Relationship between serum uric acid level and vascular injury markers in hemodialysis patients.

PURPOSE: It has been reported that hyperuricemia causes vascular endothelial injury. Most hemodialysis patients present with hyperuricemia and also with vascular injury, resulting in cardiovascular diseases (CVD). However, the association of serum uric acid (sUA) with vascular injury markers in hemodialysis patients remains unclear. This study aimed to investigate this and discuss the mechanism by which uric acid causes vascular injury. METHODS: We enrolled 48 Japanese maintenance hemodialysis patients without any history of CVD. The association between sUA level and three vascular injury markers (reactive hyperemia index [RHI], ankle-brachial index [ABI], and cardio ankle vascular index [CAVI]) was investigated by linear- and logistic regression analyses. RESULTS: The median natural logarithm RHI (LnRHI) was 0.36. Linear regression analysis revealed a significant positive correlation between sUA level and LnRHI (ß = 0.42, p = 0.001) in all patients. Moreover, a significant, strongly positive correlation was observed between sUA and LnRHI in patients who were treated with xanthine oxidase inhibitors (XOIs) (ß = 0.75, p = 0.001). Further, the linear analysis showed a significant negative correlation between sUA level and CAVI in patients who were treated with XOIs (ß = - 0.52, p = 0.049). sUA level was not significantly associated with ABI abnormality. CONCLUSIONS: It is possible that a high level of sUA is significantly associated with better vascular endothelial function and condition of vascular tone in hemodialysis patients who were treated with XOIs. The findings suggest a significant paradox between sUA level and vascular endothelial function in hemodialysis patients; however, the opposite has been reported in patients without hemodialysis.

Thrombotic Thrombocytopenic Purpura Treated with Rituximab Associated with Primary Sjögren's Syndrome and Primary Hypothyroidism.

A 47-year-old man was admitted to our hospital because of thrombocytopenia and consciousness disturbance. As his laboratory data showed undetectable activity of a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13 (ADAMTS13) and the presence of ADAMTS13 inhibitor, he was diagnosed with acquired thrombotic thrombocytopenic purpura (TTP). Asymptomatic primary Sjögren's syndrome (SS) and primary hypothyroidism were incidentally diagnosed on screening. After initial plasma exchange therapy and pulse corticosteroid therapy, the patient received rituximab therapy for refractory TTP with "inhibitor boosting" and recovered. TTP secondary to primary SS is rare but can trigger refractory TTP. Treatment with rituximab, which is considered "inhibitor boosting," should be considered when re-exacerbation occurs.

Coexistence of Anti-Glomerular Basement Membrane Glomerulonephritis and Membranous Nephropathy in a Female Patient with Preserved Renal Function.

Renal prognosis for anti-glomerular basement membrane (GBM) glomerulonephritis is poor. The greater the amount of anti-GBM antibody binding the antigen (type IV collagen of the glomerular basement membrane), the greater the number of crescents that develop in glomeruli, resulting in progression of renal impairment. Immunofluorescence staining reveals linear IgG depositions on glomerular capillary walls. Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in middle-aged to elderly patients. Immune complex is deposited in the sub-epithelial space of the glomerulus resulting in the development of a membranous lesion. Immunofluorescence staining reveals granular IgG depositions on glomerular capillary walls. Coexisting anti-GBM glomerulonephritis and MN are rare and, here we report a case of coexisting anti-GBM glomerulonephritis and MN with preserved renal function. There are some cases of coexisting anti-GBM glomerulonephritis and MN do not show severely decreased renal function. A 76-year-old Japanese woman presented with nephrotic syndrome, microscopic hematuria, and was positive for anti-GBM antibody. Kidney biopsy revealed linear and granular IgG depositions in glomerular capillary walls, crescent formations, and electron-dense deposits in the sub-epithelial space. She was diagnosed with anti-GBM glomerulonephritis and MN. Steroid and cyclosporine therapy achieved complete remission, and kidney function was preserved. In conclusion, coexisting anti-GBM glomerulonephritis and MN can have preserved renal function. IgG subclass of deposited anti-GBM antibody may be associated with the severity of anti-GBM glomerulonephritis. In addition, in the case of nephrotic syndrome with hematuria, we should consider the possibility of coexisting anti-GBM glomerulonephritis and MN.