Association between glycated albumin and sudden death in patients undergoing hemodialysis.

BACKGROUND: The frequency of sudden death and its risk factors in patients undergoing hemodialysis are unknown. This study was performed to examine the association between glycated albumin (GA) and sudden death in Japanese patients undergoing hemodialysis. METHODS: In total, 260 patients undergoing hemodialysis aged ≥18 years were retrospectively followed for a mean of 4.6 years. The patients' serum GA levels were divided into tertiles, and the patients' sex, age, albumin level, C-reactive protein (CRP) level, and cardiothoracic ratio (CTR) were selected as adjustment factors. A logistic regression model was used to calculate the odds ratio (OR) for the occurrence of sudden death by GA level. RESULTS: Ninety-one patients died during follow-up. Of the 91 deaths, 23 (25.2%) were defined as sudden deaths. Compared with non-sudden death cases, sudden death cases were significantly younger (p = 0.002) and had a higher proportion of men (p = 0.03), a higher proportion of diabetes (p = 0.008), and higher GA levels (p = 0.023). Compared with patients with the lowest GA levels (<15.2%), those with the highest GA levels (≥18.5%) had a sex- and age-adjusted OR for sudden death of 5.40 [95% confidence interval (CI): 1.35-21.85]. After adjusting for the albumin level, CRP level, and CTR in addition to sex and age, the OR for sudden death of patients with the highest GA levels increased to 6.80 (95%CI: 1.64-28.08); the relationship did not change. CONCLUSION: Serum GA levels were significantly associated with sudden death in patients undergoing hemodialysis.

Fibroblast growth factor 23 is associated with carotid artery calcification in chronic kidney disease patients not undergoing dialysis: a cross-sectional study.

BACKGROUND: Fibroblast growth factor 23 (FGF23) is an important hormone in the regulation of phosphate metabolism. It is unclear whether FGF23 is associated with carotid artery calcification (CAAC) in predialysis patients. The present study aimed to clarify the relationship between FGF23 and CAAC in patients with chronic kidney disease (CKD) who were not on dialysis. METHODS: One-hundred ninety-five predialysis CKD patients were enrolled in this cross-sectional study. CAAC was assessed using multidetector computed tomography, and the prevalence of CAAC was examined. Intact FGF23 was measured in each patient. The risk factors for CAAC were evaluated using a logistic regression model. RESULTS: We found CAAC in 66% of the patients. The prevalence of CAAC significantly increased across CKD stages: it was 37% in CKD stages 1-2, 58% in stage 3; 75% in stage 4, and 77% in stage 5 (p < 0.01). In multivariate analysis, smoking, diabetes mellitus and log FGF23 were each identified as risk factors for CAAC. The study population was divided in quartiles of FGF23 levels. Compared with the lowest FGF23 quartile, each subsequent quartile had a progressively higher odds ratio (OR) for CAAC, adjusted for confounders (ORs [95% confidence interval] of 2.34 [0.78 to 7.31], 5.28 [1.56 to 19.5], and 13.6 [2.92 to 74.6] for the second, third, and fourth quartiles, respectively. CONCLUSIONS: The prevalence of CAAC is increased with the decline in the kidney function. FGF23 is independently related to CAAC in patients with CKD who are not on dialysis.

Carotid artery calcification at the initiation of hemodialysis is a risk factor for cardiovascular events in patients with end-stage renal disease: a cohort study.

BACKGROUND: Vascular calcification has been recognized as a risk factor for cardiovascular (CV) events in patients with end-stage renal disease (ESRD). However, the association of carotid artery calcification (CAAC) with CV events remains unknown. The aim of this study was to elucidate whether CAAC is associated with composite CV events in ESRD patients. METHODS: One-hundred thirty-three patients who had been started on hemodialysis between 2004 and 2008 were included in this retrospective cohort study. These patients received multi-detector computed tomography to assess CAAC at the initiation of hemodialysis. Composite CV events, including ischemic heart disease, heart failure, cerebrovascular diseases, and CV deaths after the initiation of hemodialysis, were examined in each patient. RESULTS: CAAC was found in 94 patients (71%). At the end of follow-up, composite CV events were seen in 47 patients: ischemic heart disease in 20, heart failure in 8, cerebrovascular disease in 12, and CV deaths in 7. The incidence of CAAC was 87% in patients with CV events, which was significantly higher than the rate (62%) in those without. Kaplan-Meier analysis showed a significant increase in composite CV events in patients with CAAC compared with those without CAAC (p = 0.001, log-rank test). Univariate analysis using a Cox hazards model showed that age, smoking, common carotid artery intima-media thickness and CAAC were risk factors for composite CV events. In multivariate analysis, only CAAC was a significant risk factor for composite CV events (hazard ratio, 2.85; 95% confidence interval, 1.18-8.00; p = 0.02). CONCLUSIONS: CAAC is an independent risk factor for CV events in ESRD patients. The assessment of CAAC at the initiation of hemodialysis is useful for predicting the prognosis.

A case of IgA nephropathy and renal hemosiderosis associated with primary hemochromatosis.

IgA nephropathy associated with liver cirrhosis is a common disease, unlike hemochromatosis-associated renal involvement, which is uncommon. A 55-year-old man was admitted to our hospital for the acute deterioration of renal function. Laboratory tests showed extremely high transferrin saturation and serum ferritin level. Furthermore, magnetic resonance imaging revealed low-intensity signals in both T1- and T2-weighted images within the liver, diagnosed as primary hemochromatosis. Renal biopsy showed mesangial IgA deposition with cellular crescent and hemosiderin in both glomerular and tubular epithelial cells. Renal function worsened progressively after admission, and thus steroid pulse therapy was started. Renal dysfunction improved, but the patient died of cerebral hemorrhage. The present case was considered IgA nephropathy and renal hemosiderosis secondary to primary hemochromatosis. To our knowledge, this is the first report that describes the above complications in association with primary hemochromatosis.

Tocilizumab-induced remission of nephrotic syndrome accompanied by secondary amyloidosis and glomerulonephritis in a patient with rheumatoid arthritis.

Rheumatoid arthritis (RA) is an autoimmune-mediated systemic disorder that primarily affects the musculoskeletal system. Patients with RA often present with kidney diseases, such as nephrotic syndrome. Causes of nephrotic syndrome include membranous nephropathy, IgA nephropathy and secondary amyloidosis. Recently, biological agents, including anti-tumor necrosis factor alpha and anti-interleukin 6 (IL-6) receptor antibodies, have been used for the treatment of RA. Anti-IL-6 receptor antibody therapy is believed to ameliorate RA-related kidney diseases, as IL-6 plays a central role in the pathogenesis of RA. We, herein, present the case of a patient with RA and related nephrotic syndrome whose proteinuria completely disappeared 1 month after tocilizumab treatment. A light microscopic examination of the pretreatment kidney biopsy specimen showed active glomerulonephritis with fibrocellular crescents and the deposition of amorphous substances stained weakly with hematoxylin-eosin and strongly with the Dylon method. Electron microscopy revealed the accumulation of microtubules ranging from 10 to 20 µm in width, primarily in the mesangial lesion. Amyloid A (AA) protein was positively stained in the mesangial area and vascular wall on immunohistochemistry. The final histologic diagnosis was RA-related glomerulonephritis and secondary AA amyloidosis. This case indicates that biological treatment targeting IL-6 is a promising therapeutic option for the treatment of kidney diseases associated with RA.