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P Naish

Publications and source records attributed to P Naish.

13 recordsLinked to original sources

Quantitative assessment of the effects of platelet depletion in the autologous phase of nephrotoxic serum nephritis.

The effects of platelet depletion with antibody have been studied in two models of the autologous phase of nephrotoxic nephritis in the rabbit. In the 'telescoped' model (animals pre-immunized to sheep IgG injected with sheep nephrotoxic antibody), platelet depletion did not alter intraglomerular fibrin deposition or evidence of glomerular damage, but did significantly reduce proteinuria during the first 3 days of the 5 day experiment. In the 'passive' model (animals injected with hyperimmune rabbit antiserum to sheep IgG 48 hr after sheep nephrotoxic antibody and killed 3 hr later), platelet depletion was associated with significantly fewer intraglomerular polymorphonuclear leucocytes (PMN), but again did not alter intraglomerular fibrin deposition. The results indicate that platelets are involved in the initiation of glomerular PMN localization in the autologous phase, but that fibrin-induced glomerular injury is platelet-independent.

Animals

The mediation of the localization of polymorphonuclear leucocytes in glomeruli during the autologous phase of nephrotoxic nephritis.

A passive model of the autologous phase of nephrotoxic nephritis (NTN) in rabbits was developed to study the events at the initiation of this stage of the disease. Intravenous injection of sheep anti-rabbit glomerular basement membrane antiserum was followed 48 hr later by 125I trace labelled rabbit anti-sheep IgG. Animals were killed 3 hr after the second antibody injection. Experiments were undertaken to investigate whether or not a reaction between the passive antibody Fc piece and polymorphonuclear leucocyte (PMN) Fc receptor occurred, causing the localization of PMN in glomeruli in the autologous phase of NTN. The results indicate that such a reaction is an important, but not exclusive, factor in glomerular PMN localization. The complement independence of the localization was confirmed. In addition, it appeared that PMN-dependent intraglomerular fibrin deposition was mediated exclusively by a reaction between antibody Fc piece and PMN Fc receptor.

Animals

Urinary fibrinogen derivative excretion and intraglomerular fibrin deposition in glomerulonephritis.

The relations between glomerular fibrin deposition, urinary excretion of fibrinogen derivatives (F.D.), and proteinuria were explored in 81 patients with glomerulonephritis. A positive correlation existed between proteinuria and F.D. excretion even when no fibrin could be detected in the glomerulus. In two patients with tubular proteinuria F.D. excretion was also raised, suggesting that tubular reabsorption or catabolism of F.D. or both normally occur.Disproportionately high titres of F.D. were observed when fibrin was deposited in an extracapillary site, but mesangial fibrin deposition was not accompanied by a higher excretion of F.D. than that observed in patients in whom intraglomerular fibrin was not detected. These observations suggest that the immunofluorescent findings on renal biopsies should be the major criteria on which a trial of anticoagulants in proliferative glomerulonephritis might be instituted and that measurement of urinary F.D. is likely to be of value in monitoring therapy in patients with extracapillary fibrin deposition.

Biopsy