hr following injection of a standard dose of sheep anti-rabbit GBM antibody (mean, 42.0 +/- 26.3; range, 18.4 to 83.5 mg protein/mg creatinine, N = 5). In contrast, C6D rabbits excreted a mean of only 5.1 +/- 5.5 mg/mg creatinine (range, 0.06 to 14.4, N = 6, P = 0.002). Protein excretion in normal rabbits was less than 0.06 mg/mg creatinine. Both control and C6D rabbits had similar deposits of sheep anti-rabbit GBM IgG in glomeruli when measured by radiolabeling techniques (control 15.8 +/- 2.71, N = 5; C6D 18.7 +/- 1.99 micrograms of sheep IgG/10(4) glomeruli, N = 6, P greater than 0.05). Control rabbits had a greater rise in serum creatinine in the first 24 hr (1.74 +/- 1.15 vs. 0.53 +/- 0.44 mg/dl, P less than 0.05). Both groups had similar deposits of sheep IgG and rabbit C3 by IF. By light microscopy at 4 and 24 hr, both groups had qualitatively similar proliferative changes and similar numbers of neutrophils infiltrating glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Role of the terminal complement pathway in experimental membranous nephropathy in the rabbit.

Our recent observations of a complement-mediated, cell-independent mechanism of altered glomerular permeability in rat membranous nephropathy suggested a possible role for the terminal complement pathway in the mediation of proteinuria in certain forms of glomerular disease. To directly determine whether the membranolytic terminal complement components (C5b-C9) are involved in glomerular injury, we studied the development of proteinuria in normal and C6-deficient (C6D) rabbits, in both of which a membranous nephropathy-like lesion develops early in the course of immunization with cationized bovine serum albumin (cBSA) (pI 8.9-9.2). C6 hemolytic activity of C6D was 0.01% that of control rabbits. After 1 wk of daily intravenous injections of cBSA, proteinuria developed in 71% of controls (median 154, range 1-3,010 mg/24 h, n = 24), whereas none of C6D were proteinuric (median 6, range 2-12 mg/24 h, n = 12, P less than 0.01). After 1 wk of cBSA, both groups had qualitatively identical glomerular deposits of BSA, rabbit IgG, and C3 on immunofluorescence microscopy, predominantly subepithelial electron-dense deposits on electron microscopy, and minimal glomerular inflammatory cell infiltration of glomeruli. Glomeruli were isolated from individual animals after 1 wk of cBSA and deposits of rabbit IgG antibody were quantitated by a standardized in vitro assay using anti-rabbit IgG-125I. Rabbit IgG deposits were found to be similar in control (29.8 +/- 13.2, range 12.7-48.6 micrograms anti-IgG/2,000 glomeruli, n = 6) and C6D rabbits (32.6 +/- 13.8, range 16.8-48.8 micrograms anti-IgG/2,000 glomeruli, n = 5, P greater than 0.05). After 2 wk, coincident with a prominent influx of mononuclear cells and neutrophils, proteinuria developed in C6D rabbits. These results document, for the first time, a requirement for a terminal complement component in the development of immunologic glomerular injury. Since the only known action of C6 is in the assembly of the membrane attack complex, these observations suggest that the membranolytic properties of complement may contribute to glomerular damage.

Animals↗