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Biomedical subjects

A G Birtch

Publications and source records attributed to A G Birtch.

At least 19 recordsLinked to original sources
PubMed1979

Urinary tract infections in kidney transplant recipients.

In 65 kidney transplant recipients who were followed up for a mean period of 14.7 months, the incidence of urinary tract infection (UTI), and how the incidence was affected by length of graft survival, age, HLA-A and HLA-B matches, complications, duration of Foley catheter use, and other aspects, were examined. The total incidence of infection included an unexpectedly high rate of late infections. The incidence was found to be statistically increased with nephrectomy, splenectomy, recatheterization, and age older than 40 years. There was no correlation noted with graft source, antigen match, graft loss, or previous history of UTI. A group of patients with persistent UTI was noted and an inability to suppress UTI with long-term therapy with antibiotics was found. The asymptomatic nature of most of the UTIs confirmed the need for frequent periodic cultures of urine in the immunosuppressed patient.

Adult↗
PubMed1979

False positive 51Cr release tests during post-transplant immunological monitoring due to recipient serum radioactive contamination.

The occurrence of false positive 51Cr release test results in post-transplant immunological monitoring of human kidney graft recipients due to 131I carryover from renograms is described. False positivity was detected in 7 instances in 4 recipients, and suspected in 12 instances in 7 recipients, in a series of 46 consecutive transplant recipients. Technical methods and controls to detect and prevent such false positivity are described.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1976

Hyperacute renal allograft rejection in the primate. Therapeutic limitations of antiplatelet agents alone and combined with heparin.

Two antiplatelet drugs, pyridinolcarbamate and Sudoxicam, were tested separately and in combination with heparin for their ability to modify experimental hyperacute renal allograft rejection in primates. Pyridinolcarbamate delayed and amerliorated tissue injury and obstructive thrombosis but only minimally prolonged renal blood flow over that seen in untreated allografts, suggesting that graft failure was primarily due to vasoconstriction. Sudoxicam, an antiinflammatory agent, resulted in higher initial blood flow, but the duration of flow and graft survival were again only minimally prolonged. However, functional changes including C3, Factor II and X consumption were prevented, a net increase in Factor VIII activity was minimized, and fibrinolysis was inhibited. The combined effects of pyridinolcarbamate and heparin resembled those of heparin alone. Combination of Sudoxicam with heparin was more effective than heparin along in preventing intrarenal complement consumption, sequestration of formed elements, activation of coagulation, and inhibition of fibrinolysis. However, the latter combination also failed to prolong venous flow and graft survival over that seen with heparin alone.

Animals↗
PubMed1975

Hyperacute renal allograft rejection in the primate. Intrarenal effects of heparin and associated net release of factor VIII activity and kallikrein activation.

Two groups of specifically presensitized Macaca speciosa monkeys received renal allografts via anastomosis to an indwelling arteriovenous (A-V) shunt. One group was pretreated with heparin (2 mg/kg) intravenously and the other was also treated with constant heparin infusion (1 mg/kg/hr) directly into the renal artery. These studies were performed to evaluate the effects of heparin within the kidney on total and compartmental blood flow, complement (C3) levels, sequestration of formed elements, and activation of the coagulation, fibrinolytic, and kinin-forming systems during the initial 3 hours of hyperacute rejection. The results are compared with those previously reported in unmodified control allografts. Heparin prolonged blood clotting time to infinity, markedly prolonged total renal venous blood flow, and normalized compartmental distribution in both groups despite antibody deposition similar to that in controls. With heparin pretreatment only, initial morphologic injury was much reduced but then progressed rapidly. Marked initial cortical cyanosis with mottling appeared to change constantly and was associated with fluctuations in renal turgor, total blood flow, and sequestration of formed elements, all of which suggested repetitive local cortical arterial spasm and incremental destruction of the grafts. Activation of coagulation Factors II and XII was also revealed and marked net Factor VIII activity was observed in the venous effluent. The latter reflects either formation and release of this factor by the injured kidney, or provides in vivo documentation of the "hyperactivation" of Factor VIII by thrombin known to occur in vitro. The addition of intrarenal artery heparin infusion resulted in greater improvement in early total blood flow rates and more uniformly progressive cyanosis and loss of turgor, but the diffuse initial morphologic injury suggested more uniform perfusion of injured areas. Intrarenal consumption of C3 and sequestration of formed elements was similar to that in controls. Paradoxically, prompt activation and consumption of all coagulation factors, plasminogen, and prekallikrein were observed, but formed fibrin was sparse. The exess amount of Factor XIIa present during heparin blockade may have been diverted to production of plasminogen activator and kallikrein formation. The enormous numbers of neutrophils observed within vessels of grafts which showed the greatest kallikrein activation provide the probable in vivo demonstration of the chemotactic properties of kallikrein noted by others in vitro. Heparin-induced platelet aggregation may have played an important role in the failure of these grafts. These studies elucidate the intrarenal effects of heparin during hyperacute rejection and again suggest that vasoconstriction is the most important early determinant of graft failure, as blood flow appeared unrelated to the degree of vascular injury and apparent obstruction. Also, heparin may exer a beneficial effect on blood flow by other than its known action on coagulation.

Animals↗