Search PubMed⌕ Search

Biomedical subjects

J S Cameron

Publications and source records attributed to J S Cameron.

At least 199 records · Page 11Linked to original sources

Adult-onset minimal change nephrotic syndrome: a long-term follow-up.

A series of 89 adult-onset nephrotic patients with minimal changes on renal biopsy was analyzed to compare the rate of response to corticosteroids and cytotoxic agents and the stability of remission or frequency of relapses at different ages. Severe hypertension and diminished renal function were more common in patients aged over 60 years, who formed 22.5% of the group. Seventy-five patients were given a first course of prednisolone in an initial dose of 60 mg/24 hr. After an eight week course of tapering doses of corticosteroids, only 45 of the 75 patients were in complete remission, 55 patients after 16 weeks and eventually 58 lost their proteinuria. The respective estimates of remission were 60%, 76% and 81%. Subsequently, of the 58 treated patients who responded, 24% never relapsed. Fifty-six percent of the patients relapsed on a single occasion or infrequently, and only 21% were frequent relapsers. Cyclophosphamide was used in 36 patients, in two as initial treatment, in 11 because of corticosteroid resistance, and in the remainder because of relapses. The time-course of loss of proteinuria was similar to that following treatment with corticosteroids, 25 (69%) losing proteinuria within 16 weeks. Only four patients failed to lose their nephrotic syndrome. Two of them had presented in acute renal failure and all four were over 60 years of age. The stability of remission after cyclophosphamide was better than that reported for children, only 13 of 36 showing relapses and 66% being in remission at five years, after which no further relapses were seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗

The Goodpasture antigen in Alport's syndrome: studies with a monoclonal antibody.

A mouse monoclonal antibody (MCA-P1), which recognizes an antigenic determinant in human glomerular basement membrane against which autoantibodies are directed in Goodpasture's syndrome, was used in indirect immunofluorescence studies to investigate glomerular basement membrane structure in Alport's syndrome. We found reduced or absent binding of MCA-P1 to glomerular and distal tubular basement membranes in renal biopsy tissue from ten patients with Alport's syndrome. Antiglomerular basement membrane antibody eluted from the kidneys of a patient who had died from Goodpasture's syndrome was used to confirm these findings. In contrast, there was bright linear fluorescence of MCA-P1 on glomerular and tubular basement membranes of normal renal material and renal biopsy tissue obtained from patients with a variety of glomerulonephritides. These results suggest an abnormality or a variable quantity of the immunoreactive autoantigen in the glomerular basement membrane of patients with Alport's syndrome. Furthermore, MCA-P1 may be of value in the diagnostic interpretation of renal biopsies from patients with familial nephritis.

Anti-Glomerular Basement Membrane Disease↗

Platelet-associated IgG in idiopathic glomerulonephritis and the nephritis of systemic lupus erythematosus.

We studied platelet-associated IgG (PAIgG) in patients with the nephritis of systemic lupus erythematosus (SLE) and with idiopathic glomerulonephritis (IGN), and found no increase in PAIgG in the patients with IGN, and an increase in only a minority of patients with SLE, all of whom had active disease. Patients with IGN and a nephrotic syndrome had both a low serum IgG and a low PAIgG. The increase in PAIgG in the patients with SLE correlated with the titres of antibody against dsDNA in the serum, but not with the platelet-agglutinating immune complexes also present. Intraplatelet serotonin, however, was reduced in both groups, and this correlated with the amounts of platelet-agglutinating complexes in the serum of the SLE patients. Immune complexes may associate with platelets in vivo to cause this release, but if so this must be a reversible phenomenon ('hit and run' immune platelet injury); alternatively, the Fc binding to the platelet surface may be weak and insufficient to survive the ex vivo washing procedures.

Blood Platelets↗

Morphological differentiation between rejection and cyclosporin nephrotoxicity in renal allografts.

In a prospective study of renal dysfunction in 60 consecutive allograft recipients treated with cyclosporin and prednisolone routine renal biopsies at one week and one month after transplantation, as well as for all episodes of renal dysfunction, were performed. The one year graft survival of this group was 88%. In a retrospective clinical analysis of these patients 35 episodes of dysfunction due to rejection, defined by a response to antirejection treatment alone, and 30 episodes due to cyclosporin nephrotoxicity, defined by a response to reduction in cyclosporin dose alone, were identified. The morphological findings from these biopsies were compared with 20 samples from routine biopsies taken from patients with stable renal function. All patients diagnosed as having rejection had a diffuse, interstitial mononuclear cell infiltrate (32 of 35) or arteritis (19 of 35), or both. In contrast, focal mononuclear cell infiltrates were common in both patients with nephrotoxicity and those with stable function (17 of 30 and 14 of 20, respectively). There were no important differences between biopsies from those with nephrotoxicity and those with stable function, except that arteriolar hyalinosis was considerably more common in the nephrotoxic patients than in those with stable function. Many patients with stable function were, in retrospect, in a state of stable mild nephrotoxicity. In our experience rejection should only be diagnosed when there is at least a diffuse interstitial infiltrate or an arteritis. Focal mononuclear cell infiltrates do not denote rejection. The development of arteriolar lesions in the absence of rejection is indicative of nephrotoxicity.

Adolescent↗

Platelet-associated DNA and anti-DNA antibody in systemic lupus erythematosus with nephritis.

We report DNA and specific anti-dsDNA antibody (dsDNAb) in excess of controls, associated with platelets from 35 patients with systemic lupus erythematosus (SLE). Deoxyribonuclease (DNase) treatment of intact platelets resulted not only in a drop in platelet-associated DNA, but also a dramatic fall in platelet-associated dsDNAb. This suggests that at least some DNA and virtually all the dsDNAb is bound to the platelet surface, probably in the form of an immune complex. The quantity of platelet-associated DNA did not correlate with amounts of platelet-associated anti-dsDNA antibody (PAdsDNAb); perhaps because platelets also have receptors for DNA itself. Total platelet-associated IgG was elevated in only six patients with normal PAdsDNab.

Antibodies, Antinuclear↗

Role of antigenic charge and antibody avidity on the glomerular immune complex localization in serum sickness of mice.

Passive injection of mice with preformed immune complexes (IC) made from cationized bovine serum albumin (BSA) and anti-native BSA antibody gave immune deposits along the glomerular capillary walls at predominantly subepithelial sites, while similar quantities of complexes made with native, anionized BSA did not deposit. Peripheral localization could be obtained also using low avidity antibody and a great excess of native BSA. Ultracentrifugation analysis showed that the size of IC in the animals given complexes containing cationized BSA was a little larger than 7 S, whereas those formed with the native or anionized BSA were around 19 S. The anti-native BSA antibody had a low avidity for cationized BSA in vitro, and thus all the IC which could deposit peripheral capillary walls were small and contained low avidity antibody. Chemical cationization of BSA alters the precipitability of the antibody and also the size and stability of the complexes formed. In an active model, injection of cationized BSA into mice preimmunized with cationized BSA caused localization of the BSA and its antibody in the peripheral capillary walls. Analysis of the circulating IC formed in this model also revealed low avidity of antibody and small-sized IC. From these results, it is clear that chemical cationization of antigen changes the characteristics of the antigen-antibody interaction, e.g. low precipitating efficiency and the formation of small-sized IC. Therefore, in addition to interaction of cationized IC with the polyanion layer of the glomerular basement membrane (GBM), the properties of antigen-antibody interaction play an important role in the deposition of IC along the peripheral capillary walls in a model of membranous glomerulonephritis.

Animals↗

Effects of amrinone on contraction and K+-induced contracture of normal and subacutely failed cat ventricular muscle.

Normal right ventricular muscles and similar preparations obtained from cats with signs of subacute right ventricular failure (RVF) (3 to 14 days after pressure overload induced by pulmonary artery coarctation) were studied during stimulation (at 0.5 Hz) and exposure to high-K+ Tyrode's solution. Twitch force, rate of force development (dP/dt), and rate of relaxation (-dP/dt) were significantly lower in RVF muscles compared with control muscles; duration of the twitch was significantly longer. Time to peak force was unchanged. Amrinone (5.3 x 10(-4)M) increased twitch force and dP/dt in normal muscle; however, the drug had no significant effects on twitch force and dP/dt in RVF muscles. Also unlike its action in control muscle, duration of the twitch was reduced by amrinone in failed muscle. Amrinone reduced K+ contracture force similarly in control and RVF muscle. In control and RVF muscles, isoproterenol (1.0 x 10(-6)M) significantly increased twitch force and dP/dt and reduced K+ contracture, while ouabain increased twitch force, dP/dt, and K+ contracture. The differential effects of amrinone on RVF and control muscles may reflect cellular defects associated with experimental ventricular failure.

Aminopyridines↗

Renal transplantation in patients treated with haemodialysis and short term and long term continuous ambulatory peritoneal dialysis.

Forty two adult patients who had been treated with continuous ambulatory peritoneal dialysis for one to 142 weeks (mean (SD) 38 (36)) received a total of 44 allografted kidneys. Twenty one had been treated with continuous ambulatory peritoneal dialysis for less than 26 weeks (mean 11 (8)) and the other 21 for longer than 26 weeks (mean 64 (35)). These two groups were compared with 55 patients who had been treated with haemodialysis and received a total of 63 grafts. In the group of patients treated with continuous ambulatory peritoneal dialysis azathioprine and low dose prednisolone were used as the immunosuppressive regimen for 20 transplantations in 18 patients, and 24 patients receiving 24 grafts were treated with cyclosporin A and low dose prednisolone. In the group of patients treated with haemodialysis 38 patients receiving 43 grafts were treated with azathioprine and low dose prednisolone, and 20 patients receiving 20 grafts were treated with cyclosporin A and low dose prednisolone. Actuarial survival of patients and grafts at two years was 95% and 72%, respectively, in the continuous ambulatory peritoneal dialysis group compared with 89% and 58%, respectively, in the haemodialysis group. No difference was found in graft survival between short term treatment with continuous ambulatory peritoneal dialysis (72% graft survival) and long term treatment (65% graft survival). In conclusion, continuous ambulatory peritoneal dialysis is suitable treatment for patients awaiting renal transplantation.

Adolescent↗

Differentiation between allograft rejection and cyclosporin nephrotoxicity in renal-transplant recipients.

In a retrospective study of 60 renal-transplant patients immunosuppressed with cyclosporin no specific clinical features differentiated allograft dysfunction responsive to anti-rejection therapy from dysfunction responsive to reduction in cyclosporin dosage. Histologically, allograft dysfunction responsive to anti-rejection therapy was strongly associated with diffuse interstitial infiltration by mononuclear cells, oedema, and haemorrhage, vascular endothelial-cell proliferation, and infiltration of arterial walls by mononuclear cells. Arteriolar medial hypertrophy and hyalinosis were more commonly found in biopsy specimens from allografts with dysfunction responsive to reduction in cyclosporin dose than in those with dysfunction responsive to anti-rejection therapy and those with stable or improving function. Whole-blood cyclosporin concentrations were significantly lower in patients with dysfunction reversed by anti-rejection therapy than in those with dysfunction reversed by reduction in cyclosporin dose or in those with stable function. There was, however, considerable overlap between these groups, so that individual cyclosporin measurements were of little diagnostic value.

Adolescent↗

Myocardial infarction in the guinea pig: cellular electrophysiology.

The cellular electrophysiology of left ventricular preparations from guinea pig hearts was studied 1 hour, 24 hours, and 4-6 weeks after myocardial infarction produced by 6-8 single ties of the distal left coronary artery system or after sham operation. Microelectrode recordings were used to monitor cells from the endocardial surface of each preparation in tissue bath. All coronary ligated preparations displayed accelerated spontaneous activity compared to normal and sham operated preparations. Single and multiple premature ventricular depolarizations occurred frequently in coronary ligated and rarely in normal and sham operated preparations. Premature stimuli delivered to areas overlying and bordering the area of infarction, induced short bursts of self-terminating rapid repetitive ventricular activity in 4 of 8 (50%) acute (1-hour), 5 of 9 (55%) subacute (24-hour), and 14 of 20 (70%) healed (4-6-week) infarcted preparations. Such activity could not be induced in normal and sham operated preparations. The preparations with healed infarction were unique in that they demonstrated runs of self-terminating repetitive ventricular activity which occurred spontaneously or was inducible with premature stimulation. Recordings from multiple sites in acute, subacute, and healed preparations revealed a variety of transmembrane action potential abnormalities (i.e., reduced action potential amplitude and resting potential, decreased and increased action potential duration, and depressed maximum rates of phase 0 depolarization) in cells overlying and bordering areas of infarction. Only Purkinje fiber action potentials were recorded over the healed infarcts. These data demonstrate that a spectrum of electrophysiological alterations occur in response to ischemic injury and persist after healing of the injury in this new model of myocardial infarction utilizing the guinea pig.

Action Potentials↗

Long-term outcome for children with minimal-change nephrotic syndrome.

A retrospective study was undertaken to assess the outcome of a cohort of 183 unselected children who presented with the nephrotic syndrome between 1963 and 1969. All subjects showed minimal glomerular changes in biopsy samples and were given conventional steroid therapy. Information was available on 152 children, now aged 14-32 years. Activity persisted longer in patients presenting at an early age. The outcome for most of the children was favourable. Only 10 patients (5.5%), all of whom presented with initial symptoms before their 6th birthday, continued to have steroid-responsive relapses in adult life. There were 11 deaths, of which 7 (4% of the series) were from avoidable complications of the disorder.

Adolescent↗

Why do patients with lupus nephritis die?

Over 20 years 42 of 138 patients with systemic lupus erythematosus "died"--that is, suffered actual death or went into terminal renal failure, or both; data from 41 were available for analysis. In most patients the causes of death were multiple. Twenty seven patients went into terminal renal failure, of whom 25 were offered dialysis treatment. Three regained renal function later, 12 survived on dialysis or with functioning kidney allografts--almost all with inactive lupus--but 13 died after starting dialysis, most within a few weeks or months. The principal causes were active lupus or infection. In those patients with renal failure after rapid deterioration in renal function (n = 14) there were nine deaths, while of 10 patients with a slow evolution into renal failure, only four died. Four patients with impaired and 10 with normal renal function died, again most often from complications of lupus or from infection. Vascular disease was a major cause of death in seven patients, all but two of whom were young; of 15 postmortem examinations, eight showed severe coronary artery atheroma, and three surviving patients required coronary bypass operations. Analysis of the timing of death or entry into renal failure showed that in 12 out of 13 patients who died within two years of onset the lupus was judged to be active, while this was true in only eight out of 19 patients who died later. Six of the seven vascular deaths occurred later than two years from onset, while only nine of 26 renal "deaths" occurred before two years; deaths from infections (n = 13) were distributed equally. Despite this and aggressive treatment of active disease, the principal cause of actual death was uncontrolled lupus.

Adolescent↗

Differential effects of calcium antagonists on viability of adult rat ventricular myocytes.

This study was designed to determine whether the various classes of Ca2+ channel blockers have differential protective effects on isolated adult rat ventricular myocytes exposed to high K+ under anoxic (100% N2) conditions. Calcium-tolerant myocytes were incubated under control (4mM K+) aerobic conditions and then subjected to high K+ (75 mM) and N2. The cells were assessed by morphological criteria (i.e. absence of blebbing, granulation etc.), maintenance of ATP levels, exclusion of trypan blue, and the presence or absence of spontaneous contractile activity. Under control conditions, the cells were quiescent and declined at a rate of approximately 10%/h. In the absence of O2, the rate of cell decline was significantly faster. Verapamil, diltiazem and the dihydropyridines had no significant effects on cell decline under these conditions. Cells exposed to 75 mM K0+ exhibited contractile activity and accelerated rate of decline under anoxic conditions; these effects were independent of lowering Na0+ to 75mM. Cells in high K0+ and N2 were significantly protected (i.e. contractile activity and rate of decline were decreased) by verapamil, less so by diltiazem, and not at all by the dihydropyridines. The uptake of 45Ca2+ into cells in high K0+ was not significantly altered by verapamil or diltiazem. Caffeine induced the immediate cessation of contractile activity of cells incubated in high K0+, but did not affect the accelerated rate of cell declined under anoxic conditions. Verapamil and diltiazem still conferred significant protection in this non-beating cell preparation. Neither verapamil nor diltiazem had any effect on the oscillation frequency of skinned heart cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

The continued care of pediatric patients with renal disease into adult life.

The transition in continuing care of children with chronic or relapsing renal diseases to units of adult internal medicine has received surprisingly little attention. The types of children with renal disease requiring continuing care into adult life are reviewed and the practical problems of making the transfer discussed.

Adolescent↗

Glomerular thrombi in renal allografts associated with cyclosporin treatment.

We have found glomerular capillary thrombi or afferent arteriolar thrombosis in eight renal biopsy specimens from seven renal allograft recipients. All patients were receiving cyclosporin and prednisolone. Biopsies were performed either routinely one and four weeks after transplantation or during periods of renal dysfunction. None of the patients whose biopsy material contained glomerular thrombi was considered, in retrospect, to have been undergoing rejection at the time of biopsy. Thrombi consisted of finely granular material partially obstructing glomerular capillaries. By light microscopy the staining characteristics of the thrombi were compatible with platelet-fibrin aggregates, and this was confirmed by immunoperoxidase examination. Such thrombi have not previously been seen in biopsy material from patients treated with prednisolone and azathioprine, except rarely associated with acute vascular injection. In none of these patients was there haematological evidence of the haemolytic uraemic syndrome as has been reported in bone marrow recipients treated with cyclosporin.

Adult↗