Background/Aims:  Rituximab is known to be associated with high hepatitis B virus (HBV) reactivation rate in patients with resolved HBV infection and hematologic malignancy. However, data regarding HBV reactivation (HBVr) in rheumatic patients receiving rituximab is limited. To assess the HBVr rate in hepatitis B surface antigen (HBsAg)-negative patients receiving rituximab for autoimmune diseases in a large real-world cohort. Methods:  From March 2006 to December 2019, 900 patients with negative HBsAg receiving at least one cycle of rituximab for autoimmune diseases in a tertiary medical center in Taiwan were retrospectively reviewed. Clinical outcome and factors associated with HBVr were analyzed. Results: After a median follow-up period of 3.3 years, 21 patients developed HBVr, among whom 17 patients were positive for hepatitis B core antibody (anti-HBc) and four were negative. Thirteen patients had clinical hepatitis flare, while eight patients had HBsAg seroreversion without hepatitis. Old age, anti-HBc positivity, undetectable serum hepatitis B surface antibody level at rituximab initiation and a higher average rituximab dose were associated with a higher HBVr rate. There was no significant difference in the HBVr risk between rheumatoid arthritis and other autoimmune diseases. Among anti-HBc-negative patients, subjects without HBV vaccination at birth had an increased risk of HBVr (4/368, 1.1%) compared with those who received vaccination (0/126, 0%). Conclusions In HBV endemic areas where occult HBV is prevalent, anti-HBc-negative patients, may still be at risk for HBVr after rituximab exposure. HBVr may still be considered in HBsAgnegative patients developing abnormal liver function after rituximab exposure, even in patients with negative anti-HBc.

Background: Larger middle molecules are important substances associated with cardiovascular complications in end- stage renal disease. Unfortunately, larger middle molecules are not reliably removed by a high-flux dialyzer. A medium cut-off (MCO) membrane could effectively remove larger middle molecules. This study aimed to identify the long -term effect of the MCO membrane for changes of larger middle molecules. Methods: Thirty-four patients were prospectively analyzed for 12 months. The enrolled patients were divided into control and MCO groups. We measured the plasma levels of growth differentiation factor 15, sclerostin, and fibroblast growth factor 23 in larger middle molecules and those of biomarkers including small solutes. Single-pool Kt/V (spKt/V) and reduction ratios also were evaluated. Results: Plasma sclerostin did not increase significantly in patients using the MCO dialyzer (135.3 [–637.7 to 908.3], p = 0.715). And there was a significant difference in change of plasma sclerostin level between the two groups (–1,646.9 [–3,015.2 to –278.7], p = 0.033). Furthermore, a negative association between calcium and sclerostin was not observed in the MCO group (r = –0.142, p = 0.587). Solute clearance of larger middle molecules in the MCO group was significantly higher. Moreover, spKt/V values for patients in the MCO group were significantly increased without albumin loss. Values are presented as mean (95% confidence interval [CI]) or adjusted mean (95% CI). Conclusion The MCO dialyzer can increase dialytic adequacy and suppress the increase in plasma sclerostin level without significant albumin loss in patients with end-stage renal disease.

Background: Larger middle molecules are important substances associated with cardiovascular complications in end- stage renal disease. Unfortunately, larger middle molecules are not reliably removed by a high-flux dialyzer. A medium cut-off (MCO) membrane could effectively remove larger middle molecules. This study aimed to identify the long -term effect of the MCO membrane for changes of larger middle molecules. Methods: Thirty-four patients were prospectively analyzed for 12 months. The enrolled patients were divided into control and MCO groups. We measured the plasma levels of growth differentiation factor 15, sclerostin, and fibroblast growth factor 23 in larger middle molecules and those of biomarkers including small solutes. Single-pool Kt/V (spKt/V) and reduction ratios also were evaluated. Results: Plasma sclerostin did not increase significantly in patients using the MCO dialyzer (135.3 [–637.7 to 908.3], p = 0.715). And there was a significant difference in change of plasma sclerostin level between the two groups (–1,646.9 [–3,015.2 to –278.7], p = 0.033). Furthermore, a negative association between calcium and sclerostin was not observed in the MCO group (r = –0.142, p = 0.587). Solute clearance of larger middle molecules in the MCO group was significantly higher. Moreover, spKt/V values for patients in the MCO group were significantly increased without albumin loss. Values are presented as mean (95% confidence interval [CI]) or adjusted mean (95% CI). Conclusion The MCO dialyzer can increase dialytic adequacy and suppress the increase in plasma sclerostin level without significant albumin loss in patients with end-stage renal disease.

No abstract available.
Eating* ; Nephrosis, Lipoid* ; Toxicodendron*

BACKGROUND: Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI. METHODS: Pax8–rtTA/tetracycline response element–human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI. RESULTS: Results of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the collagen 3a1 gene in folic acid-treated transgenic mice overexpressing human CD 36 compared with folic acid-treated wild type mice. CONCLUSION: Human CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease.
Acute Kidney Injury* ; Albuminuria ; Animals ; Collagen ; Fibrosis ; Folic Acid ; Humans* ; Hyperglycemia ; Hypertension ; Kidney Diseases ; Mice* ; Mice, Transgenic ; Renal Insufficiency ; Renal Insufficiency, Chronic ; Risk Factors ; RNA, Messenger

No abstract available.
Hernia, Obturator* ; Polycystic Kidney, Autosomal Dominant*

No abstract available.
Glomerulonephritis, IGA* ; Immunoglobulin A* ; Immunoglobulins*

BACKGROUND/AIMS: Advanced glycation end-products (AGEs) exert various toxic effects through the receptor for AGEs (RAGE). Soluble RAGE (sRAGE) is a naturally occurring inhibitor of AGE-RAGE. Recent studies have suggested that inhibition of angiotensin-converting enzyme (ACE) reduces the accumulation of AGEs in diabetes partly by increasing the production and secretion of sRAGE into the plasma. This report describes the relationship between sRAGE and ACE polymorphism in maintenance hemodialysis patients. METHODS: The levels of sRAGE and advanced oxidation protein products (AOPPs) were assessed by enzyme-linked immunosorbent assay (ELISA), and ACE polymorphism was detected by PCR amplification. RESULTS: The distributions of ACE genotypes in 105 hemodialysis patients were as follows: II, 56 (35.9%); ID, 29 (18.6%); and DD, 20 (12.8%). According to the ACE genotypes, the study group consisted of II (n = 56) and ID + DD group (n = 49). sRAGE was correlated with age (r = -0.24; p = 0.013). There were significant differences in sRAGE, AOPP, age, duration of dialysis, C-reactive protein, or 24-h urine volume between two genotype groups. There were no significant differences in sRAGE levels, even though the effect of age was treated as a covariate. CONCLUSIONS: Our findings suggested that sRAGE may be affected only by age, and not by ACE polymorphism in maintenance hemodialysis patients.
Advanced Oxidation Protein Products ; C-Reactive Protein ; Dialysis ; Enzyme-Linked Immunosorbent Assay ; Genotype ; Humans ; Plasma ; Polymerase Chain Reaction ; Rage ; Renal Dialysis* ; Urine