Low-dose cyclosporine therapy combined with standard immunosuppression in pediatric renal transplantation

So, Samuel; Najarían, John S.; Nevins, Thomas E.; Fryd, David S.; Knaak, M.; Chavers, Blanche M.; Mauer, S. Michael; Simmons, Richard L.

doi:10.1016/s0022-3476(87)80048-3

Cited by 17 publications

(7 citation statements)

References 9 publications

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“…50 to 200 /LgfL) may be sufficient to effectively manage a variety of clinical conditions. This assertion is supported by recent reports of successful immunosuppressive therapy with low dose cyclosporine in paediatric renal allograft recipients (Conley et al 1985;Geary 1987;So et al 1987).…”

Section: Cyclosporine Immunosuppressionmentioning

confidence: 73%

“…At present, the mechanisms of action for cyclosporine appear to include inhibition of T -cell-dependent B cell activation, expansion ofunprimed T helper and cytotoxic T cell subsets, clonal expansion of alloreactive cells and induction of 'Y-interferon secretion (Gerson 1987). The primary therapeutic uses of cyclosporine in paediatric patients have been to prevent or ameliorate rejection of kidney (Conley et al 1985;Geary et al 1987;Kahan et al 1987;Salaman et al 1987;Sheldon et al 1985;So et al 1987;Tejani et al 1986), liver (Esquivel et al 1987), cardiac (Addonizio & Rose 1987) and bone marrow allografts (Beveridge et al 1982;Deeg et al 1985;Kay 1982;Yee et al 1986). Recently, how-43 ever, the use of this agent in infants and children has been broadened with successful therapeutic trials for autoimmune enteropathy (Roth et al 1987;Siedman et al 1987), autoimmune chronic active hepatitis (Hyams et al 1987), systemic lupus erythematosus (Feutren et al 1987), relapsing nephrotic syndrome (Tejani et al 1987), dermatomyositis (Girardin et al 1988) and type I diabetes mellitus (Bach 1987;Stiller et al 1987).…”

Section: Cyclosporine Immunosuppressionmentioning

confidence: 99%

See 1 more Smart Citation

Clinical Pharmacokinetics in Infants and Children A Reappraisal

Kearns

Reed

1989

Clinical Pharmacokinetics

174

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A significant increase in the knowledge base in paediatric clinical pharmacology has occurred over the past 2 decades and has largely been the result of important scientific and sociological advancements pertaining to paediatric therapeutics. Although the data on drug disposition in infants and children have increased considerably over the past few years, pharmacokinetic-pharmacodynamic interactions, particularly the effect of development on pharmacodynamics, remain poorly understood.The impact of developmental physiology on drug absorption, distribution, metabolism and elimination in infants and children is reviewed and contrasted to the determinants of clinical pharmacokinetics in neonates. The most notable differences in drug disposition between in/ants and children when compared with neonates and young adults centre around alterations in body water and serum protein composition and the affinity/capacity for hepatic biotransformation of xenobiotics.As opposed to examining the effect of age on the disposition of specific compounds, the differences in developmental pharmacology are highlighted by the review of important and/or emerging pharmacokinetic-pharmacodynamic controversies in infants and children. These include the issues of altered drug distribution and metabolism in cysticjibrosis, pharmacokinetic determinants of successful antimicrobial therapy in bacterial meningitis and the pharmacokinetic determinants of immunosuppression treatment with cyclosporin. The pharmacological differences which are characteristic of development in both infants and children are also reviewed by examination of considerations for clinical pharmacokinetic evaluations such as specific routes and techniques for both drug administration and determination of sampling strategies.Clinical pharmacokinetics will continue to function as a bridge between the generation of new information and the practical application of this knowledge. Consequently, pharmacokinetics provides a pharmacological tool for use in research and clinical care. The clinical application of this tool is examined by a review of the pertinent assumptions and limitations, as well as useful mathematical techniques for use in paediatric patients. Additionally, 'non-traditional' uses of clinical pharmacokinetics (forensic application and use to evaluate organ function) in infants and children are discussed as are considerations for research use of clinical pharmacokinetic data.

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Section: Cyclosporine Immunosuppressionmentioning

confidence: 73%

Section: Cyclosporine Immunosuppressionmentioning

confidence: 99%

Clinical Pharmacokinetics in Infants and Children A Reappraisal

Kearns

Reed

1989

Clinical Pharmacokinetics

174

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“…In the early years of transplantation only a few centers performed this procedure in children and then mostly from a living‐related source ( 2). As immunosuppression became safer and more stable ( 3, 4) pediatric renal transplant activity increased markedly; however, with 73 pediatric centers across the country, the volume at each center is too small to derive meaningful information regarding outcome and the quality of life of children, post‐transplantation.…”

mentioning

confidence: 99%

The 1997 Annual Renal Transplantation in Children Report of the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS)

Benfield

McDonald

Sullivan

et al. 1999

Pediatric Transplantation

150

108

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This report of the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS), covering the years 1987-96 (January 15, 1997), analyzed data on 4898 patients who received 5362 transplants. Over the 10 yr of the study, 21.3% of the patients were under the age of 6 yr. Of the disorders that lead to end-stage renal disease (ESRD), structural and developmental anomalies of aplasia, dysplasia, and obstructive uropathy accounted for over 1500 patients. Despite the potential therapies for focal segmental glomerulosclerosis (FSGS), there has been little change in its incidence and this lesion continues to be the most common cause of renal failure and transplantation among acquired diseases. Eighty-nine per cent of patients with a functioning graft continue to receive cyclosporin A (CsA) 5 yr post-transplantation, and 84% of patients continue to receive azathioprine (AZA), whereas 26% of patients receive alternate-day steroid therapy at 4 yr post-transplant. Thirty-seven per cent of the living donor (LD) recipients and 47% of cadaver donor (CD) recipients were treated with the polyclonal T-cell antibody ATG/ALG for induction, and the monoclonal T-cell antibody, OKT3, was utilized for induction in 12% of LD patients and in 19% of CD patients. Twenty-five per cent of the 5362 transplants (1333) have failed over the 10-yr period. Graft survival is 90% at 1 yr and 74% at 6 yr for LD kidneys, and is 80% at 1 yr and 58% at 6 yr for CD patients. The most common cause for graft failure (30%) is chronic rejection. For recipients of LD grafts, relative risk (RR) factors for graft survival are African-American race (RR = 2.1, p < 0.001) and greater than five prior transfusions (RR = 1.6, p < 0.001). Prophylactic anti-T-cell antibody reduces the risk of graft failure (RR = 0.76, p = 0.009). For recipients of cadaver kidneys, risk factors are: recipient age < 2 yr (RR = 2, p < 0.001), donor age < 6 yr (RR = 1.3, p = 0.005), and absence of induction T-cell antibody (RR = 1.31, p < 0.001).

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“…Urinary oxalate excretion was elevated at 1.2 mM/day (normal, G0.6 mM/day). Cyclosporin was ceased given the association with hyperoxaluria and hypocitraturia, renal calcium-oxalate deposition (3), and poor kidney transplantation outcomes (4,5). The serum creatinine stabilized at 150 KM/L after 5 weeks.…”

mentioning

confidence: 99%