Quality of Life and Depression Among Mexican Americans on Hemodialysis: A Preliminary Report.

Health-related quality of life (QOL) and depression burden of Mexican Americans with end-stage renal disease (ESRD) are not known. This observational cross-sectional study assessed QOL and depression and examined their inter-relatedness in Mexican Americans with type 2 diabetes and ESRD on maintenance hemodialysis (HD) treatment. Prevalent Mexican Americans on HD (N = 40) completed the Kidney Disease Quality of Life-Short Form (KDQOL-SF) and the Beck Depression Inventory II. The overall median scores for the mental component summary and the physical component summary scales in the KDQOL-SF were 40.9 and 34.0, respectively. The prevalence of severe depression was 40%. The most significant differences between depressed and non-depressed groups were symptom/problem list, cognitive function, and emotional well- being (P < 0.0001 for all). Mexican Americans with depression endure a more dismal QOL compared to non-depressed peers. Significant negative correlations between depression and several QOL scales underscore plausible interactions between the two conditions which warrants further evaluation.

Tryptophan Metabolism in Patients With Chronic Kidney Disease Secondary to Type 2 Diabetes: Relationship to Inflammatory Markers.

OBJECTIVE: Type 2 diabetes (T2D) is the primary case of chronic kidney disease (CKD). Inflammation is associated with metabolic dysregulation in patients with T2D and CKD. Tryptophan (TRP) metabolism may have relevance to the CKD outcomes and associated symptoms. We investigated the relationships of TRP metabolism with inflammatory markers in patients with T2D and CKD. METHODS: Data were collected from a well-characterized cohort of type 2 diabetic individuals with all stages of CKD, including patients on hemodialysis. Key TRP metabolites (kynurenine [KYN], kynurenic acid [KYNA], and quinolinic acid [QA]), proinflammatory cytokines (tumor necrosis factor-α [TNF-α] and interleukin-6 [IL-6]), and C-reactive protein were measured in plasma. The KYN/TRP ratio was utilized as a surrogate marker for indoleamine 2,3-dioxygenase 1 (IDO1) enzyme activity. RESULTS: There was a significant inverse association between circulating TRP level and stages of CKD (P< 0.0001). Downstream bioactive TRP metabolites KYN, KYNA, and QA were positively and robustly correlated with the severity of kidney disease (P < 0.0001). In multiple linear regression, neither TNF-α nor IL-6 was independently related to KYN/TRP ratio after adjusting for estimated glomerular filtration rate (eGFR). Only TNF-α was independently related to KYN after taking into account the effect of eGFR. CONCLUSIONS: Chronic kidney disease secondary to T2D may be associated with accumulation of toxic TRP metabolites due to both inflammation and impaired kidney function. Future longitudinal studies to determine whether the accumulation of KYN directly contributes to CKD progression and associated symptoms in patients with T2D are warranted.

Ergocalciferol treatment does Not improve erythropoietin utilization and hospitalization rate in hemodialysis patients.

BACKGROUND: Vitamin D (25-hydroxyvitamin D; 25[OH]D) deficiency (VDD) is highly prevalent in chronic kidney disease. The aim of this study was to evaluate the effect of oral ergocalciferol supplementation on requirement of erythropoietin (EPO) and active vitamin D analogues, and hospitalization rate in maintenance hemodialysis (HD) patients. METHODS: This retrospective cohort study included 186 patients who were on HD for 3 months and had 25(OH)D levels < 30 ng/ml. Over 1-year period, 107 patients were supplemented with protocol-based ergocalciferol (D2 group) and 79 were not (control). Parameters of erythropoiesis and bone-mineral metabolism, and monthly doses of EPO and paricalcitol were assessed at 6- and 12- months of ergocalciferol supplementation. Total hospitalizations were recorded for the same year. RESULTS: Baseline characteristics were similar across two arms except higher serum ferritin, transferrin saturation and prevalence of stroke in D2 and higher coronary artery disease in control group with overall mean ± SD 25(OH)D level of 16.8 ± 7 ng/ml. At 12 months, 25(OH)D levels increased significantly in D2 group compared to control (30.5 ± 11.7 vs. 14.2 ± 9.3 ng/ml; p < 0.001). The EPO dose remained same with no difference in hemoglobin values between the two groups during the intervention period. On multivariate regression which included above variables there was no effect of ergocalciferol treatment on EPO dose (p = ns). Hospitalization rate was similar in two arms; however, ergocalciferol treatment inversely associated with paricalcitol dose (ß ± SE = -10.4 ± 2.8; p < 0.001). CONCLUSIONS: One-year of ergocalciferol supplementation was not associated with reduction in EPO requirement or hospitalization rate in HD patients with VDD. Further studies are warranted to determine definitive role of nutritional vitamin D in these patients.

Hydralazine induces myeloperoxidase and proteinase 3 anti-neutrophil cytoplasmic antibody vasculitis and leads to pulmonary renal syndrome.

We report a case of hydralazine-induced ANCA-associated glomerulonephritis with pulmonary hemorrhage. A 62-year-old Hispanic man with hypertension, who was being treated with hydralazine 100 mg three times a day for four and half years, presented to the hospital with severe anemia. He had acute kidney injury and urinalysis showed proteinuria, dysmorphic RBCs, and rare RBC cast. CT scan of the chest revealed bilateral pulmonary ground-glass infiltrates. Transbronchial biopsy was consistent with pulmonary hemorrhage. Serologic tests showed high titer PR3 ANCA and, to a lesser extent, MPO ANCA. Kidney biopsy revealed focal segmental necrotizing glomerulonephritis with crescents, without evidence of immune complex deposits. Hydralazine was discontinued and the patient was treated with corticosteroids and intravenous cyclophosphamide. At one-year follow-up, he had no symptoms and anemia had resolved. Kidney function improved dramatically. Serology showed undetectable PR3 ANCA and minimally elevated MPO ANCA. To our knowledge, hydralazine-associated PR3 ANCA has not been previously reported. The possibility of ANCA systemic vasculitis should be included in the differential diagnosis of any patient with hydralazine use and pulmonary renal syndrome. This is a potentially life threatening condition requiring prompt cessation of the drug and treatment with glucocorticoids and immunosuppression.