In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.

Rheumatoid arthritis (RA) is regarded as a high risk factor for myocardial infarction. Hypertension is a major modifiable risk factor contributing to increased risk of myocardial infarction (MI). Dual blood pressure (BP)-lowering and anti-inflammatory effect of renin-angiotensin-system (RAS) inhibitors may possess protective effect from MI in RA population. However, treatment of hypertension with RAS inhibitors and MI in RA population remains unclear. We investigated whether RAS blockade could decrease risk of incident MI in hypertensive patients with RA. We identified patients with RA and hypertension from the Registry for Catastrophic Illness, a nation-wide database encompassing almost all of the RA patients in Taiwan from 1995 to 2008. The primary endpoint was MI and the median duration of follow up was 2,986 days. Propensity score weighting and Cox proportional hazards regression models were used to estimate hazard ratios for MI. Among 27,335 subjects, 9.9% received angiotensin-converting enzyme inhibitors (ACEIs), 25.9% received angiotensin II receptor blockers (ARBs) and 20.0% received ACEIs or ARBs alternatively. The incidence of MI significantly decreased in patients treated with ACEIs (hazard ratio 0.707; 95% confidence interval 0.595–0.840), ARBs (0.641; 0.550–0.747) and ACEIs/ARBs (0.631; 0.539–0.739). The protective effect of ACEI or ARB therapy was significantly better in patients taking longer duration. The effect remained robust in subgroup analyses. Therapy of ACEIs or ARBs is associated with a lower risk of MI among patients with RA. Hence, hypertension in patients with RA could comprise a compelling indication for RAS inhibitors.

Isolated pulmonary valve infective endocarditis caused by Candida is rare in chronic hemodialysis patients. The 2009 Infectious Diseases Society of America guidelines suggest the combined use of surgery and antibiotics to treat candidiasis; however, successful nonsurgical treatment of Candida endocarditis has been reported. A 63-year-old woman with end-stage kidney disease was admitted to our hospital after experiencing disorientation for 5 days. The patient was permanently bedridden because of depression, and denied active intravenous drug use. She received maintenance hemodialysis through a tunneled-cuffed catheter. An initial blood culture grew Candida guilliermondii without other bacteria. Subsequent blood cultures and tip culture of tunneled-cuffed catheter also grew C. guilliermondii, even after caspofungin replaced fluconazole. A 1.2-cm mobile mass was observed on the pulmonary valve. Surgical intervention was suggested, but the family of the patient declined because of her multiple comorbidities. The patient was discharged with a prescription of fluconazole, but she died soon after. Our patient is the first case with isolated pulmonary valve endocarditis caused by C. guilliermondii in patients with uremia. Hematologic disorders, in addition to long-term central venous catheter use, prolonged antibiotic intravenous injection, and congenital cardiac anomaly, predispose to the condition. The diagnosis “isolated” pulmonary IE is difficult, and combing surgery with antifungal antibiotics is the appropriate therapeutic management for Candida related pulmonary IE.

Although renin-angiotensin system (RAS) blockade has been shown to reduce cardiovascular disease (CVD) in the general population and high-risk subjects, their protective effect in autosomal dominant polycystic kidney disease (ADPKD) patients under dialysis was still unknown. By using the database from 1995 to 2008 Taiwan National Health Insurance Research Database (Registry for Catastrophic Illnesses), we included 387 ADPKD patients who received dialysis therapy, aged ≥ 18 year-old, and with no evidence of CVD events in 1997 and 1998. We utilized Cox proportional hazards regression analysis and propensity score matching to evaluate adjusted hazard ratios for all-cause mortality and CVD events in users (n=231) and nonusers (n = 156) of an angiotensin-converting enzymes inhibitor (ACEI) / angiotensin II receptor blocker (ARB) during the 12 years of follow-up. All study subjects were followed up for more than 3 months. There was no significant difference between the ACEI/ARB treatment group and the control group in incident CVD events except ischemic stroke and transient ischemic accident (TIA). The results remain similar between groups before and after propensity score matching. Moreover, there was no significant difference in outcomes between ACEI/ARB treatment over 50% of follow-up period and without ACEI/ARB treatment after propensity score matching. This nationwide cohort study failed to prove the protective effects of long-term ACEI or ARB on incident CVD events among APKD dialysis patients. Further larger scale, multicenter and randomized control trials are warranted to show the causal association