Diverse associations between oxidative stress and thromboxane A2 in hypertensive glomerular injury.

We examined the potential contributions of oxidative stress and thromboxane A2 (TXA2) to the development of regional heterogeneity in hypertensive glomerular injury using stroke-prone spontaneously hypertensive rats (SHRSP), an animal model of human essential hypertension. We also examined the effect of antioxidant treatment on the regional expression of thromboxane synthase (TXAS) mRNA using a microdissection method. Increases in the glomerular expression of TXAS mRNA were observed in the SHRSP at 15 weeks of age compared with those in the age-matched normotensive control Wistar-Kyoto (WKY) rats: 2.4-fold and 3.1-fold in the superficial and juxtamedullary glomeruli, respectively (P < 0.05). The heme oxygenase-1 mRNA expression was markedly increased (greater than eightfold, P < 0.05) in both the superficial and juxtamedullary glomeruli in the SHRSP compared with the expression in the WKY rats. In contrast to our expectations, the treatment of SHRSP with tempol (a superoxide dismutase mimetic) significantly (P < 0.05) increased the TXAS mRNA expression in the superficial glomeruli and did not improve the histological injury or albuminuria, which were both aggravated. Moreover, ozagrel (a TXAS inhibitor) had a suppressive effect on the TXAS mRNA expression and significantly (P < 0.05) improved the histological injury. These results indicated that although TXA2 and oxidative stress are linked to each other, TXA2 rather than oxidative stress may be a better therapeutic target to improve hypertensive glomerular injury.

Efficacy of Cryofiltration for Treatment of Mixed Cryoglobulinemia: A Report of Four Cases.

Cryoglobulinemia can induce systemic vasculitis affecting various organs such as skin, peripheral nerves, and kidney. The disease can induce chronic organ failure and even be life-threatening. Cryofiltration has been applied for the treatment of cryoglobulinemic vasculitis. We have experienced four cases with mixed cryoglobulinemia showing severe and progressive clinical manifestations, including skin purpura, nephrotic syndrome, acute kidney injury, and peripheral neuropathy. Cryofiltration in conjunction with conventional pharmacological therapies appeared to be safe and effective. After the treatments, plasma cryoglobulins were markedly reduced and the disease was well controlled. Although its efficacy has not yet been well established, this report can be another evidence showing efficacy of cryofiltration for treatment of mixed cryoglobulinemia.

[Senile-onset recurrent myelitis with anti-aquaporin-4 antibody].

An 81-year-old man presented with sudden-onset paraplegia. Cerebrospinal fluid examination revealed an increased cell count and an elevated protein level; the patient also tested positive for the oligoclonal band (OCB). Gadolinium-enhanced MRI revealed a thoracic cord lesion. On the basis of these results, his condition was diagnosed as acute myelitis. The steroid pulse therapy was ineffective, but intravenous immunogloblin treatment (IVIg) resulted in a slight improvement in the muscle strength of his lower limbs. However, three weeks later, a new thoracic spinal cord lesion developed. He was then diagnosed with multiple sclerosis (MS), and was once again, administered IVIg which proved ineffective then. Furthermore, one and a half month later, his condition relapsed with long lesions extending from the brainstem to cervical cord with respiratory muscles involvement. This time, steroid pulse therapy was effective, and he was able to breathe without, the assistance of a respirator. Anti-aquaporin-4 (AQP4) antibodies were detected in the patient's serum, and hence he was administered oral prednisolone in order to prevent the recurrence of lesions. This was not atypical case of neuromyelitis optica (NMO) because of the patient's advanced age at onset, the presence of OCB, and the absence of optic symptoms. However, the pathogenesis may be similar to that of NMO. In the case of acute myelitis of senile onset, examination for anti-AQP-4 antibodies may be required to administer the appropriate therapy.