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J M Bone

Publications and source records attributed to J M Bone.

70 records · Page 4Linked to original sources
PubMed1977

On the origin of urinary fibrin-fibrinogen-related antigen in glomerulonephritis.

A model of antiglomerular basement membrane nephritis in the rat was used to elucidate the origin of urinary fibrin-fibrinogen-related antigen (FRA). The intrarenal distribution and excretion of 125I-rat fibrinogen was examined to determine whether there was increased filtration of bibrinogen or fibrin degradation products (FDP) or lysis of intraglomerular fibrin. 125I-protein appeared in the urine immediately after injection of 125I-fibrinogen and fell in parallel with the fall in plasma 125I-fibrinogen. Renal retention of 125I-fibrin averaged less than 0.2 percent of the administered dose of 125I-fibrinogen. The infusion of epsilon aminocaproic acid (EACA) had no significant effect on either FRA excretion or 125I-protein excretion. Plasma FDP levels and the elution patteren of 125I-protein from the urine were not significantly changed by EACA infusion. These observations support the view that ruinary FRA excretion in glomerulonephritis is derived predominantly from increased filtration of plasma fibrinogen rather than from breakdown of intraglomerular fibrin.

Aminocaproates↗
PubMed1977

Oral or parenteral iron therapy in haemodialysis patients?

In 28 haemodialysis patients, in whom there was a high incidence of depleted marrow iron stores, a significant rise in Hb, and Hct, occasionally to a normal level, was achieved as effectively with oral as with i.v. iron supplements. There was a variable response to iron in individuals which could not be predicted from the initial iron status. No patient in whom marrow iron stores were reassessed after iron therapy developed increased marrow iron stores. Routine iron supplements are recommended in haemodialysis patients with regular monitoring of body iron stores.

Administration, Oral↗
PubMed1976

Calcifediol in chronic renal insufficiency. Skeletal response.

Quantitative histology of thin, nondecalcified sections was performed on sequential bone biopsy specimens from five patients undergoing long-term hemodialysis and treated with calcifediol (25-hydroxycholecalciferol) for periods of three to nine months. With increase of intestinal absorption of calcium and decline of circulating immunoreactive parathyroid hormone and alkaline phosphatase, the bones of each patient exhibited striking histological improvement. The group as a whole showed statistically significant decreases in osteoclast number and in the percentages of osteoid surface covered by active osteoblasts. Marrow fibrosis was either eliminated or strikingly decreased in each patient. Osteoid volume significantly declined in four of five patients. In patients with osteitis fibrosa as the predominant histological lesion, calcifediol therapy resulted in decreased calcification front activity. Increased activity was the result when osteomalacia predominated.

Adult↗
PubMed1976

Intracellular acid-base heterogeneity in nucleated avian erythrocytes.

1. Intracellular hydrogen ion activity, [H+]i, was extimated in human erythrocytes and in nucleated avian erythrocytes from measurements of the distribution of ammonia and 5,5'-dimethyloxazolidine-2,4'-dione (DMO) between intracellular and extracellular fluid. 2. In human erythrocytes there was no difference between values for [H+]i derived from measurements of either DMO or ammonia. 3. In avian erythrocytes, [H+]i(ammonia) was consistently greater than [H+]i(DMO), indicating significant acid-base heterogeneity of the intracellular water. The degree of heterogeneity was assessed by reference to a theoretical model of two compartments of equal size. 4. Experiments with nuclei isolated from avian erythrocytes suggested that DMO is not bound to nucleoproteins, and that the nucleus may be more acidic than the cytoplasm.

Animals↗
PubMed1975

Heparin therapy in anti-basement membrane nephritis.

The effect of heparin on the development and progression of a form of antiglomerular basement membrane nephritis was examined in the rat. Animals which received heparin before and throughout the period of immunological insult developed lesions which were as severe, and perhaps more severe, than rats which did not receive heparin. Inulin clearances were lower in heparin-treated animals than in untreated rats. Animals in both groups exhibited renal fibrin-fibrinogen deposition and had increased rates of urinary fibrin-fibrinogen related antigen excretion. These results indicate that heparin per se has no beneficial effect on the development of this form of glomerulonephritis in this species.

Animals↗
PubMed1968

Intracellular pH.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMedDate not supplied

Renal tubular peptide catabolism in chronic vascular rejection.

Chronic vascular rejection (CR) is the commonest cause of renal transplant loss, with few clues to etiology, but proteinuria is a common feature. In diseased native kidneys, proteinuria and progression to failure are linked. We proposed a pathogenic role for this excess protein at a tubular level in kidney diseases of dissimilar origin. We demonstrated in both nephrotic patients with normal function and in those with failing kidneys increased renal tubular catabolism and turnover rates of a peptide marker, Aprotinin (Apr), linked to increased ammonia excretion and tubular injury. These potentially injurious processes were suppressed by reducing proteinuria with Lisinopril. Do similar mechanisms of renal injury and such a linkage also occur in proteinuric transplanted patients with CR, and if so, is Lisinopril then of beneficial value? We now examine these aspects in 11 patients with moderate/severe renal impairment (51CrEDTA clearance 26.2+/-3.3 mL/min/1.73 m2), proteinuria (6.1+/-1.5 g/24 h) and biopsy proven CR. Lisinopril (10-40 mg) was given daily for 2 months in 7 patients. Four others were given oral sodium bicarbonate (Na HCO3) for 2 months before adding Lisinopril. Renal tubular catabolism of intravenous 99mTc-Apr (Apr* 0.5 mg, 80MBq), was measured before and after Lisinopril by gamma-ray renal imaging and urinary radioactivity of the free radiolabel over 26 h. Fractional degradation was calculated from these data. Total 24 h urinary N-acetyl-beta-glucoaminidase (NAG) and ammonia excretion in fresh timed urine collections were also measured every two weeks from two months before treatment. After Lisinopril proteinuria fell significantly (from 7.8+/-2.2 to 3.4+/-1.9 g/24 h, p<0.05). This was associated with a reduction in metabolism of Apr* over 26 h (from 0.5+/-0.05 to 0.3+/-0.005% dose/h, p < 0.02), and in fractional degradation (from 0.04+/-0.009 to 0.02+/-0.005/h, p<0.01). Urinary ammonia fell, but surprisingly not significantly and this was explained by the increased clinical acidosis after Lisinopril, (plasma bicarbonate fell from 19.1+/-0.7 to 17.4+/-0.8 mmol/L, p < 0.01), an original observation. Total urinary NAG did fall significantly from a median of 2108 (range 1044-3816) to 1008 (76-2147) micromol/L, p < 0.05. There was no significant change in blood pressure or in measurements of glomerular hemodynamics. In the 4 patients who were given Na HCO3 before adding Lisinopril, both acidosis (and hyperkalemia) were reversed and neither recurred after adding Lisinopril. These observations in proteinuric transplanted patients after Lisinopril treatment have not been previously described.

Adult↗
PubMedDate not supplied

Energy and nitrogen balance and changes in midupper-arm circumference with multiple organ failure.

Energy intake and energy expenditure, nitrogen intake, and urinary nitrogen excretion (or urea production rates) were measured in 35 intravenously fed patients with multiple organ failure over the course of their illness to determine to what extent nutrient requirements were met despite fluid retention. Energy and nitrogen balance were related to serial measurements of midupper-arm circumference (MAC). The target feeding regimen of 176 kJ (42 kcal)/kg fat-free mass (FFM) was achieved in only three patients and the target of 0.24 g N/kg FFM in only four. Two patterns of change in MAC were noted: a steady decrease with time and no change with time. Serial muscle biopsy data indicated that all the patients were wasting away; the maintenance of MAC in the group with no change over time was due to fluid retention. Abnormal losses were not measured, but energy and nitrogen balance in the group in which arm circumference decreased had no apparent effect on the rate of wasting.

Adolescent↗