Background and objectives: As well as being a marker of body iron stores, serum ferritin (sFerritin) has also been shown to be a marker of inflammation in hemodialysis (HD) patients. The aim of this study was to analyze whether sFerritin is a reliable marker of the iron stores present in bone marrow of HD patients.Design: Histomorphometric analysis of stored transiliac bone biopsies was used to assess iron stores by determining the number of iron-stained cells per square millimeter of bone marrow.Results: In 96 patients, the laboratory parameters were hemoglobin ‫؍‬ 11.3 ؎ 1.6 g/dl, hematocrit ‫؍‬ 34.3 ؎ 5%, sFerritin ‫؍‬ 609 ؎ 305 ng/ml, transferrin saturation ‫؍‬ 32.7 ؎ 22.5%, and C-reactive protein (CRP) ‫؍‬ 0.9 ؎ 1.4 mg/dl. sFerritin correlated significantly with CRP, bone marrow iron, and time on HD treatment (P ‫؍‬ 0.006, 0.001, and 0.048, respectively). The independent determinants of sFerritin were CRP (␤-coef ‫؍‬ 0.26; 95% CI ‫؍‬ 24.6 to 132.3) and bone marrow iron (␤-coef ‫؍‬ 0.32; 95% CI ‫؍‬ 0.54 to 2.09). Bone marrow iron was higher in patients with sFerritin >500 ng/ml than in those with sFerritin <500 ng/ml. In the group of patients with sFerritin <500 ng/ml, the independent determinant of sFerritin was bone marrow iron (␤-coef ‫؍‬ 0.48, 95% CI ‫؍‬ 0.48 to 1.78), but in the group of patients with sFerritin >500 ng/ml, no independent determinant of sFerritin was found.Conclusions: sFerritin adequately reflects iron stores in bone marrow of HD patients.

The presence of ectopic and supernumerary PT in patients with renal hyperparathyroidism is significant. Although preoperative imaging tests did not locate most of ectopic glands, MIBI may be important for identifying ectopic PT in the mediastinal and thymic regions.

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Background/Aims: Hypovitaminosis D is highly prevalent among patients with chronic kidney disease (CKD) and has been associated with poor outcome. We aimed to test the effect of a protocol of cholecalciferol supplementation on the restoration of vitamin D status and on parathyroid hormone (PTH) levels in patients with CKD. Methods: This was a prospective interventional study of 6 months. Forty-five CKD patients (stages 3 and 4) with 25-hydroxyvitamin D deficiency [25(OH)D <15 ng/ml] were included. Patients received a weekly dose of 50,000 IU of cholecalciferol during 3 months, and 50,000 IU/month thereafter for those who had achieved 25(OH)D ≥30 ng/ml. Results: At 3 months, 78% of the patients restored their vitamin D status. At 6 months, only 43% of those patients maintained adequate vitamin D status. PTH decreased at 3 months (p = 0.02) but returned to baseline levels after 6 months. Fibroblast growth factor 23 increased at 3 months (p = 0.001) and returned to initial levels at 6 months. No changes were found in serum 1,25(OH)₂D, ionized calcium and phosphorus. Conclusions: A weekly dose of 50,000 IU of cholecalciferol for 3 months restored the vitamin D status of most patients and led to a reduction in PTH. The monthly dose of 50,000 IU appears not to be sufficient to maintain the levels of 25(OH)D.

Background and objectives: The aim of this study was to determine the role of host factors and bacterial virulence genes in the development of pyelonephritis caused by Escherichia coli in renal transplant (Tx) recipients.Design, setting, participants, & measurements: A total of 328 E. coli isolates from cases of cystitis (Cys; n ‫؍‬ 239) or pyelonephritis (PN; n ‫؍‬ 89), with 169 from renal Tx recipients, were subjected to molecular analyses to identify P-fimbria subunits (PapC, PapG II, and PapGIII), G-and M-fimbriae, and aerobactin. The presence of antibiotic resistance was also determined. Parameters such as gender, age, immunosuppression regimens, causes of ESRD, kidney donor, intraoperative anastomosis, use of double J stent, trimethoprim/sulfamethoxazole (TMP/SMZ) prophylaxis, and time after Tx were evaluated.Results: A multivariate analysis showed a significant association between PN and renal Tx. In renal Tx recipients, the risk of occurrence of PN was significantly higher among males and for those no longer receiving TMP/SMZ prophylaxis. E. coli strains isolated from PN presented a lower prevalence of papGIII and lower rates of resistance to pipemidic acid. Although papGII was more prevalent in PN than in Cys, it was not independently associated with PN.Conclusions: These findings suggested that renal Tx increases the risk for PN, and the male sex represented a host factor independently associated with risk, whereas the prophylaxis with TMP/SMZ was protective. The lack of papGIII and low resistance to first-generation quinolones were bacterial-independent risk factors for PN in Tx.