G C Francos

Thomas Jefferson University Hospitals, Filadelfia, Pennsylvania, United States

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Publications (18)97.37 Total impact

  • George C. Francos ·

    Seminars in Dialysis 09/2007; 1(4):209 - 212. DOI:10.1111/j.1525-139X.1988.tb00730.x · 1.75 Impact Factor

  • Transplantation 04/2000; 69(Supplement):S224. DOI:10.1097/00007890-200004271-00426 · 3.83 Impact Factor
  • J. F. Burke · G. C. Francos · B. B. Francos ·

    Transplantation 04/1999; 67(7). DOI:10.1097/00007890-199904150-00600 · 3.83 Impact Factor
  • M S Islam · G C Francos · S R Dunn · J F Burke ·

    Transplantation Proceedings 09/1998; 30(5):2230-1. DOI:10.1016/S0041-1345(98)00601-0 · 0.98 Impact Factor
  • B Michael · G C Francos · J F Burke · W I Gaughan ·

    Transplantation Proceedings 11/1994; 26(5):3046-7. · 0.98 Impact Factor
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    ABSTRACT: Orthoclone OKT3 (Ortho Biotech Inc, Raritan, NJ) is a potent immunosuppressive agent effective in the therapy of acute renal allograft rejection. Following the first one or two doses, patients often exhibit a "flu-like" illness ascribed to OKT3-induced release of cytokines. Systemic reactions resulting from the cytokines include pyrexia, pulmonary edema, bronchospasm, photophobia, headache, hypotension, rigors, hypertension, gastrointestinal disturbances, and arthralgias/myalgias. The cyclooxygenase inhibitor indomethacin has been shown to ameliorate the pyrexia associated with OKT3 administration. We conducted a retrospective analysis with the purposes of (1) confirming that indomethacin reduces pyrexia and (2) determining the effect of indomethacin on the other aforementioned adverse side effects. Group 1 patients (n = 28) received indomethacin during the initial 48 hours of OKT3 antirejection therapy. Group 2 patients (n = 28) received OKT3 without indomethacin. The incidence of fever (P < 0.0001), headache (P < 0.030), and gastrointestinal disturbances (P < 0.030), and the number of adverse effects (P < 0.0001) were significantly less in the indomethacin-treated group. There were no differences between the groups in pre- and post-OKT3 serum creatinine levels. The indomethacin was well tolerated. We conclude that the widely available and relatively inexpensive cyclooxygenase inhibitor indomethacin safely and significantly reduces adverse effects associated with OKT3 therapy of acute renal allograft rejection.
    American Journal of Kidney Diseases 09/1994; 24(3):486-90. DOI:10.1016/S0272-6386(12)80906-1 · 5.90 Impact Factor
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    ABSTRACT: Although acute interstitial nephritis has been well described with the histamine H2-receptor antagonist cimetidine, we found only one previous case report of ranitidine-induced interstitial nephritis in the literature. We describe an additional patient who developed acute interstitial nephritis after taking ranitidine. Electron microscopy showed focal fusion of the epithelial cell foot processes that was not described in the previous report of ranitidine-induced interstitial nephritis.
    American Journal of Kidney Diseases 09/1993; 22(2):337-40. DOI:10.1016/S0272-6386(12)70328-1 · 5.90 Impact Factor
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    ABSTRACT: A role for histamine in the pathogenesis of uremic pruritus was investigated in maintenance hemodialysis patients. Venous plasma histamine levels, as determined by radioenzymatic assay, were significantly higher (p less than 0.05) in hemodialysis patients with pruritus (368 +/- 103 pg/ml [mean +/- SEM], n = 6) than in those without pruritus (146 +/- 22 pg/ml, n = 5) and in normal controls (142 +/- 16, n = 5). Arteriovenous fistula histamine levels (202 +/- 52 pg/ml, n = 6) were significantly lower (p less than 0.05) than simultaneously drawn venous samples. Markedly elevated histamine-degrading enzyme (histaminase) activities were found in both hemodialysis patients with (2.95 +/- 0.18 pg histamine degraded/minute) and without (2.44 +/- 0.28) pruritus, but was undetectable in normal controls. Histaminase activities did not significantly differ in simultaneously drawn venous and fistula samples. With hemodialysis, histaminase activities fell significantly (p less than 0.01), whereas plasma histamine did not change. We further examined the effects of ketotifen, a putative mast cell stabilizer, on severe uremic pruritus. Five of five patients had significant (p less than 0.01) reductions in pruritus, as judged on a six-point pruritus index, after 8 weeks of drug (x = 2.3), as compared to conventional therapy (x = 5.9). Despite these improvements, no significant differences were noted in pre- versus post-drug plasma histamine levels, histaminase activities, or the histamine content per gram of skin biopsy specimen. These data support prior hypotheses that mast cell activation contributes to the pruritus of uremia.
    International Journal of Dermatology 01/1992; 30(12):884-9. DOI:10.1111/j.1365-4362.1991.tb04360.x · 1.31 Impact Factor
  • C S Ben-Maimon · J F Burke · A Besarab · B E Jarrell · G C Francos · S S Moyer ·

    Transplantation Proceedings 03/1991; 23(1 Pt 2):1260-2. · 0.98 Impact Factor
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    ABSTRACT: There has been concern that cyclosporine's nephrotoxicity increases the incidence of delayed graft function (DGF), prolongs periods of oliguria, and reduces graft survival. In order to further study whether CsA should be used in DGF, we conducted a randomized prospective trial of the effect of CsA versus antilymphocyte globulin on the effects of DGF. Between 12/22/85 and 3/11/88, all patients with DGF after an initial 12-24 hr of CsA were randomized to either daily Minnesota ALG and prednisone or lower-dose CsA (10 mg/kg/day) and prednisone. Resolution of DGF was defined as a lack of dialysis dependency and a 25% fall in the serum creatinine (CR). If DGF was not resolved by 2 weeks, transplant renal biopsies were performed to assess the presence of occult rejection. CsA (10 mg/kg/day) was initiated in the ALG group only after resolution of the DGF. Of the 45 patients who recovered graft function, 19 received ALG and 26 received CsA. CsA significantly prolonged the duration of DGF (ALG 9.74 days, CsA 13.69 days, P = 0.035) but did not result in a prolongation of hospitalization. No difference in CR was found between the two groups at 1 month, 3 months, 6 months, or 12 months. Mean CR at 12 months was 1.98 mg/dl for ALG versus 1.96 mg/dl for CsA. Overall graft survival did not differ in the CsA and ALG groups (P = 0.33). CsA does slightly increase the duration of DGF as compared with ALG but has no effect on one-year serum CR or one-year graft survival. Since there appeared to be no harmful long-term effects of the slight lengthening of DGF, a lower-dose of CsA protocol with biopsy surveillance for occult rejection can be used in patients with DGF.
    Transplantation 12/1989; 48(5):805-8. DOI:10.1097/00007890-198911000-00016 · 3.83 Impact Factor
  • A Besarab · B E Jarrell · J F Burke · G Francos · J Caro · E Mallon ·

    Transplantation Proceedings 07/1988; 20(3 Suppl 3):945-7. · 0.98 Impact Factor
  • G C Francos · J F Burke · A Besarab · B E Jarrell · M J Marcolina · E Mallon ·

    Transplantation Proceedings 03/1988; 20(1 Suppl 1):449-52. · 0.98 Impact Factor
  • Anatole Besarab · Jaime Caro · Bruce E Jarrell · George Francos · AJ Erslev ·
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    ABSTRACT: We examined the temporal dynamics of the correction of anemia following renal transplantation in 65 recipients using a sensitive radioimmunoassay for erythropoietin to determine the effects of modern immunosuppressive agents, delayed graft function, and early acute rejection. Pretransplant mean erythropoietin (25.6 +/- 3.3 mU/ml) was only 25% of the expected value at the mean hematocrit of 27.2 +/- 0.7, and erythropoietin correlated positively with hematocrit (r = 0.37, P less than 0.05). Following onset of graft function, erythropoietin increased to 109 +/- 13 mU/ml and then decreased in a negative feedback fashion over the next several months. Delayed graft function was associated with delay in the assumption of this orderly process irrespective of the immunosuppressive regimen used. Cyclosporine A produced a biphasic response despite delayed graft function in recipients with underlying adult polycystic kidney disease. Correction of anemia required resumption of graft function. Onset of acute graft rejection within the first month posttransplantation (14 episodes in 11 patients) abrogated the hematopoietic response until the rejection was successfully reversed. We conclude that a major cause for the anemia of renal failure is subnormal production of erythropoietin. Following transplantation, anemia corrects in an orderly manner with restoration of the normal biofeedback process between erythropoietin and red cell mass. This process is delayed by failure of graft to function initially and interrupted by acute early rejection, re-commencing following successful reversal.
    Kidney International 11/1987; 32(4):526-36. DOI:10.1038/ki.1987.241 · 8.56 Impact Factor
  • J F Burke · G C Francos ·
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    ABSTRACT: Medical management of the surgical patient with renal dysfunction revolves primarily around the application of sound medical principles used in the care of all patients. In this article, the unique peculiarities associated with renal failure are stressed. Knowledge of these points is vital in securing a favorable outcome for the patient.
    Medical Clinics of North America 06/1987; 71(3):489-97. · 2.61 Impact Factor
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    ABSTRACT: The effect of delayed graft function and immunosuppressive drugs on posttransplant erythropoiesis was studied prospectively in 18 living-related (LR) and 84 cadaver-donor (CD) recipients. Eight of 18 LR and 20 of 84 CD recipients received antilymphoblast globulin (ALG) in addition to azathioprine and prednisone. Sixty-four CD recipients received cyclosporine (CsA) with prednisone. In the absence of rejection reticulocytosis began 6.7 +/- 0.2 days following graft implantation in azathioprine-only-treated LR recipients. This was lengthened by ALG to 9.4 +/- 0.3 and 9.9 +/- 0.7 days in LR and CD recipients, respectively, whose grafts functioned immediately. Delayed graft function prolonged onset of reticulocytosis to 15.9 +/- 0.9 days in ALG-treated but not in CsA-treated recipients (5.8 +/- 0.4 days). The shortest latency was noted in CsA-treated recipients (4.9 +/- 0.5 days) with immediately functioning grafts. The earlier onset of reticulocytosis of CsA-treated recipients was followed by statistically significant blunting of peak reticulocytosis, which correlated with a slower rate of correction of anemia (delta Hct = 0.19/day) compared with non-CsA-treated recipients (delta Hct = 0.34/day). Early rejection was associated with abrogation of reticulocytosis and correction of anemia without regard to immunosuppressive regimen) until rejection was reversed. Erythropoietin (EPO) was measured sequentially in 5 patients with immediate function. In 4 of 5 cases changes in EPO preceded those in reticulocytosis. EPO rose from a mean of 13 mU/ml pretransplant to a peak of 50 within 3 weeks and decreased to 18 mU/ml within 6 weeks of graft implantation. At six months posttransplant, normalized reticulocyte counts were only 55% higher (1.75 vs. 1.13%) but hematocrit had increased from 26 +/- 1% to 42 +/- 1%. Hematocrit varied inversely with serum creatinine, which was highest in CsA-treated patients with initial delayed graft function. We conclude that correction of anemia posttransplantation is driven by EPO but other factors may also be important, that neither ATN nor ALG-therapy have clinically important effects on erythropoiesis, and that CsA reduced "effective" erythropoiesis and influences correction of anemia--particularly if delayed graft function complicates the initial course posttransplantation.
    Transplantation 01/1986; 40(6):624-31. DOI:10.1097/00007890-198512000-00010 · 3.83 Impact Factor
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    ABSTRACT: Hypoxemia during hemodialysis may result from several differing processes. We initially studied patients undergoing standard acetate hemodialysis. At 15 minutes of dialysis, leukopenia (primarily neutropenia), a decline of platelet count, and hypoxemia occurred, but without a significant change in mean minute ventilation. Complement activation (V/A ratios of C5a greater than 1.0) persisted throughout dialysis. Leukocyte count returned to baseline by one hour. To separate the effects of solute and/or gas fluxes from those of blood-membrane interaction we studied changes in Po2, WBC, C5a, TxB2, and PGI2 during a period of blood membrane interaction without dialysis, and during subsequent acetate dialysis. Patients were studied with both polyacrylonitrile (PAN) and cuprophan membranes containing different priming solutions during membrane contact alone. Despite leukopenia and complement activation, hypoxemia failed to occur during membrane contact alone. At 15 minutes of subsequent acetate dialysis, significant hypoxemia occurred with both membranes. However, the degree of hypoxemia was twice as great with a cuprophan membrane primed with acetate (18.6 +/- 3.3 mm Hg) compared with air or bicarbonate (9.1 +/- 1.4 and 7.0 +/- 2.0 mm Hg, respectively), or compared with PAN (8 +/- 2.8 mm Hg). Changes in thromboxane B2, PGI2, and C5a did not correlate with changes in Po2. We conclude that there are two major components to dialysis related hypoxemia. One is membrane independent, and may relate to the metabolic effects of acetate or to dialyzer CO2 loss. The remaining portion is membrane dependent, occurring with cuprophan, but not with PAN, and is conditioned by an acetate dependent interaction between blood and membrane.
    American Journal of Kidney Diseases 04/1985; 5(3):191-8. DOI:10.1016/S0272-6386(85)80050-0 · 5.90 Impact Factor
  • G C Francos · Anatole Besarab · R E Joseph ·

    The Lancet 02/1984; 1(8370):219. DOI:10.1016/S0140-6736(84)92135-4 · 45.22 Impact Factor

  • Transactions - American Society for Artificial Internal Organs 02/1983; 29(1):140-5.

Publication Stats

288 Citations
97.37 Total Impact Points


  • 1983-2007
    • Thomas Jefferson University Hospitals
      • • Division of Hospital Medicine
      • • Department of Medicine
      Filadelfia, Pennsylvania, United States
  • 1987-1998
    • Thomas Jefferson University
      • • Division of Nephrology
      • • Division of Hospital Medicine
      • • Department of Medicine
      Filadelfia, Pennsylvania, United States