Search PubMed⌕ Search

Biomedical subjects

J S Cameron

Publications and source records attributed to J S Cameron.

At least 361 records · Page 20Linked to original sources
PubMed1976

IgA and glomerular disease.

Serum IgA levels are raised in a proportion of children with Henoch-Schönlein disease (H. S. P.), patients with Berger's mesangial IgA disease, and in patients with glomerular lesions in association with hepatic cirrhosis. These conditions are all characterized by mesangial staining with anti-IgA antisera on immunofluorescence. It has been suggested that elevated serum IgA levels are of value in the diagnosis of these diseases. We have measured serum IgA levels by radial immunodiffusion in a variety of primary and secondary glomerular diseases. High serum IgA levels were confined to patients with glomerular IgA deposition, but were not restricted to H. S. P. and Berger's disease, nor to patients with deposition of IgA only in a mesangial pattern. Elevated salivary IgA levels were found in 3/4 patients with high serum IgA levels but we found no evidence for involvement of the secretory system in glomerular mesangial IgA deposition.

Adolescent↗
PubMed1975

Local infusion of urokinase and heparin into renal arteries in impending renal cortical necrosis.

Two patients with presumed impending cortical necrosis, after haemolytic uraemic syndrome in one and after concealed accidental haemorrhage in the other, were treated by local infusion of urokinase and heparin into the renal artery. Both recovered and one regained normal renal function. Local infusion of anticoagulants or thrombolytic drugs into one renal artery offers the possibility of a controlled examination of the efficacy of this treatment in preventing cortical necrosis.

Adult↗
PubMed1975

Intrarenal platelet consumption in the diffuse proliferative nephritis of systemic lupus erythematosus.

1. Platelet survival and an index of the localization of platelets in the kidney were studied in patients with the proliferative nephritis of systemic lupus erythematosus, either focal or diffuse, and in control subjects. Platelet survival was reduced in patients with proliferative lupus nephritis, more in those with diffuse rather than focal renal involvement. 2. The index of renal platelet localization in patients with diffuse proliferative nephritis suggested an intrarenal platelet consumption not found in other groups. 3. A patient with the classical platelet autoantibody disease, idiopathic thrombocytopenic purpura, also showed reduced platelet survival but localization of platelets was in the spleen rather than the kidney. 4. Intrarenal platelet consumption in diffuse proliferative lupus nephritis may be an epiphenomenon of pre-existing scarring or platelet aggregation secondary to immune complex-formation, which contributes to the progressive sclerosing lesions of this form of nephritis.

Adult↗
PubMed1975

Seasonal nephrotic syndrome. Description and immunological findings.

Three cases are described showing a seasonal exacerbation of their nephrotic syndrome in association with an atopic trait and grass pollen allergy. The first patient has a history of four consecutive seasonal relapses each requiring steroid therapy. Following a course of desensitization injections he has now been free of relapse for 3 consecutive years. The second patient has also had a recurrent steroid-sensitive nephrotic syndrome often associated with the pollen season and allergic rhinitis. In this patient a course of cyclophosphamide has reduced his tendency to relapse. The third patient who has been on continuous prednisone therapy shows a seasonal increase in proteinuria. Serum changes in the first two patients include: a seasonal rise in total and grass pollen specific IgE; the continued presence of grass pollen specific IgG throughout the year but with a reduction during the pollen season in association with a more pronounced fall in the total IgG level; a depression in the C3 level in association with each major relapse; a mild rise in the I-K titre and a positive result in the Clq test for circulating complexes. A renal biopsy performed on the first patient when in relapse showed minor histological changes only and IgG, IgM, IgA, IgD, IgE, C3 and fibrinogen were undetectable by immunofluorescent examination. The probable mechanism for the development of proteinuria in these patients is discussed.

Adolescent↗
PubMed1975

Renal biopsy in the pig.

In the pig, needle renal biopsy proved a safe and simple procedure which caused little discomfort to the animal. It proved a valuable method for following serial changes in renal histology and can therefore be applied to the study of both spontaneous and experimental renal diseases in pigs.

Acepromazine↗
PubMed1975

Membranous nephropathy. Long-term follow-up and association with neoplasia.

Sixty-six patients of all ages whose renal biopsy appearances satisfied strict criteria for the histopathological diagnosis of membranous nephropathy were studied and followed for a mean of 5-4 years (range 1 to 20 years). From initial investigation seven patients were found to have associated neoplasia, and in two patients the condition followed treatment with a mercurial diuretic and gold. One patient was Australia antigen positive. Two patients developed renal vein thrombosis, but in both this appeared to follow not precede their nephrotic syndrome. In the remaining 56 patients there was no associated factor. During the follow-up period, approximately one-quarter of the patients (15) died, nine from renal failure; one-quarter (10) had a persistent nephrotic syndrome, another one-quarter (15) proteinuria of lesser degree. The final one-quarter (16) are now in complete remission. The prognosis of the 54 patients with an initial nephrotic syndrome was poorer than the 12 with lesser proteinuria and no oedema at onset; five of 11 children were in complete remission when last seen. All but one of the nine patients who developed terminal chronic renal failure 4 to 18 years from onset had an unremitting nephrotic syndrome, eight of the 10 currently alive with a persistent nephrotic syndrome have reduced renal function. Renal functional deterioration did not occur in the absence of proteinuria. There was only slight correspondence between the stage of biopsy appearance, glomerular filtration rate at time of biopsy, time of the biopsy from apparent onset, or status at last follow-up. Staging is therefore of limited prognostic value. Twenty-two patients were treated with corticosteroids for 2 to 36 months; we detected no short or long-term benefit when compared to patients not so treated.

Adolescent↗
PubMed1975

Experimental crystal nephropathy (one year study in the pig).

An acute crystal nephropathy was produced in pigs by feeding a mixture of guanine and allopurinol. The pathogenesis of the lesion produced was studied by serial histology and renal function tests over 12 months. Tubular blockage by the crystals produced erosion of the basement membrane and an accompanying interstitial nephritis. Tubular degeneration around the crystal mass transferred the crystals to the interstitium. Despite rapid subsequent disappearance of these crystals the interstitial nephritis was still evident nine months later. An early return of renal function to near normal was not sustained beyond nine months. It was shown that even brief periods of intratubular crystal deposition caused irreversible changes, resulting eventually in a reduction in kidney size, nephron population and renal function.

Allopurinol↗