MicroRNA-29a promotion of nephrin acetylation ameliorates hyperglycemia-induced podocyte dysfunction.

Podocyte dysfunction is a detrimental feature in diabetic nephropathy, with loss of nephrin integrity contributing to diabetic podocytopathy. MicroRNAs (miRs) reportedly modulate the hyperglycemia-induced perturbation of renal tissue homeostasis. This study investigated whether regulation of histone deacetylase (HDAC) actions and nephrin acetylation by miR-29 contributes to podocyte homeostasis and renal function in diabetic kidneys. Hyperglycemia accelerated podocyte injury and reduced nephrin, acetylated nephrin, and miR-29a levels in primary renal glomeruli from streptozotocin-induced diabetic mice. Diabetic miR-29a transgenic mice had better nephrin levels, podocyte viability, and renal function and less glomerular fibrosis and inflammation reaction compared with diabetic wild-type mice. Overexpression of miR-29a attenuated the promotion of HDAC4 signaling, nephrin ubiquitination, and urinary nephrin excretion associated with diabetes and restored nephrin acetylation. Knockdown of miR-29a by antisense oligonucleotides promoted HDAC4 action, nephrin loss, podocyte apoptosis, and proteinuria in nondiabetic mice. In vitro, interruption of HDAC4 signaling alleviated the high glucose-induced apoptosis and inhibition of nephrin acetylation in podocyte cultures. Furthermore, HDAC4 interference increased the acetylation status of histone H3 at lysine 9 (H3K9Ac), the enrichment of H3K9Ac in miR-29a proximal promoter, and miR-29a transcription in high glucose-stressed podocytes. In conclusion, hyperglycemia impairs miR-29a signaling to intensify HDAC4 actions that contribute to podocyte protein deacetylation and degradation as well as renal dysfunction. HDAC4, via epigenetic H3K9 hypoacetylation, reduces miR-29a transcription. The renoprotective effects of miR-29a in diabetes-induced loss of podocyte integrity and renal homeostasis highlights the importance of post-translational acetylation reactions in podocyte microenvironments. Increasing miR-29a action may protect against diabetic podocytopathy.

Analgesic use, parents' clan, and coffee intake are three independent risk factors of chronic kidney disease in middle and elderly-aged population: a community-based study.

Chronic kidney disease (CKD) is a world-wide public health problem. The purpose of this study was to identify the role of some controversial potential risk factors in development of CKD. "Community Complex Health Screening" is a large-scale, free, health program for individuals ≥40 years of age that has been available since January 2002 in Chiayi County, Taiwan. A questionnaire was administered to study participants, collecting information on ethnicity, use of analgesics, and life habits. Age, sex, and blood biochemical analyses were considered as potential confounders. A high prevalence and low awareness of CKD were noted in this population. Females with CKD had a lower awareness of their illness than males. Analgesic users had a significantly lower estimated glomerular filtration rate (eGFR). Age (OR = 1.095), females (OR = 0.348), fasting plasma glucose (OR = 1.005), level of uric acid (UA) (OR = 1.517), and analgesic usage (OR = 1.512) remained independent predictors of CKD. Multivariate linear regression found that use of analgesics, father' clan from Fujian, mother' clan from Fujian, and coffee intake were independent determinants of renal outcome with coefficient of regression (ß) of -0.102, -0.192, 0.210 and 0.88, respectively. The prevalence of CKD decreased with advanced education. Further, there was no significant difference between education background and analgesics use. In conclusion, analgesic use, parents' clan, and coffee intake were independent risk factors for CKD in middle-aged and elderly Taiwanese. Thus, an effective educational program that increases the awareness of such individuals residing in rural counties is warranted.

Educational intervention in CKD retards disease progression and reduces medical costs for patients with stage 5 CKD.

BACKGROUND: Nephrologist-based multidisciplinary care (MDC) has a positive impact on slowing chronic kidney disease (CKD) progression. However, the benefits of MDC in patients with stage 5 CKD remain unclear. METHODS: Stage 5 CKD patients who visited the Chang Gung Memorial Hospital, Chiayi, Taiwan during the period of 2002-2008 were enrolled. The incident dialysis and medical cost were compared between MDC recipients and nonrecipients. The MDC recipients were divided into two groups by educational duration to observe the clinical renal outcome and medical care expenses. The effect of MDC on renal disease progression was also compared in MDC recipients with and without diabetes. RESULTS: Out of 307 patients, 171 received MDC. For MDC recipients, the temporary usage of catheter was reduced (54.7% vs. 79.4%, p < 0.001), the hospital stay was shorter (18.64 ± 1.20 vs. 24.63 ± 1.22 months, p = 0.001), and the total medical cost was lower [New Taiwan dollars (NTD) 105,948.54 ± 9,967.22 vs. NTD 160,388.61 ± 16,373.97, p = 0.005] than for nonrecipients. Out of the 171 MDC recipients, those with MDC for more than 1 year had slower renal disease progression (0.76 ± 0.27 mL/min per 1.73 m(2) per year) and had an estimated per- capita annual cost savings of about NTD 336,500.66. MDC recipients with diabetes had a higher risk of requiring dialysis than those without diabetes. CONCLUSIONS: MDC could significantly reduce temporary use of the catheter, hospital stay, and total medical costs in patients with stage 5 CKD. Furthermore, longer (>1 year) MDC could preserve renal function and deliver annual medical cost savings.

Obstructive sleep apnea: a stand-alone risk factor for chronic kidney disease.

BACKGROUND: Previous studies have found an association between obstructive sleep apnea (OSA) and chronic kidney disease (CKD). However, subjects with confounding factors such as diabetes and hypertension were not excluded. The purpose of the present study was to determine whether patients with OSA without meeting criteria for diabetes or hypertension would also show increased likelihood of CKD. METHODS: We prospectively enrolled adult patients with a chief complaint of habitual snoring. Overnight polysomnography, fasting blood triglyceride, cholesterol, glucose, insulin, creatinine, albumin and hemoglobin A1c, and first voiding urine albumin and creatinine were examined. Estimated glomerular filtration rate (eGFR), urine albumin-to-creatinine ratio (UACR), homeostatic model assessment-insulin resistance and percentage of CKD were calculated. RESULTS: The final analyses involved 40 patients who were middle-aged [44.8 (8.6) years] predominantly male (83%), obese [body mass index, 28.2 (5.1) kg/m(2)] and more severe OSA, with an apnea-hypopnea index (AHI) of 51.6 (39.2)/h. The mean eGFR and UACR were 85.4 (18.3) mL/min/1.73m(2) and 13.4 (23.4) mg/g, respectively. The prevalence of CKD in severe OSA subjects is 18%. With stepwise multivariate linear regression analysis, AHI and desaturation index were the only independent predictor of UACR (ß = 0.26, P = 0.01, R(2) = 0.17) and eGFR (ß = 0.32, P < 0.01, R(2) = 0.32), respectively. CONCLUSIONS: High prevalence of CKD is present in severe OSA patients without hypertension or diabetes. Significantly positive correlations were found between severity of OSA and renal function impairment.

Reversibility of albuminuria and continuous positive airway pressure compliance in patients of obstructive sleep apnea syndrome.

A positive correlation between albuminuria and severity of obstructive sleep apnea syndrome (OSAS) has been demonstrated, as indexed by urine albumin-to-creatinine ratios (UACRs). However, the effect of continuous positive airway pressure (CPAP) treatment on albuminuria in OSAS patients has not been established.Sixty subjects, with apnea-hypopnea indices >15 events per hour and no other diagnoses associated with albuminuria, underwent overnight polysomnography for sleep apnea and were examined for UACR at baseline and after 6 months of CPAP therapy. CPAP compliance rates were also recorded.Significant improvement in UACR was found in OSAS patients with good compliance to CPAP treatment after 6 months of therapy (baseline vs 6-month follow-up, 32.0 ±â€Š9.5 vs 19.2 ±â€Š6.5 mg/g, respectively, P = 0.007), whereas slight worsening in UACRs was noted in patients with poor compliance to CPAP treatment (baseline vs 6-month follow-up, respectively, 16.7 ±â€Š4.4 vs 19.1 ±â€Š6.3 mg/g, respectively, P = 0.39). Change in UACR was significant between poor compliance versus good compliance groups (2.4 ±â€Š2.7 vs -12.8 ±â€Š4.4 mg/g, respectively, t = 2.9, P = 0.005). A significant correlation between improvement in UACR and CPAP compliance rates was also noted (Spearman's correlation coefficient: -0.37, P = 0.007). Baseline UACR, good CPAP compliance, and body mass index were independent predictors of changes in UACR.Adequate CPAP treatment improves albuminuria in OSAS patients. In addition to monitoring CPAP adherence and subjective sleepiness, UACR may offer an objective physiological index of CPAP therapeutic effectiveness.

Nitric oxide donors rescue diabetic nephropathy through oxidative-stress-and nitrosative-stress-mediated Wnt signaling pathways.

AIMS/INTRODUCTION: The role of the renal nitric oxide (NO) system in the pathophysiology of diabetic nephropathy constitutes a very challenging and fertile field for future investigation. The purpose of the present study was to investigate whether NO donors can attenuate diabetic renal fibrosis and apoptosis through modulating oxidative-and nitrosative-stress, and Wnt signaling using in vivo diabetic models. MATERIALS AND METHODS: Diabetic rat was induced by a single intraperitoneal injection of streptozotocin. Rats in each group were intraperitoneally given 2,2'-(hydroxynitrosohydrazino)bis-ethanamine (1 U/kg/day) and vehicle for 28 and 56 consecutive days. Expression of the oxidative-and nitrosative-stress, and Wnt signaling components were examined in kidneys from diabetic animals by quantitative reverse transcription polymerase chain reaction, western blot analysis and immunohistochemical staining. RESULTS: NO donor treatment significantly reduced the ratio of kidney weight to bodyweight and proteinuria. This treatment also significantly restored the suppressive effect of diabetes on urinary NO2 + NO3 levels. Immunohistochemistry showed that NO donor treatment significantly reduced transforming growth factor (TGF)-ß1, fibronectin, cleaved caspase-3 and triphosphate-biotin nick end-labeling expression in the glomeruli of diabetic rats. We found that diabetes promoted 8-hydroxy-2'-deoxyguanosine, and peroxynitrite expression coincided with reduced endothelial NO synthase expression in glomeruli. Interestingly, NO donor treatment completely removed oxidative stress and nitrosative stress, and restored endothelial NO synthase expression in diabetic renal glomeruli. Immunohistomorphometry results showed that NO donor treatment significantly restored suppressed Wnt5a expression and ß-catenin immunoreactivities in glomeruli. Based on laser-captured microdissection for quantitative reverse transcription polymerase chain reaction, diabetes significantly increased TGF-ß1, and fibronectin expression coincided with depressed Wnt5a expression. NO donor treatment reduced TGF-ß1, fibronectin activation, and the suppressing effect of diabetes on Wnt5a and ß-catenin expression in renal glomeruli. CONCLUSIONS: NO donor treatment alleviates extracellular matrix accumulation and apoptosis in diabetic nephropathy in vivo by not only preventing the diabetes-mediated oxidative and nitrostative stress, but also restoring downregulation of endothelial NO synthase expression and Wnt/ß-catenin signaling. These findings suggest that modulation of NO is a viable alternative strategy for rescuing diabetic renal injury.

Cannabinoid receptor 1 disturbance of PPARγ2 augments hyperglycemia induction of mesangial inflammation and fibrosis in renal glomeruli.

UNLABELLED: Intensive fibrosis in the glomerular microenvironment is a prominent feature of diabetic nephropathy. Cannabinoid receptor 1 (CB1R) reportedly mediates diabetes-induced renal injury. However, studies on the molecular events underlying CB1R promotion of renal dysfunction are limited. This study is undertaken to investigate whether CB1R signaling via Ras or PPARγ pathway regulates mesangial fibrosis in diabetic kidneys. In streptozotocin-induced diabetic rats, hyperglycemia induced glomerular hypertrophy and fibrosis in association with increased IL-1ß, fibronectin, and CB1R expressions and reduced PPARγ2 signaling. CB1R transgenic mice gained kidney weight, and renal glomeruli strongly displayed IL-1ß and fibrotic matrices. Disruption of CB1R by antisense oligonucleotides or inverse agonist AM251 restored PPARγ2 signaling and reduced the promotional effects of hyperglycemia on the expression of fibrogenic transcription factor c-Jun, inflammation regulator SOCS3, proinflammatory cytokines, and accumulation of fibrotic matrix. PPARγ agonist rosiglitazone reduced the hyperglycemia-mediated enhancement of CB1R signaling, inflammation, and glomerular fibrosis in diabetic animals. In vitro, CB1R antagonism restored PPARγ2 action and reduced the promotional effects of high glucose on Ras, ERK, c-Jun, SOCS3 signaling, IL-1ß, and fibronectin expression in renal mesangial cells. Activation of PPARγ2 reduced the high glucose-induced CB1R expression in mesangial cells. Taken together, CB1R signaling contributes to the hyperglycemia disturbance of PPARγ2 signaling and increases inflammatory cytokine secretion and fibrotic matrix deposition in renal glomeruli. CB1R mediates the hyperglycemia-induced inflammation and fibrosis in mesangial cells by regulating Ras, ERK, and PPARγ2 signaling. CB1R blockade has a therapeutic potential to reduce the deleterious actions of hyperglycemia on renal glomerular integrity. KEY MESSAGE: Hyperglycemia increases glomerular fibrosis, inflammation, and CB1R signaling. CB1R signaling promotes fibrosis and inflammation of renal tissue. Loss of CB1R function alleviates diabetes-mediated renal deterioration. PPARγ agonist decreases CB1R expression in diabetic renal glomeruli. Ras and ERK mediated CB1R promotion of fibrosis matrix deposition in mesangial cells.

Hyperuricemia is an independent risk factor for new onset micro-albuminuria in a middle-aged and elderly population: a prospective cohort study in taiwan.

BACKGROUND: Hyperuricemia is now regarded as a risk factor for cardiovascular disease. Micro-albuminuria is associated with increased risk for cardiovascular disease and chronic kidney disease. We hypothesized that elevated serum uric acid (UA) is associated with development of micro-albuminuria in the general population. METHODOLOGY/PRINCIPAL FINDINGS: We conducted a community-based prospective cohort study. A total of 1862 subjects from southern Taiwan, all older than 40 years, were screened and 993 of these participants without micro-albuminuria were followed for 4 years. Urinary albumin-to-creatinine ratio was measured two times per year. A multiple linear regression model indicated that serum UA was independently associated with ln(ACR) after adjustment for 8 factors (age, sex, and 6 metabolic metrics) (ß = 0.194, p<0.01). Logistic regression analysis indicated that each 1 mg/dL increase of UA was associated with a 1.42-fold increased risk of micro-albuminuria after adjustment for the same 8 factors (OR = 1.42, 95% CI: 1.27-1.59, p<0.01). A Cox regression model using subjects with serum UA less than 5 mg/dL as reference group indicated higher hazard ratios (HRs) only found in subjects with serum UA more than 7 mg/dL (HR = 3.54, 95% CI: 2.11-5.93, p<0.01) and not in subjects with serum UA of 5 to 7 mg/dL (HR = 1.30, 95% CI: 0.82-2.07, p = 0.15). CONCLUSION: Hyperuricemia is significantly associated with micro-albuminuria in middle-aged and elderly males and females from a general population in Taiwan. Elevated serum UA is an independent predictor for development of micro-albuminuria in this population.

Sustained Wnt/ß-catenin signaling rescues high glucose induction of transforming growth factor-ß1-mediated renal fibrosis.

INTRODUCTION: Although diabetic nephropathy is attributable to transforming growth factor-ß1 (TGF-ß1) overproduction in glomer-ular mesangial cells, the biological role of Wnt/ß-catenin signaling in controlling high glucose-induced TGF-ß1 has not yet been elucidated. METHODS: This study found that sustained Wnt/ß-catenin signaling was required to protect glomerular mesangial cells from high glucose induction of TGF-ß1-mediated fibrosis using in vitro and in vivo diabetic models. RESULTS: High glucose down-regulated the Wnt signaling associated with increased TGF-ß1 and fibronectin messenger RNA expression in glomerular mesangial cells. Restoring Wnt4, Wnt5a and cytosolic ß-catenin levels by transfecting Wnt4, Wnt5a and stable ß-catenin alleviated the stimulatory effect of high glucose on c-Jun mediated TGF-ß1 fibrosis. Transfection of kinase-active glycogen synthase kinase-3ß (GSK-3ß) also abrogated high glucose promotion of nuclear c-Jun levels, TGF-ß1 and fibronectin messenger RNA expression in mesangial cells. Pharmacological modulation of GSK-3ßß and ßß-catenin signaling by recombinant Wnt5a or GSK-3ß inhibitor (BIO or LiCl) suppressed high glucose promotion of TGF-ß1-mediated fibrosis. Exogenous BIO and SB216763 alleviated TGF-ß1-mediated fibrogenic expression in the kidneys of diabetic rats. Immunohistochemistry showed that GSK-3ß inhibitor significantly reversed the diabetic attenuation of TGF-ß1 and c-Jun coinciding with fibronectin immunoreactivity within glomeruli. Immunofluorescence demonstrated that cells within the glomeruli restored ß-catenin expression after BIO and SB216763 treatment in cells within diabetic glomeruli colocalized with fragmented nuclei by 4',6-diamidino-2-phenylindole staining. CONCLUSIONS: Sustained Wnt signaling reduced c-Jun-dependent TGF-ß1-mediated fibronectin accumulation in mesangial cells. These findings suggest that modulation of Wnt signaling is a viable alternative strategy to rescue the TGF-ß1-mediated fibrotic signaling pathway in diabetic renal injury.

Hyperuricemia as an independent risk factor of chronic kidney disease in middle-aged and elderly population.

INTRODUCTION: Hyperuricemia in the general population remains controversial, in terms of it being considered a risk factor for chronic kidney disease (CKD). Within this context, we evaluated the effects of hyperuricemia on renal function in older Taiwanese adults. METHODS: From January 2002 to December 2006, we conducted a community-based medical screening program involving 31,331 subjects older than 40 years. According to the National Kidney Foundation guidelines, stage 3 to 5 patients with CKD were included for analysis. Age, body mass index, systolic blood pressure, fasting plasma glucose, triglyceride, cholesterol and proteinuria were considered potential confounders. RESULTS: Participants with hyperuricemia tended to have higher systolic blood pressure, sugar levels, body mass index, and cholesterol and triglyceride levels but lower estimated glomerular filtration rate (eGFR) levels; eGFR negatively correlated with serum uric acid level. By using multiple logistic regression models before and after adjusting for any confounding factors, we noted that participants with hyperuricemia had a 4.036-fold (odds ratios = 4.036) and 3.649-fold (odds ratios = 3.649) increased risk for CKD, respectively, compared with the control group. We used multiple linear regression analysis to examine the association of serum uric acid level and eGFR at different stages of CKD; significance was found only in participants with stage 3 CKD and not in participants with stages 4 or 5. CONCLUSIONS: Hyperuricemia is an independent risk factor for CKD in middle-aged and elderly Taiwanese adults. Thus, an effective screening program that identifies people with hyperuricemia is warranted.

Hypertriglyceridemia: an independent risk factor of chronic kidney disease in Taiwanese adults.

BACKGROUND: The prevalence and incidence of chronic kidney disease (CKD) are relatively high in Taiwanese patients than in patients of other countries, particularly in the older age groups. Dyslipidemia in patients with CKD has been recognized as a risk factor for disease progression but the role of triglycerides (TGs) remains controversial. With this regard, we evaluated the effects of hypertriglyceridemia on renal function in Taiwanese adults (aged >or=40 years). METHODS: From January 2002 to December 2006, we conducted a community-based medical screening program in Chiayi County with 18,422 subjects (aged >or=40 years). The CKD was defined as an estimated glomerular filtration rate of <60 mL min 1.73 m. Age, body mass index, systolic blood pressure, fasting plasma glucose, and serum total cholesterol were considered as potential confounders. RESULT: The CKD was prevalent in 24.2% of the middle-aged and elderly population. By using multiple logistic regression models, we determined that old age and elevated levels of body mass index, systolic blood pressure, fasting plasma glucose, and cholesterol were associated with CKD. The adjusted odds ratios of CKD in participants with serum TG >==200 mg/dL was 1.901 (95% confidence interval: 1.07-3.36; P < 0.05) and in participants with serum TG > 500 mg/dL it increased to 2.205 (1.33-3.64, P < 0.05). CONCLUSION: Hypertriglyceridemia is an independent risk factor for CKD in Taiwanese adults. Thus, an effective screening program that identifies people with hypertriglyceridemia is warranted.

Methylglyoxal-induced fibronectin gene expression through Ras-mediated NADPH oxidase activation in renal mesangial cells.

BACKGROUND: The formation of methylglyoxal (MGO), a highly reactive dicarbonyl compound, is accelerated under diabetic conditions. Although recent studies have suggested that apoptotic cell death is involved in diabetic nephropathy, the precise mechanism of MGO-induced renal fibrosis remains to be elucidated. METHODS: Rat kidney mesangial cells with or without pretreatment with inhibitors, including superoxide dismutase, catalase, L-NAME, diphenylene iodonium, rotenone, allopurinol, PD98059, SB203580 and SP600125 were cultured in medium containing 100 microM MGO. In the MGO-treated cell culture system, fibrosis-related signalling pathway was assessed by enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction and western blotting. RESULTS: Expression of fibronectin induced by MGO was highest after 48 h treatment. Superoxide production rapidly increased after 2 h and remained at a high level for 24 h. Scavenging O(2) (-) reversed transforming growth factor beta 1 (TGF-beta1) and fibronectin mRNA level. Pretreatment with diphenylene iodonium significantly suppressed MGO-induced superoxide, TGF-beta1 expression and fibronectin gene expression, indicating that NADPH oxidase is responsible for inducing superoxide formation and subsequently induced renal fibrosis. High MGO rapidly enhanced Ras activation in 1 h and progressively increased cytosolic p38 activation. Additionally, SB203580 pretreatment reduced MGO promotion of fibronectin gene activation suggesting that cytosolic p38 activation might affect MGO-induced renal mesangial fibrosis. Inhibiting Ras activity with manumycin A significantly reduced the promoting effect of MGO on superoxide synthesis, and fibronectin expression. CONCLUSION: Induction of superxoide by Ras via p38 pathway activates fibrotic gene transcription of mesangial cells. Reduction of oxidative stress by scavenging superoxide may offer an alternative strategy for controlling MGO-induced renal fibrosis.

Ras activation modulates methylglyoxal-induced mesangial cell apoptosis through superoxide production.

AIMS: While previous studies have demonstrated that diabetic nephropathy is attributable to glucose-derived dicarbonyl compounds, methylglyoxal (MGO)-inducing apoptosis in renal mesangial cells, the molecular mechanism of upper stream redox signaling modulation, has not been fully elucidated. METHODS: Rat mesangial cells pretreated with or without superoxide dismutase, diphenyloniodium, SB203580, and manumycin A were cultured in methylglyoxal stress-induced apoptosis. Signaling protein expression, flow cytometry, and morphological features of apoptotic cell death were assessed. RESULTS: Methylglyoxal decreased cell viability in mesangial cells. Superoxide mediated methylglyoxal-induced caspase 3 cleavage. Pretreatment with diphenyloniodium, SB203580, and manumycin A reduced methylglyoxal augmentation of superoxide synthesis and caspase-3 activation. Methylglyoxal rapidly enhanced Ras activation and progressively increased cytosolic P38 and nuclear c-Jun activation. Scavenging of superoxide by superoxide dismutase or diphenyloniodium, inhibiting P38 by SB203580, and inhibiting Ras with manumycin A successfully reduced the promoting effect of methylglyoxal on P38 and c-Jun phosphorylation (activation). Furthermore, pretreatment with superoxide dismutase, diphenyloniodium, SB203580, and manumycin A significantly attenuated methylglyoxal induction of apoptosis on the basis of Annexin-V assay and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labelling (TUNEL) staining. CONCLUSIONS: This study has shown that methylglyoxal increased Ras modulation of superoxide-mediated P38 activation and c-Jun activation, which resulted in increased apoptosis.

Octreotide therapy for chylous ascites in a chronic dialysis patient.

Chylous ascites, a rare complication in patients receiving continuous peritoneal dialysis, often presents with turbid dialysate. This characteristic makes it frequently confused with peritonitis. Conservative treatments including bowel rest and dietary intervention with medium chain triglycerides are advised by many authors in the literature. However, this approach usually takes a long time before the lymphorrhagia are eventually resolved. Here, a case of chylous ascites that was successfully treated with subcutaneous octreotide, a somatostatin analogue, is reported. By shortening the bowel rest period, this treatment avoids the nutritional and immunological adverse effects. A series of peritoneal equilibrium tests were performed after administration of octreotide and the results showed that octreotide did not alter the peritoneal function in the short term. Therefore, subcutaneous octreotide administration is a safe and effective therapy in peritoneal dialysis patient with chylous ascites.