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Rivelli GG, Lima MLD, Mazzali M. Therapy for persistent hypercalcemic hyperparathyroidism post-renal transplant: cinacalcet versus parathyroidectomy. ACTA ACUST UNITED AC 2021; 42:315-322. [PMID: 32720971 PMCID: PMC7657049 DOI: 10.1590/2175-8239-jbn-2019-0207] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/24/2019] [Accepted: 05/04/2020] [Indexed: 01/14/2023]
Abstract
Background: Persistent hyperparathyroidism post-transplant is associated with increases in the incidence of cardiovascular events, fractures, and deaths. The aim of this study was to compare both therapeutic options available: parathyroidectomy (PTX) and the calcimimetic agent cinacalcet. Methods: A single center retrospective study including adult renal transplant recipients who developed hypercalcemia due to persistent hyperparathyroidism. Inclusion criteria: PTH > 65 pg/mL with serum calcium > 11.5 mg/dL at any time after transplant or serum calcium persistently higher than 10.2 mg/dL one year after transplant. Patients treated with cinacalcet (n=46) were compared to patients treated with parathyroidectomy (n=30). Follow-up period was one year. Clinical and laboratory data were analyzed to compare efficacy and safety of both therapeutic modalities. Results: PTX controlled calcemia faster (month 1 x month 6) and reached significantly lower levels at month 12 (9.1±1.2 vs 9.7±0.8 mg/dL, p < 0.05); PTX patients showed significantly higher levels of serum phosphate (3.8±1.0 vs 2.9±0.5 mg/dL, p < 0.05) and returned PTH to normal levels (45±51 pg/mL). Cinacalcet, despite controlling calcium and phosphate in the long term, decreased but did not correct PTH (197±97 pg/mL). The proportion of patients that remained with PTH above normal range was 95% in the cinacalcet group and 22% in the PTX group. Patients treated with cinacalcet had better renal function (creatinine 1.2±0.3 vs 1.7±0.7 mg/dL, p < 0.05). Conclusions: Surgical treatment was superior to cinacalcet to correct the metabolic disorders of hyperparathyroidism despite being associated with worse renal function in the long term. Cinacalcet proved to be a safe and well tolerated drug.
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Affiliation(s)
- Gabriel Giollo Rivelli
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Clínica Médica, Campinas, SP, Brasil.,Universidade Estadual de Campinas, Laboratório de Investigação em Transplante, Campinas, SP, Brasil
| | - Marcelo Lopes de Lima
- Universidade Estadual de Campinas, Laboratório de Investigação em Transplante, Campinas, SP, Brasil.,Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Cirurgia, Campinas, SP, Brasil
| | - Marilda Mazzali
- Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Clínica Médica, Campinas, SP, Brasil.,Universidade Estadual de Campinas, Laboratório de Investigação em Transplante, Campinas, SP, Brasil
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Eren M, Place AT, Thomas PM, Flevaris P, Miyata T, Vaughan DE. PAI-1 is a critical regulator of FGF23 homeostasis. SCIENCE ADVANCES 2017; 3:e1603259. [PMID: 28924605 PMCID: PMC5597312 DOI: 10.1126/sciadv.1603259] [Citation(s) in RCA: 22] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 12/22/2016] [Accepted: 08/11/2017] [Indexed: 05/29/2023]
Abstract
Elevated levels of fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic hormone, are associated with a number of pathologic conditions including chronic kidney disease, cardiac hypertrophy, and congestive heart failure. Currently, there are no specific treatments available to lower plasma FGF23 levels. We have recently reported that genetic plasminogen activator inhibitor-1 (PAI-1) deficiency provided a significant reduction in circulating FGF23 levels while simultaneously prolonging the life span of Klotho-deficient mice. We extend our investigations into the effect of PAI-1 on FGF23 homeostasis. Transgenic overexpression of PAI-1 resulted in threefold increase in FGF23 levels compared to wild-type littermates. Moreover, pharmacological modulation of PAI-1 activity with the small-molecule PAI-1 antagonist TM5441 significantly reduced FGF23 levels in PAI-1 transgenic and Klotho-deficient mice. In addition, TM5441 treatment or PAI-1 deficiency significantly accelerated the clearance of endogenous FGF23 and recombinant human FGF23 from circulation in mice with acute kidney injury. On the basis of these observations, we studied the effects of plasminogen activators (PAs), tissue-type PA (tPA) and urokinase-type PA (uPA), on FGF23. We demonstrate that both PAs directly cleave FGF23; however, it is not known whether the PA-generated FGF23 peptides retain or acquire functions that affect binding and/or signaling properties of intact FGF23. PAI-1 inhibits the PA-dependent cleavage of FGF23, and TM5441 inhibition of PAI-1 restores the proteolysis of FGF23. Furthermore, top-down proteomic analysis indicates that tPA cleaves FGF23 at multiple arginines including the proconvertase sensitive site R176. In summary, our results indicate that PAI-1 prevents the PA-driven proteolysis of FGF23 and PAI-1 inhibition provides a novel therapeutic approach to prevent the pathologic consequences of increased FGF23.
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Affiliation(s)
- Mesut Eren
- Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
- Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
| | - Aaron T. Place
- Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
- Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
| | - Paul M. Thomas
- Proteomics Center of Excellence, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
| | - Panagiotis Flevaris
- Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
- Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
| | - Toshio Miyata
- United Centers for Advanced Research and Translational Medicine, Tohoku University Graduate School of Medicine, Miyagi, Japan
| | - Douglas E. Vaughan
- Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
- Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
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Wada Y, Iyoda M, Iseri K, Arai-Nunota N, Saito T, Hamada T, Tachibana S, Ikeda M, Shibata T. Combination Therapy of Denosumab and Calcitriol for a Renal Transplant Recipient with Severe Bone Loss due to Therapy-Resistant Hyperparathyroidism. TOHOKU J EXP MED 2017; 238:205-12. [PMID: 26947314 DOI: 10.1620/tjem.238.205] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022]
Abstract
Denosumab (DMAb), a complete human type monoclonal antibody directed against the receptor activator of nuclear factor-κB ligand, has gained attention as a novel treatment for osteoporosis. However, its efficacy in patients with chronic kidney disease (CKD) remains unclear. We describe a 64-year-old man with severe bone loss and persistent secondary hyperparathyroidism (SHPT) after renal transplantation, whose condition failed to respond to conventional pharmacologic or surgical interventions. He underwent parathyroidectomy with left forearm autograft of crushed tiny parathyroid gland (PTG) particles. However, the autografted PTGs became swollen and caused persistent SHPT in spite of two additional parathyroidectomies of the left forearm. A single subcutaneous administration of DMAb induced hypocalcemia, which was corrected by calcium supplementation and high-dose calcitriol. Eventually, combination therapy with DMAb and calcitriol led to a decline in the patient's elevated serum parathyroid hormone levels, normalization of laboratory markers of bone metabolism, and improvement in bone mineral density in a short period of time. To the best of our knowledge, this is the first case report of severe bone loss with persistent SHPT in a renal transplant recipient effectively treated with the combination therapy of DMAb and vitamin D (VD). Although DMAb itself exerts no direct effects on PTGs, the DMAb treatment improved the patient's bone loss. In addition, administration of DMAb allowed for high-dose VD therapy which ultimately controlled SHPT and prevented DMAb-induced hypocalcemia. Therefore, this combination therapy might be a reasonable therapeutic strategy to reverse severe bone loss due to therapy-resistant SHPT in patients with CKD.
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Affiliation(s)
- Yukihiro Wada
- Division of Nephrology, Department of Medicine, Showa University School of Medicine
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Biancone L, Leonardi G, Gai M, Segoloni GP. Secondary Hyperparathyrodism in Adult Predialysis and Dialysis Patients. Updates Surg 2016. [DOI: 10.1007/978-88-470-5758-6_17] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
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Muirhead N, Zaltman JS, Gill JS, Churchill DN, Poulin-Costello M, Mann V, Cole EH. Hypercalcemia in renal transplant patients: prevalence and management in Canadian transplant practice. Clin Transplant 2013; 28:161-5. [PMID: 24329899 DOI: 10.1111/ctr.12291] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 11/04/2013] [Indexed: 12/11/2022]
Abstract
Hypercalcemia, occurring in up to 25% of patients within 12 months following renal transplantation, and persistent hyperparathyroidism were evaluated following renal transplantation, by retrospective chart review of 1000 adult patients transplanted between January 1, 2003 and January 31, 2008 with at least six months follow-up. Serum calcium, parathyroid hormone, and phosphate levels were recorded at 12, 24, 36, and 48 months. Average follow-up was 766 (535) d (mean (SD); median 668 d). Majority were first transplants (85%); deceased donor 57%. Point prevalence of hypercalcemia (serum Ca(2+) > 2.6 mM) was 16.6% at month 12, 13.6% at month 24, 9.5% at month 36, and 10.1% at month 48. Point prevalence of serum parathyroid hormone (PTH) > 10 pM was 47.6% at month 12, 51.1% at month 24, 43.4% at month 36, and 39.3% at month 48. Estimated glomerular filtration rate (GFR) was maintained throughout and was not different between patients with or without hypercalcemia or elevated PTH. Cinacalcet was prescribed in 12% of patients with hypercalcemia and persistent hyperparathyroidism; parathyroidectomy was performed in 112/1000 patients, 15 post-transplant. Persistent hyperparathyroidism, often accompanied by hypercalcemia, is common following successful renal transplantation, but the lack of clear management suggests the need for further study and development of evidence-based guidelines.
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Affiliation(s)
- N Muirhead
- London Health Sciences Centre, London, ON, Canada
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Alshayeb HM, Josephson MA, Sprague SM. CKD-mineral and bone disorder management in kidney transplant recipients. Am J Kidney Dis 2012; 61:310-25. [PMID: 23102732 DOI: 10.1053/j.ajkd.2012.07.022] [Citation(s) in RCA: 52] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/05/2012] [Accepted: 07/09/2012] [Indexed: 12/11/2022]
Abstract
Kidney transplantation, the most effective treatment for the metabolic abnormalities of chronic kidney disease (CKD), only partially corrects CKD-mineral and bone disorders. Posttransplantation bone disease, one of the major complications of kidney transplantation, is characterized by accelerated loss of bone mineral density and increased risk of fractures and osteonecrosis. The pathogenesis of posttransplantation bone disease is multifactorial and includes the persistent manifestations of pretransplantation CKD-mineral and bone disorder, peritransplantation changes in the fibroblast growth factor 23-parathyroid hormone-vitamin D axis, metabolic perturbations such as persistent hypophosphatemia and hypercalcemia, and the effects of immunosuppressive therapies. Posttransplantation fractures occur more commonly at peripheral than central sites. Although there is significant loss of bone density after transplantation, the evidence linking posttransplantation bone loss and subsequent fracture risk is circumstantial. Presently, there are no prospective clinical trials that define the optimal therapy for posttransplantation bone disease. Combined pharmacologic therapy that targets multiple components of the disordered pathways has been used. Although bisphosphonate or calcitriol therapy can preserve bone mineral density after transplantation, there is no evidence that these agents decrease fracture risk. Moreover, bisphosphonates pose potential risks for adynamic bone disease.
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Affiliation(s)
- Hala M Alshayeb
- Department of Medicine, Section of Nephrology, University of Chicago, Chicago, IL, USA
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Douthat WG, Chiurchiu CR, Massari PU. New options for the management of hyperparathyroidism after renal transplantation. World J Transplant 2012; 2:41-5. [PMID: 24175195 PMCID: PMC3782233 DOI: 10.5500/wjt.v2.i3.41] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/22/2011] [Revised: 04/08/2012] [Accepted: 06/01/2012] [Indexed: 02/05/2023] Open
Abstract
The persistence and severity of hyperparathyroidism (HPT) post-renal transplantation is relatively frequent and primarily associated with the timing and its magnitude in the pre-transplant period and with the presence of parathyroid adenomas. HPT after renal transplantation is clinically manifested with hypercalcemia, hypophosphatemia, bone pain, fractures, and in more serious cases with cardiovascular calcifications that affect the survival. The primary clinical objective for patients with secondary HPT after renal transplantation is to obtain a level of parathyroid hormone (PTH) adequate to the renal transplanted function and to normalize levels of calcium, phosphorus and vitamin D. In many cases during this period, the development of hypercalcemia and/or hypophosphatemia makes it necessary to take different therapeutic measures. The use of vitamin D or its analogues has been extrapolated from the management of pre-transplant HPT obtaining variable outcomes, although its use is limited by its capacity to produce hypercalcemia. Calcimimetics are drugs that have proven be effective in reducing PTH levels in patients with HPT on dialysis and has been effective in reducing up to 50% PTH levels in moderate to severe HPT in post-renal transplantation.When HPT persists after renal transplantation and does not respond to medical treatment, invasive management by percutaneous ethanol injection therapy of parathyroid glands or parathyroidectomy should be considered. The emergence of new methods for the management of HPT expands the availability of therapeutic tools for transplant patients.
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Affiliation(s)
- Walter Guillermo Douthat
- Walter Guillermo Douthat, Carlos Raul Chiurchiu, Pablo Ulises Massari, Bone and Mineral Metabolism Section, Renal Service, Hospital Privado, Centro Médico de Córdoba, 5016 Córdoba, Argentina
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8
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Prevalence and Progression of Chronic Kidney Disease after Renal Transplantation. Transplant Proc 2011; 43:2587-91. [DOI: 10.1016/j.transproceed.2011.05.055] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/25/2011] [Accepted: 05/24/2011] [Indexed: 11/17/2022]
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Copley JB, Wüthrich RP. Therapeutic management of post-kidney transplant hyperparathyroidism. Clin Transplant 2011; 25:24-39. [PMID: 20572835 DOI: 10.1111/j.1399-0012.2010.01287.x] [Citation(s) in RCA: 33] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
Left uncontrolled, persistent post-kidney transplant hyperparathyroidism (HPT) may lead to or exacerbate pre-existing bone and cardiovascular disease. Parathyroidectomy has long been the primary treatment option for long-term uncontrolled HPT in post-kidney transplant patients. However, patients with contraindications for surgery and parathyroidectomy-associated complications, including graft loss, highlight the need for other approaches. Conventional medical therapies have limited impact on serum calcium (Ca) and parathyroid hormone (PTH) levels. Bisphosphonates and calcitonin, used to spare bone loss, and phosphorus supplementation, to correct hypophosphatemia, do not directly regulate PTH or Ca. Although vitamin D supplementation can reduce PTH, it is often contraindicated because of hypercalcemia. Studies of the calcimimetic cinacalcet in patients with post-kidney transplant HPT suggest that it can rapidly reduce serum PTH and Ca concentrations while increasing serum phosphorus concentrations toward the normal range. Although the clearest application for cinacalcet is the non-surgical treatment of hypercalcemic patients with persistent HPT, current indications for other transplant patients are as yet uncertain. Further studies are needed to determine the utility of cinacalcet in patients with spontaneous resolution of HPT or low bone turnover. This review discusses the pathophysiology of post-kidney transplant HPT, associated complications, and current options for clinical management.
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Complications of pediatric live-donor kidney transplantation: a single center's experience in Egypt. Pediatr Nephrol 2008; 23:2067-73. [PMID: 18071759 DOI: 10.1007/s00467-007-0669-x] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/13/2007] [Revised: 09/25/2007] [Accepted: 10/01/2007] [Indexed: 10/22/2022]
Abstract
Our objective was to study the complications of chronic renal failure (CRF) among pediatric live-donor kidney transplant recipients. Between March 1976 and December 2005, 1,785 live-donor kidney transplantations were carried out at our center. Of the recipients, 292 were 20 years old or younger (mean age 12.8 years, ranging from 4 years to 20 years). Clinical and laboratory parameters of these 292 patients were analyzed retrospectively. They were 182 boys and 110 girls. Patients who had received transplants before 1988 were treated with prednisolone and azathioprine as combined therapy. From 1988 to 1998, a triple regimen comprising prednisolone, azathioprine and cyclosporine A (CsA) was administered. Tacrolimus and mycophenolate mofetil (MMF) were introduced as primary therapy in 1998. Growth, anemia, infections, and surgical, cardiac, neurologic, bone and other medical complications were assessed. Triple-drug immunosuppression (prednisone + CsA + azathioprine) was used in 68.2% of transplants. Acute rejection rate was 47.6%; chronic rejection rate was 31%. Hypertension (62%) was the commonest complication. Anemia was diagnosed in 61%. A substantial proportion of patients (48%) were short, with height standard deviation scores (SDSs) of less than -1.88. The overall infection rate was high, and the majority (54%) was bacterial. Malignancy was diagnosed in eight (3%) patients. The incidence of urological complications was 14%, and that of vascular complications was 1%. Cardiac complications included left ventricular hypertrophy (LVH) in 47.9% of patients, left atrial enlargement (31.5%) and left ventricular dilatation and systolic dysfunction (13.7% for each). Neuropathic changes were found in 19% of our cases, with the distal muscles of lower limbs more affected. Other complications included avascular bone necrosis in 8% (all of them in the hip joint) and bone loss in 60% of patients. We concluded that, despite the long-term success of pediatric renal transplantation in a developing country, there is a risk of significant morbidity.
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Mirone V, Longo N, Fusco F, Verze P, Creta M, Parazzini F, Imbimbo C. Renal transplantation does not improve erectile function in hemodialysed patients. Eur Urol 2008; 56:1047-53. [PMID: 18835084 DOI: 10.1016/j.eururo.2008.09.020] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/06/2008] [Accepted: 09/16/2008] [Indexed: 12/14/2022]
Abstract
BACKGROUND Effects of renal transplantation (RT) on erectile dysfunction (ED) is a controversial issue. OBJECTIVE To verify the efficacy of RT in restoring erectile function (EF) in hemodialysed patients. DESIGN, SETTING, AND PARTICIPANTS We conducted a prospective, interventional, nonrandomised study from September 2001 to September 2005 on 78 hemodialysed male patients undergoing RT. EF was evaluated during the baseline visit and 1 yr after RT, using the International Index of Erectile Function (IIEF) questionnaire. A subanalysis was performed by splitting the total cohort into two age groups: <45 yr and ≥45 yr. INTERVENTION RT was performed. MEASUREMENTS EF was evaluated using the IIEF scoring system. RESULTS AND LIMITATIONS Before RT, 68 patients with a mean total IIEF score of 42.46 complained about ED. One year after RT, 71 patients reported ED, and the mean total IIEF score had decreased to 39.97. The mean pre-RT IIEF EF domain score was 18.48, and it decreased to 17.55 after RT. Patients aged≥45 yr reported no significant variations in any IIEF domain, while patients aged<45 yr reported a significant decrease in mean total IIEF score due to variations in domain scores for erectile function, sexual desire, and overall satisfaction. In the younger age group, we found significant differences between baseline and post-RT IIEF scores in dyslipidaemic patients and in those patients using immunosuppressive (methylprednisolone and cyclosporin) or antihypertensive (ACE-inhibitors, β-blockers, and Ca-antagonists) drugs. The main limitations were the absence of any aetiological characterisation of ED and the small number of patients. CONCLUSIONS After RT, EF worsens in patients<45 yr but is not modified in patients≥45 yr.
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Affiliation(s)
- Vincenzo Mirone
- Department of Urology, University Federico II of Naples, Naples, Italy
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White CT, Schisler T, Er L, Djurdjev O, Matsuda-Abedini M. CKD Following Kidney Transplantation in Children and Adolescents. Am J Kidney Dis 2008; 51:996-1004. [DOI: 10.1053/j.ajkd.2008.03.001] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/03/2007] [Accepted: 03/03/2008] [Indexed: 12/17/2022]
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Feber J, Wong H, Geier P, Chaudry B, Filler G. Complications of chronic kidney disease in children post-renal transplantation - a single center experience. Pediatr Transplant 2008; 12:80-4. [PMID: 18186892 DOI: 10.1111/j.1399-3046.2007.00782.x] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
Similar to adults, CKD may persist after pediatric RTx. Clinical and laboratory parameters were analyzed retrospectively in 23 RTx recipients (13 males, age 11.9 +/- 5.2 yr), initially treated with prednisone, calcineurin inhibitor (TAC = 18, cyclosporine neoral = 5), and MMF at four months post-RTx (T1) and at 3.4 +/- 2.8 yr post-RTx (T2). Mean (+/-s.d.) cystatin C GFR (mL/min/1.73 m(2)) was 72 +/- 19 at T1 and 70 +/- 22 at T2 (NS). At T2, CKD stage I was present in five patients (22%), stage II in eight patients (35%), and stage III in 10 patients (43%). At T2, calcineurin inhibitors were utilized in 19, MMF in 13, and SIR in 13 patients. The prevalence of hypertension was 69% at T1 and 87% at T2 (p = NS). Anemia was diagnosed in 61% at T1 and 69% at T2 with average therapeutic MMF (2.78 +/- 1.3 mg/mL) and SIR (7.62 +/- 2.3 mg/mL) trough levels. Hypercholesterolemia was detected in 44.0% at T1 and 47% at T2. Bone disease was diagnosed in 26.0% at T1 and 21.7% at T2. Mean height Z-scores were -1.0 +/- 1.2 (T1) and -1.0 +/- 1.59 (T2, NS), with 21% at T1 and 30% at T2 below two SDS. We observed suboptimal growth, hypertension, hypercholesterolemia, bone disease, and anemia in a significant proportion of transplanted children.
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Affiliation(s)
- Janusz Feber
- Department of Pediatrics, CHEO, Ottawa, ON, Canada.
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