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Biomedical subjects

W A Border

Publications and source records attributed to W A Border.

101 records · Page 6Linked to original sources
PubMed1979

IgA antibasement membrane nephritis with pulmonary hemorrhage.

Goodpasture's syndrome has characteristically been described as being mediated by IgG antibodies. We have recently seen a 55-year-old man who developed renal failure and hemoptysis; a renal biopsy showed linear deposits of IgA and C3 involving glomerular and tubular basement membrane. Serologic tests for detecting (IgG) antiglomerular basement membrane antibodies were negative. Elution studies of kidney and lung showed the presence of an IgA antibasement membrane antibody only. The patient's serum contained IgA, but not IgG, antibodies reactive with glomerular and tubular basement membrane of normal human kidney and alveolar basement membrane of normal human lung. Attempts to transfer disease with the patient's IgA antibody to a monkey and to Lewis and Brown-Norway rats were unsuccessful. Immunoglobulin A antibasement membrane antibody must be considered in the design of immunoserologic procedures for the diagnosis of Goodpasture's syndrome.

Animals↗
PubMed1978

Renal damage with intestinal bypass.

Renal function and biopsies were studied in 18 patients, 7 to 108 months after intestinal bypass. Enteropathy was found in 12 and hyperoxaluria in 16. Every biopsy showed a type of focal interstitial nephritis, tubular atrophy, fibrosis, and glomerular hyalinization. Damage ranged from minimal to extensive and renal function from normal to end-stage failure. Tubular injury had resulted partly from oxalate deposits. However, in 10 patients no oxalate crystals were seen. In eight others, most of the damaged areas were remote from crystal deposits. Immunoglobulin M and C3 deposits, found in glomerular capillaries and the messangium in six of 11 specimens, and the presence of circulating immune complexes in five of 10 patients, in addition to the extraintestinal organ involvement, suggested immune complex mesangial injury as one factor in bypass nephropathy. With progressive impairment of renal function, a biopsy appears justified. If damage is significant, the bypass should be dismantled.

Adult↗
PubMed1977

Partial lipodystrophy, C3 nephritic factor and clinically inapparent mesangiocapillary glomerulonephritis.

A case of partial lipodystrophy with C3 nephritic factor was found to be associated with mesangiocapillary glomerulonephritis although all clinical parameters of renal function were normal. Diagnosis of mesangiocapillary glomerulonephritis required renal biopsy. Nephriti factor obtained from this patient was immunochemically related to nephritic factor isolated from the serum of patients with typical mesangiocapillary glomerulonephritis without partial lipodystrophy.

Adult↗
PubMed1977

Detection of circulating immune complexes in patients with glomerulonephritis.

A panel of three immune complex (IC) assays was used in this study to test sera from patients with glomerulonephritis (GN): the Raji cell radioimmune assay (IRCA), the radio-labeled C1q binding assay (IC1qBA), and the microcomplement consumption test (MCT). The sensitivity and specificity of each assay was evaluated in preliminary studies, and the greater sensitivity (5 to 10microgram of aggreagated human gamma-globulin (AHG) per ml of serum) and IgG specificity of the IRCA was apparent. Problems related to the preliminary heat inactivation of test sera, the interaction of C1q with substances other than IC, and the effects of suboptimal storage of test sera were experienced with the MCT and, to a lesser extent the IC1qBA. The individual reactivities of the different assays were exploited by using them in combination. Thus ICs were detected by one or more of the assays in 87% of patients with systemic lupus erythematosus (SLE), 65% of patients with GN associated with other systemic diseases, and 39% of patients with primary GN. ICs were detected more frequently in patients with acute GN than chronic GN, and in patients with low serum C3, C4, and properdin factor B (C3PA) levels.

Acute Disease↗
PubMed1976

Nephritic factor: Description of a new quantitative assay and findings in glomerulonephritis.

A sensitive quantitative test for nephritic factor (NF) in human serum is reported. The test is based on the capacity of NF to initiate fluid phase consumption of the third complement (C) component in the presence of magnesium ions (Mg++) and of factors of the alternative pathway of C activation. These factors as well as C3 and C5 were supplied by the incorporation of normal human serum (NHS) into the assay mixture. In order to prevent C3 (and C5) consumption via the Ca++- and Mg++-dependent classical pathway, the test was performed in the presence of the chelating agent Mg-ethylene bis (oxyethylene-nitrilo) tetraacetic acid (Mg EGTA) which interacts preferentially with Ca++. The Mg EGTA concentration was found to be critical, a final concentration of 5 mM in the assay mixture being required for optimal results. By its heat stability (54 degrees to 56 degrees C, 30 min), NF could be distinguished from other, heat-labile NF-like factors. The NF test was applied to five categories of patients with glomerulonephritis (GN). Heat-stable NF activity was found in seven of 17 sera in the membranoproliferative glomerulonephritis (MPGN) group. Two of the 12 acute poststreptococcal GN sera had NF-like activity which disappeared upon heating. Serum C3 and proactivator (PA) concentrations varied widely in all groups but a clear positive relationship was found between the presence of NF and low serum C3 concentrations in MPGN. Renal immunofluorescence in MPGN indicated a lesser amount of lg deposited in glomeruli from patients with NF when compared to the NF-negative patients. Both groups had heavy C3 deposits. The availability of a sensitive, quantitative assay for NF may help to provide further insight into the various pathogenic mechanisms in different forms of MPGN.

Acute Disease↗
PubMed1975

Failure of heparin to affect two types of experimental glomerulonephritis in rabbits.

Anticoagulation has been reported to ameliorate antiglomerular basement membrane glomerulonephritis (anti-GBM-GN) while its effect on chronic immune complex glomerulonephritis (IC-GN) as studied in the NZB mouse is unclear. Chronic serum sickness IC-GN was induced in rabbits by injecting bovine serum albumin (BSA) daily. Anti-GBM-GN was induced by i.v. injection of a known amount of heterologous anti-GBM antibody. Heparin was administered beginning at two to six weeks after the first BSA injections or before the administration of anti-GBM antibody, on various schedules from 5000 U every 12 hr to 8000 U every 8 hr. With this dosage the partial thromboplastin time remained greater than 1-1/2 to 2-1/2 times the control at the time of the subsequent heparin injection. Heparinized and nonheparinized groups were matched according to duration of disease, maximum anti-BSA concentrations or anti-GBM antibody dosage--and no significant differences were found in proteinuria; severity of the glomerular histologic lesions; or immunofluorescence patterns of immunoglobulin G (IgG), third component of complement (C3), BSA or fibrinogen-related antigen(s) (FRA). Crescent formation was not prevented. This study shows that heparin in the maximum permissible dosage is ineffective in preventing glomerular FRA deposition or altering the progression of experimental IC-GN or anti-GBM-GN in rabbits.

Animals↗