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Biomedical subjects

J M Bone

Publications and source records attributed to J M Bone.

At least 55 records · Page 3Linked to original sources
PubMed1988

Hypoglycaemia following treatment of hyperkalaemia with insulin and dextrose.

We describe four patients who developed symptomatic hypoglycaemia following treatment of hyperkalaemia with insulin and dextrose. Two patients had a delayed onset of hypoglycaemia, between 5 and 6 hours after treatment despite use of a 'soluble' type of insulin. A review of the literature revealed a variety of insulin and dextrose regimes but no research to assess the metabolic effects of such therapy in patients with renal failure. The possibility of significant hypoglycaemia following use of insulin and dextrose in the recommended dosages is rarely mentioned. The cases we describe demonstrate that there is no 'correct' dose of insulin and dextrose to suit every circumstance. Regular blood glucose estimations should be performed in all patients receiving such therapy for hyperkalaemia.

Adult↗
PubMed1988

Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure.

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.

Blood Pressure↗
PubMed1988

Sepsis: a cause of aluminum release from tissue stores associated with acute neurological dysfunction and mortality.

We report six cases of patients with renal failure and exposure to aluminum who developed septicemia. In all cases the serum aluminum increased markedly. This may have contributed to the neurological dysfunction seen in five, and the deaths of four of the patients. We suggest that the rise in serum aluminum was due to the release of tissue-bound aluminum, resulting in an increase in free, diffusable aluminum and that this jeopardized both neurological function and immunocompetence.

Acute Disease↗
PubMed1988

Increased incidence of anti-glomerular basement membrane antibody (anti-GBM) nephritis in the Mersey Region, September 1984-October 1985.

We report an increase in the incidence of anti-glomerular basement membrane antibody nephritis in the Mersey Region over the 13 months from September 1984 to October 1985. During this period anti-glomerular basement membrane antibody nephritis was diagnosed in 10 patients: seven cases occurred between 1 June and 31 October 1985. We could identify no common infective agent or history of toxic exposure. Although outbreaks of parvovirus infection were reported in the region during this period, no patient had serological evidence of recent infection with parvo- or other virus. The only atypical feature was the high incidence of allergic rash which was seen in four of six patients treated with antibiotics before admission. Only two patients recovered sufficient renal function to make dialysis unnecessary. Both had a longer duration of prodromal symptoms, lower levels of circulating anti-glomerular basement membrane antibody antibodies and histological evidence of less aggressive disease.

Adult↗
PubMed1987

Effect of cyclosporin, previous third-party transfusion, and pregnancy on antibody development after donor-specific transfusion before renal transplantation.

Non-cytotoxic and cytotoxic antibodies were sought after donor-specific transfusion (DST) in 12 potential renal transplant recipients given concomitant cyclosporin therapy and 13 given DST alone. Non-cytotoxic antibodies, which have been shown to develop after third-party transfusion and to be associated with successful transplantation, developed after DST whether or not cyclosporin was given. Donor and panel reactive lymphocytotoxic antibodies developed relatively infrequently after DST with or without cyclosporin. Donor-specific sensitisation occurred only in patients who were multiparous or had over 10 third-party transfusions. Non-cytotoxic Fc-receptor-blocking antibodies may play a part in the improved survival of one-haplotype-mismatched transplants pretreated with DST.

Antibodies↗
PubMed1985

Follow-up prednisolone dosage in rapidly progressive crescentic glomerulonephritis successfully treated with pulse methylprednisolone or plasma exchange.

Of nineteen patients with RPCGN who responded promptly to initial treatment with PMP or PX, and who were subsequently maintained on oral immunosuppression with prednisolone (reducing dosage from 30mg/day) and azathioprine/cyclophosphamide (1-3 mg/kg/day), five showed progressive loss of renal function within one year of responding to treatment. Both the daily dose at four weeks and the cumulative dose of prednisolone at six months were significantly lower (p less than 0.01) in the group whose renal function deteriorated. We suggest that the follow-up dosage of prednisolone may be critical in maintaining continued stable renal function in the first few months after starting PMP or PX.

Adolescent↗
PubMed1983

Aggressive treatment with pulse methylprednisolone or plasma exchange is justified in rapidly progressive glomerulonephritis.

Rapidly progressive crescentic glomerulonephritis (RPGN) carries a poor prognosis, but early immunosuppression may reverse renal impairment. We have given intensive therapy to 27 patients with biopsy proven RPGN from 1977-1981. Fourteen patients received pulse methylprednisolone (PMP) and 13 patients plasma exchange (Px). These patients fared significantly better than 17 patients seen from 1972-1979 who had neither PMP nor Px. Both groups received oral prednisolone and other immunosuppressive agents. PMP and Px were equally effective in prolonging survival without dialysis and had no serious side effects; prognostic factors affecting the outcome of treatment were identified. Early aggressive immunosuppressive therapy is indicated in RPGN.

Adolescent↗
PubMed1979

The relationship of biochemical and histometric determinants of uremic bone.

Simultaneous histometric and biochemical analyses were performed on 16 bone biopsy specimens taken from eight patients with chronic renal failure. The bone calcium and phosphorus contents are inversely related to the relative volume of microscopically measured, nonmineralized bone matrix (osteoid) and to the percentage of trabecular surface covered by this tissue. The magnesium content of uremic bone is positively correlated with the quantity of osteoid. Skeletal calcium and phosphorus contents correlate inversely with the osteoblast population, and phosphorus relates directly to the volume of trabecular bone. Bone hydroxyproline content does not correlate significantly with any histometric variable. As one may now infer biochemical conclusions about the uremic skeleton from morphological observations, these data may facilitate interpretation of nondecalcified histological sections of bone.

Bone and Bones↗