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Background: Few studies have investigated the relationship between serum total carbon dioxide (CO2) concentration and bicarbonate ion (HCO3 -) concentration in patients undergoing hemodialysis. We determined the agreement and discrepancy between serum total CO2 and HCO3 - concentrations and the diagnostic accuracy of serum total CO2 for the prediction of low (HCO3 - < 24 mEq/L) and high (HCO3 - ≥ 24 mEq/L) bicarbonate concentrations in hemodialysis patients. Methods: One hundred forty-nine arteriovenous blood samples from 84 hemodialysis patients were studied. Multiple linear regression analysis was used to determine factors correlated with HCO3 - concentration. Diagnostic accuracy of serum total CO2 was evaluated using receiver operating characteristic curve analysis and a 2 × 2 table. Agreement between serum total CO2 and HCO3 - concentrations was assessed using Bland-Altman analysis. Results: Serum total CO2 concentration was closely correlated with HCO3 - concentration (β = 0.858, P < 0.001). Area under the curve of serum total CO2 for the identification of low and high bicarbonate concentrations was 0.989. Use of serum total CO2 to predict low and high bicarbonate concentrations had a sensitivity of 100%, specificity of 50.0%, positive predictive value of 96.5%, negative predictive value of 100%, and accuracy of 96.6%. Bland-Altman analysis showed moderate agreement between serum total CO2 and HCO3 - concentrations. Discrepancies between HCO3 - and serum total CO2 concentrations (serum total CO2 - HCO3 - ≤ -1) were observed in 89 samples. Conclusion: Serum total CO2 concentration is closely correlated with HCO3 - concentration in hemodialysis patients. However, there is a non-negligible discrepancy between serum total CO2 and HCO3 - concentrations.

Introduction: Near-infrared spectroscopy has been used to measure the regional oxygen saturation (rSO2) of the brain, and decreases in cerebral rSO2 have been reported to lead to cognitive impairment in patients undergoing hemodialysis. However, reports about the association between changes in cerebral oxygenation and clinical parameters at hemodialysis initiation, including hemoglobin level, are lacking. Methods: This study included 33 patients at the hemodialysis initiation phase. Cerebral rSO2 was monitored using an INVOS 5100C. Included patients were assessed twice (at hemodialysis initiation and 42.7 ± 20.8 days after the first measurement), and changes in cerebral rSO2 were compared with changes in clinical parameters. Results: Cerebral rSO2 at the second measurement significantly increased compared with that at hemodialysis initiation (57.2 ± 6.8% vs 54.4 ± 8.8%, p Conclusion: Cerebral rSO2 was low in the presence of low hemoglobin levels at hemodialysis initiation and improved in response to hemoglobin increase in addition to changes in serum albumin levels. Attention should be paid to changes in hemoglobin levels even at hemodialysis initiation to prevent the deterioration of cerebral oxygenation, and this might contribute to the maintenance of cognitive function in patients undergoing hemodialysis.

Background: We report a unique case of renal cholesterol crystal embolism (CCE) induced by carotid artery stenting that was successfully treated with evolocumab, a fully human monoclonal antibody against proprotein convertase subtilisin kexin type 9 (PCSK9). Case presentation: A 77-year-old man with hypertension, hyperlipidemia, and chronic kidney disease was referred to our department for decreased estimated glomerular filtration rate (eGFR)—from 32.0 to 13.9 mL/min/1.73 m2—5 weeks after carotid artery stenting. Further examination revealed livedo reticularis in the bilateral toes and eosinophilia (723/μL). Skin biopsy from livedo reticularis tissue in the bilateral toes showed cholesterol clefts in the small arteries. The patient was therefore diagnosed with CCE. After 25 weeks’ administration of evolocumab at a dose of 140 mg subcutaneously administered every 2 weeks, his eGFR had improved from 10.7 to 18.1 mL/min/1.73 m2. Conclusion: Evolocumab may have a beneficial effect on renal involvement in patients with CCE.

Carnitine deficiency contributes to developing various pathological conditions, such as cardiac dysfunction, muscle weakness, and erythropoietin-resistant anemia in patients undergoing hemodialysis. However, a conclusion has not been reached concerning the prevalence and the effect of carnitine deficiency in patients undergoing peritoneal dialysis (PD). In this study, the prevalence of carnitine deficiency and the clinical factors associated with carnitine deficiency were investigated in 60 patients undergoing PD. The median age of the patients was 62.5 years (52.5–72.5 years), the proportion of male sex was 44/60 (73.3%), and the median PD period was 24 months (12–45 months). Carnitine deficiency (acyl carnitine/free carnitine ratio >0.4) was detected in 56/60 (93%) patients. Multiple regression analysis showed that the erythropoietin resistance index was independently associated with carnitine deficiency (β = 0.283, p = 0.04). These results suggest that carnitine plays pivotal roles in hematogenesis in patients undergoing PD.

Keiji Hirai, Junki Morino, Saori Minato, Shohei Kaneko, Katsunori Yanai, Yuko Mutsuyoshi, Hiroki Ishii, Momoko Matsuyama, Taisuke Kitano, Mitsutoshi Shindo, Akinori Aomatsu, Haruhisa Miyazawa, Kiyonori Ito, Yuichiro Ueda, Susumu Ookawara, Yoshiyuki Morishita Division of Nephrology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University, Saitama, JapanCorrespondence: Keiji HiraiDivision of Nephrology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University, 1-847 Amanuma-Cho, Omiya-Ku, Saitama City, Saitama 330-8503, JapanTel +81-48-647-2111Fax +81-48-647-6831Email keijihirai@kfy.biglobe.ne.jpIntroduction and Objectives: We investigated the efficacy and safety of sodium-glucose cotransporter-2 (SGLT-2) inhibitors as an add-on therapy in patients with advanced-stage diabetic kidney disease taking renin-angiotensin system (RAS) blockers.Materials and Methods: Changes in glycated hemoglobin (HbA1c), urine protein-to-creatinine ratio (UACR), body weight, systolic blood pressure, and annual change in estimated glomerular filtration rate (eGFR) were retrospectively analyzed in 20 patients after 12 months of SGLT-2 inhibitor administration (mean eGFR: 22.8 ± 9.7 mL/min/1.73 m2). All patients had advanced-stage diabetic kidney disease and were taking RAS blockers. Twenty patients matched with similar propensity scores who were not taking SGLT-2 inhibitors served as the control group.Results: The annual change in eGFR improved significantly from − 8.6 ± 12.5 mL/min/1.73 m2/year to − 2.6 ± 5.0 mL/min/1.73 m2/year after 12 months by SGLT-2 inhibitor administration (p < 0.05), but did not change in the control group. Other clinical parameters, such as HbA1c, UACR, body weight, blood pressure, serum lipids, and electrolytes did not change in either group. No adverse effects were observed by taking SGLT-2 inhibitors.Conclusion: Using SGLT-2 inhibitors as an add-on therapy may have beneficial effects on renal function in patients with advanced-stage diabetic kidney disease taking RAS blockers without any adverse effects.Keywords: advanced-stage diabetic kidney disease, renin-angiotensin system blocker, sodium-glucose cotransporter-2 inhibitor

A 71-year-old man undergoing hemodialysis (HD) was admitted to our hospital with congestive heart failure (CHF) and pneumonia. After admission, ultrafiltration with HD was urgently performed because of a lack of respiratory improvement despite the use of noninvasive positive pressure ventilation. During HD, cerebral regional saturation of oxygen (rSO2) was monitored by INVOS 5100c oxygen saturation monitor (Covidien Japan, Japan) to evaluate changes in tissue oxygenation. At HD initiation, cerebral rSO2 was very low at 34% under the fraction of inspiratory oxygen (FiO2) of 0.4. Ultrafiltration was performed at the rate of 0.5 L/h thereafter, cerebral rSO2 gradually improved even as inhaling oxygen concentration decreased. At the end of HD, cerebral rSO2 improved at 40% under a FiO2 of 0.28 as excess body fluid was removed. After pneumonia and CHF improved, he was discharged. Reports of the association between cerebral oxygenation and acute CHF status in patients undergoing HD are limited; therefore, in our experience with this case, cerebral oxygenation deteriorated with the CHF status but was improved by adequate body-fluid management during HD.

Background Proteinase 3-antineutrophil cytoplasmic antibody has been reported to be positive in 5–10% of cases of renal injury complicated by infective endocarditis; however, histological findings have rarely been reported for these cases. Case presentation A 71-year-old Japanese man with a history of aortic valve replacement developed rapidly progressive renal dysfunction with gross hematuria and proteinuria. Blood analysis showed a high proteinase 3-antineutrophil cytoplasmic antibody (163 IU/ml) titer. Streptococcus species was detected from two separate blood culture bottles. Transesophageal echocardiography detected mitral valve vegetation. Histological evaluation of renal biopsy specimens showed necrosis and cellular crescents in glomeruli without immune complex deposition. The patient met the modified Duke criteria for definitive infective endocarditis. On the basis of these findings, the patient was diagnosed with proteinase 3-antineutrophil cytoplasmic antibody-positive necrotizing crescentic glomerulonephritis complicated by Streptococcus infective endocarditis. His renal disease improved, and his proteinase 3-antineutrophil cytoplasmic antibody titer normalized with antibiotic monotherapy. Conclusion Few case reports have described histological findings of proteinase 3-antineutrophil cytoplasmic antibody-positive renal injury complicated with infective endocarditis. We believe that an accumulation of histological findings and treatments is mandatory for establishment of optimal management for proteinase 3-antineutrophil cytoplasmic antibody-positive renal injury complicated with infective endocarditis.

Background: We investigated the effects of roxadustat on the anemia, iron metabolism, peritoneal membrane function, and residual renal function; and determined the factors associated with the administration of roxadustat in patients who were undergoing peritoneal dialysis.Methods: We retrospectively analyzed the changes in hemoglobin, serum ferritin, transferrin saturation (TSAT), 4-h dialysate/plasma creatinine, and renal weekly urea clearance over the 24 weeks following the change from an erythropoiesis-stimulating agent (ESA) to roxadustat in 16 patients who were undergoing peritoneal dialysis and had anemia (Roxadustat group). Twenty-three peritoneal dialysis patients who had anemia and continued ESA served as a control group (ESA group).Results: There were no significant differences in hemoglobin, serum ferritin, TSAT, 4-h dialysate/plasma creatinine, or renal weekly urea clearance between the two groups at baseline. The hemoglobin concentration was significantly higher in the Roxadustat group than in the ESA group after 24 weeks (11.6 ± 1.0 g/dL vs. 10.3 ± 1.1 g/dL, p < 0.05), whereas the ferritin concentration and TSAT were significantly lower (139.5 ± 102.0 ng/mL vs. 209.2 ± 113.1 ng/mL, p < 0.05; and 28.1 ± 11.5% vs. 44.8 ± 10.4%, p < 0.05, respectively). The changes in 4-h dialysate/plasma creatinine and renal weekly urea clearance did not differ between the two groups. Linear regression analysis revealed that the serum potassium concentration correlated with the dose of roxadustat at 24 weeks (standard coefficient = 0.580, p = 0.019).Conclusion: Roxadustat may improve the anemia and reduce the serum ferritin and TSAT of the peritoneal dialysis patients after they were switched from an ESA, without association with peritoneal membrane function or residual renal function.

Background:Although cerebral regional oxygen saturation (rSO2) is significantly lower in hemodialysis (HD) patients than that in healthy controls, investigations on cerebral oxygenation in peritoneal dialysis (PD) patients are limited. We aimed to confirm the cerebral oxygenation status and identify the factors affecting cerebral rSO2in PD patients.Methods:Thirty-six PD patients (21 men and 15 women; mean age, 62.8 ± 12.7 years) were recruited. In addition, 27 healthy volunteers (17 men and 10 women; mean age, 43.5 ± 18.8 years) were recruited as a control group. Cerebral rSO2was monitored at the forehead using an INVOS 5100c oxygen saturation monitor.Results:Cerebral rSO2was significantly lower in PD patients than that in healthy controls (57.0 ± 7.3% vs 68.9 ± 8.6%, p 2was significantly correlated with natural logarithm (Ln)-PD duration ( r = −0.389, p = 0.019) and serum albumin concentration ( r = 0.370, p = 0.026) in a simple linear regression analysis. Multivariable linear regression analysis was performed using variables that showed a significant correlation and p 2. Cerebral rSO2was independently associated with Ln-PD duration (standardized coefficient: −0.339) and serum albumin concentration (standardized coefficient: 0.316).Conclusions:Cerebral rSO2was significantly affected by the PD duration and serum albumin concentration. Further prospective studies are needed to clarify whether preventing a decrease in serum albumin concentration leads to the maintenance of cerebral oxygenation in patients undergoing PD.

A 79-year-old woman who was on chronic hemodialysis due to diabetic nephropathy and had previously undergo surgery for radiocephalic arteriovenous fistula (AVF) in her right wrist needed percutaneous transluminal angioplasty (PTA) for stenosis at the juxta-anastomotic access site. After successful PTA, the systemic blood pressure decreased from 144/93 mm Hg to 117/67 mm Hg in response to the increase in AVF blood flow. Furthermore, the regional oxygen saturation (rSO2) value in her dorsal hand decreased from 67.9% to 64.9% and, simultaneously, the cerebral rSO2 decreased from 63.6% to 60.1%. Our experience indicates that the PTA procedure may affect the rapid deterioration of systemic oxygenation, including that in the hand and brain, in association with the increase in the AVF blood flow and change in systemic circulation.

Background Endotoxin contamination of dialysate has serious adverse effects on patients undergoing hemodialysis. Therefore, endotoxin activity in dialysate is closely monitored. Limulus amebocyte lysate (LAL) has been used as a reagent to measure endotoxin activity. Here, we investigated the efficacy of an automatic LAL kinetic turbidimetric test (Toxinometer ET-mini) for screening endotoxin activity in dialysate. Methods In total, endotoxin activity was measured in 110 dialysate samples obtained from several sites within hemodialysis circuits between June 2012 and March 2018. The results were compared with those from a conventional chromogenic substrate LAL test conducted by a clinical examination laboratory. Results Both the automatic LAL test and the chromogenic substrate LAL test had a minimum detection level of 0.001 endotoxin units (EU)/mL. Endotoxin activity levels measured via the automatic LAL test showed a strongly positive correlation (concordance correlation coefficient: 0.9933; 95% CI: 0.9902-0.9954) and good agreement (mean difference: 0.00±0.01 EU/mL) with those obtained using the chromogenic substrate LAL test. Conclusion The results suggest that the automatic LAL test may be useful for endotoxin activity screening in hemodialysis facilities.

Background : We investigated the relationship between serum total carbon dioxide (CO2) and bicarbonate ion (HCO3−) concentrations in pre-dialysis chronic kidney disease (CKD) patients and devised a formula for predicting low bicarbonate (HCO3−< 24 mmol/L) and high bicarbonate (HCO3− ≥ 24 mmol/L) using clinical parameters. Methods : In total, 305 samples of venous blood collected from 207 pre-dialysis patients assessed by CKD stage (G1 + G2, 46; G3, 50; G4, 51; G5, 60) were investigated. The relationship between serum total CO2 and HCO3− concentrations was analyzed using Pearson's correlation coefficient. An approximation formula was developed using clinical parameters correlated independently with HCO3− concentration. Diagnostic accuracy of serum total CO2 and the approximation formula was evaluated by receiver operating characteristic curve analysis and a 2 × 2 table. Results : Serum total CO2 correlated strongly with HCO3− concentration (r = 0.91; P < 0.001). The following approximation formula was obtained by a multiple linear regression analysis: HCO3− (mmol/L) = total CO2 − 0.5 × albumin − 0.1 × chloride − 0.01 × (estimated glomerular filtration rate + blood glucose) + 15. The areas under the curves of serum total CO2 and the approximation formula for detection of low bicarbonate and high bicarbonate were 0.981, 0.996, 0.993, and 1.000, respectively. This formula had superior diagnostic accuracy compared with that of serum total CO2 (86.6% vs. 81.3%). Conclusion : Serum total CO2 correlated strongly with HCO3− concentration in pre-dialysis CKD patients. An approximation formula including serum total CO2 showed superior diagnostic accuracy for low and high bicarbonate compared with serum total CO2.

A 44-year-old man undergoing automated peritoneal dialysis (PD) developed headache and dizziness with truncal ataxia and ataxic gait. Severe hypertension (systolic blood pressure/diastolic pressure: 193/83 mm Hg) and lower extremity edema were present, and his PD efficiency (weekly KT/V: 1.49) was inadequate. Magnetic resonance imaging revealed diffuse hyperintensities in the brain stem and bilateral cerebellar hemispheres on fluid-attenuated inversion recovery and apparent diffusion coefficient mapping imaging. Based on these findings, the patient was diagnosed with posterior reversible encephalopathy syndrome due to hypertension and uremia. He was treated with antihypertensive agents, and we changed the PD prescription to improve PD efficiency. Thereafter, his symptoms gradually improved, and abnormal findings on brain magnetic resonance imaging disappeared in accordance with lowering blood pressure.

We herein report two cases of advanced stage rapidly progressive diabetic nephropathy that were effectively treated with combination therapy including renin–angiotensin–aldosterone system (RAS) blocker [angiotensin II receptor blocker (ARB)], glucagon-like peptide-1 (GLP-1) receptor agonist and sodium glucose transporter-2 (SGLT-2) inhibitor. A 30-year-old woman with advanced stage diabetic nephropathy [estimated glomerular filtration rate (eGFR): 20.7 mL/min/1.73 m(2); proteinuria: 13.2 g/gCr], showing a rapidly progressive pattern (annual eGFR change: − 60.0 mL/min/1.73 m(2)/year), had improvement in proteinuria (5.9 g/gCr) and eGFR change (+ 4.3 mL/min/1.73 m(2) over 15 weeks) after administration of ARB (irbesartan 25 mg/day), GLP-1 receptor agonist (liraglutide 0.3 mg/day) and SGLT-2 inhibitor (canagliflozin 50 mg/day). A 59-year-old man with advanced stage diabetic nephropathy (eGFR: 32.4 mL/min/1.73 m(2); proteinuria: 8.90 g/gCr), showing a rapidly progressive pattern (annual eGFR change: − 21.2 mL/min/1.73 m(2)/year), had an improvement in proteinuria (0.02 g/gCr) and annual eGFR change (+ 0.1 mL/min/1.73 m(2)/year) after combination therapy with ARB (olmesartan 40 mg/day), GLP-1 receptor agonist (liraglutide 0.9 mg/day) and SGLT-2 inhibitor (tofogliflozin 10 mg/day). These results suggest that this triple combination therapy has renoprotective effects on advanced stage rapidly progressive diabetic nephropathy.

Near-infrared spectroscopy has been used to measure regional oxygen saturation (rSO2), and intradialytic tissue rSO2 measurements have been playing an important role in evaluating changes in tissue oxygenation in various clinical settings of hemodialysis (HD) therapy.However, few reports have described changes in hepatic oxygenation associated with body fluid management in overhydrated HD patients. We herein report an HD patient with congestive heart failure (CHF) that had improved systemic and tissue oxygenation, including in the brain and liver, during HD with ultrafiltration. A 73-year-old man undergoing HD was admitted to our hospital with CHF. After admission, HD with ultrafiltration was performed to adequately manage his body fluid excess. Because of deterioration of systemic oxygenation on admission, we monitored his percutaneous arterial oxygen saturation (SpO2) using a pulse oximeter and regional oxygen saturation (rSO2) in the brain and liver using an INVOS 5100c oxygen saturation monitor during HD. At HD initiation, his cerebral and hepatic rSO2 levels were relatively low, at 43.2% and 34.1%, respectively, in addition to the SpO2 of 88%. During HD with ultrafiltration, systemic oxygenation evaluated by SpO2 and tissue oxygenation by cerebral and hepatic rSO2 improved. Interestingly, the hepatic rSO2 ratio, defined as the ratio of rSO2 values at t (min) during HD and the initial rSO2 value before HD, increased larger than the cerebral rSO2 ratio during HD. After the adjustment of body fluid condition under the maintained SpO2 values, we confirmed the hepatic and cerebral SO2 ratio again during HD, and these two values changed nearly in the same manner. Throughout our experience, in this case, we confirmed a remarkable increase in hepatic rSO2 ratio relative to cerebral rSO2 ratio under a CHF status during HD, and these differences disappeared after the adjustment of the body fluid status.

The microRNAs (miRNAs) that can regulate diabetic kidney disease (DKD) have not been fully characterized. The aim of this study was to identify the miRNAs that affect DKD and could be used as specific biomarkers or therapeutic agents. First, kidney tissues from two DKD mouse models and control mice were screened for differences in miRNA expression by microarray analysis followed by quantitative real-time reverse transcription-PCR. Six miRNAs were differentially expressed from controls in both DKD mouse models. Among them, miRNA-125b-5p and miRNA-181b-5p were exclusively downregulated in the DKD mouse model. Next, we administered miRNA-181b-5p-mimic to DKD mice, which reduced the albuminuria and abnormal mesangial expansion. Pathway analysis and database research revealed that overexpression of miRNA-181b-5p significantly altered the expression of seven mRNAs in six known signaling pathways in the kidneys of DKD mice. Furthermore, the serum level of miRNA-125b-5p was significantly higher in patients with DKD (1.89±0.40-fold, p

This study investigated the effects of evolocumab on vulnerable coronary plaques and factors associated with the change in stability and size of plaques in patients taking statins. Vulnerable coronary plaques were defined using coronary computed tomography (CT) angiography as having a density of &lt, 50 HU within the region of interest and a remodeling index &ge, 1.1. The changes in minimum CT density, remodeling index, and percent stenosis of vulnerable coronary plaques after six months of evolocumab administration were retrospectively analyzed in 136 vulnerable coronary plaques from 98 patients (68 men and 30 women, mean age: 72.9 &plusmn, 8.7 years) treated with a statin. The administration of evolocumab significantly increased the minimum CT density (39.1 &plusmn, 8.1 HU to 84.9 &plusmn, 31.4 HU, p &lt, 0.001), reduced the remodeling index (1.29 &plusmn, 0.11 to 1.19 &plusmn, 0.10, p &lt, 0.001), and decreased the percent stenosis (27.0 &plusmn, 10.4% to 21.2 &plusmn, 9.8%, p &lt, 0.001). Multiple linear regression analysis revealed that baseline percent stenosis (standard coefficient (&beta, ) = &minus, 0.391, p = 0.002) independently correlated with the change in minimum CT density, whereas the baseline remodeling index (&beta, = &minus, 0.368, p &lt, 0.001) independently correlated with a change in the remodeling index. Evolocumab stabilized vulnerable coronary plaques and reduced their size. These results suggest that evolocumab protects against coronary artery disease progression in patients taking statins.

Background: Zinc deficiency is common and is associated with erythropoietin resistant anemia, dysgeusia, and hypogonadism in patients undergoing hemodialysis. However, the prevalence and clinical effects of zinc deficiency in patients undergoing peritoneal dialysis (PD) have not been determined.Methods: This was a retrospective, cross-sectional study. The prevalence of serum zinc deficiency and the clinical factors related to serum zinc concentration were determined in 49 patients undergoing PD [mean age 59.5 years (±14.8 years), 38/49 were men (78.6%), median PD period 24.0 months (12.5–45.0 months)]. A serum zinc concentration

Diabetic nephropathy is one of the major complications of diabetes mellitus and is the leading cause of end-stage renal disease worldwide. Podocyte injury contributes to the development of diabetic nephropathy. However, the molecules that regulate podocyte injury in diabetic nephropathy have not been fully clarified. MicroRNAs (miRNAs) are small non-coding RNAs that can inhibit the translation of target messenger RNAs. Previous reports have described alteration of the expression levels of many miRNAs in cultured podocyte cells stimulated with a high glucose concentration and podocytes in rodent models of diabetic nephropathy. The associations between podocyte injury and miRNA expression levels in blood, urine, and kidney in patients with diabetic nephropathy have also been reported. Moreover, modulation of the expression of several miRNAs has been shown to have protective effects against podocyte injury in diabetic nephropathy in cultured podocyte cells in vitro and in rodent models of diabetic nephropathy in vivo. Therefore, this review focuses on miRNAs in podocyte injury in diabetic nephropathy, with regard to their potential as biomarkers and miRNA modulation as a therapeutic option.

We determined the effects of evolocumab, a fully human monoclonal antibody targeting proprotein convertase subtilisin/kexin type 9, on carotid intima-media thickness (IMT) and the factors associated with the change in carotid IMT in patients taking a statin. The change in carotid mean and maximum IMT before and after the initiation of evolocumab treatment was retrospectively analyzed in 229 statin-treated patients. The changes in clinical parameters, including serum lipid concentrations, were also evaluated. Evolocumab significantly reduced the increase in carotid mean and maximum IMT (0.09 &plusmn, 0.13 mm/year to &minus, 0.04 &plusmn, 0.16 mm/year, p &lt, 0.001 and 0.17 &plusmn, 0.38 mm/year to 0.08 &plusmn, 0.47 mm/year, p = 0.02). Evolocumab reduced serum total cholesterol, low-density lipoprotein-cholesterol, triglyceride, and lipoprotein (a) concentrations (each p &lt, 0.001), and increased serum high-density lipoprotein (HDL)-cholesterol concentrations (p = 0.01). Multiple linear regression analysis revealed that the change in HDL-cholesterol (standard coefficient (&beta, ) = &minus, 0.120, p = 0.04) and carotid mean IMT (&beta, = &minus, 0.467, p &lt, 0.001) were independently correlated with the change in carotid mean IMT during the administration of evolocumab, whereas the change in HDL-cholesterol (&beta, 0.208, p = 0.002) and log-triglyceride (&beta, 0.167, p = 0.01) independently correlated with the change in carotid maximum IMT. Evolocumab reduced the increase in carotid IMT in patients taking a statin. These results suggest that evolocumab is protective against carotid atherosclerosis in patients undergoing statin therapy.

Sarcopenia, which is characterized by the loss of skeletal muscle, has been reported to contribute to development of physical disabilities, various illnesses, and increasing mortality. MicroRNAs (miRNAs) are small non-coding RNAs that inhibit translation of target messenger RNAs. Previous studies have shown that miRNAs play pivotal roles in the development of sarcopenia. Therefore, this systematic review focuses on miRNAs that regulate sarcopenia.

Background: Patients with chronic kidney disease (CKD) are at risk for bone loss and sarcopenia because of associated mineral and bone disorders (MBD), malnutrition, and chronic inflammation. Both osteoporosis and sarcopenia are associated with a poor prognosis; however, few studies have evaluated the relationship between muscle mass and bone mineral density (BMD) in hemodialysis (HD) patients. The present study examined the association between skeletal muscle mass index (SMI) and BMD in the lumbar spine and femoral neck in HD patients. Methods: Fifty HD patients (mean age, 69 ± 10 years; mean HD duration, 9.0 ± 8.8 years) in Minami-Uonuma City Hospital were evaluated. BMD was measured by dual-energy X-ray absorptiometry, and SMI was measured by bioelectrical impedance analysis (InBodyTM) after HD. The factors affecting lumbar spine and femoral neck BMD were investigated, and multivariate analysis was performed. Results: In simple linear regression analysis, the factors that significantly affected the lumbar spine BMD were sex, presence of hypertension, presence of diabetes mellitus, body mass index, triglyceride level, grip strength, and SMI; the factors that significantly affected the femoral neck BMD were sex, HD duration, serum creatinine level, tartrate-resistant acid phosphatase 5b level, undercarboxylated osteocalcin (ucOC) level, N-terminal propeptide of type I procollagen level, grip strength, and SMI. In multivariate analysis, SMI (standardized coefficient: 0.578) was the only independent factor that affected the lumbar spine BMD; the independent factors that affected the femoral neck BMD were SMI (standardized coefficient: 0.468), ucOC (standardized coefficient: −0.366) and sex (standardized coefficient: 0.231). Conclusion: SMI was independently associated with the BMD in the lumbar spine and femoral neck in HD patients. The preservation of skeletal muscle mass could be important to prevent BMD decrease in HD patients, in addition to the management of CKD-MBD.

Summary Background and aims The use of the psoas muscle mass index (PMI) using computed tomography (CT) has become a marker of interest to evaluate whole body muscle mass. However, in hemodialysis (HD) patients, reports about the clinical significance of psoas muscle evaluation are limited. We aimed to clarify the association between PMI and skeletal muscle mass index (SMI) using bioelectrical impedance analysis (BIA), and to investigate factors affecting PMI in HD patients. Methods In this prospective observational study, to evaluate muscle mass, SMI was measured using BIA after HD, and PMI was measured by the manual trace method on routinely available CT scans. PMI measurement was assessed twice by two physicians to compute intra-rater and inter-rater reliability. The correlations between PMI and the clinical factors were evaluated using Pearson's correlation coefficient and a linear regression analysis. Variables with a p-value Results Fifty HD patients were recruited (31 males and 19 females; HD duration, 9.0 ± 8.8 years). The SMI was 6.10 ± 1.20 kg/m2, and the PMI was 4.79 ± 1.61 cm2/m2. Regarding the reliability of PMI measurements, intra-rater reliability [intra-class correlation (ICC) = 0.999] and inter-rater reliability (ICC = 0.998) were high in this study. The mean PMI of male patients was 5.40 ± 1.62 cm2/m2, while that of female patients was significantly lower (3.78 ± 0.98 cm2/m2; p Conclusions PMI assessed with CT positively correlated with SMI measured using BIA. PMI might be one of the methods for evaluating the muscle mass in HD patients, when CT scans are taken as part of routine care.

A 49-year-old woman developed eosinophilic peritonitis 2 months after starting continuous ambulatory peritoneal dialysis because of congenital right kidney hypoplasia and chronic glomerulonephritis. This was shown to have been induced by sucroferric oxyhydroxide, an iron-based phosphate binder, using a drug-induced lymphocyte stimulation test. Her eosinophilic peritonitis was improved after stopping the administration of sucroferric oxyhydroxide without providing any immunosuppressive agents.

Background:Several reports indicate that extracellular volume predicted by bioimpedance analysis method is associated with hydration status of hemodialysis patients.Theory:Fundamentally, uric acid does not cross cell membranes by simple diffusion, either by facilitated diffusion or by active transport. In addition, uric acid cannot move through cell membranes in most tissues other than those involved in uric acid excretion. These facts support the interpretation that uric acid distribution volume would therefore correlate with extracellular volume.Methods:We examined correlation between uric acid distribution volume calculated by uric acid mass-balance modeling from regular blood test results and extracellular volume predicted by bioimpedance analysis predicted by BCM (Fresenius Medical Care) in 53 patients.Results:There was a significant correlation between uric acid distribution volume ( x) and extracellular volume predicted by bioimpedance analysis ( y): y = 0.69 x + 3.39, r2 = 0.61, p Conclusion:Uric acid distribution volume calculated by uric acid mass-balance modeling from regular blood test results may be an alternative marker of extracellular volume predicted by bioimpedance analysis.

Cardiovascular disease is one of the most important risk factors for mortality and morbidity in patients with Chronic Kidney Disease (CKD). This systematic review focuses on the protective effects of diuretics against the development of cardiovascular disease in patients with CKD. Among various kinds of diuretics, spironolactone, a mineralocorticoid receptor antagonist, has been shown to have protective effects against cardiovascular disease in patients with all stages of CKD, including predialysis, hemodialysis, and peritoneal dialysis. Low-dose loop diuretics have also been shown to have cardioprotective effects in patients with CKD during the pre-dialysis and hemodialysis stages; however, high-dose loop diuretics have failed to show these cardioprotective effects. The protective effects of other classes of diuretics, including thiazide and tolvaptan, against cardiovascular diseases in patients with CKD remain unclear.

Keiji Hirai,1 Shigeki Imamura,2 Aizan Hirai,2 Kazuo Misumi,3 Susumu Ookawara,1 Yoshiyuki Morishita1 1Division of Nephrology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University, Saitama, Japan; 2Department of Internal Medicine, Chiba Cerebral and Cardiovascular Center, Chiba, Japan; 3Division of Cardiology, Heart Institute, Chiba-Nishi General Hospital, Chiba, Japan Background: This study investigated the factors associated with coronary artery stenosis in outpatients. Furthermore, the usefulness of maximum carotid intima–media thickness (maximum-IMT) as a surrogate marker of coronary artery stenosis was evaluated. Methods: We conducted a single-center retrospective study. A total of 601 outpatients (338 males; 263 females; mean age, 69.8±10.0 years) who underwent coronary computed tomography angiography between April 2006 and March 2012 were analyzed. The associations between coronary artery stenosis (≥75%) as determined by coronary computed tomography angiography and clinical and laboratory parameters were evaluated by multivariate logistic regression. Validation of maximum-IMT as measured by ultrasonography as a surrogate marker of coronary artery stenosis was analyzed by receiver operating characteristic (ROC) curve analysis. Results: The estimated glomerular filtration rate (eGFR: mL/min/1.73 m2) (odds ratio [OR] 0.985, p

High concentrations of lactate are considered to contribute to impairment of the peritoneal membrane. We investigated the longer-period effects of bicarbonate/lactate-buffered neutral peritoneal dialysis fluid (PDF) in patients undergoing PD for about 2 years. Patients undergoing PD were changed from a lactate-buffered neutral PDF to a bicarbonate/lactate-buffered neutral PDF. We then investigated the patients' clinical outcomes and peritoneal membrane functions as well as the surrogate markers in the drained dialysate. Fourteen patients undergoing PD were enrolled. Peritonitis was observed in one patient. No other adverse events were observed. Peritoneal function did not change as the ultrafiltration volume decreased. Fibrin degradation products and vascular endothelial growth factor in the drained dialysate decreased while the interleukin level increased. These results suggest that bicarbonate/lactate-buffered neutral PDF may have beneficial effects in terms of peritoneal preservation and can be safely used in patients undergoing PD.

A 55-year-old man with Marfan syndrome taking warfarin for anticoagulant therapy after aortic valve replacement developed acute kidney injury (serum creatinine level of 9.01 mg/dL) and gross macrohematuria. Renal biopsy showed red cell casts in the renal tubules, glomerular crescent formation in the glomeruli with immunoglobulin A deposition, and global sclerosis. Based on these findings, the patient was diagnosed with warfarin-related nephropathy with acute kidney injury characterized by immunoglobulin A nephropathy with crescents. The warfarin was withdrawn, and his hematuria and renal function improved without immunosuppressive agents.

Background: Hemodialysis (HD) patients frequently suffer from severe anemia caused by various hemorrhagic disorders in addition to renal anemia. Intradialytic blood transfusion is sometimes performed; however, the cerebral oxygenation changes associated with this procedure remain unclear. Methods: Sixteen HD patients with severe anemia who required intradialytic blood transfusion were included (12 men and 4 women; mean age, 64.8 ± 9.8 years). Cerebral regional oxygen saturation (rSO2) was monitored using near-infrared spectroscopy, and cerebral fractional oxygen extraction (FOE) was calculated before and after HD. Twenty-five HD patients with well-maintained hemoglobin (Hb) levels were included as a control group. Results: Cerebral rSO2 values were significantly lower in HD patients with severe anemia than in the control group (42.4 ± 9.9 vs. 52.5 ± 8.5%, p = 0.001). Following intradialytic blood transfusion (385 ± 140 mL of concentrated red blood cells), Hb levels significantly increased (from 7.2 ± 0.9 to 9.1 ± 1.1 g/dL, p < 0.001), and cerebral rSO2 values significantly improved after HD (from 42.4 ± 9.9 to 46.3 ± 9.0%, p < 0.001). Cerebral FOE values before HD in patients with severe anemia were significantly higher than those in the control group (severe anemia, 0.56 ± 0.10; controls, 0.45 ± 0.08; p < 0.001). After HD with intradialytic blood transfusion, these values significantly decreased (0.52 ± 0.09 after HD versus 0.56 ± 0.10 before HD, p = 0.002). Conclusion: HD patients with severe anemia represented cerebral oxygen metabolism deterioration, which could be significantly improved by intradialytic blood transfusion.

Background. Near-infrared spectroscopy revealed that the regional saturation of oxygen (rSO2) in cerebral tissue is lower in hemodialysis (HD) patients than in healthy subjects. However, no study has examined the changes in cerebral oxygenation by aortic arch calcification (AAC) progression in HD patients. Methods. A total of 104 HD patients were divided into four groups by AAC grade determined using chest radiography: 23 patients at grade 0, 24 at grade 1, 30 at grade 2, and 27 at grade 3. Differences in clinical parameters, including cerebral rSO2, among AAC grades were investigated and atherosclerotic parameters affecting cerebral rSO2 values were identified. Results. Cerebral rSO2 significantly decreased as AAC progressed (AAC grade 3 versus grade 0, p<0.01 versus grade 1, p<0.05). Multivariate logistic regression analysis was performed using parameters with p values < 0.20 in univariate analysis between cerebral rSO2 values less than the mean and atherosclerotic parameters. AAC grades 2 and 3, serum phosphate level, and history of smoking were factors associated with the cerebral rSO2 decrease. Conclusions. Cerebral rSO2 significantly decreased as AAC progressed and was independently associated with higher AAC grade, serum phosphate level, and history of smoking.

Objective This study aimed to (i) compare the extent of urinary potassium (K+) excretion in addition to the changes in serum K+ concentration: and (ii) clarify the association between changes in serum K+ concentration, urinary K+ excretion, and acid-base status with or without renin-angiotensin-aldosterone system (RAAS) inhibitors in patients with advanced chronic kidney disease (CKD) stages. Methods Six hundred and ninety-one patients with advanced CKD (CKD G3b, 161; G4, 271; G5, 259) were retrospectively evaluated. Differences in serum K+ concentration, urinary K+ excretion, and serum sodium and chloride differences (Na+−Cl-) were compared among patients with RAAS inhibitors, RAAS inhibitors and diuretic agents, and without either medication in each CKD stage. Results Serum K+ concentrations in patients with RAAS inhibitors were significantly higher than in those with RAAS inhibitors and diuretics in CKD stage G3b and the other two treatment groups in CKD stage G4. Urinary K+ excretion among the three groups did not differ significantly in each CKD stage. Serum Na+−Cl- differences in patients with RAAS inhibitors were significantly smaller than in those with RAAS inhibitors and diuretics in CKD stages G3b (p = 0.006) and the other two groups in CKD stage G4 (vs. RAAS inhibitors and diuretics, p

A 76-year-old woman on hemodialysis (HD) for diabetic nephropathy was admitted to our hospital with occasional intradialytic hypotension (IDH). We continuously monitored the regional oxygen saturation (rSO2) in the brain, liver, and lower limb muscle during HD. The time course of changes in rSO2 ratios in each region was evaluated throughout HD. The rSO2 ratio was defined as the ratio of rSO2 value at t (min) during HD to the rSO2 value before HD. During the early phase of HD, blood pressure (BP) gradually decreased and both hepatic and lower limb muscle rSO2 ratios decreased with changes in BP, whereas the cerebral rSO2 ratio was relatively maintained. At around 90 min after HD initiation, the BP decreased to 71/46 mmHg (mean BP, 54 mmHg) and the previously maintained cerebral rSO2 ratio also suddenly decreased. Soon after the onset of IDH, ultrafiltration was stopped, normal saline was infused, and intravenous noradrenaline infusion was started. After the BP recovered, cerebral and hepatic rSO2 ratios improved, but the lower limb muscle rSO2 ratio remained low. After restarting ultrafiltration, improvement in the lower limb muscle rSO2 ratio was delayed, although cerebral and hepatic oxygenation were maintained. This observation aids in our understanding of the effect of IDH on regional tissue oxygenation.

An 88-year-old man with congenital hemophilia A developed end-stage renal disease due to microscopic polyangiitis. He was at risk for catheter-related infection because he was taking immunosuppressive agents for the treatment of polyangiitis. He was also unable to manipulate the peritoneal dialysis device. Therefore, hemodialysis using an arteriovenous fistula was induced for renal replacement therapy. Recombinant coagulation factor VIII (1000 IU) was administered via the venous chamber of the hemodialysis circuit 10 min before the end of each hemodialysis session, and nafamostat mesylate (25 mg/h) was employed as an anticoagulant during hemodialysis. His clotting factor VIII activity level increased to > 50% and activated partial thromboplastin time decreased to 50 s at the end of each hemodialysis session. This method allowed him to achieve hemostasis at the puncture site of the arteriovenous fistula and undergo stable hemodialysis with no complications, including bleeding. This case suggests that hemodialysis using an arteriovenous fistula with coagulation factor replacement and nafamostat mesylate in each hemodialysis session is a therapeutic option for end-stage renal disease in patients of advanced age with hemophilia at high risk of bleeding.

BackgroundDietary management is highly important for the maintenance of renal function in patients with chronic kidney disease (CKD). Cerebral oxygen saturation (rSO2) was reportedly associated with the estimated glomerular filtration rate (eGFR) and cognitive function. However, data concerning the association between cerebral rSO2 and dietary intake of CKD patients is limited.MethodsThis was a single-center observational study. We recruited 67 CKD patients not undergoing dialysis. Cerebral rSO2 was monitored using the INVOS 5100c oxygen saturation monitor. Energy intake was evaluated by dietitians based on 3-day meal records. Daily protein and salt intakes were calculated from 24-h urine collection.ResultsMultivariable regression analysis showed that cerebral rSO2 was independently associated with energy intake (standardized coefficient: 0.370) and serum albumin concentration (standardized coefficient: 0.236) in Model 1 using parameters with p < 0.10 in simple linear regression analysis (body mass index, Hb level, serum albumin concentration, salt and energy intake) and confounding factors (eGFR, serum sodium concentration, protein intake), and the energy/salt index (standardized coefficient: 0.343) and Hb level (standardized coefficient: 0.284) in Model 2 using energy/protein index as indicated by energy intake/protein intake and energy/salt index by energy intake/salt intake in place of salt, protein and energy intake.ConclusionsCerebral rSO2 is affected by energy intake, energy/salt index, serum albumin concentration and Hb level. Sufficient energy intake and adequate salt restriction is important to prevent deterioration of cerebral oxygenation, which might contribute to the maintenance of cognitive function in addition to the prevention of renal dysfunction in CKD patients.

Background Sleep apnea syndrome (SAS) is a sleep disturbance, which is frequently comorbid in dialysis patients. SAS induces hypoxia, and therefore, systemic and cerebral oxygenation would be low. Near-infrared spectroscopy (NIRS) has recently been used to measure regional saturation of oxygen (rSO2), as a marker of tissue oxygenation. Although cerebral rSO2 was measured in patients in various clinical settings, few reports have previously shown the associations of changes in cerebral rSO2 and systemic oxygenation using measurement of peripheral arterial oxygen saturation (SpO2) in patients undergoing hemodialysis (HD) with SAS. We herein report a first HD case with SAS-induced reduction in cerebral oxygenation during sleep. Case presentation A 74-year-old woman underwent HD therapy for 1 month, because of advanced CKD caused by hypertension and obesity. In addition, she was diagnosed with obstructive sleep apnea with polysomnography about 4 years prior. Her apnea-hypopnea index (AHI) was 77.5 per hour, and therefore, continuous positive airway pressure (CPAP) was started. Thereafter, her AHI was improved to 3 to 6 per hour. However, she discontinued CPAP therapy at HD initiation. Since her oxygenation without CPAP would deteriorate, we evaluated her SpO2 and cerebral rSO2 by NIRS monitoring during sleep. We confirmed the deterioration in cerebral rSO2 according to the SpO2 decrease, and furthermore, the improvement in cerebral rSO2 was apparently delayed even after the improvement in her SpO2. The patient’s cerebral oxygenation under CPAP therapy could not be evaluated because she refused to receive CPAP therapy after HD initiation. Therefore, as a comparison, we evaluated a 69-year-old male HD patient without SAS and found that in contrast to a patient with SAS, his SpO2 and cerebral rSO2 were maintained throughout sleep. Conclusion We observed deterioration in cerebral oxygenation during sleep in addition to a decrease in systemic oxygenation in a patient with SAS undergoing HD. Real-time cerebral NIRS monitoring during sleep might be a useful method for detection of SAS.

Rationale Herein, we report 3 hemodialysis patients with idiopathic hypereosinophilic syndrome who were successfully treated using corticosteroid therapy. Patient concerns Case 1 was a 63-year-old man who was undergoing hemodialysis because of bilateral nephrectomy and developed hypereosinophilia with digestive symptoms, myocardial injury, and intradialytic hypotension. Case 2 was an 83-year-old man who was undergoing hemodialysis because of nephrosclerosis and developed hypereosinophilia with pruritus, myocardial injury, and intradialytic hypotension. Case 3 was a 59-year-old man who was undergoing hemodialysis because of diabetic nephropathy and developed hypereosinophilia with pruritus, myocardial injury, and intradialytic hypotension. Diagnoses All 3 patients presented with hypereosinophilia (eosinophil count ≥1500 /μL for more than 1 month) and multiple-organ involvement (intradialytic hypotension, cardiac injury, digestive symptoms, and allergic dermatitis). A specific cause for the hypereosinophilia was not identified by systemic computed tomography, electrocardiography, echocardiography, bone marrow examination, or blood tests. Furthermore, Case 2 and 3 had not recently started taking any new drugs and drug-induced lymphocyte stimulation tests were negative in Case 1. Therefore, they were diagnosed with idiopathic hypereosinophilic syndrome. Interventions All 3 patients received corticosteroid therapy with prednisolone at a dose of 40 mg/d, 30 mg/d, and 60 mg/d in Case 1, 2, and 3, respectively. Outcomes Their digestive symptoms, pruritus, intradialytic hypotension, and serum troponin I concentrations were immediately improved alongside reductions in their eosinophil counts. Lessons There have been few case reports of idiopathic hypereosinophilic syndrome in patients undergoing hemodialysis. We believe that recording of the clinical findings and treatments of such patients is mandatory to establish the optimal management of idiopathic hypereosinophilic syndrome.

Background: Hyperkalemia is one of the more serious complications of chronic kidney disease (CKD), and the cause of potassium retention is a reduction in urinary potassium excretion. However, few studies have examined the extent of the decrease of urinary potassium excretion in detail with respect to decreased renal function. Methods: Nine hundred eighty-nine patients with CKD (CKD stages G1 and G2 combined: 135; G3a: 107; G3b: 170; G4: 289; and G5: 288) were evaluated retrospectively. Values for urinary potassium excretion were compared between CKD stages, and the associations between urinary potassium excretion and clinical parameters, including diabetes mellitus status and use of renin–angiotensin–aldosterone system inhibitors, were analyzed using a multivariable linear regression analysis. Results: Urinary potassium excretion gradually decreased with worsening of CKD (G5: 24.8 ± 0.8 mEq/d, P

Intradialytic exercise-induced blood volume (BV) reduction may cause intradialytic hypotension in hemodialysis (HD) patients. However, BV recovery time after intradialytic exercise remains unknown. Hemodialysis patients were recruited, and their relative BV change (%ΔBV) were measured with intradialytic exercise (n = 12). After confirming the linearity of %ΔBV for 30 min, patients exercised using a stationary cycle in the supine position. The target exercise intensity was a 10% increase in heart rate (HR), corresponding to relatively low-intensity exercise. Baseline %ΔBV (assumed baseline) were calculated for the 30 min before exercise using linear regression analysis. The mean intradialytic exercise start and end times after HD initiation were 93.0 ± 8.4 and 116.4 ± 8.3 min, respectively, a mean exercise duration of 23.5 ± 2.6 min. Percentage change in blood volume declined rapidly upon exercise initiation and gradually increased above the assumed baseline throughout HD. At the end of HD, %ΔBV in the exercise group was significantly higher than the assumed baseline (measured - assumed baseline %ΔBV: 2.17 ± 0.62%; p = 0.02). Intradialytic exercise with low intensity in the supine position attenuated ultrafiltration-induced BV reduction at the end of HD. Therefore, intradialytic exercise may prevent intradialytic hypotension during later HD, although its intensity was relatively low level.

The following conventional calcium correction formula (Payne) is broadly applied for serum calcium estimation: corrected total calcium (TCa) (mg/dL) = TCa (mg/dL) + (4 - albumin (g/dL)); however, it is inapplicable to chronic kidney disease (CKD) patients. A total of 2503 venous samples were collected from 942 all-stage CKD patients, and levels of TCa (mg/dL), ionized calcium ([iCa(2+) ] mmol/L), phosphate (mg/dL), albumin (g/dL), and pH, and other clinical parameters were measured. We assumed corrected TCa (the gold standard) to be equal to eight times the iCa(2+) value (measured corrected TCa). Then, we performed stepwise multiple linear regression analysis by using the clinical parameters and derived a simple formula for corrected TCa approximation. The following formula was devised from multiple linear regression analysis: Approximated corrected TCa (mg/dL) = TCa + 0.25 × (4 - albumin) + 4 × (7.4 - p H) + 0.1 × (6 - phosphate) + 0.3. Receiver operating characteristic curves analysis illustrated that area under the curve of approximated corrected TCa for detection of measured corrected TCa ≥ 8.4 mg/dL and ≤ 10.4 mg/dL were 0.994 and 0.919, respectively. The intraclass correlation coefficient demonstrated superior agreement using this new formula compared to other formulas (new formula: 0.826, Payne: 0.537, Jain: 0.312, Portale: 0.582, Ferrari: 0.362). In CKD patients, TCa correction should include not only albumin but also pH and phosphate. The approximated corrected TCa from this formula demonstrates superior agreement with the measured corrected TCa in comparison to other formulas.

Hemoglobin (Hb) is associated with cerebral oxygenation status owing to its important role of carrying oxygen to systemic tissues. However, data concerning the associations between Hb levels and cerebral regional oxygen saturation (rSO2) of hemodialysis (HD) patients is limited. We aimed to identify these associations to consider a target Hb level for renal anemia management. This study included 375 HD patients. Cerebral rSO2 before HD was monitored using the INVOS 5100c oxygen saturation monitor. Multivariable linear regression analysis showed that cerebral rSO2 was independently associated with natural logarithm (Ln)-HD duration (standardized coefficient: -0.36), mean blood pressure (standardized coefficient: 0.13), pH (standardized coefficient: -0.10), serum albumin (standardized coefficient: 0.14), presence of diabetes mellitus (standardized coefficient: -0.20), and Hb level (standardized coefficient: 0.29). Furthermore, a generalized linear model with restricted cubic spline function was used to investigate the non-linear association between cerebral rSO2 and Hb levels. In the multivariable analysis for the adjustment with Ln-HD duration, mean blood pressure, pH, serum albumin, and presence of diabetes mellitus, a linear relationship was demonstrated between the two variables (p for linearity = 0.79). Hb levels revealed the positive and significant association with cerebral rSO2 in this study. Moreover, the relationship between cerebral rSO2 and Hb level was proven to be linear. Therefore, the target Hb level in renal anemia management would be considered to be the upper limits for the appropriate management of renal anemia by previous guidelines and position statement from the viewpoint of maintaining cerebral oxygenation in HD patients.

Introduction The use of warfarin in patients undergoing hemodialysis is associated with decreased bone mineral density and an increased incidence of bone fracture. However, no studies to date have directly estimated bone quality with bone histomorphometry in patients with bone abnormalities who are taking warfarin and undergoing hemodialysis. Patient concerns A 47-year-old female with Noonan syndrome presented with progressive bilateral lower extremity pain on walking, and skin sclerosis. She had been undergoing maintenance hemodialysis for 25 years following 2 years of peritoneal dialysis for chronic glomerulonephritis. She had been taking warfarin as an anticoagulant agent for 13 years after she underwent an aortic valve replacement. Diagnosis Warfarin-induced impairment of bone material quality. Interventions and outcomes Histomorphometric analysis of the bone biopsy specimens showed impairment in bone calcification processes, a high turnover of bone remodeling, low bone volume, and mild fibrosis. The bone abnormality could not be categorized into any type of representative bone disease classification such as osteitis fibrosa, osteomalacia, adynamic bone disease, uremic osteodystrophy, or hyperparathyroidism, but was consistent with warfarin-induced impairment of bone material quality. Conclusion Warfarin can induce impairment of bone material quality in a patient undergoing hemodialysis.

Background A decline in estimated glomerular filtration rate (eGFR) is reportedly associated with increased prevalence rates of cognitive impairment. However, data concerning the association between the cerebral saturation of oxygen (rSO2) and cognitive function of patients with chronic kidney disease (CKD) is limited. This study aimed to (i) elucidate the clinical factors associating with cerebral rSO2 and (ii) investigate the association between cerebral rSO2 and cognitive assessment in CKD patients. Methods A total of 40 CKD patients not requiring dialysis (26 men and 14 women; mean age, 61.0 ± 2.7 years) were recruited. The numbers of patients at each CKD stage were as follows: G1, 5; G2, 8; G3a, 6; G3b, 5; G4, 11; and G5, 5. Cerebral rSO2 was monitored at the forehead using the oxygen saturation monitor INVOS 5100C. The cognitive function of each patient was confirmed using the Mini-Mental State Examination (MMSE). Results Cerebral rSO2 levels were significantly higher in CKD patients than in hemodialysis patients (63.8 ± 1.5% vs. 44.9 ± 2.2%, p < 0.001). Multiple regression analysis showed that cerebral rSO2 was independently associated with eGFR (standardized coefficient: 0.530), serum albumin concentration (standardized coefficient: 0.365), and serum sodium concentration (standardized coefficient: 0.224). Furthermore, MMSE showed a significantly positive correlation with cerebral rSO2 (r = 0.624, p < 0.001). Conclusions Cerebral rSO2 was affected by eGFR and serum albumin and sodium concentrations in CKD patients. Furthermore, cerebral rSO2 monitoring, which reflected MMSE scores, might be a useful method for assessing cognitive function in CKD patients.

Objectives: Dulaglutide and liraglutide are glucagon-like peptide-1 receptor agonists. We investigated the effects of once-weekly dulaglutide on glycemic control and renal function compared to once-daily liraglutide in patients with advanced-stage diabetic nephropathy. Methods: Changes over a 12-month period in levels of glycated hemoglobin, urine protein/creatinine ratio, and annual change in estimated glomerular filtration rate were retrospectively analyzed in 10 patients with advanced-stage diabetic nephropathy after changing from once-daily liraglutide (0.9 mg/day) to once-weekly dulaglutide (0.75 mg/week) (dulaglutide group). The control group comprised 10 patients with advanced-stage diabetic nephropathy who had continued once-daily liraglutide (0.9 mg/day) (liraglutide group). Results: The glycated hemoglobin level significantly decreased in the dulaglutide group after switching from liraglutide to dulaglutide (-0.81 ± 1.03% at 12 months from baseline, P < 0.05), but no change occurred in the liraglutide group. The urine protein/creatinine ratio and annual change in estimated glomerular filtration rate did not change in either groups. Conclusions: Once-weekly dulaglutide may be more advantageous for glycemic control compared to once-daily liraglutide in patients with advanced-stage diabetic nephropathy.

Background: Chronic inflammation of the peritoneum causes peritoneal injury in patients on peritoneal dialysis. Intercellular adhesion molecule-1 and its circulating form, soluble intercellular adhesion molecule-1, play pivotal roles in inflammation. However, their role in peritoneal injury is unclear. Methods: We measured changes in intercellular adhesion molecule-1 expression in the peritoneum of a peritoneal injury model in rats. The associations between soluble intercellular adhesion molecule-1 levels in drained dialysate and the solute transport rate (D/P-Cr and D/D0-glucose) determined by the peritoneal equilibration test, and matrix metalloproteinase-2 levels in drained dialysate were investigated in 94 peritoneal drained dialysate samples. Results: Intercellular adhesion molecule-1 expression was increased in the peritoneum of rats with peritoneal injury. Soluble intercellular adhesion molecule-1 levels in drained dialysate were significantly positively correlated with D/P-Cr (r = .51, p

Renal fibrosis is the final common pathway leading to end-stage renal failure regardless of underlying initial nephropathies. No specific therapy has been established for renal fibrosis. Gene therapy is a promising strategy for the treatment of renal fibrosis. Nano-sized carriers including viral vectors and non-viral vectors have been shown to enhance the delivery and treatment effects of gene therapy for renal fibrosis in vivo. This review focuses on the mechanisms of renal fibrosis and the in vivo technologies and methodologies of nano-sized carriers in gene therapy for renal fibrosis. RESPONSIBLE EDITOR Alexander Seifalian Director of Nanotechnology & Regenerative Medicine Ltd., The London BioScience Innovation Centre, London, UNITED KINGDOM

A 54-year-old Japanese man noticed painful swelling and redness of his left leg. He was admitted for treatment of cellulitis, which was accompanied with increased anti-streptolysin O and anti-streptokinase titers in his clinical course. After Piperacillin/Tazobactam administration, the skin lesion resolved. However, the patient then developed arthritis, palpable purpura, and intermittent abdominal pain, later found to be secondary to a severe duodenal ulcer. He was diagnosed with cellulitis-associated anaphylactoid purpura and was given prednisolone, which dramatically improved his symptoms. The anaphylactoid purpura was likely caused by Streptococcus-induced cellulitis, which was successfully treated with prednisolone. Association between these diseases is rare.