Objective To evaluate the effect of a modified method of percutaneous catheter placement without a break-in procedure on the development of catheter-related complications in patients on continuous ambulatory peritoneal dialysis (CAPD). Design A prospective, observational clinical study. Setting Peritoneal dialysis (PD) units of two university-based hospitals. Patients and Methods This study included 51 consecutive patients on CAPD. A straight double-cuffed Tenckhoff catheter with a straight intraperitoneal segment was used, and all catheters were inserted using a modified percutaneous placement method under local anesthesia. The catheter was introduced directly into the deep pelvis through an intramuscular tract, which had been created by tapered dilators. Peritoneal dialysis was initiated immediately after catheter insertion without a break-in procedure. Catheter-related complications were surveyed during the 12 months after initiation of CAPD. Results Within the first month, only 1 pericatheter leakage (1.9%) was detected. There were no cases of visceral perforation or severe hemorrhage during catheter insertions. Catheter malfunction due to catheter tip migration, exit-site infection, and peritonitis developed in only 1.9%, 3.9%, and 3.9% of patients, respectively. After 1 month following catheter insertion, no further incidences of pericatheter leakage occurred during the follow-up period. All catheters, except one that was reinserted due to tip migration, survived throughout the study period. Conclusion The rates of pericatheter leakage and other catheter-related complications are relatively low in CAPD patients using our percutaneous catheter placement method without a break-in procedure. This procedure is comparatively simple and less invasive than other catheter placement methods, and allows for immediate start of PD after catheter insertion, without a break-in procedure.

Increased podocyte cyclooxygenase-2 (COX-2) expression is seen in rats after renal ablation and Thy-1 nephritis and in cultured murine podocytes in response to mechanical stress. For investigation of whether COX-2 overexpression plays a role in podocyte injury, transgenic B6/D2 mice in which COX-2 expression was driven by a nephrin promoter were established. Selective upregulation of COX-2 expression in podocytes of transgenic mouse kidneys was confirmed by immunoblotting and immunohistochemistry. Whether upregulation of podocyte-specific COX-2 expression enhanced sensitivity to the development of Adriamycin nephropathy was examined. Adriamycin administration induced dramatically more albuminuria and foot process effacement and reduced glomerular nephrin mRNA and immunoreactivity in transgenic mice compared with wild-type littermates. Adriamycin also markedly increased immunoreactive COX-2 expression in podocytes from transgenic mice compared with the wild-type mice. Reverse transcriptase-PCR indicated that this increase represented a stimulation of endogenous COX-2 mRNA expression rather than COX-2 mRNA driven by the nephrin promoter. Balb/C mice, which are susceptible to renal injury by Adriamycin, also increased podocyte COX-2 expression and reduced nephrin expression in response to administration of the drug. Long-term treatment with the COX-2-specific inhibitor SC58236 ameliorated the albuminuria that was induced by Adriamycin in the transgenic mice. SC58236 also reduced Adriamycin-induced foot process effacement in both the COX-2 transgenic mice and Balb/C mice. Therefore, overexpression of COX-2 may predispose podocytes to further injury.

Chronic volume overload is associated with left ventricular hypertrophy and high cardiovascular mortality in patients undergoing dialysis. Therefore, estimating body fluid status is important in these patients. However, most dry-weight assessments are still performed clinically, while attempts have been made to measure the volume status and dry weight of patients undergoing dialysis using bioimpedance analysis (BIA). BIA uses the electrical properties of the human body to alternate current flow and measures resistance values to estimate body water content and composition. BIA is divided into single-frequency BIA, multi-frequency BIA, and bioimpedance spectroscopy (BIS) according to the number of frequencies used, and into whole-body and segmental BIA according to whether or not the whole body is divided into segments. Extracellular water (ECW), intracellular water, and total body water (TBW) contents can be measured with BIA. Dry weight can be estimated by measuring the volume overload of the patient through the ECW/TBW and ECW-to-body weight ratios. Other estimation methods include the normovolemia/hypervolemia slope method, a resistance-reactance (RXc) graph, overhydration measurements using a body composition monitor, and calf BIS. In this review, we will examine the principles of BIA, introduce various volume status measurement methods, and identify the optimal method for patients undergoing dialysis.

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Previous studies from our own group and others have demonstrated that cyclooxygenase-2 (COX-2) inhibitors could reduce proteinuria in some experimental models of progressive renal disease. To investigate a possible role of COX-2 in podocytes during the course of self-limited glomerular injury, we administered puromycin nucleoside (PAN) on day 1 (15 mg/100 g BW) and day 3 (30 mg/100 g BW) to wild-type and transgenic mice with podocyte-specific COX-2 expression driven by a nephrin promoter. An additional group received both PAN and the COX-2-specific inhibitor, SC58236 (6 mg/l in drinking water). There was no significant difference in the albumin (µg)/creatinine (mg) ratio between wild-type (26.3 ± 4.2, n = 8) and transgenic (28.9 ± 2.3, n = 8) mice under baseline conditions. PAN induced significant albuminuria only in the transgenic mice with a peak at day 3: 72.1 ± 8.9 µg/mg creatinine (n = 12, p < 0.05, compared with basal level), which remitted by day 10 (37.4 ± 4.4 µg/mg, n = 7, p < 0.05, compared with day 3). Electron microscopy demonstrated that PAN caused 56.7 ± 4.2% foot process effacement in transgenic mice compared with 38.8 ± 4.1% in wild type at day 3. PAN increased immunoreactive COX-2 in glomeruli from transgenic mice (day 3: 1.47 ± 0.08 fold; day 10: 1.25 ± 0.16 fold, n = 5–9, p < 0.05 compared with basal level), which was restricted to podocytes. Real time PCR indicated that endogenous COX-2 mRNA increased (2.6 ± 0.1 fold of wild-type control at day 3 and 2.2 ± 0.2 at day 10, n = 4, p < 0.05), while the nephrin-driven COX-2 mRNA was unchanged. Nephrin mRNA and protein expression were decreased by PAN in the transgenic mice. The COX-2-specific inhibitor, SC58236, reduced foot process effacement in transgenic mice administered PAN to 21.7 ± 5.2% and significantly reduced the albuminuria at day 3 (42.2 ± 3.8, n = 13, p < 0.05 compared with untreated) without significantly altering COX-2 expression. In summary, in transgenic mice with podocyte COX-2 overexpression, PAN increased albuminuria and induced foot process fusion. Thus, increased COX-2 expression increased podocyte susceptibility to further injury.