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J S Cameron

Publications and source records attributed to J S Cameron.

At least 37 records · Page 2Linked to original sources
PubMed1999

European best practice guidelines for the management of anaemia in patients with chronic renal failure.

Best practice guidelines recommend management strategies and attempt to set standards for optimal patient care. The momentum towards formulating guidelines comes not only from health care professionals, but also from health care management organizations, who need some way of measuring the quality of the services they purchase. The European Best Practice Guidelines for the Management of Anaemia in Patients with Chronic Renal Failure have been drawn up by a Working Party including representatives of the European Renal Association/European Dialysis and Transplantation Association (ERA-EDTA) and the national nephrology societies of a cross-section of European countries. The guidelines draw on the National Kidney Foundation-Dialysis Outcomes Quality Initiative (NKF-DOQI) Clinical Best Practice Guidelines for the Treatment of Anemia in Chronic Renal Failure, but reflect European clinical practice and experience. They include additional publications, and new analysis and interpretation of the evidence base. Topics covered in the European guidelines include diagnosis of the anaemia of chronic renal failure, indications for starting treatment with epoetin, recommended minimum target haemoglobin concentrations, epoetin dosage and route of administration, assessing and optimizing iron stores, causes and management of epoetin resistance, and possible adverse effects of epoetin treatment. The guidelines are not intended to be prescriptive but rather to provide clinical guidance based on the best available evidence. The evidence supporting each guideline is graded, so that physicians may judge its reliability.

Anemia↗
PubMed1999

The very long-term prognosis and complications of lupus nephritis and its treatment.

Although the short- and medium-term (5-10 years) outcome of patients with lupus nephritis has been studied extensively, there are very few data on the second and subsequent decades. We studied outcome in 110 local patients investigated at a single centre before 1986, who all had potential follow-up of more than 10 years (actual 2-31 years, median 15.5 years). At last follow-up, 40 patients were dead and 70 alive, nine of whom were on maintenance dialysis or transplanted, actuarial survivals being 84%, 72%, 62%, 61% and 54% at 5, 10, 15, 20 and 25 years for the group as a whole. Survival was better in the cohort 1976-86 (n = 60) than in that from 1963-75 (n = 50) (90, 81 and 76% vs. 78, 56 and 43% at 5, 10 and 15 years, p < 0.001). Sepsis (12) and myocardial infarction (8) were the principal causes of death. Of living patients with renal function, 38% had normal urine and renal function, 11 were off all treatment (19%), 62% had persistent proteinuria and 18% had reduced but generally stable renal function. Renal failure, in those patients who developed it, occurred during the first decade and none of 67 patients actually followed more than 10 years subsequently went into renal failure. Induction treatment was with prednisolone, combined with azathioprine in more severe forms of nephritis, and from the middle 1970s to 1986, 30 with methylprednisolone and in 12 cases plasma exchange. Seventeen other patients were treated using oral cyclophosphamide during the 1960s. No patient received i.v. cyclophosphamide as induction therapy, although nine patients had this form of treatment later, largely because of non-compliance. Serious complications of lupus and/or its treatment occurred in 49%: sepsis in 32, ischaemic heart disease in 20, thrombosis in one and avascular necrosis of bone in eight. In contrast, fracturing osteoporosis occurred in only three, and cataracts requiring surgery and diabetes mellitus in none. The very long-term outlook of lupus nephritis, especially its more severe forms, has improved, but that with current management strategies only a minority of patients are able to stop treatment altogether, and the incidence of serious complications is high.

Adolescent↗
PubMed1999

Regulation of neuronal K(+) currents by target-derived factors: opposing actions of two different isoforms of TGFbeta.

The developmental expression of macroscopic Ca(2+)-activated K(+) currents in chick ciliary ganglion neurons is dependent on an avian ortholog of TGFbeta1, known as TGFbeta4, secreted from target tissues in the eye. Here we report that a different isoform, TGFbeta3, is also expressed in a target tissue of ciliary ganglion neurons. Application of TGFbeta3 inhibits the functional expression of whole-cell Ca(2+)-activated K(+) currents evoked by 12 hour treatment with either TGFbeta1 or beta-neuregulin-1 in ciliary ganglion neurons developing in vitro. TGFbeta3 had no effect on voltage-activated Ca(2+) currents. A neutralizing antiserum specific for TGFbeta3 potentiates stimulation of Ca(2+)-activated K(+) currents evoked by a target tissue (iris) extract in cultured ciliary ganglion neurons, indicating that TGFbeta3 is an inhibitory component of these extracts. Intraocular injection of TGFbeta3 causes a modest but significant inhibition of the expression of Ca(2+)-activated K(+) currents in ciliary ganglion neurons developing in vivo. Further, intraocular injection of a TGFbeta3-neutralizing antiserum stimulates expression of Ca(2+)-activated K(+) currents in ciliary ganglion neurons developing in vivo, indicating that endogenous TGFbeta3 regulates the functional expression of this current. The normal developmental expression of functional Ca(2+)-activated K(+) currents in ciliary ganglion neurons developing in vivo is therefore regulated by two different target-derived isoforms of TGFbeta, which produce opposing effects on the electrophysiological differentiation of these neurons.

Animals↗
PubMed1999

Lupus nephritis.

Explore the source record for details and available documents.

Autoimmunity↗
PubMed1998

Presymptomatic detection of familial juvenile hyperuricaemic nephropathy in children.

We studied 34 apparently healthy children and 2 propositi from kindreds with familial juvenile hyperuricaemic nephropathy (FJHN) - a disorder characterised by early onset, hyperuricaemia, gout, familial renal disease and a similarly low urate clearance relative to glomerular filtration rate (GFR) [fractional excretion of uric acid (FEur) 5.1+/-1.6%] in young men and women. In addition to the propositi, 17 asymptomatic children were hyperuricaemic -- mean plasma urate (368+/-30 micromol/l), twice that of controls (154+/-41 micromol/l). Eight of them had a normal GFR ( > 80 ml/min per 1.73 m2), and 11 renal dysfunction, which was severe in 5. The FEur in the 14 hyperuricaemic children with a GFR > 50 ml/min was 5.0+/-0.5% and in the 5 with a GFR < or =50 ml/min was still low (11.5+/-0.2%) compared with controls (18.4+/-5.1%). The 17 normouricaemic children (185+/-37 micromol/l) had a normal GFR (>80 ml/min) and FEur (14.0+/-5.3%). The results highlight the dominant inheritance, absence of the usual child/adult difference in FEur in FJHN and presence of hyperuricaemia without renal disease in 42% of affected children, but not vice versa. Since early allopurinol treatment may retard progression to end-stage renal failure, screening of all relatives in FJHN kindreds is essential.

Adolescent↗
PubMed1998

Developmental regulation of neuronal K+ channels by target-derived TGF beta in vivo and in vitro.

The functional expression of Ca2+-activated K+ channels (KCa) in developing chick ciliary ganglion (CG) neurons requires interactions with target tissues and preganglionic innervation. Here, we show that the stimulatory effects of target tissues are mediated by an isoform of TGFbeta. Exposure of cultured CG neurons to TGFbeta1, but not TGFbeta2 or TGFbeta3, caused robust stimulation of KCa. The KCa stimulatory effects of target tissue extracts were blocked by a neutralizing pan-TGFbeta antiserum but not by specific TGFbeta2 or TGFbeta3 antisera. Intraocular injection of TGFbeta1 caused robust stimulation of KCa, whereas intraocular injection of pan-TGFbeta antiserum inhibited expression of KCa in CG neurons developing in vivo. The effects of TGFbeta1 were potentiated by beta-neuregulin-1, a differentiation factor expressed in preganglionic neurons.

Animals↗
PubMed1998

ATP-sensitive K+ channels in cardiac muscle from cold-acclimated goldfish: characterization and altered response to ATP.

ATP-sensitive potassium channels (K(ATP)) play an important, if incompletely defined, role in myocardial function in mammals. With the discovery that K(ATP) channels are also present at high densities in the hearts of vertebrate ectotherms, speculation arises as to their function during periods of cold-acclimation and depressed ATP synthesis. We used single-channel and intracellular recording techniques to examine the possibility that channel activity would be altered in cardiac muscle from goldfish (Carassius auratus) acclimated at 7+/-1 degrees C relative to control (21+/-1 degrees C). As previously observed in mammals, K(ATP) channels in isolated ventricular myocytes were inwardly rectified with slope conductances of 63 pS. However, channel mean open-time and overall open-state probability (Po) were significantly increased in cells from the cold-acclimated animals. In addition, K(ATP) channels in cells from fish acclimated at 7 degrees were nearly insensitive to the inhibitory effects of 2 mM ATP, whether studied at 7 or at 21 degrees C. Transmembrane action potential duration (APD) in hearts of cold-acclimated fish studied at 21 degrees was significantly shorter than that observed in hearts of warm-acclimated fish at the same temperature; this difference was eliminated by the K(ATP) channel antagonist glibenclamide (5 microM). These data suggest that K(ATP) channels in the hearts of cold-acclimated animals are more active and less sensitive to ATP-inhibition than those in warm-acclimated fish, possibly reflecting a functional adaptation to promote tolerance of low temperatures in this species.

Acclimatization↗
PubMed1997

The introduction of renal biopsy into nephrology from 1901 to 1961: a paradigm of the forming of nephrology by technology.

'Biopsy' (Besnier 1895) became useful towards the end of the 19th century with the development of good histology and microbiology. Needle biopsy of the liver, although first performed in 1895, did not become current until 50 years later. Surgical biopsy of the kidney at incidental operations, particularly the then fashionable renal decapsulation, was performed from 1900 to 1930. Percutaneous needle renal biopsy was introduced after first, the successful liver biopsy and second, demonstration of the value of aspiration needle biopsy in tumours of the kidney. In addition, a number of physicians obtained renal tissue by accident and without problems during intended biopsies of the liver. Nils Alwall of Sweden performed the first systematic aspiration needle biopsies of the kidney in 1944, but did not publish his results because of an early death which led him to abandon the technique. However, when Iversen and Brun in Copenhagen described their results in 1951, a number of physicians around the world immediately began to attempt renal biopsy, using cutting as well as aspiration techniques. Success was inconsistent and operator dependent: the refinements of technique and needles introduced by the group in Chicago led by Robert Kark, plus their advocacy of the technique and their training of many physicians in its performance rapidly led to widespread acceptance. New techniques of immunofluorescence and electron microscopy arrived at the same time so that the technique could be fully exploited. The performance and interpretation of renal biopsies became, along with classical whole-organ and nephron physiology and the introduction of dialysis and transplantation, powerful agents determining the emergence of Nephrology as a specialty around 1960.

Biopsy, Needle↗
PubMed1996

Trypsin alters ATP sensitivity of KATP channels in control and hypertrophied myocytes.

Increased ATP-sensitive potassium (KATP) channel activity in cardiac muscle during hypertension and myocardial hypertrophy may be induced by the release of endogenous proteases, altering inhibitory binding sites for intracellular ATP. To test this hypothesis, we studied the effects of trypsin (1.5 mg/ml) on channel sensitivity to ATP in myocytes from control (WKY) and spontaneously hypertensive rats (SHR). Trypsin increased channel activity in 63% of membrane patches from WKY rats, but in only 29% from SHR. Pre-treatment with trypsin decreased sensitivity to the inhibitory effects of ATP in both groups. These results support the possibility that KATP channel modification during chronic metabolic stress is caused by intracellular proteolysis, which decreases sensitivity to [ATP]i.

Adenosine Triphosphate↗
PubMed1996

Don't forget sickled cells in the urine when investigating a patient for haematuria.

Haematuria is a well-known complication of sickle cell disease. A South African coloured patient with repeated episodes of gross haematuria is described in whom the diagnosis of sickle cell disease was suggested after the finding of sickled erythrocytes in the urine sediment. The diagnosis was then confirmed by haemoglobin electrophoresis, which revealed sickle cell trait (Hb-AS). It is concluded that sickle erythrocytes must be looked for when urine is microscopically scrutinized to determine the source of a haematuria.

Adolescent↗
PubMed1996

Impaired outcome of continuous ambulatory peritoneal dialysis in immunosuppressed patients.

BACKGROUND: Although immunodeficiency predisposes to CAPD peritonitis with fungal or unusual organisms, the role of immunosuppression as a predisposing factor for CAPD peritonitis, as well as the outcome of such episodes, remains uncertain. METHODS: The incidence, spectrum of infectious organisms, and outcome of CAPD peritonitis was retrospectively reviewed in 39 immunosuppressed and 146 non-immunosuppressed patients treated with CAPD over the calendar year 1993. RESULTS: Immunosuppressed patients were younger (mean 44 vs 57 years, P<0.001) and had an increased incidence of previous transplantation, glomerulonephritis, systemic lupus erythematosus, and vasculitis. Immunosuppressed patients had more episodes of peritonitis (69/29 patients vs 99/147, P<0.001), required more frequent hospital admission (25/39 vs 33/146, P<0.001), had more days off CAPD (331 vs 242, P<0.001), and required more laparotomies to remove infected CAPD catheters (11/39 vs 14/146, P<0. 01). Immunosuppression was associated with increased infection due to S.aureus and fungi, which may have contributed towards increased morbidity in this group. Current immunosuppression or a recent history of immunosuppression appeared to be equally potent risk factors for infection. There was a trend for the incidence of infection to parallel the aggressiveness of immunosuppression. CONCLUSIONS: Immunosuppression is an important risk factor for CAPD peritonitis. A high index of suspicion for infection and aggressive chemotherapy are mandatory. CAPD may not be the initial therapy of choice in this high-risk group.

Adult↗