Hepatic Oxygenation Changes and Symptomatic Intradialytic Hypotension.

INTRODUCTION: Clinical studies on differences among changes in cerebral and hepatic oxygenation during hemodialysis (HD) in patients with and without intradialytic hypotension (IDH) are limited. We investigated changes in intradialytic cerebral and hepatic oxygenation before systolic blood pressure (SBP) reached the nadir during HD and compared these differences between patients with and without symptomatic IDH. METHODS: We analyzed data from 109 patients with (n = 23) and without (n = 86) symptomatic IDH who were treated with HD. Cerebral and hepatic regional oxygen saturation (rSO2), as a marker of tissue oxygenation and circulation, was monitored during HD using an INVOS 5100c oxygen saturation monitor. Changes in cerebral or hepatic rSO2 when SBP reached the nadir during HD were compared between the groups of patients. RESULTS: The cerebral rSO2 before HD in patients with and without symptomatic IDH was 49.7 ± 11.2% and 51.3 ± 9.1% (p = 0.491). %Changes in cerebral rSO2 did not significantly differ between the two groups from 60 min before the SBP nadir during HD. Hepatic rSO2 before HD in patients with and without symptomatic IDH was 58.5 ± 15.4% and 57.8 ± 15.9% (p = 0.869). The %changes in hepatic rSO2 were significantly lower in patients with symptomatic IDH than in those without throughout the observational period (p < 0.001). We calculated the area under the receiver operating characteristic curve (AUC) and estimated cutoff values for changes in hepatic rSO2 as a symptomatic IDH predictor. The predictive ability at 5 and 40 min before symptomatic IDH onset was excellent, with AUCs and cutoff values of 0.847 and 0.841, and -10.9% and -5.0%, respectively. CONCLUSIONS: Hepatic oxygenation significantly decreased more in patients with symptomatic IDH before its onset, than in those without symptomatic IDH, whereas changes in cerebral oxygenation did not differ. Evaluating changes in hepatic oxygenation during HD might help to predict symptomatic IDH.

Steroid-resistant minimal change nephrotic syndrome associated with thymoma treated effectively with rituximab following thymectomy and cyclosporine: a case report.

BACKGROUND: Minimal change nephrotic syndrome (MCNS) can be complicated by thymoma; however, no standard therapy for thymoma-associated MCNS has yet been established. We herein describe a case of steroid-resistant MCNS associated with thymoma, treated effectively with rituximab. CASE PRESENTATION: A 71-year-old Japanese man was referred to our department with severe proteinuria (20 g/gCr). Renal biopsy showed minimal change disease and computed tomography revealed an anterior mediastinal mass. Based on these findings, he was diagnosed with thymoma-associated MCNS. He was treated with oral prednisolone (50 mg/day) and cyclosporine, and underwent thymectomy and plasma exchange. However, no improvement in proteinuria was observed. He therefore received intravenous rituximab 500 mg, resulting in a marked decrease in proteinuria from 5328 to 336 mg/day after 1 week. CONCLUSIONS: This case suggests that rituximab might be an effective therapy in patients with steroid-resistant MCNS associated with thymoma.

Cerebral oxygenation changes in response to post-hemodialysis standing.

Few reports have examined the association between changes in cerebral oxygenation and clinical factors, including blood pressure (BP), upon standing after hemodialysis (HD). This study aimed to clarify the factors affecting the changes in cerebral regional oxygen saturation (rSO2) upon standing after HD and monitor the differences in cerebral rSO2 changes that occur upon standing after HD in patients with and without diabetes mellitus (DM). Changes in mean BP and cerebral rSO2 were tracked in 43 HD patients during 120 s of standing after HD using an INVOS 5100c oxygen saturation monitor. The post-HD cerebral rSO2 at rest was 55.8 ± 10.2%, while that at 120 s of standing decreased to 51.9 ± 9.6%; therefore, the percentage change in cerebral rSO2 at 120 s of standing was - 6.8 ± 6.4%, which was significantly lower than before HD (p < 0.001). This change was significantly correlated with the presence of DM, HD duration, mean BP at 120 s of standing, and percentage change in mean BP at 120 s of standing. A multivariable linear regression analysis showed that percentage change in cerebral rSO2 at 120 s of standing was independently associated with the percentage change in mean BP at 120 s of standing (standardized coefficient: 0.432; p = 0.004). Furthermore, there were significant decreases in percentage changes in cerebral rSO2 throughout the standing period in HD patients with versus without DM. Therefore, cerebral oxygenation deterioration upon standing after HD should receive attention, particularly in HD patients with DM.

Changes in tissue oxygenation in response to sudden intradialytic hypotension.

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.

Continuous monitoring of changes in cerebral oxygenation during hemodialysis in a patient with acute congestive heart failure.

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.

Successful treatment of cholesterol crystal embolism with anti-proprotein convertase subtilisin/kexin type 9 (PCSK9) antibody: a case report.

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.

Association between carnitine deficiency and the erythropoietin resistance index in patients undergoing peritoneal dialysis: a cross-sectional observational study.

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 (ß = 0.283, p = 0.04). These results suggest that carnitine plays pivotal roles in hematogenesis in patients undergoing PD.

Differences in cerebral and hepatic oxygenation in response to intradialytic blood transfusion in patients undergoing hemodialysis.

Hemodialysis (HD) patients frequently experience severe anemia, requiring intradialytic blood transfusion. Severe anemia leads to deterioration of systemic tissue oxygenation. However, few reports have examined the effect of intradialytic blood transfusion on tissue oxygenation changes. This study aimed to (i) monitor the differences in tissue oxygenation in the brain and liver during intradialytic blood transfusion, and (ii) elucidate the clinical factors affecting cerebral and hepatic oxygenation. Thirty-eight HD patients with severe anemia requiring intradialytic blood transfusion were included (27 men, 11 women; mean age, 70.2 ± 1.6 years). Cerebral and hepatic regional oxygen saturation (rSO2) values were monitored using near-infrared spectroscopy (INVOS 5100c oxygen saturation monitor). Cerebral and hepatic rSO2 were significantly higher after than before blood transfusion (p < 0.001, both). Furthermore, hepatic rSO2 was significantly higher than cerebral rSO2 after transfusion (p = 0.004). In multivariable linear regression analysis, cerebral rSO2 changes were independently associated with the natural logarithm of hemoglobin (Hb) ratio (Hb after/before transfusion) (standardized coefficient: 0.367, p = 0.023), whereas hepatic rSO2 changes were independently associated with the natural logarithm of [Hb ratio/colloid osmotic pressure ratio (colloid osmotic pressure after/before transfusion)] (standardized coefficient: 0.378, p = 0.019). In conclusion, throughout intradialytic blood transfusion, brain and liver tissue oxygenation improved. Hepatic rSO2 was significantly higher than cerebral rSO2 at the end of HD. Furthermore, cerebral oxygenation changes were associated with only transfusion-induced Hb increase, whereas hepatic oxygenation changes were associated with both transfusion-induced Hb increase (positive changes) and ultrafiltration-induced colloid osmotic pressure increase (negative changes).

Differences in tissue oxygenation and changes in total hemoglobin signal strength in the brain, liver, and lower-limb muscle during hemodialysis.

Near-infrared spectroscopy has been used to measure regional saturation of oxygen (rSO2) based on the total hemoglobin (t-Hb) signal strength. To date, few studies have investigated the changes of systemic oxygenation and t-Hb signal strength during hemodialysis (HD). This study aimed to (1) monitor rSO2 and t-Hb signal strength in the brain, liver, and lower-limb muscle during HD and (2) clarify the differences in rSO2 and t-Hb signal strength in each compartment. Fifty-three patients receiving 4-h HD were included and divided into three groups according to the compartments in which tissue oxygenation was measured as follows: brain (n = 44), liver (n = 42), and lower-limb muscle (n = 40). The rSO2 and t-Hb signal strength was monitored using an INVOS 5100c (Covidien Japan, Tokyo, Japan). The rSO2 levels were significantly lower in the brain than in the liver from HD initiation to the end (HD initiation: rSO2 in the brain and liver, 46.5 ± 1.3 and 52.4 ± 1.7%, respectively, p = 0.031). Furthermore, compared to the t-Hb signal strength ratio [value at t (min) during HD/initial value before HD] in the brain during HD, there were significant increases in the liver and lower-limb muscle, respectively. In conclusion, deterioration of cerebral oxygenation was remarkable compared to the hepatic oxygenation in HD patients. Our results, which revealed significant differences among the t-Hb signal strength ratios in the brain, liver, and lower-limb muscle during HD, might reflect the non-uniform body-fluid reduction within systemic tissues induced by ultrafiltration.

Glucose and GTP-binding protein-coupled receptor cooperatively regulate transient receptor potential-channels to stimulate insulin secretion [Review].

In pancreatic ß-cells, glucose-induced closure of the ATP-sensitive K+ (KATP) channel is an initial process triggering glucose-stimulated insulin secretion (GSIS). This KATP-channel dependent pathway has been believed to be a central mechanism for GSIS. However, since the resting membrane potential of cells is determined by the balance of the net result of current amplitudes in outward and inward directions, it must be taken into consideration that not only KATP channel inhibition but also inward current via the basal opening of non-selective cation channels (NSCCs) plays a crucial role in membrane potential regulation. The basal activity of NSCCs is essential to effectively evoke depolarization in concert with KATP channel closure that is dependent on glucose metabolism. The present study summarizes recent findings regarding the roles of NSCCs in GSIS and GTP-binding protein coupled receptor-(GPCR) operated potentiation of GSIS.

[A case of rapidly progressive glomerulonephritis exhibiting granulomatosis with polyangiitis (GPA) and extremely high level of PR3-ANCA with improvement of renal dysfunction after plasma exchange therapy].

A 68-year-old Japanese man was diagnosed with left otitis media with effusion and left uveitis more than 5 months before admission. He was urgently admitted to our hospital for progressive deterioration of his renal function [serum creatinine(Cr) 7.59 mg/dL] with proteinuria and urinary red blood cell casts, inflammation, and anemia. Additionally, his serum proteinase 3 antinuclear antibody (PR3-ANCA) level, determined by using the chemiluminescence enzyme immunoassay method, had increased to more than 3,500 U/mL. Hemodialysis (HD) was initiated on the third day after admission and renal biopsy was performed on the eighth day. The histological findings showed necrotic cellar crescents, hence, he was diagnosed as granulomatosis with polyangiitis on the basis of the clinical criteria. Methylprednisolone pulse therapy was administered from the 11th day. Thereafter, the administration of oral prednisolone (PSL) was started, and plasma exchange was initiated for the purpose of RP3-ANCA removal. In his clinical course, PSL was tapered as soon as possible because of the development of steroid psychosis, and we started intravenous cyclophosphamide on the 25th day instead of tapering the PSL. Subsequently, his renal function improved even without HD, and he was discharged on the 49th day. Although his PR3-ANCA level was still high after discharge, the administration of azathioprine led to a decrease in the PR-3 ANCA levels. About 2 years after discharge, the PR3-ANCA level decreased to 10.0 U/mL, and there has been no sign of GPA recurrence.

Factors affecting the progression of renal dysfunction and the importance of salt restriction in patients with type 2 diabetic kidney disease.

BACKGROUND: Type 2 diabetic kidney disease (DKD) is the most common cause of end-stage renal failure, and the prevention of its progression has been a topic of discussion. METHODS: Sixty type 2 DKD patients were retrospectively evaluated for 1 year. Factors independently affecting the annual Ccr decline were examined by multivariable linear regression analysis. Patients were further divided into 2 groups based on their degree of renal function, and between-group differences at study initiation were evaluated. RESULTS: Ccr values were 21.0 ± 11.8 mL/min/1.73 m(2) at study initiation, and 15.7 ± 10.9 mL/min/1.73 m(2) after 1 year of observation. The multivariable linear regression analysis indicated salt intake (standardized coefficient: -0.34, P = 0.010) and urinary protein excretion (standardized coefficient: -0.33, P = 0.011) to be factors independently affecting the annual Ccr decline. Although decliners (-9.8 ± 4.7 mL/min/1.73 m(2)/year) had a significantly higher salt intake than non-decliners (-1.1 ± 3.8 mL/min/1.73 m(2)/year) at study initiation, this difference disappeared at the end of the study as a result of intensive dietary education. In 21 decliners with an additional year of follow-up, the annual Ccr decline significantly improved from -10.1 ± 5.3 to -5.3 ± 7.4 mL/min/1.73 m(2)/year (P = 0.02). CONCLUSION: Salt intake and urinary protein excretion were associated with annual Ccr decline in type 2 DKD patients. Furthermore, dietary education covering salt intake may have positively affected the change in Ccr.

Renoprotective effects of thiazides combined with loop diuretics in patients with type 2 diabetic kidney disease.

BACKGROUND/AIMS: Type 2 diabetic kidney disease (DKD) is frequently accompanied by uncontrollable hypertension due to the sodium sensitivity inherent in DKD and to diuretic-resistant edema. In general, diuretics are effective in treating this condition, but thiazide diuretics are thought to be innocuous in advanced chronic kidney disease (CKD). We examined the renoprotective effects of combination therapy with thiazides and loop diuretics in type 2 DKD patients with CKD stage G4 or G5. METHODS: This study included 11 patients with type 2 DKD and an estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m(2) who were suffering from severe edema even with loop diuretics. Each patient received additional hydrochlorothiazide (HCTZ) therapy, which was continued for more than 12 months. We examined clinical parameters including blood pressure (BP), proteinuria, and eGFR before and after the addition of HCTZ. RESULTS: Patients received a 13.6 ± 3.8 mg/day dose of HCTZ in addition to loop diuretics (azosemide: 120 mg/day in 6 cases, 60 mg/day in 3 cases and furosemide: 80 mg/day in 1 case, 120 mg/day in 1 case). Side effects of HCTZ were not observed in all patients. After the addition of HCTZ therapy, systolic and diastolic blood pressures (S-BP, D-BP) as well as proteinuria significantly decreased (S-BP: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month, D-BP: at 12 months, p < 0.05 vs. 0 month, proteinuria: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month). The annual decline in eGFR was not significantly different before and after HCTZ therapy (-7.7 ± 8.5 and -8.4 ± 4.8 mL/min/1.73 m(2)/year, respectively). CONCLUSION: Our findings suggest that the combination of HCTZ and loop diuretics improves BP levels, and decreases proteinuria even in advanced stage type 2 DKD patients with severe edema. The addition of HCTZ therapy was not found to negatively affect the change in eGFR in the present study.

Low-density lipoprotein apheresis ameliorates monthly estimated glomerular filtration rate declines in patients with renal cholesterol crystal embolism.

The incidence of cholesterol crystal embolism (CCE) has increased along with increases in the prevalence of atheromatous diseases and intravascular procedures. CCE frequently results in the deterioration of renal function, which sometimes leads to end-stage renal failure. Although there has been no established therapy for CCE, the possibility that low-density lipoprotein apheresis (LDL-A) is an effective therapy for renal CCE was previously reported. However, whether LDL-A improves renal CCE remains uncertain. This study aimed to evaluate the effectiveness of LDL-A in renal CCE patients. Twelve renal CCE patients (9 men and 3 women, mean age 70.6 ± 1.7 years) were included in this retrospective study. All patients had received LDL-A therapy, and estimated glomerular filtration rate (eGFR) values were examined before and after LDL-A. In addition, monthly changes in eGFR before and after LDL-A were calculated for each patient. At initial diagnosis of renal CCE, the eGFR was 35.2 ± 4.8 mL/min/1.73 m(2). At the initiation of LDL-A, the eGFR significantly decreased to 11.0 ± 1.2 mL/min/1.73 m(2), and monthly changes in eGFR reached -7.2 ± 2.5 mL/min/1.73 m(2)/month. After the initiation of LDL-A, the progression of renal dysfunction stabilized in nearly two-thirds of patients, and monthly changes in eGFR after LDL-A significantly diminished to -0.3 ± 0.7 mL/min/1.73 m(2)/month (p < 0.05 vs. before LDL-A). Although 4 patients had to undergo hemodialysis, all patients were alive over 1 year after the initiation of LDL-A. LDL-A therapy ameliorated renal dysfunction in renal CCE patients.

Evaluation of cerebral oxygenation in patients undergoing long-term hemodialysis.

BACKGROUND/AIMS: Patients undergoing hemodialysis (HD) have higher occurrence rates of cerebral diseases, including uremic encephalopathy, cognitive impairment, dementia, and cerebrovascular disease, than the general population. During HD, ultrafiltration is performed to maintain an adequate fluid condition and is associated with subsequent blood volume (BV) reduction. We aimed to (1) monitor changes in cerebral oxygenation and BV reduction during HD, and (2) clarify the mechanism that influences cerebral oxygenation in HD patients. METHODS: Eighteen HD patients and 12 healthy controls were recruited. Regional saturation of oxygen (rSO2) was continuously monitored in the frontal cortex using INVOS 5100C before, during, and after HD, and in healthy controls. Relative change in BV (%ΔBV) was simultaneously monitored during HD using a BV monitor. RESULTS: Before HD, patients had significantly lower rSO2 values than controls (56.1 ± 1.4 vs. 70.4 ± 2.5%, p < 0.001). Although %ΔBV significantly decreased from 20 min to the end of HD (20 min: -3.3 ± 0.3%, p < 0.05; end of HD: -12.0 ± 1.0%, p < 0.01), changes in rSO2 values during HD were not significant. No relationship existed between rSO2 values and blood pressure levels, hemoglobin levels, oxygen pressure, HCO3(- ), oxygen saturation, and arterial O2 content before and after HD. Furthermore, changes in rSO2 were not correlated with changes in these parameters. CONCLUSION: rSO2 values before HD were significantly lower in HD patients than in healthy controls. rSO2 values were maintained during HD and were not influenced by BV reduction.

Factors Affecting Psoas Muscle Mass Index in Patients Undergoing Peritoneal Dialysis.

INTRODUCTION: Many patients with chronic kidney disease (CKD), including peritoneal dialysis (PD), have sarcopenia. It is important to evaluate muscle mass to prevent sarcopenia in the field of CKD management. Recently, muscle mass assessment using psoas muscle evaluated by computed tomography (CT) has been reported in patients undergoing hemodialysis. However, few clinical studies have investigated the clinical factors associated with the evaluation of psoas muscle in patients undergoing PD. METHODS: Psoas muscle mass index (PMI) was measured in cross-sectional areas of the bilateral psoas muscles at the third lumbar spine level to evaluate psoas muscle status. The associations between PMI and possible clinical factors were investigated in 68 patients undergoing PD. RESULTS: The mean PMI was 6.3 ± 2.0 cm2/m2, and the PMI was higher in men than in women (p < 0.001). In a multivariable linear regression analysis of the factors associated with PMI, male gender (standardized coefficient: 0.331), body mass index (standardized coefficient: 0.283), serum creatinine concentration (standardized coefficient: 0.289), serum albumin concentration (standardized coefficient: 0.235), and the use of vitamin D (standardized coefficient: 0.195) were independently identified. CONCLUSION: PMI was independently and significantly associated with gender, BMI, serum creatinine concentration, serum albumin concentration and the use of vitamin D. Further prospective studies are needed to clarify whether the maintenance of nutritional status or vitamin D administration could affect muscle mass in patients undergoing PD.

Effects to cerebral oxygenation by arteriovenous fistula creation in patients with chronic kidney disease.

BACKGROUND: Vascular access, including arteriovenous fistula (AVF), is essential in patients undergoing hemodialysis (HD). However, the presence of AVF is non-physiological in humans and could pose a burden to the systemic circulation or tissue microcirculation, potentially affecting tissue oxygenation, including in the brain. Recently, near-infrared spectroscopy has been used to measure regional oxygen saturation (rSO2) as a marker of cerebral oxygenation in various settings, including in patients undergoing HD. Thus far, no studies have reported changes in cerebral rSO2 before and after AVF creation. This study aimed to monitor the differences in cerebral oxygenation before and after AVF creation and to clarify the clinical factors affecting the changes in cerebral rSO2. METHODS: Forty-eight patients (34 men, 14 women) with chronic kidney disease (CKD) who were not undergoing dialysis and newly created AVF were recruited. Cerebral rSO2 values before and after AVF creation were evaluated using near-infrared spectroscopy (INVOS 5100c). RESULTS: Cerebral rSO2 values were significantly changed from 60.3% ± 7.5% to 58.4% ± 6.8% before and after AVF creation in all patients (p < 0.001). Cerebral rSO2 were also lower in patients with diabetes mellitus (DM) than in those without DM (57.5 ± 7.1 vs 63.7 ± 6.5, p = 0.003) before surgery; however, no differences of changes in cerebral rSO2 were observed between the two groups after AVF creation. Additionally, multivariate regression analysis identified changes in HR (standardized coefficient: 0.436) as independent factors associated with changes in cerebral rSO2. CONCLUSION: Surgically created AVF was associated with the deterioration of cerebral rSO2 in patients with CKD not undergoing dialysis. Notably, AVF could cause cerebral hypoxia, and thus further studies are needed to clarify the clinical factors influencing changes in cerebral oxygenation after AVF creation.