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Decline of estimated glomerular filtration rate (eGFR) is associated with increased cardiovascular (CV) morbidity and mortality, but the predictive value of different eGFR on CV outcomes is limited in Southeast Asian populations.We aimed to stratify CV outcomes according to renal function among Thai patients with high atherosclerosis risk.We performed a secondary analysis in a 5-year national cohort entitled "CORE-Thailand study." Subjects were classified in 6 groups according to baseline kidney function: group I, eGFR ≥ 90; group II, eGFR 60-89; group IIIa, eGFR 45-59; group IIIb, eGFR 30-44; group IV, eGFR 15-29; group V, eGFR 15 ml/min/1.73 mA total of 6376 subjects (3467 men and 2909 women) were categorized in 6 groups. After adjusting covariates in the Cox proportional hazards model, compared to group I, subjects in groups II-V had a 1.65-fold, 2.17-fold, 2.67-fold, 4.24-fold, and 4.87-fold risk for 4-point MACE, respectively, with statistical significance at P 0.05 in all groups. Kaplan-Meier analysis illustrated stepwise lower survivals from 4-point MACE following the groups with lower baseline eGFR (log-rank test with P 0.001). All secondary outcomes showed similar trends as the primary outcome, except nonfatal stroke.Lower baseline kidney function was independently associated with increased risk of CV events and all-cause mortality in Thai populations at high CV risk.

BACKGROUND Low ankle-brachial index (ABI) related ischemic events are common among individuals with chronic kidney disease (CKD). It is also associated with an increased risk of rapid renal function decline. The presence of peripheral artery disease (PAD) with low ABI among patients with high cardiovascular (CV) risk increases limb loss and mortality. AIMS To estimate the association between abnormal ABI and renal endpoints and all-cause mortality. METHODS A multicenter prospective cohort study was conducted among subjects with high CV risk or established CV diseases in Thailand. The subjects were divided into 3 groups based on ABI at baseline > 1.3, 0.91-1.3, and ≤ 0.9, respectively. Primary composite outcome consisted of estimated glomerular filtration rate (eGFR) decline over 40%, eGFR less than 15 mL/min/1.73 m2, doubling of serum creatinine and initiation of dialysis. The secondary outcome was all-cause mortality. Cox regression analysis and Kaplan-Meier curve were performed. RESULTS A total of 5543 subjects (3005 men and 2538 women) were included. Cox proportional hazards model showed a significant relationship of low ABI (ABI ≤ 0.9) and primary composite outcome and all-cause mortality. Compared with the normal ABI group (ABI 0.91-1.3), subjects with low ABI at baseline significantly had 1.42-fold (95% CI 1.02-1.97) and 2.03-fold (95% CI 1.32-3.13) risk for the primary composite outcome and all-cause mortality, respectively, after adjusting for variable factors. CONCLUSION Our study suggested that PAD independently predicts the incidence of renal progression and all-cause mortality among Thai patients with high CV risk.

A precise description of renal histological lesions and an appropriate classification of lupus nephritis are both essential for nephrologists to guide treatment and predict prognosis among patients. The prognostic value of ISN/RPS 2003 classification is controversial. A new classification for lupus nephritis was recently proposed, namely, the revised ISN/RPS 2018 classification. The study aimed to evaluate the predictive value of the clinical and pathological factors according to ISN/RPS 2018 classification on renal remission among patients with proliferative lupus nephritis. A total number of 41 patients with proliferative lupus nephritis on adequate renal biopsy specimen between 2017 and 2018 were included. Clinical and histological variables were tested for their association with renal remission. Univariate and multivariate logistic regression analysis were performed to identify independent predictors of renal remission after 24 weeks of induction therapy. After induction therapy, 56.1% of patients reached complete and partial remission and 43.9% reached no remission. In univariate analyses, baseline glomerular filtration rate (GFR), presence of anti-DNA titer, cellular crescents, interstitial inflammation, glomerulosclerosis, interstitial fibrosis, tubular atrophy and total chronicity index strongly impacted renal response. After multivariate logistic regression analysis, we identified aging, presence of cellular crescents, and high total renal chronicity index as independent predictors of renal remission. Receiver operating characteristic (ROC) analysis revealed that baseline estimated GFR (AUC = 0.708; 95% CI 0.527–0.888), anti-DNA titer (AUC = 0.674; 95% CI 0.491–0.858), cellular crescent (AUC = 0.750; 95% CI 0.585–0.915) and renal chronicity index (AUC = 0.765; 95% CI 0.585–0.915) predicted renal remission. Combining all factors achieved a perfect score predicting renal response (AUC 0.924; 95% CI 0.840–1.000). The study identified baseline GFR, anti-DNA titer, cellular crescent, and high chronicity index according to revised ISN/RPS 2018 classification as important predictors of renal response after induction therapy in proliferative lupus nephritis.

PURPOSE Nephrotoxicity is a major dose-limiting toxicity among patients with cancer who were treated with cisplatin. Although no standard approach is available to prevent cisplatin-induced nephrotoxicity, administering intravenous isotonic saline is recommended. Additionally, mannitol combined with hydration has been evaluated, but none of them have been established. Our study aimed to determine the efficacy of mannitol combined hydration to prevent cisplatin-induced nephrotoxicity. PATIENTS AND METHODS This study was a phase II, randomized, placebo-controlled design. All patients with solid cancers who were treated with cisplatin (n = 48) were randomly assigned to receive either placebo (n = 25) or 20 g of mannitol (n = 23) after completing 2 L of prehydration and receiving cisplatin. Serum creatinine, blood urea nitrogen, electrolyte, and glomerular filtration rate (GFR) were measured at baseline and days 2 and 7. Moreover, GFR was calculated based on the 24-hour urine creatinine clearance rate to assess renal function at baseline and 48 hours after receiving cisplatin. Severity of nausea and vomiting was evaluated using Common Terminology Criteria for Adverse Events. RESULTS No difference was found regarding baseline characteristics between the two groups. Seven of 23 patients (37.4%) in the mannitol group and 10 of 25 patients (40%) in the placebo group increased serum creatinine level ≥ 0.3 mg/dL at 48 hours after intervention ( P value = .48). Patients receiving mannitol exhibited significantly lower incidence of 24-hour urine GFR below 60 mL/min/1.73 m than those in the placebo group (13.6% v 48.0% in the placebo group; P value = .012). Univariate analysis showed the greatest benefit for administering mannitol among patients receiving cisplatin > 80 mg/m2, or patients receiving concomitant radiation. CONCLUSION Mannitol combined with hydration significantly prevented cisplatin-induced nephrotoxicity. Additionally, mannitol should be particularly considered among patients with cancer, treated with cisplatin > 80 mg/m2, or patients receiving concomitant radiation.

BACKGROUND Intradialytic hypotension (IDH) is one of the most critical adverse events during maintenance haemodialysis. Previous studies reported the association of fluid removal rate with the occurrence of IDH. OBJECTIVE We aimed to identify the optimal threshold of ultrafiltration rate to prevent the occurrence of IDH events. DESIGN, PARTICIPANTS AND MEASUREMENTS: Prognostic factor research with a retrospective case-control design was conducted. Patient data were gathered from four haemodialysis units from January to December 2017. All the haemodialysis records were independently justified, whether IDH occurred or not, based on the standard definition. A total of 10 haemodialysis sessions were sampled from each patient's pool based on the incidence of events. The association of ultrafiltration rates and IDH events was explored by multivariable multilevel logistic regression. RESULTS A total of 1080 haemodialysis sessions from 108 patients were included: 149 (13.8%) with IDH and 931 (86.2%) without IDH. After adjusting for all pre-specified risk factors and imbalance baselines, the odds ratio of IDH were 1.22 (95% confidence interval [CI]: 0.59, 2.52) for rate 10-12 ml/kg/h; 2.52 (95% CI: 1.20, 5.29) for rate 12-14 ml/kg/h; 4.02 (95% CI: 1.61, 10.03) for rate 14-16 ml/kg/h; and 7.41 (95% CI: 2.53, 21.68) for rate >16 ml/kg/h comparing to the referent rate of

BACKGROUND Increased arterial stiffness is linked to markers of endothelial dysfunction and vasculopathy such as albuminuria, vascular calcification, left ventricular hypertrophy and cardiovascular (CV) diseases. Studies of arterial stiffness on renal progression are limited. OBJECTIVE The study aimed to evaluate the association between high cardio-ankle vascular index (CAVI) and renal endpoint and all-cause mortality in a Thai population with high atherosclerosis risk. METHODS A multicenter prospective cohort study was conducted among subjects with high CV risk or established CV diseases in Thailand. Subjects were divided into 3 groups with mean CAVI

BACKGROUND There is increasing awareness of the impact of obesity and underweight on cardiovascular (CV) disease, chronic kidney disease (CKD) and mortality. Abnormal body mass index (BMI) might be associated with worse clinical outcomes, including CKD progression, but limited evidence exists among Asian patients with high CV risk. OBJECTIVE To investigate the association of BMI with progressive loss of kidney function and all-cause mortality in Thai patients with high CV risk. METHODS In a national cohort of 5887 high CV risk subjects, we assessed the association of high BMI with the composite renal outcome (estimated glomerular filtration rate [eGFR] decline over 40%, eGFR less than 15 mL/min/1.73 m2 , doubling of serum creatinine, initiation of dialysis and death related to renal causes) and with all-cause mortality in Cox proportional hazards models. RESULTS A total of 5887 participants (3217 male and 2670 female) with high CV risk were enrolled. Participants were classified into five groups by their baseline BMI

Background Novel potential tubular biomarkers in diabetic nephropathy could improve risk stratification and prediction. The study aimed to evaluate the association of tubular damage markers with rapid renal progression and incidence of end stage renal disease (ESRD) in type 2 diabetes (T2DM). Methods A prospective cohort study, involving a total of 257 patients with T2DM, was included. The baseline values of urine albumin, cystatin-C, angiotensinogen, kidney injury molecule-1 (KIM-1) and neutrophil-gelatinase associated lipocalin (NGAL) were measured. The composite outcomes included a rapid glomerular filtration rate (GFR) decline or incident of ESRD at 3-year follow-up. Main findings The composite outcomes were noted in 26.1%. Using univariate followed by multivariate COX proportional hazard regression analysis, the patients with highest quartiles of urine cystatin-C (HR 2.96, 95% CI, 1.38–6.35), urine angiotensinogen (HR 2.93, 95% CI, 1.40– 6.13) urine KIM-1 (HR 2.77, 95% CI, 1.27-6.05) and urine NGAL (HR 2.53, 95% CI, 1.11-5.76) were significantly associated with rapid renal progression when compared with the patients with the lowest quartiles of all tubular biomarkers. Conclusions Patients with T2DM with high levels of baseline urine tubular biomarkers (cystatin-C, angiotensinogen, KIM-1 and NGAL) had a greater incidence of ESRD and rapid GFR decline.

Background Albuminuria is an established risk marker for both cardiovascular and renal outcomes. In this study, we expected to use portable and inexpensive test strips to detect urine albumin level for risk stratification in cardiovascular and renal outcomes among rural Thai community. Objective To evaluate the relationship between urine albumin dipstick and cardiovascular and renal complications in rural Thai population. Methods We conducted a retrospective study in 635 rural Thai adults who tested urine albuminuria by using commercial urine albumin dipstick and the Micral-albumin test II strips at baseline. The subjects were divided into normoalbuminuria (albumin 200 mg/L). We collected data on the incidences of primary composite outcomes including cardiovascular or renal morbidity and mortality. Incident density and cox regression were analyzed to evaluate the association between albuminuria status and primary composite outcome. Results During an average 14-year follow-up, 102 primary composite events occurred including 59 (13.1%), 32 (20.6%) and 11 (39.3%) among 452, 155, and 28 subjects with normoalbuminuria, microalbuminuria, and macroalbuminuria, respectively. Incident densities of primary composite outcome were elevated continually according to the degree of albuminuria (9.36, 17.11 and 38.12 per 1000 person-years). Compared with the subjects without albuminuria, subjects with microalbuminuria and macroalbuminuria at baseline had higher risk for primary composite outcome in univariate model. After multivariate analysis was performed, the effect of macroalbuminuria was only persisted with 3.13-fold risk (adjusted HR 3.13; 95% CI 1.40–6.96, P= 0.005). Conclusion Albuminuria from semi-quantitative methods is an important factor predicting cardiovascular and renal risk among subjects in Thai rural population. Our findings support to also incorporating urine albumin dipstick into assessments of cardiovascular risk in the general population.

Introduction. Dipeptidyl peptidase-4 (DPP-4) inhibitors improve glycemic control and have pleiotropic effects on kidney injury, albuminuria, and vascular inflammation, especially in animal models. We evaluated the effects of a potent DPP4 inhibitor (gemigliptin) on these processes among patients with diabetic kidney disease (DKD). Methods. This study employed a multicenter, prospective, randomized, placebo-controlled design. A total of 201 participants were enrolled and randomly assigned to one of two groups, one received treatment with 50 mg gemigliptin daily along with standard care for diabetes mellitus for 6 months. The changes in the coronary calcium score (CAC score), cardio-ankle vascular index (CAVI), estimated glomerular filtration rate (eGFR), vascular calcification level, and tubular renal injury marker expression were evaluated at baseline and 6 months. Results. In total, 182 patients completed the study. Significant reductions in hemoglobin A1C levels were observed in both groups. The changes in the CAC score, CAVI, eGFR, and level of proteinuria over the 6 months of the study did not significantly differ between the gemigliptin and control groups. However, biomarkers of vascular calcification, including serum bone alkaline phosphatase and kidney injury, including urine neutrophil gelatinase-associated lipocalin (NGAL)/Cr and urine liver fatty acid-binding protein (L-FABP)/Cr, were improved significantly in the gemigliptin treatment group compared with the control group. No serious adverse events were observed during the study. Conclusion. Our study showed that gemigliptin significantly improved the expression of renal tubular injury biomarkers and vascular calcification levels among patients with DKD; however, gemigliptin did not affect renal function or coronary calcification compared with those observed in the control. A larger study with a longer follow-up is essential to verify these beneficial effects. Clinical Trials. This trial is registered with ClinicalTrials.Gov Identifier NCT04705506.

Background Activation of the transforming growth factor beta (TGF-β) pathway is a significant contributor to the pathogenesis of diabetic nephropathy. Carnosine is a dipeptide that can inhibit TGF-β synthesis. We tested the hypothesis that carnosine supplement added to standard therapy will result in reduced urinary TGF-β levels among patients with diabetic nephropathy. Methods We randomly assigned 40 patients with diabetic nephropathy and albuminuria 30–299 mg/day to treatment with carnosine (2 g/day) or placebo for 12 weeks. Urinary TGF-β level was determined using ELISA, urine albumin was ascertained by immunonephelometric assay, and renal function and metabolic profiles were determined at baseline and during 12 weeks of active treatment. Primary outcome was decrease in urinary levels of TGF-β. Results The 2 groups were comparable for baseline characteristics, blood pressure, urine albumin, urine TGF-β and renal function measurements. Urinary TGF-β significantly decreased with carnosine supplement (− 17.8% of the baseline values), whereas it tended to increase with placebo (+ 16.9% of the baseline values) (between-group difference P Conclusions These data indicated an additional renoprotective effect of oral supplementation with carnosine to decrease urinary TGF-β level that serves as a marker of renal injury in diabetic nephropathy. Trial registration Thai Clinical Trials, TCTR20200724002. Retrospectively Registered 24 July 2020.

Background. Type 2 diabetic mellitus (T2DM) patients with impaired renal function have a higher risk of mortality, and often progress to end-stage renal disease. The study aims to determine the prevalence of kidney disease and investigate the relationship between various factors and impaired renal function in a large population of patients with T2DM. Methods. We conducted a cross-sectional study among 30,377 patients from a nationwide diabetes study involving 602 Thai hospitals. Impaired glomerular filtration rate (GFR) was defined as 2. Multivariate logistic regression was used to determine the association between standard risk factors and impaired GFR. Results. The prevalence of impaired GFR in a T2DM population was 39.2%. After adjusting for multiple risk factors, advanced age (adjusted OR 11.69 (95%CI=3.13 to 43.61)), macroalbuminuria (adjusted OR 3.54 (95%CI=1.50 to 8.40)), high serum uric acid (adjusted OR 2.06 (95%CI=1.73 to 2.46)), systolic BP 130-139 mmHg (adjusted OR 3.21 (95%CI=1.30 to 7.96)), hemoglobinA1C (HA1C) 95%CI=1.65 to 8.32)), and HA1C >7% (adjusted OR 2.53 (95%CI=1.38 to 4.63)) were found to be associated with a significantly increased risk of impaired GFR among T2DM patients. Conclusion. Almost 40% of patients with T2DM in a nationwide cross-sectional study in Thailand had impaired GFR. Advanced age, albuminuria, hyperuricemia, hypertension, HA1C 7% were independently associated with increased prevalence of impaired GFR.

Background Tubulointerstitial injury is important to predict the progression of lupus nephritis (LN). Urine neutrophil gelatinase-associated lipocalin (NGAL) has been reported to detect worsening LN disease activity. Thus, urine NGAL may predict renal outcomes among lupus patients. Methods We conducted a prospective multi-center study among active LN patients with biopsy-proven. All patients provided urine samples for NGAL measurement by ELISA collected from all patients at baseline and at 6-month follow-up after induction therapy. Results In all, 68 active LN patients were enrolled (mean age 31.7 ± 10.0 years, median UPCR 4.8 g/g creatinine level with interquartile range (IQR) 2.5 to 6.9 and mean estimated glomerular filtration rate (GFR) 89.6 ± 33.7 mL/min/1.73 m2). At baseline measurement, median urinary NGAL in complete response, partial response and nonresponse groups was 10.86 (IQR; 6.16, 22.4), 19.91 (IQR; 9.05, 41.91) and 65.5 (IQR; 18.3, 103) ng/mL, respectively (p = 0.006). Urinary NGAL (ng/mL) correlated positively with proteinuria and blood pressure, and correlated negatively with serum complement C3 level and estimated GFR. Based on ROC analysis, urinary NGAL (AUC; 0.724, 95%CI 0.491–0.957) outperformed conventional biomarkers (serum creatinine, urine protein, and GFR) in differentiating complete and partial response groups from the nonresponse group. The urine NGAL cut-off value in the ROC curve, 28.08 ng/mL, discriminated nonresponse with 72.7% sensitivity and 68.4% specificity. Conclusion Urine NGAL at baseline performed better than conventional markers in predicting a clinical response to treatment of active LN except serum complement C3 level. It may have the potential to predict poor response after induction therapy.

Currently, the data on independent risk factors for the progression of kidney disease in type 2 diabetes mellitus (T2DM) patients with CKD are limited. This study aimed to investigate CKD progression in T2DM patients who have reduced kidney function with baseline estimated glomerular filtration rate (eGFRs) between 15 and 59 mL/min/1.73 m2 . This study was composed of a nationwide retrospective cohort of adult T2DM patients from 831 public hospitals in Thailand during the year 2015. T2DM patients with CKD stages 3 and 4 were followed up, until development of CKD stage 5, requirement of chronic dialysis, loss to follow-up, death, or 31 May 2018, whichever came first. Cox proportional hazard regression was utilized for analysis. A total of 8464 participants were included; 30.4% were male. The mean age was 69 ± 10 years. The mean eGFR was 45 ± 11 mL/min/1.73 m2 . The incidence of CKD stage 5 or the need for chronic dialysis was 16.4 per 1000 person-years. The annual rate of eGFR decline during a mean follow-up of 29 months was -2.3 mL/min/1.73 m2 ; 14.4% had a rapid decline in eGFR. The risk factors associated with progression to CKD stage 5 or the need for chronic dialysis were diabetes duration, systolic blood pressure, serum uric acid, albuminuria, and baseline eGFR. Conversely, older age and the use of renin-angiotensin aldosterone system blockade were associated with decreased risks for rapid CKD progression and incidence CKD stage 5 or dialysis. This study identifies multiple predictive risk factors that support a multifaceted approach to prevent progression of advanced CKD.

Background: Among people with diabetes, those with kidney disease have exceptionally high rates of cardiovascular (CV) morbidity and mortality and progression of their underlying kidney disease. Finerenone is a novel, nonsteroidal, selective mineralocorticoid receptor antagonist that has shown to reduce albuminuria in type 2 diabetes (T2D) patients with chronic kidney disease (CKD) while revealing only a low risk of hyperkalemia. However, the effect of finerenone on CV and renal outcomes has not yet been investigated in long-term trials. Patients and Methods: The Finerenone in Reducing CV Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD) trial aims to assess the efficacy and safety of finerenone compared to placebo at reducing clinically important CV and renal outcomes in T2D patients with CKD. FIGARO-DKD is a randomized, double-blind, placebo-controlled, parallel-group, event-driven trial running in 47 countries with an expected duration of approximately 6 years. FIGARO-DKD randomized 7,437 patients with an estimated glomerular filtration rate ≥25 mL/min/1.73 m2 and albuminuria (urinary albumin-to-creatinine ratio ≥30 to ≤5,000 mg/g). The study has at least 90% power to detect a 20% reduction in the risk of the primary outcome (overall two-sided significance level α = 0.05), the composite of time to first occurrence of CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. Conclusions: FIGARO-DKD will determine whether an optimally treated cohort of T2D patients with CKD at high risk of CV and renal events will experience cardiorenal benefits with the addition of finerenone to their treatment regimen. Trial Registration: EudraCT number: 2015-000950-39; ClinicalTrials.gov identifier: NCT02545049.

Aims: Arterial stiffness is known to be an important surrogate marker for atherosclerosis and predictor of peripheral vascular and cardiovascular (CV) disease. Whether high cardio-ankle vascular index (CAVI) is associated with the development of rapid glomerular filtration rate (GFR) decline remains uncertain. The study aimed to determine the relationship between CAVI and renal function progression among patients with high CV risk. Methods: This study employed a prospective cohort design with 1-year follow-up among patients with high CV risk. Arterial stiffness was measured using CAVI method. GFR was estimated using the chronic kidney disease (CKD) epidemiology collaboration equation, and rapid decline in GFR was defined with decrease in GFR ≥ 5 mL/min/1.73 m2 yearly. Results: Of 352 patients with mean age 67.8 ± 10.1 years, 224 patients (63.6%) were suspected to have arteriosclerosis (CAVI ≥ 9), and 208 patients (59.1%) had CKD (GFR < 60 mL/min/1.73 m2). Annual decline of GFR was −0.75 [interquartile range (IQR), −1.16 to 6.08] mL/min/1.73 m2/year, and 30.1% of patients experienced a rapid decline in GFR. Compared with normal CAVI (CAVI < 8), high CAVI (CAVI ≥ 9) and borderline CAVI (CAVI 8–8.9) in all subjects and subgroup of baseline GFR > 60 mL/min/1.73 m2 were associated with rapid GFR decline. Multivariable analysis showed that high CAVI and borderline CAVI were associated with 2.47-fold (95% CI, 0.89–6.84; P = 0.082) and 4.04-fold (95% CI, 1.46–11.18; P = 0.007) increased odds ratio of rapid GFR decline, respectively. Conclusion: Among patients with high risk of CV with or without CKD, high CAVI (cut point of ≥ 9) was independently associated with a rapid decline in GFR, suggesting that systemic vascular stiffness predicted a decrease in renal function in this population.

Determining insulin requirements for hemodialysis patients with end-stage renal disease (ESRD) is difficult. We performed a randomized crossover study among type 2 diabetes (T2DM) patients with ESRD on continuous hemodialysis and receiving standard insulin for glycemic control. The patients were randomized in 2 groups: daily insulin needed on the day after hemodialysis and a 25% decrease in daily insulin needed on the day after hemodialysis. A total of 51 T2DM patients with ESRD were enrolled. The adjusted-insulin group had higher plasma glucose levels at the 2nd hour of dialysis than those of the nonadjusted-insulin group. Incidence of hypoglycemia per dialysis session (3.3% vs. 0.7%, P=0.02) and symptoms related to hypoglycemia (6.9% vs. 0.7%, P=0.001) were more frequent in the nonadjusted-insulin group. A reduced insulin administration of 25% among T2DM patients undergoing hemodialysis on the day of dialysis was associated with sustained glycemic efficacy and the production of fewer hypoglycemic symptoms. This trial is registered with TCTR20180724002.

The evidence for an association between renal function and neurological diseases among type 2 diabetes mellitus (T2DM) patients, particularly in the Asian population, is limited. This study aimed to assess the association between glomerular filtration rate (GFR) and various neurological diseases among T2DM patients in Thailand using a nationwide patient sample.We conducted a nationwide cross-sectional study based on the DM/HT study of the Medical Research Network of the Consortium of Thai Medical Schools. This study evaluated adult T2DM patients receiving care at public Thailand hospitals in the year 2014. GFR was categorized into ≥60, 30-59, and 30 mL/min/1.73 mA total of 30,423 T2DM patients with available GFR data were included in the analysis. The mean GFR was 68.18 ± 26.45 mL/min/1.73 mDecreased GFR was associated with increased ischemic stroke/TIA, all cerebrovascular diseases, and peripheral neuropathy. GFR should be monitored in diabetic patients for neurological disease awareness and prevention.

Background Increased monocyte chemoattractant protein-1 (MCP-1) and decreased epidermal growth factor (EGF) are promising biomarkers to predict progressive decline in kidney function in non-diabetic kidney diseases. We aimed to evaluate the performance of urinary EGF, MCP-1 or their ratio in predicting rapid decline of GFR in a cohort of Type 2 diabetic patients (T2DM) with diabetic kidney disease (DKD). Methods T2DM patients (n = 83) with DKD at high risk for renal progression were followed up prospectively. The baseline urine values of MCP-1 to creatinine ratio (UMCP-1), EGF to creatinine ratio (UEGF), EGF to MCP-1 ratio (UEGF/MCP-1) and albumin to creatinine ratio (UACR) were measured. The primary outcome was a decline in estimated glomerular filtration rate (GFR) of ≥25% yearly from baseline. Results During follow-up time of 23 months, patients with rapid decline in estimated GFR of ≥25% yearly from baseline had significantly higher baseline levels of UMCP-1, and UACR and lower UEGF and UEGF/MCP-1 ratio. All renal biomarkers predicted primary outcomes with ROC (95%CI) for UMCP-1=0.73 (0.62-0.84), UEGF=0.68 (0.57-0.80), UEGF/MCP-1=0.74 (0.63-0.85), and UACR =0.84 (0.75-0.93). By univariate analysis, blood pressure, GFR, UACR, UMCP-1, UEGF, and UEGF/MCP-1 were associated with rapid decline GFR. By multivariate analysis, UACR, systolic blood pressure, and UMCP-1 or UEGF/MCP-1 were independently associated with rapid GFR decline. Conclusions UMCP-1 or UEGF/MCP-1 ratio were associated with rapid renal progression independent from conventional risk factors in DKD.

Calcineurin inhibitors added to standard-of-care induction therapy for lupus nephritis (LN) may increase complete renal remission (CRR) rates. The AURA-LV study tested the novel calcineurin inhibitor voclosporin for efficacy and safety in active LN. AURA-LV was a Phase 2, multicenter, randomized, double-blind, placebo-controlled trial of two doses of voclosporin (23.7 mg or 39.5 mg, each twice daily) versus placebo in combination with mycophenolate mofetil (2 g/d) and rapidly tapered low-dose oral corticosteroids for induction of remission in LN. The primary endpoint was CRR at 24 weeks; the secondary endpoint was CRR at 48 weeks. Two hundred sixty-five subjects from 79 centers in 20 countries were recruited and randomized to treatment for 48 weeks. CRR at week 24 was achieved by 29 (32.6%) subjects in the low-dose voclosporin group, 24 (27.3%) subjects in the high-dose voclosporin group, and 17 (19.3%) subjects in the placebo group (OR=2.03 for low-dose voclosporin versus placebo). The significantly greater CRR rate in the low-dose voclosporin group persisted at 48 weeks, and CRRs were also significantly more common in the high-dose voclosporin group compared to placebo at 48 weeks. There were more serious adverse events in both voclosporin groups, and more deaths in the low-dose group compared to placebo and high-dose voclosporin groups (11.2%, 1.1%, and 2.3%, respectively). These results suggest that the addition of low-dose voclosporin to mycophenolate mofetil and corticosteroids for induction therapy of active LN results in a superior renal response compared to mycophenolate mofetil and corticosteroids alone, but higher rates of adverse events including death were observed.

BACKGROUND Many renal transplant recipients develop complications such as obesity, posttransplantation diabetes mellitus, and dyslipidemia. There have been few studies of metabolic syndrome (MS) in Asian renal transplant recipients. MATERIAL AND METHODS This cross-sectional study was performed in 303 patients in 5 transplant centers in Bangkok, Thailand. The diagnosis of MS was based on the criteria of the modified NCEP-ATPIII, and chronic allograft dysfunction was defined as estimated glomerular filtration rate (eGFR)

Background Obesity is a risk factor for cardiovascular disease and cardiovascular mortality in renal transplant recipients (RTRs). There are limited studies of prevalence and associated factors of obesity in Asian RTRs. Methods A cross-sectional study was conducted from July to December 2012 in 4 kidney transplant centers in Bangkok, Thailand. Obesity was diagnosed based on the International Obesity Taskforce-proposed classification. At risk of obesity, obese I, and obese II were defined as having a body mass index (BMI) of 23–24.9 kg/m 2 , 25–29.9 kg/m 2 , and ≥30 kg/m 2 , respectively. Results Of 263 recipients studied, 50 (19.0%), 70 (26.6%), and 17 (6.5%) were at risk of obesity, obese I, and obese II, respectively. The prevalence of obesity was 12.6% in the 1st year, was 28.6% in the first 3 years, and rose to 39.7% after 3 years after transplantation. Age (odds ratio [OR], 1.04; 95% CI, 1.01–1.07), systolic blood pressure ≥130/85 mm Hg (OR, 2.82; 95% CI, 1.51–5.26), number of antihypertensive medications (OR, 1.99; 95% CI, 1.42–2.79), fasting plasma glucose (OR, 1.03; 95% CI, 1.01–1.04,) and high-density lipoprotein (HDL) cholesterol (OR, 0.96; 95% CI, 0.94–0.98) were associated with obesity. Compared with 100 RTRs with normal BMI, obese patients tended to have higher prevalence of chronic kidney disease (OR, 1.59; 95% CI, 0.89–2.83). Conclusions The study demonstrates the high prevalence of obesity in Thai RTRs especially after 3 years after transplantation. Obesity is more prevalent with advanced age and variable components of metabolic syndrome in the RTR population. Obese RTRs had significantly higher blood pressure and required more antihypertensive medication when compared with RTRs with normal BMI.

BACKGROUND Post-transplantation diabetes mellitus is a major metabolic adverse effect of tacrolimus (TAC). The objective of this study was to determine if the conversion from tacrolimus twice-daily (TAC-BID) to extended-release tacrolimus once-daily (TAC-OD) in stable renal transplant recipients had any effect on beta cell function (HOMA-b), insulin resistance (HOMA-IR), patient preference, and expense. MATERIAL AND METHODS Twenty-eight renal transplant recipients were recruited and converted from TAC-BID to TAC-OD at the same dose. Primary outcomes were beta cell function and insulin resistance in stable renal transplant recipients at 4, 8, and 16 weeks after conversion. Secondary outcomes were patient satisfaction and expense of medication. RESULTS No significant change in the HOMA-β and HOMA-IR was found in any of the 28 renal transplant recipients. However, HOMA-β increased from 60 (37.33, 109.71) to 78.5 (44.3, 108.4) (p=0.02) in 15 patients who had the conversion within 4 years after renal transplantation. In multivariate regression analysis, the conversion from TAC-BID to TAC-OD significantly increased HOMA-b at 4 months at 1.21 mIU/mmol (95%CI 0.54-1.88 mIU/mmol, p=0.01) in this subgroup. The renal transplant recipients reported the conversion was more satisfactory and cost of treatment was comparable. CONCLUSIONS In short-term follow-up, conversion from TAC-BID to TAC-OD is safe in stable renal transplant recipients and might be beneficial in term of improved beta cell function in the early years after renal transplantation. The conversion caused comparable cost and was preferred by renal transplant recipients.

Summary Background and objectives Sarcopenia is common in hemodialysis patients. This study examined whether the anabolic steroid oxymetholone improves muscle mass and handgrip strength in hemodialysis patients and possible mechanisms that might engender such changes. Design, setting, participants, & measurements Forty-three eligible hemodialysis patients were randomly assigned to ingest oxymetholone or placebo for 24 weeks. Body composition, handgrip strength, and quality of life were measured during the study. Muscle biopsies were performed and analyzed for mRNA levels for myostatin, IGF-I, IGF binding proteins, and myosin heavy chains and protein expression. Muscle fiber types and diameter were assessed by reduced nicotinamide–adenine dinucleotide staining. Results There was a significantly greater increase in fat-free mass and handgrip strength and decrease in fat mass in the oxymetholone compared with the placebo group. Moreover, compared with baseline values, patients given oxymetholone exhibited an increase in fat-free mass, handgrip strength, physical functioning scores, and type I muscle fiber cross-sectional area and a decrease in fat mass, whereas patients receiving placebo did not undergo changes. There was a significantly greater increase in muscle mRNA levels for myosin heavy chain 2×, IGF-I, and IGF-II receptor with oxymetholone treatment than placebo. Liver enzyme rose significantly in the oxymetholone group, but the number of values greater than three times the upper limit of normal were not different between these groups. Conclusions In hemodialysis patients, ingesting oxymetholone was associated with an increase in fat-free mass, handgrip strength, and muscle mRNA levels for several growth factors and a decrease in fat mass, but it also induced liver injury.

Hyperuricemia has been associated with increased risk of endothelial dysfunction, cardiovascular, and renal disease. Allopurinol is a potent xanthine oxidase inhibitor used in hyperuricemic patients. It has been shown to decrease cardiovascular disease and hypertension. However, studies have reported conflicting evidence on its effects on blood pressure (BP) and estimated glomerular filtration rate (GFR) in chronic kidney disease (CKD) patients.To demonstrate the effect of allopurinol on BP and estimated GFR in CKD patients.Patients with CKD stage II-III were screened for possible study enrollment. All patients received allopurinol 50 mg once daily for 12 weeks. The main outcomes were to observe the changes of BP and GFR after given treatment.Forty-four patients were eligible with mean age of 70.14 ± 8.50 years and mean estimated GFR of 43.22 ± 14.44 mL/ min/1.73 m². Serum uric acid decreased significantly from 8.11 ± 2.68 to 7.05 ± 2.38 mg/dL (p = 0.012) at the end of the study. Allopurinol had also statistically significant lower systolic BP (137.72 ± 14.72 to 131.34 ± 12.10 mmHg, p = 0.019) and diastolic BP (79.63 ± 11.56 to 75.43 ± 9.80 mmHg, p = 0.037) at 12 weeks when compared to baseline. There was significant increased in GFR after treatment (43.22 ± 14.44 vs. 45.34 ± 16.09, mL/min/1.73 m², p = 0.029). No serious adverse effects were noted in any of the treated subjects. Two patients (4.5%) in the treatment group had minor skin reaction.The study results confirmed that 12 weeks of allopurinol treatment affects the values of serum uric acid, BP and GFR in early stage of CKD patients who already received standard antihypertensive agents without any significant serious adverse effects.

BK virus nephropathy (BKVN) is an important clinical problem in kidney transplant (KT) recipients. The sequence of disease is usually viruria, viremia and then nephropathy. Diagnosis of BK virus (BKV) infection includes checking BKV DNA in the urine, in the plasma and histology on renal biopsy. This last method is used to diagnose BKVN. We describe a KT patient with BKVN without detectable BK viremia. A 62-year-old female with hypertensive nephropathy underwent renal transplant from a living relative donor in December 2011. Fourteen months after transplantation, her serum creatinine(SCr) rose up from 1.2 to 1.6 mg/dl with biopsy-proven acute antibody-mediated and cellular rejection. After pulse methylprednisolone, plasmapheresis and intravenous immunoglobulin, her SCr decreased to baseline but she subsequently developed cytomegalovirus infection with pancytopenia and transaminitis. The SCr rose to 1.9 mg/dl despite ganciclovir treatment. Renal ultrasound and antegrade pyelogram showed partial obstruction of the proximal ureter with moderate hydronephrosis. A quantitative polymerase chain reaction (PCR) assay for BKV DNA was negative (less than 10 copies/ml). A renal biopsy was performed and the pathology revealed viral cytopathic changes in the tubular epithelium with interstitial inflammation. The renal biopsy also showed BKV nucleic acid sequences by in-situ hybridization confirming BKVN. Immunosuppression regimen was changed to cyclosporine, low-dose prednisolone and leflunomide. A temporary percutaneous nephrostomy was performed. Her renal function improved within one week. The diagnosis of BKVN should be considered in a KT recipient with a rising SCr with or without BK viremia and should be made by renal biopsy.

We sought to find a urinary biomarker for chronic kidney disease and tested hematopoietic growth factor inducible neurokinin-1 (HGFIN, also known as Gpnmb/Osteoactivin) as it was found to be a kidney injury biomarker in microarray studies. Here, we studied whether HGFIN is a marker of kidney disease progression. Its increase in kidney disease was confirmed by real-time PCR after 5/6 nephrectomy, in streptozotocin-induced diabetes, and in patients with chronic kidney disease. In the remnant kidney, HGFIN mRNA increased over time reflecting lesion chronicity. HGFIN was identified in the infarct portion of the remnant kidney in infiltrating hematopoietic interstitial cells, and in distal nephron tubules of the viable remnant kidney expressed de novo with increasing time. In vitro, it localized to cytoplasmic vesicles and cell membranes. Epithelial cells lining distal tubules and sloughed luminal tubule cells of patients expressed HGFIN protein. The urine HGFIN-to-creatinine ratio increased over time after 5/6 nephrectomy; increased in patients with proteinuric and polycystic kidney disease; and remained detectable in urine after prolonged freezer storage. The urine HGFIN-to-creatinine ratio compared favorably with the urine neutrophil gelatinase-associated lipocalin (NGAL)-to-creatinine ratio (both measured by commercial enzyme-linked immunosorbent assays (ELISAs)), and correlated strongly with proteinuria, but weakly with estimated glomerular filtration rate and serum creatinine. Thus, HGFIN may be a biomarker of progressive kidney disease.

Background Choices of hypoglycemic agents for patients with type 2 diabetes and chronic kidney disease (CKD) are limited. Available data among patients with CKD suggest that pioglitazone was effective and safe, with no increase in serious adverse effects. However, weight gain and fluid retention are major clinical problems for pioglitazone among patients with CKD. We conducted this study to compare the efficacy and side effects of low dose pioglitazone with standard dose pioglitazone among patients with type 2 diabetes and CKD. Methods A total of 75 patients with type 2 diabetes and CKD and inadequate glycemic control receiving any pharmacological antidiabetic treatment were randomly assigned to 2 groups. One group consisted of 37 patients treated with standard dose pioglitazone (15 mg/day) and another group consisted of 38 patients treated with low dose pioglitazone (7.5 mg/day). Glycosylated hemoglobinA1c (HbA1c) and metabolic profiles were monitored every 8 weeks for 24 weeks. Body composition was assessed using bio-electrical impedance analysis (BIA). Results After 6 months of therapy, HbA1c levels decreased in both standard and low dose pioglitazone groups. The mean changes in HbA1c for standard and low dose pioglitazone were 1.1±1.6 and -1.4±1.5 (P = 0.543), respectively. Compared with low dose pioglitazone, standard dose pioglitazone treatment led to a greater increase in body weight, fat mass, total body water and extracellular water composition. No major adverse effects including hypoglycemia, congestive heart failure and abnormal liver function were identified. Conclusion Pioglitazone 7.5 mg once daily treatments presented similar glycemic control to standard dose pioglitazone and exhibited beneficial effects on weight gain and fluid retention among patients with type 2 diabetes and CKD.

Aim: Elevated serum uric level has been suggested as a risk factor for chronic kidney disease (CKD). The relationship between serum uric acid level, and CKD in a Southeast Asian population was examined. Methods: In a cross-sectional study, authors surveyed 5618 subjects, but 5546 participants were included. The glomerular filtration rate (GFR) values were calculated by the Modification of Diet in Renal Disease (MDRD) equation. CKD was defined as a GFR of less than 60 mL/min per 1.73 m2. Multivariate binary logistic regression was used to determine the association between serum uric acid level and CKD. Results: The prevalence of CKD in serum uric acid quartiles: first quartile, 5.3 mg/dL or less; second quartile, 5.4–6.4 mg/dL; third quartile, 6.5–7.6 mg/dL; and fourth quartile, 7.7 mg/dL or more were 1.8%, 3.6%, 5.5% and 11.9%, respectively (P

SUMMARY: Aim: Insulin resistance is a predictor of cardiovascular mortality in patients with end-stage renal disease. Although some clinical studies demonstrated that angiotensin II receptor blockers (ARB) improve insulin action in hypertensive patients, the role of ARB among patients with maintenance haemodialysis (MHD) remains controversial. The aim was to evaluate the effect of the ARB on insulin resistance in patients with MHD. Methods: The authors examined 10 patients with MHD who regularly underwent haemodialysis at least two visits per week. After 4, 8 and 12 weeks of treatment with valsartan, blood pressure monitoring, insulin resistance by homeostasis model assessment (HOMA-IR), fasting plasma glucose, fasting plasma insulin and blood chemistries were measured and compared with baseline values. Results: Ten patients with MHD aged 16–74 years participated in the study. The causes of end-stage renal disease included hypertension (four cases), diabetes (three cases), glomerulonephritis (one case) and unknown cause (two cases). Fasting insulin levels significantly reduced from 11.9 ± 5.7 μU/mL to 8.0 ± 6.8 μU/mL (P

Vitamin D deficiency/insufficiency is common in chronic kidney disease (CKD) patients and it contributes to secondary hyperparathyroidism, which occurs early in CKD. It is not clear whether the Kidney Disease Outcomes Quality Initiative (K/DOQI) recommended doses of ergocalciferol are adequate for correction of vitamin D insufficiency and hyperparathyroidism.To evaluate the parathyroid hormone (PTH)-lowering effect, safety, and tolerability of high-dose ergocalciferol compared with conventional-dose ergocalciferol in CKD subjects.We enrolled CKD stage III-IV patients who had 25-hydroxyvitamin D (25-OH-D) level30 ng/mL. The patients were randomized into two groups, control group treated with ergocalciferol as recommended by K/DOQI guidelines, and treatment group treated with double dosage of ergocalciferol from the recommendation. We compared serum 25-OH-D, intact-PTH, phosphate, calcium, and bone biomarker levels, during the 8-week intervention.Sixty-eight patients were included (34 controls and 34 treatments). Baseline characteristics of both groups were similar except calcium level 9.12 ± 0.56 mg/dL in control group and 9.44 ± 0.38 mg/dL in treatment group (p = 0.009), but not clinically significant. At the end of the 8-week, the mean 25-OH-D level significantly increased from 20.99 ± 6.68 to 33.41 ± 8.92 ng/mL in the treatment group (p = 0.001) and increased from 20.84 ± 7.21 to 23.42 ± 7.89 ng/mL in the control group (p = 0.026). There was also a significantly greater increase of 25-OH-D levels in the treatment group. Additionally, PTH levels significantly decreased from 90.75 ± 67.12 to 76.40 ± 45.97 at 8 weeks (p = 0.024) in the treatment group, and there was no change in the control group (97.14 ± 83.52 vs. 101.13 ± 95.03 pg/mL, p = 0.546). Serum calcium, phosphate, and adverse effects did not significantly change in either group throughout the study.In addition to improving vitamin D levels, oral high-dose ergocalciferol was safe and had a beneficial effect in decreasing PTH in patients with stage III-IV of CKD.

Background Improving the early detection of diabetic nephropathy remains a great challenge in disease management. Periostin is a marker of renal tubular injury and related to progressive kidney injury in animal models of chronic kidney disease. The clinical implications of urinary periostin activities in patients with type 2 diabetes have not been evaluated. Methods Urine samples were obtained from 30 healthy volunteers and 328 type 2 diabetic patients with normoalbuminuria (n=114), microalbuminuria (n=100) and macroalbuminuria (n=114). The excretion levels of urinary periostin were quantified with enzyme-linked immunosorbent assay. Immunohistochemical periostin expression was determined in kidney tissues from overt diabetic nephropathy. Results Increased periostin expression in glomeruli and tubular epithelium in diabetic renal pathology was observed. Urinary periostin levels were significantly elevated in the patients of the normoalbuminuria [3.06 (IQR: 1.12, 6.77) ng/mgCr], microalbuminuria [8.71 (IQR: 5.09, 19.29) ng/mgCr] and macroalbuminuria [13.58 (IQR: 3.99, 16.19) ng/mgCr] compared with healthy controls [1.15 (IQR: 0.60, 1.63) ng/mgCr] (P

Glycosaminoglycans or sulodexide has shown benefits in early experimental diabetic nephropathy (DN) models, but its efficacy in patients with early stage of DN is unknown.Methods. Twenty patients were randomly assigned to the placebo group and another 20 patients were randomly assigned to receive sulodexide 100 mg/day for 14 weeks. Primary outcome was a change of urinary TGF-beta1, albuminuria, and glomerular filtration rate (GFR). All patients had stable metabolic profiles for at least 90 days before randomization.Results. Urinary TGF-beta1 increased significantly in the placebo group but did not change significantly in the sulodexide group. Additionally, the mean change of urine TGF-beta1 in the placebo group was significantly higher than that in the sulodexide group (8.44±9.21versus2.17±6.96 pg/mg Cr,P=0.02). Mean changes of urinary albumin were15.05±30.09 μg/mg Cr (P=0.038) in the placebo group and13.89±32.25 μg/mg Cr (P=0.069) in the sulodexide group. No consistent patterns of side effects were observed.Conclusion. In this 14-week trial, benefits of sulodexide in preventing the increase of urinary TGF-beta1 were observed in patients with normoalbuminuric type 2 diabetes. The study suggests that sulodexide treatment may provide additional renoprotection in early stage DN. This trial is registered withTCTR20140806001.

Insufficient production oferythropoietin (EPO) is the primary cause ofanemia in patients with chronic kidney disease (CKD). The EPO treatment is an established treatment for renal anemia. The study investigated the therapeutic outcome between lyophilized powder and liquid form of EPO alpha by intravenous (IV) administration in hemoglobin maintenance of anemic treatment for CKD patients receiving hemodialysis.Forty patients were randomly assigned to either lyophilized powder of EPO alpha (treatment, n = 21) or liquidform of EPO alpha (control, n = 19) for 12 weeks by lVadministration. The hemoglobin was maintained within the target range of 10. 0 to 12.0 g/dL by adjusting the dosage of EPO. The clinical and biochemical profiles including transferrin saturation andferritin were measured. Adverse events were documented.The mean hemoglobin ofboth groups at baseline was 11.2±0.6 g/dL. Mean hemoglobin and mean hematocrit levels at baseline, and follow-up data of both groups were not statistically different. The mean weekly dosage of EPO in the treatment and control groups had no statistical significance within the same group and between groups as well. Stable hemoglobin levels were maintained without EPO dosage adjustment in the majority ofpatients in both groups (treatment group, 90.5%, control group, 94.7%). During the 12-week study period, no serious side effect was detectedThe present study demonstrated that the lyophilizedpowder ofEPO alpha was effective and safe as the standard liquid form of EPO alpha when it was administered by IV route in hemoglobin maintenance of anemia treatment.

Insulin resistance is commonly observed in uremic patients. Angiotensin II receptor blockers (ARB) are reported to act as insulin sensitizers in the animal model of hypertension and hypertensive patients. The authors investigated the effects of valsartan on insulin resistance and glucose metabolism in patients with long-term hemodialysis in the prospective, randomized controlled study.Thirty-three hemodialysis patients were randomized into two treatment groups, valsartan 80 to 320 mg/day (n = 18) or non-renin-angiotensin-aldosterone-system blocking antihypertensive agents (control, n = 15), treated for 12 weeks. Insulin resistance determined by homeostasis model assessment (HOMA-IR), fasting plasma glucose (FPG), fasting plasma insulin, and blood pressure monitoring were measured during the study.At baseline, metabolic profiles did not significantly differ between the treatment and the control groups. After 12 weeks of treatment, the valsartan group significantly improved HOMA-IR from 2.6 +/- 0.9 to 2.3 +/- 0.7 (p = 0.041) and significantly decreased FPG from 90.1 +/- 15.1 to 84.8 +/- 13.2 mg/dL (p = 0.008). In contrast, the control group was not associated with any significant changes in HOMA-IR, FPG, and fasting insulin levels. At the end of 12-week treatment, HOMA-IR, FPG, and fasting insulin levels were not significantly different between the two groups.These results indicate that the antihypertensive action of valsartan improves glucose metabolism by improving the peripheral insulin sensitivity in subjects with long-term dialysis.

Acute antibody-mediated rejection is an important cause of acute and chronic kidney allograft dysfunction and graft loss. The purpose of the present study was to evaluate our experience using plasmapheresis and intravenous immunoglobulin in treating patients who had acute antibody-mediated rejection after kidney transplant.A retrospective review of 13 patients who had biopsy proven antibody-mediated rejection was performed to determine the efficacy of plasmapheresis and intravenous immuno-globulin with or without bortezomib.All 13 patients were treated with plasmapheresis (5-18 sessions) with intravenous immunoglobulin (2 ± 1 g/kg) during and/or after plasmapheresis; 6 patients also received bortezomib. Mean age was 43 ± 10 years and median time from transplant to rejection was 4.5 months (interquartile range, 1.25-20 mo). Most patients (11 patients [85%]) had serum creatinine level return to within 20% baseline serum creatinine level before rejection. In all 13 patients, mean hospital length of stay was 27 ± 14 days. Frequency of recurrence of antibody-mediated rejection was 31%, and 1 patient resumed dialysis 7 months after treatment. Mean serum creatinine level was greater before (217 ± 111 μmol/L) than after treatment (141 ± 59 μ mol/L; P ≤ .03).The combination of intensive plasmapheresis and intravenous immunoglobulin is effective treatment for antibody-mediated rejection after kidney transplant. Long-term, prospective studies are justified to determine the effect of this regimen on graft survival.

Apolipoprotein E (ApoE) polymorphisms have been proposed as the risk factor for the development of diabetic nephropathy (DN). A number of studies have investigated the association between the ApoE isoforms and DN. However the findings remain inconclusive.To determine the association between the ApoE polymorphisms and DN.Two hundred thirty patients with type 2 diabetes were divided into two groups, patients with clinically diagnosed DN and normoalbuminuric patients. ApoE genotypes were determined by RT-PCR analysis. Student's t-test, ANOVA test, Chi-square test, odds ratio, and logistic regression was performed.The frequency of ApoE4 genotype was significantly lower in DN patients (8.7%) than in normoalbuminuric patients (21.7%). Logistical regression analysis showed that subjects with ApoE4 genotype (adjusted OR = 0.43; 95% CI: 0.19-0.99) were less likely to have DN than subjects with ApoE3 genotype. Furthermore, when analyzed only in patients with overt DN vs. patients with normoalbuminuria, the frequency of e4 allele was decreased in overt DN (2.8% vs. 21.7%, adjusted OR = 0.13; 95% CI: 0.03-0.57) and the frequency of e2 allele was increased (25.4% vs. 13.0%, adjusted OR = 2.34; 95% CI: 1.02- 5.38).ApoE4 genotype is associated with protection from type 2 DN, and subjects with e2 allele have increased risk of developing type 2 overt DN.

Obesity represents a significant problem in patients with cardiovascular disease and chronic kidney disease (CKD). The aim of the present study was to investigate the association between body mass index (BMI) and CKD in Thai individuals.Participants underwent general health screening. Overweight, weight at risk, obese I and obese II were defined as having a BMI ≥23 kg/m(2), 23-24.9 kg/m(2) , 25-29.9 kg/m(2) and ≥30 kg/m(2), respectively. Waist circumference ≥ 90 cm for men and 80 cm for women were represented by abdominal obesity. CKD was defined as a glomerular filtration rate (GFR) 60 mL/min per 1.73 m(2). An estimate of the GFR was obtained by the four-variable Modification of Diet in Renal Disease (MDRD) equation.The study population had 12 348 males and 3009 females. The survey population had a 7.5% prevalence of CKD. There was also a significant graded relationship between the degrees of overweight with the prevalence of CKD. Mean BMI were 25.36 ± 3.29 kg/m(2) for CKD subjects and 24.04 ± 3.13 kg/m(2) for non-CKD subjects (P 0.001). Prevalence of overweight and abdominal obesity in the participants with CKD were found to be higher than in those without CKD (overweight, 77.6% vs. 61.6%, P 0.001; abdominal obesity, 35.7% vs. 25.3%, P 0.001). In a multivariate logistic regression analysis, weight at risk (adjusted odds ratio 1.29; 95% CI 1.07-1.54), obese I (adjusted odds ratio 1.58; 95% CI 1.33-1.87) and obese II (adjusted odds ratio 1.65; 95% CI 1.24-2.19) were associated with CKD.Our data showed that overweight and obesity were associated with CKD in Thai members of the army population and their relatives undergoing a general health screening, independently of age, gender, blood pressure, serum lipid, uric acid and glucose levels.

Cyclosporine can cause acute and chronic nephrotoxicity. Renal biopsy is a reliable tool for the diagnosis of cyclosporine nephrotoxicity. The authors report a 56-year-old Thai female with a history of end-stage renal disease who underwent cadaveric renal transplantation. A transplanted kidney biopsy was performed on day 9 post-transplant to identify the cause of delayed graft function. Light and electron microscopic findings revealed widespread (50% involvement) numerous tubules filled with uniformly-sized vacuoles in cytoplasm (isometric vacuolization). Serum cyclosporine trough level was 534 ng/mL. Neither acute rejection nor acute tubular necrosis was seen. Diagnosis of acute cyclosporine nephrotoxicity was made. Isometric vacuolization in more than 50% involvement of the tubules is rare (3%) in biopsy specimens. The tubular isometric vacuolization might not have the strong impact to the long term graft outcome. This is the first case report of isometric tubular vacuolization due to cyclosporine toxicity in renal transplant recipient in Thailand.

Peritoneal dialysis is a convenient way of maintaining patients with end stage renal disease (ESRD) and in the present days, the Thai government supports all payments for ESRD patients. Continuous ambulatory peritoneal dialysis-(CAPD) related infections are the major cause of morbidity and mortality. The present study was conducted to identify the incidence and epidemiological data of CAPD-related infection.Medical records of 333 CAPD patients attending the Dialysis Unit of Phramongkutklao Hospital from January 1983 to June 2007 were reviewed. The historical cohort study was focused on the incidence of CAPD-related infections, causing pathogens, risk factors, and patient outcome.In total, 73.3% of episodes developed peritoneal infection. The incidences of peritonitis, exit site infection, and tunnel infection were 0.864, 0.213, and 0.034 episodes per patient per year, respectively. The most common infecting organisms were gram positive cocci (49.1%). The main pathogens were Coagulase-negative staphylococcus (15.9%), Staphylococcus aureus (15.2%) and Pseudomonas spp. (14.2%). CAPD-related infections increased in patients who had age60. A total of 81% of the infections responded to initial antibiotic therapy administered in the dialysis fluid. Overall, there were 10 episodes (1.9%) of the refractory group and 83 episodes (15.4%) of peritoneal catheter loss, with an overall mortality rate of 1.1%. Non-vancomycin based regimens were applied in 63.9% of peritoneal infected patients.The authors' center's CAPD-related infection rate achieved the International Society for Peritoneal Dialysis (ISPD) recommendation. A significantly enhanced incidence of CAPD-related infection occurred in advanced age. Coagulase-negative staphylococcus is still a very common organism that generally responds well to antibiotic therapy.

Insulin resistance is frequently recognized in uremic patients and is a predictor of cardiovascular mortality in end stage renal disease (ESRD) patients. However sparse data are available regarding the effects of different methods of renal dialysis on insulin resistance in ESRD without diabetes. The present study was conducted to evaluate the levels of insulin resistance in dialysis versus non dialysis ESRD patients without diabetes.A cross-sectional study was carried out in 45 non diabetic ESRD patients including continuous ambulatory peritoneal dialysis (CAPD), hemodialysis (HD), and non dialysis ESRD patients. The value of insulin resistance was obtained by homeostasis model assessment (HOMA). Estimation of the glomerular filtration rate (GFR) was obtained by the four-variable Modification of Diet in Renal Disease equation and ESRD was defined when GFR was below 15 ml/min/1.73 m2.Non diabetic ESRD patients were studied: 12 patients on CAPD treatment for 67.4 months, 18 patients on HD treatment for 89.3 months, and 15 patients on conservative treatment. HOMA scores (CAPD 5.4 +/- 2.3, HD 6.0 +/- 1.9 vs. non dialysis 1.5 +/- 0.9, p0.05) and fasting plasma insulin levels (CAPD 21.9 +/- 7.7 microU/mL, HD 19.5 +/- 8.4 microU/mL vs. non dialysis 4.4 +/- 2.5 microU/mL, p0.05) of the CAPD and HD groups were significantly higher than the non dialysis ESRD group, with no significant differences observed between CAPD and HD groups. However, fasting plasma glucose was significantly lower in the HD group than the CAPD and non dialysis ESRD groups (CAPD 98.2 +/- 10.6 mg/dL, non dialysis 93.0 +/- 11.5 mg/dL vs. HD 76.2 +/- 7.8 mg/dL, p0.05). All groups showed no significant differences for blood pressure, body weight, body mass index, fat free mass, body fat, and serum levels of albumin, total cholesterol, LDL-cholesterol, HDL-cholesterol, and triglycerides.Impaired insulin sensitivity in both dialysis groups after long term dialysis was still higher than that of the non dialysis ESRD group. However, no significant differences were noted between CAPD and HD treatments.

The metabolic syndrome has been documented to increase the risk of cardiovascular disease and chronic kidney disease (CKD); however, there are few studies of this in developing countries. A total of 15,357 participants of a standardized check-up, included metabolic screening, were enrolled. Metabolic syndrome was defined using criteria modified from the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) and the International Diabetes Federation (IDF). CKD was defined as a glomerular filtration rate60 m/min per 1.73 m2. Eighty point four percent of participants were men and 2,228 (14.5%) had CKD. Metabolic syndrome was more prevalent among CKD subjects than non-CKD subjects (modified NCEP-ATP III, 30.1% vs 24.4%; p0.001; modified IDF 26.9% vs 23.1%; p0.001, respectively). Abdominal obesity, high triglycerides, high blood pressure and impaired fasting glucose were significantly associated with an increased prevalence of CKD. There was also a significant graded relationship between the number of metabolic syndrome components and the prevalence of CKD. Participants with metabolic syndrome according to the modified NCEP-ATP III and modified IDF criteria had a 1.34-fold increase in adjusted odds ratio (95% CI 1.21-1.49) and a 1.20-fold increase in adjusted odds ratio (95% CI 1.08-1.33), respectively, compared to those without metabolic syndrome. Our study demonstrated metabolic syndrome defined with modified NCEP-ATP III and modified IDF criteria was significantly associated with increased prevalence of CKD in a Southeast Asian population.

Clinical studies have suggested that high levels of uric acid may contribute to the development of hypertension and kidney disease. However the relation between uric acid and chronic kidney disease (CKD) has been inconsistent.To examine the association between plasma concentration of uric acid, and estimated glomerular filtration rate (GFR) in CKD subjects.In a cross-sectional study, authors surveyed 5,558 subjects, but only 750 CKD subjects in whom GFR was between 15 and 60 ml/min/1.73 m2 were included in the study. The GFR values were calculated by Cockcroft-Gault formula.There were 65.5% males, mean age of 50.29 +/- 6.39 years and body mass index (BMI) of 21.68 +/- 2.64 kg/m2. The mean value of estimated GFR was 53.86 +/- 6.29 ml/min/1.73 m2. In subjects with serum uric acid fourth quartile displayed significantly higher BMI, higher systolic blood pressure (BP), higher diastolic BP, higher BUN, and higher serum creatinine, and lower estimated GFR as compared with the three lower quartiles. The correlation analysis showed that estimated GFR was negatively correlated with serum uric acid (r = -0.208, p0.01), age (r = -0.171, p0.01), systolic BP (r = -0.148, p0.01) and BMI (r = -0.147, p0.01). Multiple regression analysis, the presence of high serum uric acid levels were independently associated with a decline of GFR.In CKD subjects, high levels of uric acid were independent associated with GFR decline. Our finding suggests that early detection and prevention on hyperuricemia in CKD subjects are critical.

Multiple lines of evidence have indicated that the dose of hemodialysis (HD) affects patient outcome. According to K-DOQI, daily spKt/V1.2 predicts the morbidity and mortality among thrice-weekly HD. However in developing countries, about three-fourths of end stage renal disease patients undergo twice-weekly HD. No data studied the outcome and nutritional status between twice- and thrice-weekly HD patients.To compare the nutritional parameters in twice- and thrice-weekly HD patients who had weekly Kt/V3.6.The cross-sectional study was performed in the HD unit of the National Kidney Foundation of Thailand. One hundred and forty two informed consent HD patients were enrolled in the present study. Nutritional status was evaluated following a HD treatment by bioelectrical impedance analysis. All patients were interviewed for three-day food record and data were analyzed by Inmucal software program.Sixty patients had thrice-weekly HD and 82 patients were on twice-weekly HD. The characteristics and duration of dialysis of both groups were similar except age. Duration of dialysis in thrice-weekly HD group was 82.64 +/- 50 82 and twice-weekly HD group was 68.92 +/- 31.49 months. The mean age of the thrice-weekly HD group and twice-weekly HD group patients were 47.78 +/- 9.89 and 41.63 +/- 10.47 years, respectively (p0.05). Between both groups, the student t-test showed no difference in nutrition parameters except daily energy intake which was lower in the thrice-weekly HD group than twice-weekly HD group (19.21 +/- 6.42 vs. 25.02 +/- 7.70 kcal/kg/day, p0.05).HD patients with delivered weekly Kt/V3.6, nutritional status of patients undergoing twice-weekly HD are not different from that of thrice-weekly HD patients. Higher energy intake in twice-weekly HD patients might be the explanation.

A 56-year-old female patient was clinically characterized by heavy proteinuria, anemia, hypertension, and no detectable monoclonal protein in serum or urine. She had a history of diabetes with retinopathy and hypertension. Histological investigation of renal biopsy specimens revealed nodular glomerulosclerosis. Light microscopic examination did not allow discrimination between diabetic glomerulosclerosis and monoclonal immunoglobulin deposition disease (MIDD). Immunofluorescent examination showed linear capillary wall and tubular basement membrane staining with kappa, and IgG staining. Electron-microscopic examination confirmed the amorphous material along the glomerular basement. Based on these findings, the diagnosis of light chain and heavy chain monoclonal immunoglobulin deposition disease (LHCDD) and diabetic nephropathy was made. At the present after the 7th course of melphalan and prednisolone treatment, her renal function and proteinuria have progressively improved.

From a cohort of 109 patients (105 females and 4 males) treated for systemic lupus erythematosus (SLE), 20 patients (18.3%) developed new episodes of lupus nephritis and 89 patients (81.7%) remained free of renal involvement during the follow-up period. The mean duration of follow up was 39.1 +/- 54.4 months. Clinical characteristics associated with developing lupus nephritis were a high systolic blood pressure (or = 130 mmHg), photosensitivity, cutaneous vasculitis and gastrointestinal (GI) symptoms. Laboratory abnormalities associated with the development of lupus nephritis were hemoglobin10 mg/dl, hematocrit30%, blood urea nitrogen12 mg/dl, serum creatinine1.3 mg/dl, ESR60, the third component of complement (C3) level0.45 and positive antidsDNA antibody. After a multivariable analysis, only high systolic blood pressure, cutaneous vasculitis, hemoglobin10 mg/dl and serum creatinine1.3 mg/dl remained as statistically significant risk factors for developing lupus nephritis.

A 33-year-old woman without evidence of previous liver disease developed fulminant hepatic failure following the therapeutic dose of acetaminophen 3 days prior to admission. At admission, liver and renal function revealed hepatocellular injury with jaundice, and acute renal failure, total serum bilirubin 12.5 mg/ dL, direct serum bilirubin 8.1 mg/dL, aspartate aminotransferase 8460 IU/L, alanine aminotransferase 4640 IU/L, blood urea nitrogen 36 mg/dL, and serum creatinine 5.2 mg/dL. Two days later she developed multiorgan failure including hemodynamic disturbance with irreversible shock, and expired. Autopsy was performed, liver pathology showed severe centrilobular and midzonal necrosis, compatible with toxic hepatic necrosis, and renal pathology showed focal loss of tubular epithelial cells and partial occlusion of tubular lumen by cellular debris, compatible with acute tubular necrosis. Physicians should be aware of potential hepatotoxicity and nephrotoxicity of acetaminophen, even if given at therapeutic dosage in acute febrile illness.

Estimation of glomerular filtration rate (GFR) is usually determined from 24-hour urine collection, but it is time-consuming, and difficult in clinical practice. The authors attempted to select an accurate and safe, but more convenient test to obtain an estimated GFR.To compare estimation of GFR by Bioelectrical impedance analysis (BIA) with GFR calculated by 24-hour urine averaged creatinine clearance and urea clearance (Ccr-Cu-GFR).The authors examined 79 non-diabetic chronic kidney disease (CKD) patients that had estimated GFR between 15 and 89 ml/min/1. 73 m(2). Subjects were categorized into three subgroups according to K/DOQI-CKD classification: GFR of 60-89 m/min/1. 73m(2) (stage 2, 5 subjects), 30-59 ml/min/ 1.73m(2) (stage 3, 31 subjects), and 15-29 ml/min/1.73m(2) (stage 4, 43 subjects).The mean value of Ccr-Cu-GFR was 33.79+/-14.78 ml/min/1. 73 m(2) and GFR by BIA (BIA-GFR), 34.63 +/- 14.86 ml/min/1. 73 m(2) with no overall statistical differences (p = 0.838). In stage 3 CKD patients, the mean BIA-GFR and Ccr-Cu-GFR were similar (38.84+/-12.47 vs 41.16+/-9.17, p = 0. 399) while in stage 2 CKD, BIA-GFR tended to underestimate (63.50+/- 19.35 vs 70.94+/-7.82, p = 0.407) and in stage 4 CKD, BIA-GFR significantly overestimated Ccr-Cu-GFR (27.31+/-9.11 vs 23.76+/-5.68, p = 0.040).The findings suggest that BIA-GFR in non-diabetic CKD patients closely resembled with Ccr-Cu-GFR especially in stage 3 CKD patients. BIA-GFR may be considered as a more convenient test for an assessment of GFR in non-diabetic CKD patients.

A greater degree of insulin resistance may predispose to renal injury by worsening renal hemodynamics through the elevation of glomerular filtration fraction. However, there are sparse data on the relationship between insulin resistance, glomerular filtration rate (GFR) and body composition in chronic kidney disease (CKD) without diabetes.To evaluate the relationship between insulin resistance, total body fat and GFR in CKD without diabetes.The authors screened 84 non-diabetic CKD patients according to the K/DOQI definitions and only 78 patients were enrolled into the study (CKD stages 2-4, GFR between 15 and 90 ml/min/ 1.73 m2). Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR). Bioelectrical impedance analysis was performed to determine the percentage of total body fat. GFR was calculated by the average of creatinine and urea clearances.The correlation analysis showed that HOMA-IR was positively correlated with percent body fat (r = 0.32, P0.05), BMI (r = 0.46, P0.01), serum triglyceride (TG) (r =0.29, P0.01), and mean arterial pressure (r =0.25, P0.05), but not significantly correlated with GFR, age, cholesterol, HDL, uric acid and 24-hr urinary protein.In non-diabetic CKD patients, the independent factor for insulin resistance was the amount of total body fat. The insulin level and HOMA-IR were not dependent on the GFR in the present study.

Background Vitamin D insufficiency is associated with proteinuria and could be a risk factor for end-stage renal disease (ESRD). However, few studies have examined the significance of vitamin D insufficiency as a contributing factor for the development of ESRD in the Asian chronic kidney disease (CKD) population. Methods Authors examined the relationship between vitamin D status and the staging of CKD using data from an outpatient clinic-based screening in 2,895 Thai CKD patients. Serum levels of 25-hydroxyvitamin D were analyzed according to CKD stages. Vitamin D deficiency and insufficiency were defined as a serum 25-hydroxyvitamin D concentration < 10 ng/mL and 10–30 ng/mL, respectively. Results The mean (SD) 25-hydroxyvitamin D levels were significantly lower according to severity of renal impairment (CKD stage 3a: 27.84±14.03 ng/mL, CKD stage 3b: 25.86±11.14 ng/mL, CKD stage 4: 24.09±11.65 and CKD stage 5: 20.82±9.86 ng/mL, p