Assessment of fluid and nutritional status using multifrequency bioelectrical impedance analysis in peritoneal dialysis patients.

BACKGROUND/AIMS: The purpose of this study was to evaluate the clinical usefulness and relevance of bioelectrical impedance analysis (BIA) for assessing the fluid and nutritional status in peritoneal dialysis (PD) patients. METHODS: Statistical analyses between various measures of fluid and nutritional status were performed in 106 cases of 64 patients. RESULTS: Extracellular fluid/total body water (ECF/TBW) was correlated with systolic blood pressure, extremity edema, and antihypertensive medications (p = 0.042, p < 0.001, and p = 0.029, respectively). Body cell mass (BCM)/height(2) was correlated with SGA rating and PCR (p < 0.001 and p = 0.002, respectively). ECF/TBW and BCM/height(2) significantly predicted extremity edema (p < 0.001) and SGA rating (p = 0.001), respectively. ROC analysis yielded an ECF/TBW cut-off of 0.36 and a BCM/height(2) cut-off of 11.23. When the BCM/height(2) cut-off of 11.23 was applied to subclinical patients (SGA score ≥6), a significant difference in SGA rating was detected in subgroups (p = 0.010). CONCLUSION: BIA yields useful and relevant information about hydration and nutritional status in PD patients.

Effects of losartan and pentoxifylline on renal dimethylarginine dimethylaminohydrolase-1 expression in proteinuric nephropathy.

BACKGROUND/AIMS: Circulatory asymmetric dimethylarginine (ADMA) is correlated with proteinuria and endothelial dysfunction in patients with proteinuric renal diseases. However, it is not known whether proteinuria itself affects expression of dimethylarginine dimethylaminohydrolase (DDAH), a degrading enzyme of ADMA, in kidney. The aim of this study is to evaluate the direct effects of losartan and/or pentoxifylline on expression of renal DDAH-1 and its relation to oxidative stress in the setting of albuminuria. METHODS: Using NRK52E cells, DDAH-1 mRNA and protein were determined after exposure to albumin with losartan and/or pentoxifylline. Reactive oxygen species (ROS), PKC activity, and NOX-4 mRNA were also measured. In addition, the effect of losartan and/or pentoxifylline on renal expression of DDAH-1 and serum ADMA were evaluated in a rat model of proteinuric nephropathy. RESULTS: Exposure to albumin resulted in increased release of N-acetyl-ß-D-glucosaminidase along with an increase of TNF-α, 8-hydroxy-2'-deoxyguanosine, and angiotensin II in NRK52E cells. Losartan and pentoxifylline reversed albumin-induced decrease of DDAH-1 mRNA and protein expression and DDAH-1 activity. The effects of losartan and pentoxifylline on DDAH-1 mRNA were associated with reduction of ROS. In addition, treatment with losartan and pentoxifylline resulted in an attenuated change of renal DDAH-1 protein expression and serum ADMA levels in vivo. CONCLUSION: DDAH-1 was positively regulated by losartan and pentoxifylline with its antioxidative effect in albumin-exposed renal proximal tubular cells. Combined treatment with losartan and pentoxifylline has a direct beneficial effect on expression of renal DDAH-1, and, thus, at least in part, modulates the circulatory levels of ADMA in proteinuric nephropathy.

Are ex vivo mesothelial cells representative of the in vivo transition from epithelial-to-mesenchymal cells in peritoneal membrane?

BACKGROUND: We investigated whether ex vivo mesothelial cells found in peritoneal dialysis (PD) effluents were representative of the in vivo epithelial-to-mesenchymal transition (EMT) in peritoneal membrane. METHODS: Thirty-six male Sprague-Dawley rats were equally divided into three groups: Group C (control), no PD; Group D, infused with 4.25% Dianeal and Group P, infused with 4.25% Physioneal. PD infusions (25 mL) were given twice daily for 8 weeks. The in vivo study included morphometric analyses performed on the peritoneal membranes of tissue specimens obtained at the end of the study. The ex vivo study included peritoneal mesothelial cells collected from PD effluent and cultured to confluence. Cells were scored with light microscopy. RESULTS: PD for 8 weeks induced significant EMT. The in vivo expression of EMT markers (α-smooth muscle actin:E-cadherin ratio, matrix metalloproteinase-2 and Snail) was higher in Group D than in Group P. However, ex vivo EMT marker expression was similar in cells derived from Groups D and P. A significant correlation was observed among in vivo EMT markers. Moreover, the ex vivo cell score increased with time on PD. However, changes in the ex vivo cell score did not correlated with changes in the in vivo EMT marker expression. Furthermore, we found no correlation between ex vivo and in vivo cells in the expression of EMT markers. CONCLUSIONS: In this animal study, ex vivo findings did not reflect the in vivo EMT changes in the peritoneum. It may be necessary to improve the current methodology for ex vivo studies.