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  • S. Karger AG  (2)
  • Lee, Chien-Te  (2)
  • 1
    In: Blood Purification, S. Karger AG, Vol. 21, No. 6 ( 2003), p. 369-375
    Abstract: 〈 i 〉 Aims: 〈 /i 〉 Secondary hyperparathyroidism (HPT) worsens anemia and may cause hyporesponsiveness to recombinant human erythropoietin therapy (r-HuEPO). To investigate the effect of parathyroidectomy (PTX) on iron homeostasis and erythropoiesis, we conducted a prospective study in chronic hemodialysis patients who underwent PTX. 〈 i 〉 Methods: 〈 /i 〉 Thirty-two patients were enrolled in this study. Based on the increases in hemoglobin level after PTX, patients were divided into responders and nonresponders. Iron homeostasis and erythropoiesis were assessed before and 1 and 3 months after PTX, hemoglobin and parathyroid hormone levels were monitored until 6 months after PTX. 〈 i 〉 Results: 〈 /i 〉 In the responders, increased hemoglobin levels were observed in 15 patients at 1 and 3 months after PTX (8.0 ± 0.8 g/dl vs. 9.2 ± 1.3 and 10.1 ± 0.9 g/dl, p 〈 0.05). The nonresponders had higher pre-PTX hemoglobin levels than the responders (10.3 ± 1.6 g/dl vs. 8.0 ± 0.8 g/dl, p 〈 0.05). There was no further increase in hemoglobin at 6 months compared to 3 months after PTX in both groups. In neither group did PTX affect serum ferritin, transferrin saturation and serum erythropoietin level. Serum soluble transferrin receptor (sTfR) concentration was found to be higher in responders than in nonresponders (3.32 ± 1.28 mg/l vs. 1.70 ± 0.31 mg/l, p 〈 0.05). 〈 i 〉 Conclusions: 〈 /i 〉 We conclude that PTX can improve anemia in hemodialysis patients with severe hyperparathyroidism and greater resistance to r-HuEPO therapy. The reversing of anemia does not involve altering iron mobilization. Pre-PTX hemoglobin and serum sTfR levels can predict the effect of PTX on correcting anemia.
    Type of Medium: Online Resource
    ISSN: 0253-5068 , 1421-9735
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2003
    detail.hit.zdb_id: 605548-5
    detail.hit.zdb_id: 1482025-0
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  • 2
    In: Medical Principles and Practice, S. Karger AG, Vol. 28, No. 3 ( 2019), p. 273-279
    Abstract: 〈 b 〉 〈 i 〉 Objective: 〈 /i 〉 〈 /b 〉 Recent studies have reported that reduced excretion of urinary uromodulin is associated with renal tubular function and risks of progressive kidney disease. Gouty nephropathy is usually seen in patients with gout. Patients with chronic gouty nephropathy are characterized by the deposition of monosodium urate crystals primarily involving the collecting ducts in the medulla. We postulated that this correlation may be specific to gout and may serve as a useful biomarker for chronic kidney disease (CKD). 〈 b 〉 〈 i 〉 Materials and Methods: 〈 /i 〉 〈 /b 〉 〈 i 〉 〈 /i 〉 A total of 114 Taiwanese patients diagnosed with gout ( 〈 i 〉 n 〈 /i 〉 = 72), CKD ( 〈 i 〉 n 〈 /i 〉 = 26), or healthy volunteers ( 〈 i 〉 n 〈 /i 〉 = 16) were prospectively enrolled for this study from the Rheumatology and Nephrology Outpatient Clinics of our institution. We obtained urine and blood samples on patient visits to the outpatient clinics. Demographic data were obtained from medical records. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 〈 i 〉 〈 /i 〉 In patients with gout, the spot urinary uromodulin/creatinine ratio (uUMCR; mg/g) in patients with CKD was significantly lower than that in those without CKD (CKD group: 2.2; non-CKD group: 5.6, 〈 i 〉 p 〈 /i 〉 = 0.005). Multivariate analysis revealed that patients with CKD and gout had a lower uUMCR than those with gout alone ( 〈 i 〉 p = 〈 /i 〉 0.028). A significant association was not observed in our non-gout cohort. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 〈 i 〉 〈 /i 〉 The association of decreased uUMCR with CKD status was identified only in patients with gout in the present study. We believe that uUMCR might serve as an indicator of differential CKD in patients with gout.
    Type of Medium: Online Resource
    ISSN: 1011-7571 , 1423-0151
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2019
    detail.hit.zdb_id: 645108-1
    detail.hit.zdb_id: 1482963-0
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