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Biomedical subjects

C D Short

Publications and source records attributed to C D Short.

At least 55 records · Page 3Linked to original sources
PubMed1989

Fundus changes in mesangiocapillary glomerulonephritis type II: vitreous fluorophotometry.

We have described a complex abnormality of retinal pigment epithelium, Bruch's membrane, and choriocapillaris in mesangiocapillary glomerulonephritis (MCGN) type II. Patients with MCGN type II were examined by vitreous fluorophotometry which reveals that there is a breakdown of the blood retinal barrier (BRB) in those patients with the typical fundus lesions. The function of this barrier was calculated as a penetration ratio and was statistically greater in these patients when compared with a group of (a) normal persons, (b) patients with drusen, and (c) patients with other forms of glomerulonephritis.

Blood-Retinal Barrier↗
PubMed1989

Sequential development of systemic vasculitis with anti-neutrophil cytoplasmic antibodies complicating anti-glomerular basement membrane disease.

Anti-neutrophil cytoplasmic antibodies (cANCA) were detected in 3 patients with anti-glomerular basement membrane (anti-GBM) disease. All 3 cases presented late in their clinical course, with severe renal involvement and alveolar hemorrhage. Anti-neutrophil cytoplasmic antibodies were associated with clinical features outwith the lungs and kidneys; in one case cANCA were initially absent but subsequently developed concurrently with the clinical appearance of systemic vasculitis as the anti-GBM antibody titer was falling. These findings confirm that cANCA can complicate anti-GBM disease and suggest that cANCA may identify a distinct subset of patients with anti-GBM disease, supporting a pathogenic role for cANCA in the development of systemic vasculitis.

Anti-Glomerular Basement Membrane Disease↗
PubMed1988

Prognostic indicators in patients presenting with the nephrotic syndrome.

Clinical data from 246 patients presenting with a nephrotic syndrome and biopsy-proven glomerular disorder were analyzed, using statistical survival techniques, to determine which of several variables (sex, age, plasma creatinine, diastolic blood pressure and 24-hour urinary protein loss) were associated with subsequent end-stage renal failure. The best prediction of outcome could be made at one year (N = 121); then plasma creatinine (P less than 0.001) and heavy proteinuria (P = 0.049) were the best determinants. For a given plasma creatinine level, heavy urinary protein was associated with a worse outcome. The incidence of end-stage renal failure was greatest three to four years from the date edema first developed. Plasma creatinine and urinary protein values, collected four-monthly throughout the study period, were analyzed as time-dependent covariates. A relationship was found between the prevailing risk of renal failure and earlier heavy proteinuria (P less than 0.001). Spontaneous complete remission of proteinuria was associated with a highly favorable outcome (P = 0.001) and normal, or impaired but stable, renal function.

Actuarial Analysis↗
PubMed1988

Rheumatoid disease presenting as a nephrotic syndrome.

A 62 year old man with no relevant previous history presented with a nephrotic syndrome. Renal biopsy showed a membranous glomerulopathy and coincident investigation showed high serum titres of rheumatoid factors. It was not until some months later that he developed articular and extra-articular manifestations of rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1987

Methylprednisolone in patients with membranous nephropathy and declining renal function.

Fifteen consecutive patients aged 24 to 70 years, with membranous nephropathy and a progressive decline in renal function, were treated with methylprednisolone, 1 g intravenously daily for five days, followed immediately by a tapering dose of oral prednisolone. Plasma creatinine levels fell by a mean of 46 per cent (range 21-65). In 10 patients the beneficial effect was sustained, but in three it had reversed by six months. In the other two patients the progressive decline of renal function was not influenced. These observations suggest that many patients with membranous nephropathy and declining renal function could benefit from intervention with high dose steroids.

Adult↗
PubMed1986

Diagnosis of disease in renal allografts: correlation between ultrasound and histology.

Ultrasound was compared with histology in 66 cases to assess the accuracy of sonography in demonstrating abnormality in renal allografts. Patients with suspected acute, chronic or acute and chronic rejection, acute tubular necrosis and glomerulonephritis in the transplant kidney were included in the study. It was noted in this trial that ultrasound is less accurate at demonstrating abnormality in the grafted kidney than has been suggested previously in the literature. It was concluded that, where doubt exists, even when ultrasound examination is normal, biopsy should be considered.

Biopsy↗
PubMed1986

Serum and urinary high density lipoproteins in glomerular disease with proteinuria.

The serum lipoprotein concentrations, including high-density lipoprotein (HDL) subfractions and apolipoproteins Al and B were measured in 21 patients (14 male and seven female) with nephrotic range proteinuria (greater than 3g/24hr), well maintained renal function (creatinine clearance greater than 35 mliter/min/1.73m2) and biopsy-proven primary glomerular disease. In these, and in a further five patients (creatinine clearance greater than 15 mliter/min/1.73m2), urinary apolipoprotein Al output was determined. Total HDL cholesterol was similar in patients and controls, but in male patients, HDL2 was low (0.54 +/- 0.10 mmole/liter, mean +/- SEM) compared to controls (0.75 +/- 0.04 mmole/liter, P less than HDL3 was high (0.81 +/- 0.07 in patients and 0.63 +/- 0.02 mmole/liter in controls, P less than 0.01). In women, there was a similar tendency for HDL2 to be lower in patients (0.68 +/- 0.18 mmole/liter) than in controls (0.85 +/- 0.10 mmole/liter). Multiple regression analysis revealed that major determinants of the urinary apolipoprotein Al output were the urinary protein output and selectivity index (multiple r = 0.85). Furthermore, some patients lost apolipoprotein Al into their urine at rates indicating increased production of apolipoprotein Al in the nephrotic syndrome. The serum HDL subfraction concentrations in the nephrotic syndrome could be explained by a combination of increased HDL production and increased urinary loss of low molecular wt HDL.

Aged↗
PubMed1986

Impaired IgG response to tetanus toxoid in human membranous nephropathy: association with HLA-DR3.

The IgG response to tetanus toxoid (TT) immunization was quantitated by by radioimmunoassay in patients with membranous nephropathy (MN) and healthy controls. Variation in subclass (ELISA) and electrical charge (isoelectric focussing, immunofixation & autoradiography) of the IgG response were also assessed. Total IgG and igG subclass responses were impaired in MN compared to controls, although this was only significant for IgG-3 (P less than 0 X 05). Non responders to TT were more common in MN, and response was independent of disease activity. No distinctive pattern of IgG subclass response or IgG spectrotype was seen in MN. Impaired response to TT was associated with HLA-DR3 among controls, and in MN (88 X 8% of whom were DR3) markedly depressed responses occurred in apparent DR3 homozygotes.

Antibodies, Bacterial↗
PubMed1985

Effects of the calcium-channel agonist CGP 28392 on insulin secretion from isolated rat islets of Langerhans.

The rate of insulin secretion from isolated rat islets of Langerhans was affected by a number of dihydropyridine derivatives known to interact with voltage-sensitive Ca2+ channels in excitable cells. The channel antagonists nifedipine and nitrendipine were potent inhibitors of glucose-induced insulin secretion in response to both 8 mM- and 20 mM-glucose, although they did not lower the basal secretion rate observed in the presence of 4 mM-glucose. The Ca2+-channel agonist, CGP 28392, also failed to alter the basal rate of insulin secretion. In the presence of 8 mM-glucose, however, 1 microM-CGP 28392 enhanced the insulin-secretion rate to a value approximately double that with 8 mM-glucose alone. This effect was dose-dependent, with half the maximal response elicited by 0.1 microM-CGP 28392, and full enhancement at 10 microM. The response was rapid in onset, with an increase in insulin secretion evident within 2 min of CGP 28392 infusion in perifused islets. Stimulation of insulin secretion by CGP 28392 was correlated with a rapid enhancement of glucose-stimulated 45Ca2+ uptake into islets cells, and with a transiently increased rate of 45Ca2+ efflux from pre-loaded islets. Stimulation of insulin secretion by CGP 28392 was abolished in the presence of noradrenaline, although under these conditions the rapid stimulation of 45Ca2+ influx induced by CGP 28392 was only partially inhibited. In contrast with these results, when islets were incubated in the presence of 20 mM-glucose, CGP 28392 caused a dose-dependent inhibition of insulin secretion. Half-maximal inhibition required approx. 0.2 microM-CGP 28392, with maximal effects observed at 10 microM. Under these conditions, however, the extent of insulin secretion was still only decreased by about 50%, to a value which was similar to that seen in the presence of 8 mM-glucose and CGP 28392. These results suggest that dihydropyridine derivatives can alter the activity of voltage-dependent Ca2+ channels in islet cells, and are consistent with the possibility that gating of these channels plays an important role in regulating the rate of insulin secretion after glucose stimulation.

Animals↗
PubMed1983

Intoxication by aspirin and alcohol in a child. A case of child abuse by medical neglect.

Investigation of child abuse deaths is often hindered by meager or unusual autopsy findings. Circumstantial factors are crucial in such investigations for a thorough understanding of the mechanism and manner of death. We present a case of childhood poisoning from aspirin and alcohol to demonstrate the medical neglect by the parents and the blatant discrepancies between the history provided by the parents and the actual facts preceding the child's death.

Alcoholic Intoxication↗