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Acute kidney injury (AKI) poses a substantial challenge in the management of lymphoma patients and is frequently associated with diverse causative factors. Herein, we report an illustrative case involving a 47-year-old male with influenza A infection who developed severe AKI, which was incongruent with his medical history. Laboratory investigations disclosed aberrant immunoglobulin levels and urinary protein excretion, prompting further evaluation. A renal biopsy revealed the presence of infiltrating lymphoid cells and cast nephropathy, raising suspicion of an underlying hematological disorder. A comprehensive diagnostic workup, including positron emission tomography imaging and bone marrow biopsy, culminated in the definitive diagnosis of splenic marginal zone lymphoma. This case highlights the crucial significance of including lymphoma-associated kidney disorders in the evaluation of unexplained AKI, particularly when encountering unconventional clinical and laboratory results. Swift and precise intervention is of utmost importance in attaining positive results in these rare and complex clinical situations. This study underscores the persistent concern of AKI in lymphoma patients, with lymphocytic infiltration and cast nephropathy as notable elements contributing to the intricate nature of this condition.

Background Heart failure with reduced ejection fraction (HFrEF) is a chronic disease with substantial mortality. Management of HFrEF has seen significant breakthrough after the launch of neprilysin inhibitor. The PARADIGM‐HF (Prospective Comparison of ARNI with ACEI to Determine Impacton Global Mortality and Morbidity in Heart Failure) trial showed that sacubitril/valsartan significantly reduces HFrEF mortality and the heart failure hospitalization rate. However, in patients with advanced kidney disease, who have the highest prevalence of heart failure, the efficacy and safety of sacubitril/valsartan remains uncertain. We aim to study the efficiency of sacubitril/valsartan in patients with end‐stage kidney disease. Methods and Results Heart function was screened by echocardiogram among all patients with end‐stage kidney disease in 2 hospitals. Patients with HFrEF received either sacubitril/valsartan or conventional treatment. Fifteen echocardiographic parameters were compared before and after treatment. After 1‐year sacubitril/valsartan treatment, parameters of systolic (left ventricular ejection fraction 31.3% to 45.1%, P

Background Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular disease. Corin converts proatrial natriuretic peptide into its active form after being activated by PCSK6 (proprotein convertase subtilisin/kexin type 6) protease. It remains unknown whether the PCSK6/corin/atrial natriuretic peptide pathway plays a role in CKD‐induced cardiomyopathy. Methods and Results Serum corin, left ventricular mass index, and corin–left ventricular mass index correlation were compared between outpatients with versus without CKD. Cardiac corin expression and activity as well as serum corin were compared between 5/6 nephrectomy CKD animal models and sham controls. The effects of indoxyl sulfate, a uremic toxin, on cardiomyocytes were examined in vitro in H9c2 cells. A total of 543 patients were enrolled in this study. Serum corin levels were elevated in patients with CKD compared with levels in patients without CKD. Serum corin levels correlated negatively with left ventricular mass index in participants without CKD, but not in patients with CKD. Compared with sham controls, CKD mice had higher serum corin levels and increased cardiac expression of corin but reduced cardiac corin conversion activity. Indoxyl sulfate stimulated corin expression while suppressing serine protease activity in H9c2 cardiomyoblasts. Lower PCSK6 expression in CKD mouse hearts and indoxyl sulfate–treated H9c2 cardiomyoblasts may explain, at least partly, the observed CKD‐associated reduction in corin activity. Conclusions In CKD, cardiac and serum levels of corin are increased, yet corin activity is suppressed. The latter may be attributable to reduced PCSK6 expression. These findings suggest that corin dysfunction may play a significant role in the pathogenesis of CKD‐associated cardiomyopathy.

BackgroundHigher circulatory corin in patients with cardiac diseases is associated with improved cardiovascular outcomes, and chronic cardiac dysfunction is a well‐known cause of progressive renal dysfunction. This study aimed to determine the role of serum corin in predicting short‐term and long‐term renal outcomes after contrast exposure in patients with suspected coronary artery disease. Methods and ResultsFour hundred one patients who had received coronary angiography were enrolled. Serum corin levels were determined before administration of contrast media. Contrast‐induced nephropathy was defined as a rise in serum creatinine of 0.5 mg/dL or a 25% increase from baseline within 48 hours after the procedure. Progressive renal dysfunction was defined as >50% decrease in estimated glomerular filtration rate after discharge. All patients were followed up for at least 1 year or until the occurrence of death after coronary angiography. Overall, contrast‐induced nephropathy occurred in 23 (5.7%) patients. During a median follow‐up of 529 days, 44 (11.0%) cases had subsequent decline in renal function. After adjustment for demographic characteristics, kidney function, traditional risk factors, and medications, lower corin level was found to be independently associated with higher risk for progressive renal dysfunction (hazard ratio, 0.23; 95% confidence interval, 0.12–0.44) but not for contrast‐induced nephropathy. This inverse correlation remained evident in patients with underlying chronic kidney disease, coronary artery disease, or heart failure. ConclusionsLower baseline serum corin was associated with higher risk of renal function decline in patients undergoing coronary angiography. Further studies are needed to verify these results.

Coenzyme Q10 (CoQ10), an antiapoptosis enzyme, is stored in the mitochondria of cells. We investigated whether CoQ10 can attenuate high glucose-induced endothelial progenitor cell (EPC) apoptosis and clarified its mechanism. EPCs were incubated with normal glucose (5 mM) or high glucose (25 mM) enviroment for 3 days, followed by treatment with CoQ10 (10 μM) for 24 hr. Cell proliferation, nitric oxide (NO) production, and JC-1 assay were examined. The specific signal pathways of AMP-activated protein kinase (AMPK), eNOS/Akt, and heme oxygenase-1 (HO-1) were also assessed. High glucose reduced EPC functional activities, including proliferation and migration. Additionally, Akt/eNOS activity and NO production were downregulated in high glucose-stimulated EPCs. Administration of CoQ10 ameliorated high glucose-induced EPC apoptosis, including downregulation of caspase 3, upregulation of Bcl-2, and increase in mitochondrial membrane potential. Furthermore, treatment with CoQ10 reduced reactive oxygen species, enhanced eNOS/Akt activity, and increased HO-1 expression in high glucose-treated EPCs. These effects were negated by administration of AMPK inhibitor. Transplantation of CoQ10-treated EPCs under high glucose conditions into ischemic hindlimbs improved blood flow recovery. CoQ10 reduced high glucose-induced EPC apoptosis and dysfunction through upregulation of eNOS, HO-1 through the AMPK pathway. Our findings provide a potential treatment strategy targeting dysfunctional EPC in diabetic patients.

Objectives. Erythropoiesis-stimulating agents (ESA) are the main treatment for anemia in hemodialysis (HD) patients. We evaluated factors determining the response after treatment of a new ESA (continuous erythropoietin erythropoietin receptor activator (CERA)). Methods. 61 HD patients were classified by their response at two different timings. First, patients whose hematocrit (Hct) increased 1.5% in the first week were defined as initial responders (IR, n=16). We compared several parameters between IR and the rest of the study subjects (non-IR, n=45). Second, patients whose Hct increased 2% in the 4th week were defined as sustained responders (SR, n=12), and we did a similar comparison. Results. The Hct showed a waveform fluctuation. Compared with the rest, IR had significantly lower platelet counts and higher levels of ferritin, total protein, total bilirubin, and serum sodium, while SR had significantly lower levels of C-reactive protein and low-density lipoprotein (All P

The aim of the study was to explore the correlation between central corneal thickness (CCT) and the degree of myopia in Taiwanese adults. A total of 528 individuals were enrolled to undergo myopic laser refractive surgery from January 2004 to December 2006. Preoperative CCT was measured using the Orbscan corneal topography system and refractive status was determined by cycloplegic spherical equivalent. The relationship between CCT and refractive error was investigated by interindividual and intraindividual analyses. Participants had a mean age of 34.8 ± 7.3 years, and 79.9% were female. The mean refractive error was −7.27 ± 2.96 diopters and the mean CCT measurement was 560 ± 35 μm. CCT revealed that there was no association with age. However, CCT was significantly (p = 0.012) less in females than in males. The CCT also showed no significant association with refractive error (p = 0.49). Among the 67 participants with myopic anisometropia, the mean difference between both eyes was 3.09 ± 1.06 diopters. There was no association between the intereye CCT difference and refractive error (p = 0.57). The results remained the same after adjusting for age and sex. In conclusion, there was no correlation between CCT and the degree of myopia among adults in Taiwan. These data might contribute to the ongoing discussion about the role of CCT in the higher incidence of development and progression of glaucoma in myopic individuals.