PubMed Health⌕ Search

Biomedical subjects

N W Boyce

Publications and source records attributed to N W Boyce.

41 records · Page 3Linked to original sources
PubMed1985

Glomerular permselectivity in the isolated perfused rat kidney.

Glomerular permselectivity characteristics were studied in the Sprague-Dawley rat in vivo and in the isolated rat kidney perfused with an erythrocyte-free Krebs-Henseleit buffered 5% albumin solution (IPK). IPK permselectivity in vitro, assessed by fractional clearances of neutral dextran (FCND) and dextran sulfate (FCDS) with molecular radii 18-43 A, was essentially similar to that of the Sprague-Dawley rat in vivo. The negative charge barrier of the IPK glomerular filter was intact [e.g., FCND of 36 A = 0.10 +/- 0.01 (SE) vs. FCDS of 36 A = 0.01 +/- 0.00 (P less than 0.01)]. Dextrans of an intermediate size (26-34 A) had lower fractional clearances in the IPK than in vivo [e.g., FCND of 30 A in IPK = 0.23 +/- .04 vs. FCND of 30 A in vivo 0.40 +/- 0.01 (P less than 0.01)]. This decreased clearance of dextrans of an intermediate molecular size is predicted by pore theory, since the IPK has an increased afferent glomerular plasma flow rate. As glomerular permselectivity characteristics in the IPK simulate in vivo characteristics, such preparations are suitable in vitro models in which to study factors that modulate permselectivity. The demonstration that the glomerular filter in the IPK has a normal negative charge barrier indicates that the increased protein excretion in IPK systems cannot be attributed to abnormalities of this component of the filtration barrier.

Animals↗
PubMed1985

Anti-glomerular basement membrane antibody-induced experimental glomerulonephritis: evidence for dose-dependent, direct antibody and complement-induced, cell-independent injury.

The immunopathogenesis of anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM-GN) involves the triad of antibody fixation to the glomerular basement membrane, local complement activation and polymorphonuclear leucocyte (PMN) infiltration. We sought to investigate the potential for contributions to renal injury from each component of this triad (i.e., antibody, complement, and PMN). This study compares the ability of antibody to induce injury in normal, PMN-depleted and dual (i.e., PMN + complement)-depleted rabbits by assessing the quantity of kidney-fixed antibody (KFA) necessary to induce proteinuria. (The KFA levels are expressed in micrograms of antibody bound per gram renal cortex.) Normal animals developed significant proteinuria at KFA 60 +/- 6 micrograms/g. PMN-depleted animals were injury free at KFA 60 +/- 6 micrograms/g, but developed heavy proteinuria at KFA 140 +/- 5 micrograms/g. The protection from injury by PMN depletion at lower KFA levels confirms the important contribution of PMN to injury in this model. Furthermore, the demonstration of a clearcut threshold for injury despite PMN-depletion indicates that glomerular antibody deposition and complement activation can cause direct PMN-independent injury. Dual depletion studies showed a significantly higher KFA threshold for injury in PMN + complement-depleted animals than in PMN-depleted, complement intact animals (195 +/- 10 micrograms/g, cf. 140 +/- 5 micrograms/g; p less than 0.01). The occurrence of injury despite dual mediator depletion demonstrates that antibody itself can produce direct, complement and PMN independent renal injury. Together the PMN depletion and dual depletion studies indicate that antibody-induced glomerular complement activation produces direct, PMN-independent renal injury that can be prevented by complement depletion. Thus each of the potential mediators studied is individually capable of producing renal injury in anti-GBM-GN. In addition to the well established injurious role of PMN, this study demonstrates that glomerular complement activation and anti-GBM antibody deposition may both produce neutrophil-independent components of renal injury. The relative contributions of the individual mediators to injury is dependent on the quantity of antibody deposited within the glomerulus.

Animals↗
PubMed1984

Renal involvement in systemic lupus erythematosus.

A review of 28 cases of biopsy-proven lupus nephritis seen in Prince Henry's Hospital, Melbourne, in the last 12 years from 1971 to 1982 is reported. The mean follow-up period was 51 months. Renal histopathological changes were categorized according to the WHO classification of lupus nephritis. The majority of our patient population fell into two of the seven possible histological subgroups - Class IV (diffuse proliferative) disease (53.6%) and Class IIb (mesangial proliferative) disease (28.5%). Treatment with prednisolone alone or with a prednisolone/azathioprine combination resulted in an equal five-year survival (82%) and a similar overall preservation of renal function. The major single cause of death was opportunistic infection (60%). Despite overrepresentation of the more severe forms of lupus nephritis in a nephrology-unit population, there was a satisfactory outcome from therapy with either prednisolone alone or with a prenisolone /azathioprine combination. However, there were significant rates of morbidity and death associated with immunosuppressive therapy, primarily from opportunistic infection.

Acute Kidney Injury↗
PubMed1984

"Long-term" survival in light-chain myeloma with dialysis therapy alone.

We report a case of a 59 year old woman who presented in end-stage renal failure with lambda (lambda) light-chain myeloma (LLCM). Despite a large tumour burden, and refusal to accept cytotoxic chemotherapy, she was commenced on continuous ambulatory peritoneal dialysis (CAPD). With dialysis therapy alone she has shown considerable hematological improvement and remains well 18 months after diagnosis. The extremely poor prognosis attributed to light-chain myeloma is largely due to death from uremia. As the natural history of this disease in patients offered dialysis therapy is unknown, dialysis should not automatically be withheld from patients with LLCM.

Bone Neoplasms↗