Acute Kidney Injury in Patients with Acute Coronary Syndrome after Percutaneous Coronary Intervention: Pathophysiologies, Risk Factors, and Preventive Measures.

BACKGROUND: Percutaneous coronary intervention (PCI) has been an effective treatment for acute coronary syndrome (ACS) patients. Acute kidney injury (AKI) is one of the common complications after PCI, which seriously affects the living quality and survival time of patients. The approach followed for the patient with AKI after PCI depends on the clinical context and may vary by resource availability. SUMMARY: This review focuses on the pathophysiologies, influencing factors, and preventive measures of AKI in patients with ACS after PCI. The knowledge may better serve the patients and improve their outcomes. Key Messages: Many studies have been carried out for the definition and standard of AKI in the past few years. Etiologies of AKI after PCI included renal damage of contrast medium and atherosclerotic embolism, cardiac insufficiency and surgical factors on renal function. Basic conditions, treatment modalities, and perioperative changes are major risk factors of AKI. Studies have reported that the prevention of contrast-induced nephropathy, modulating the volume overload, some pharmaceuticals and blood purification treatment are helpful to prevent the occurrence of AKI.

Roxadustat for dialysis patients with erythropoietin hypo-responsiveness: a single-center, prospective investigation.

Dialysis patients with erythropoietin hypo-responsiveness suffered from refractory anemia. Roxadustat reversibly binds and inhibits hypoxia-inducible factor-prolyl hydroxylase (HIF-PHD), resulting in increased endogenous EPO which stimulates erythropoiesis, theoretically has an advantage over exogenous EPO in anti-anemia therapy. From September 2019 to October 2020, 32 dialysis patients with hypo-responsiveness to erythropoietin were evaluated. During the 24-week follow-up period, all patients were taken off erythropoietin and switched to roxadustat. Dosage adjustments were administrated according to the fluctuation of hemoglobin level during the treatment. Parameters about anemia, iron metabolism and biochemical indexes were collected, and adverse events were recorded. A total of 31 patients completed the clinical observation, with varying degrees of malnutrition-inflammation. Post treatment, the levels of transferrin and total iron-binding capacity were increased, while that of transferrin saturation and cholesterol decreased. 15 cases (accounting for 48.39%, designated as fulfilled group) met the target level of hemoglobin, while 16 cases (51.61%, non-fulfilled group) did not. The baseline conditions of the above two groups were compared. The levels of hypersensitive C-reactive protein, interleukin-6 and serum ferritin in the non-fulfilled group were higher than those in the fulfilled group, and the levels of residual renal function, serum albumin, iron, transferrin and total iron-binding capacity were lower than those in the fulfilled group. Linear regression analysis showed that increase of HsCRP had a negative effect on the improvement of Hb. One case of adverse reaction grade 3 and four cases of grade 2 occurred throughout the study, yet all were relieved after therapy. Significant anti-anemia effects could be achieved in most patients with erythropoietin hypo-responsiveness after treatment with roxadustat, accompanied by relatively mild and rare adverse reactions. The malnutrition-inflammation states of patients may interfere with the anti-anemia effect of roxadustat, and iron utilization is more important than iron storage in anemia improvement.

The role of mitofilin in left ventricular hypertrophy in hemodialysis patients.

Left ventricular hypertrophy (LVH) is a common abnormality in hemodialysis (HD) patients. Mitochondrial dysfunction contributes to the progression of LVH. As an inner mitochondrial membrane structural protein, mitofilin plays a key role in maintaining mitochondrial structure and function. The aim of this study was to investigate the relationship between mitofilin and LVH in HD patients. A total of 98 HD patients and 32 healthy controls were included in the study. Serum N-terminal proBNP (NT-proBNP), endothelin-1 (ET-1), and atrial natriuretic peptide (ANP) were examined. The protein level of mitofilin and the mitochondrial DNA (mtDNA) copy number were estimated in peripheral blood mononuclear cells (PBMCs). The left ventricle mass index (LVMI) was evaluated in all participants, and the interaction between these variables and the LVMI was assessed. The LVMI was positively correlated with the NT-proBNP, ET-1, and ANP levels, and it was negatively correlated with mtDNA copy number and mitofilin levels. Multiple regression analysis showed that the NT-proBNP, ET-1, and ANP levels as well as mitofilin levels and mtDNA copy number were associated with the LVMI. Although further research of these associations is needed, this result suggests that LVH may affect the levels of mitofilin in HD patients.

Prevalence and risk factors for vascular calcification in Chinese patients receiving dialysis: baseline results from a prospective cohort study.

OBJECTIVE: With limited data available on calcification prevalence in chronic kidney disease (CKD) patients on dialysis, the China Dialysis Calcification Study (CDCS) determined the prevalence of vascular/valvular calcification (VC) and association of risk factors in Chinese patients with prevalent hemodialysis (HD) or peritoneal dialysis (PD). METHODS: CKD patients undergoing HD/PD for ≥6 months were enrolled. Prevalence data for calcification and medical history were documented at baseline. Coronary artery calcification (CAC) was assessed by electron beam or multi-slice computed tomography (EBCT/MSCT), abdominal aortic calcification (AAC) by lateral lumbar radiography, and cardiac valvular calcification (ValvC) by echocardiography. Serum phosphorus, calcium, intact parathyroid hormone (iPTH), and 25-hydroxyvitamin D and FGF-23 were evaluated. A logistic regression model was used to evaluate the association between risk factors and VC. RESULTS: Of 1,497 patients, 1,493 (78.3% HD, 21.7% PD) had ≥1 baseline calcification image (final analysis cohort, FAC) and 1,423 (78.8% HD, 21.2% PD) had baseline calcification data complete (BCDC). Prevalence of VC was 77.4% in FAC (80.8% HD, 65.1% PD, p < .001) and 77.5% in BCDC (80.7% HD, 65.8% PD). The proportion of BCDC patients with single-site calcification were 20% for CAC, 4.3% for AAC, and 4.3% for cardiac valvular calcification (ValvC), respectively. Double site calcifications were 23.4% for CAC and AAC, 6.5% for CAC and ValvC, and 1.1% for AAC and ValvC, respectively. In total, 17.9% patients had calcification at all three sites. CONCLUSIONS: High prevalence of total VC in Chinese CKD patients will supplement current knowledge, which is mostly limited, contributing in creating awareness and optimizing VC management.

Blood glucose fluctuations in hemodialysis patients with end stage diabetic nephropathy.

OBJECTIVE: To characterize blood glucose fluctuation during hemodialysis in patients with end stage diabetic nephropathy (ESDN) by a continuous glucose monitoring system (CGMS), and aim to improve blood glucose control in this patient population. METHODS: Forty-six patients with or without type 2 diabetes mellitus (T2DM), receiving hemodialysis, were recruited in this study. Thirty-six patients had end stage diabetic nephropathy (ESDN group), the other ten patients had end stage renal disease without diabetes (ESRD group). A continuous glucose monitoring system (CGMS) was employed to monitor glycemic fluctuation for 72 hours. Blood samples were collected and analyzed. RESULTS: Mean, standard deviation (SD), maximum, and mean amplitude glycemic excursion (MAGE) of blood glucose and the ratio of blood glucose readings that was greater than 13.9 mmol/L of ESDN group, were significantly greater than those of ESRD group (p<0.01 for all) during 72 hours of observation. The mean blood glucose was significantly lower, while SD and MAGE were significantly higher in ESDN group on hemodialysis day than on days off hemodialysis (p<0.05), while these were not been observed in ESRD group. Though mean, SD, and MAGE of blood glucose during hemodialysis were significantly lower than those of peri-hemodialysis in both groups (p<0.01 or p<0.05, respectively), they were significantly higher in ESDN group than that in ESRD group (p<0.05). The mean blood glucose value calculated from HbA1c did not reflect the actual mean blood glucose measured by CGM in both groups, and gave an inaccurate impression of a significantly lower mean glucose. CONCLUSIONS: ESDN patients had larger glycemic fluctuations as compared with ESRD patients. Hemodialysis caused reduction in mean, SD, and MAGE, which in turn caused bigger glycemic fluctuations on hemodialysis day. The HbA1c in ESDN patients gave an inaccurate value, which did not truly reflect blood glucose status for a prolonged period.