Intrinsic antigen-related MN was more strongly associated with complement activation by the lectin pathway, which may contribute to a less favorable clinical outcome.

Arteriovenous fistula puncture pain is a serious problem for patients undergoing dialysis and a good indication for topical anesthetics. No previous study has compared lidocaine/prilocaine cream (EMLA) with lidocaine tape for pain relief during arteriovenous fistula puncture in patients undergoing maintenance hemodialysis. To this end, we conducted a multicenter randomized crossover study including 66 patients (mean age, 65.8 years; males, 57.6%) undergoing maintenance hemodialysis thrice/week. Subjects were assigned to Sequence EL (EMLA administration followed by lidocaine, with 1-week wash-out) or Sequence LE (reverse administration, first lidocaine then EMLA). All subjects completed the study. At each puncture site, 1 g EMLA (25 mg lidocaine + 25 mg prilocaine) or one sheet of lidocaine tape (18 mg lidocaine) was applied 1 h or 30 min prior to arteriovenous fistula puncture, respectively. The primary endpoint was puncture pain relief, which was measured using a 100-mm visual analog scale. The secondary endpoints included quality of life, which was measured by SF-36, and safety. EMLA produced a 10.1-mm greater visual analog scale improvement than lidocaine tape (P = 0.00001). However, there was no statistically significant difference in the quality of life between the two groups, and no significant carryover/period effect was observed in any analysis. Further, no drug-related adverse events were observed. Taken together, these results suggest that EMLA cream is superior to lidocaine tape for the relief of arteriovenous fistula puncture pain in patients undergoing maintenance hemodialysis.

BackgroundCardiovascular disease (CVD) due to atherosclerosis is a major cause of death in renal allograft recipients. Recently, C1q/TNF-α related protein-9 (CTRP9), which is a paralog of adiponectin (ADPN), has been suggested to be related to the prevention of atherosclerosis and the occurrence of CVD, but this relationship has not been confirmed in renal allograft recipients.

Although it has been reported that chronic kidney disease exacerbates sarcopenia progression, the mechanisms of the process remain unclear. Fifty-one patients who underwent renal transplantation at our hospital since 1998 (31 males and 20 females; aged 29-52 years at the time of transplantation) were retrospectively examined for the relationships among the psoas muscle index (PMI), intramuscular adipose tissue content (IMAC), serum adiponectin fractions (high-/low-molecularweight) and new-onset diabetes after transplantation (NODAT). Before transplantation, age at kidney transplantation negatively correlated with PMI and positively correlated with IMAC (rS = − 0.427, p < 0.01; rS = 0.464, p < 0.01, respectively). Both at 1 and 5 years after transplantation, PMI was higher than before transplantation (p < 0.01). IMAC transiently decreased to − 0.39 at 1 year after kidney transplantation but subsequently increased to − 0.36 at 5 years after kidney transplantation. Multivariate analyses revealed that the mean increase in high-molecular weight adiponectin concentrations was an exacerbating factor for the mean change in PMI (p = 0.003). Moreover, the mean increases in IMAC were exacerbating factors for NODAT. In conclusion, the increase in the PMI is associated with high-molecular weight adiponectin levels after renal transplantation. Sarcopenia is defined as loss of the mass, strength, and function of skeletal muscles 1. It is associated with not only a decline in the activities of daily living and falls, which results in the need for long-term care, but also with an increase in mortality and is a significant clinical and social problem in the developed countries 2. Sarcopenia is classified into primary sarcopenia and secondary sarcopenia 3. Primary sarcopenia is an age-associated decrease in muscle mass, whereas secondary sarcopenia is a decrease in muscle mass associated with a reduced activity level, malnutrition, organ failure, invasion and diseases, including cancer. Therefore, contributing factors for secondary sarcopenia should be considered in the same way as ageing. Metabolic acidosis and the increased expression of angiotensin II have been shown to decrease muscle mass in patients with chronic kidney disease, particularly patients on dialysis 4,5. However, studies on sarcopenia in patients with kidney transplantation are very few. Although sarcopenia is a clinically important manifestation, it is difficult to objectively evaluate its progression. As the quantity and quality of skeletal muscle is an essential component for sarcopenia, we focused on psoas muscle images on computed tomography (CT). Hamaguchi et al. reported that a decrease in muscle mass, expressed as the psoas muscle index (PMI), was related to the mortality rate after transplantation 6. Muscle quality has recently been attracting attention, and the fatty degeneration of muscle has been associated with ageing and muscle weakness 7 as well as with the development of diabetes mellitus 8. Kitajima et al. evaluated the fatty generation of muscle ...

Morphologically, early colorectal cancers are divided into two types: polypoid cancers and non-polypoid cancers. They vary in growth pattern, progression, and genetic alteration. Angiogenesis between polypoid and non-polypoid cancers may also be different. Therefore, the present study aims to evaluate angiogenesis in the early stages of colorectal malignancy, with particular attention to the morphological differences. The serial slides of all materials (48 polypoid cancers, 10 non-polypoid cancers, 20 adenomas and 10 normal tissues) were immunohistochemically stained for three endothelial cell markers (CD31, von Willebrand factor and CD105), counted for the number of microvessels in the same hot spots, and the angiogenic status was estimated. Polypoid cancers had higher microvessel counts and were more predominantly supplied by activated (CD105-positive, newly forming) microvessels than non-polypoid cancers. The present study indicated the possibility that the difference in growth pattern might be explained by the difference in angiogenesis between polypoid and non-polypoid cancers.