Dietary supplementation with concentrated RGJ improves the lipoprotein profile, reduces plasma concentrations of inflammatory biomarkers and oxidized LDL, and may favor a reduction in cardiovascular disease risk.

Background and objectives The calcimimetic cinacalcet reduced the risk of death or cardiovascular (CV) events in older, but not younger, patients with moderate to severe secondary hyperparathyroidism (HPT) who were receiving hemodialysis. To determine whether the lower risk in younger patients might be due to lower baseline CV risk and more frequent use of cointerventions that reduce parathyroid hormone (kidney transplantation, parathyroidectomy, and commercial cinacalcet use), this study examined the effects of cinacalcet in older ($65 years, n=1005) and younger (,65 years, n=2878) patients.Design, setting, participants, & measurements Evaluation of Cinacalcet HCl Therapy to Lower Cardiovascular Events (EVOLVE) was a global, multicenter, randomized placebo-controlled trial in 3883 prevalent patients on hemodialysis, whose outcomes included death, major CV events, and development of severe unremitting HPT. The age subgroup analysis was prespecified.Results Older patients had higher baseline prevalence of diabetes mellitus and CV comorbidity. Annualized rates of kidney transplantation and parathyroidectomy were .3-fold higher in younger relative to older patients and were more frequent in patients randomized to placebo. In older patients, the adjusted relative hazard (95% confidence interval) for the primary composite (CV) end point (cinacalcet versus placebo) was 0.70 (0.60 to 0.81); in younger patients, the relative hazard was 0.97 (0.86 to 1.09). Corresponding adjusted relative hazards for mortality were 0.68 (0.51 to 0.81) and 0.99 (0.86 to 1.13). Reduction in the risk of severe unremitting HPT was similar in both groups. ConclusionsIn the EVOLVE trial, cinacalcet decreased the risk of death and of major CV events in older, but not younger, patients with moderate to severe HPT who were receiving hemodialysis. Effect modification by age may be partly explained by differences in underlying CV risk and differential application of cointerventions that reduce parathyroid hormone.

Despite the increasing evidence of the benefit of corticosteroids for the treatment of moderate-severe coronavirus disease 2019 (COVID-19) patients, no data are available about the potential role of high doses of steroids for these patients. We evaluated the mortality, the risk of need for mechanical ventilation (MV), or death and the risk of developing a severe acute respiratory distress syndrome (ARDS) between high (HD) and standard doses (SD) among patients with a severe COVID-19. All consecutive confirmed COVID-19 patients admitted to a single center were selected, including those treated with steroids and an ARDS. Patients were allocated to the HD (≥ 250 mg/day of methylprednisolone) of corticosteroids or the SD (≤ 1.5 mg/kg/day of methylprednisolone) at discretion of treating physician. Five hundred seventy-three patients were included: 428 (74.7%) men, with a median (IQR) age of 64 (54-73) years. In the HD group, a worse baseline respiratory situation was observed and male gender, older age, and comorbidities were significantly more common. After adjusting by baseline characteristics, HDs were associated with a higher mortality than SD (adjusted OR 2.46, 95% CI 1.59-3.81, p < 0.001) and with an increased risk of needing MV or death (adjusted OR 2.35, p = 0.001). Conversely, the risk of developing a severe ARDS was similar between groups. Interaction analysis showed that HD increased mortality exclusively in elderly patients. Our real-world experience advises against exceeding 1-1.5 mg/kg/day of corticosteroids for severe COVID-19 with an ARDS, especially in older subjects. This reinforces the rationale of modulating rather than suppressing immune responses in these patients.

A prospective study of the evolution of serum erythropoietin level after androgen therapy was carried out in a group of 25 male patients on chronic hemodialysis treatment with nonferropenic anemia (serum ferritin > 50 ng/ml). The androgen used was nandrolone decanoate (200 mg/week intramuscularly, for 6 months). There was an increase of serum erythropoietin, that reached statistical significance in the 2nd week of treatment (8.6 ± 6.4 vs. 14.2 ± 9.8 mIU/ ml, p < 0.05), and a stabilization after 1 month (1 month: 17.8 ± 11.2 mIU/ ml, 6 months: 19.6 ± 14.9 mlU/ml). The hemoglobin also experienced a parallel increase to that observed in serum erythropoietin (basal value: 8 ± 0.9 g/ dl; at 1 month postandrogen: 9.2 ± 1.3 g/dl, p < 0.001; at 6 months: 10.7 ± 1.8 g/dl, p < 0.001). According to their response of serum erythropoietin the patients were divided into responders (15 patients) and nonresponders (10 patients). There were no differences between them concerning age, basal levels of serum erythropoietin and hemoglobin, and dose of nandrolone decanoate in relation to body weight. The evolution of hemoglobin was similar in both groups, and a correlation between serum erythropoietin and hemoglobin was not observed in the responder group. Fourteen patients were studied after androgen was discontinued. The serum erythropoietin returned to basal levels 6 weeks after the last dose of nandrolone decanoate (7.7 ± 5.4 mlU/ml). However, hemoglobin was above the basal levels 16 weeks after discontinuing androgen (9.5 ± 1.1 g/dl, p < 0.05), with no differences between the responder and nonresponder group. In conclusion, the hematopoietic effect of androgen in patients with chronic renal failure is independent of its action on the serum erythropoietin levels. The increase in the serum erythropoietin observed in 60% of patients is not the cause of the improvement in anemia and may be considered as an epiphenomenon.

Chronic kidney disease (CKD) is a silent and poorly known killer. The current concept of CKD is relatively young and uptake by the public, physicians and health authorities is not widespread. Physicians still mix up CKD with chronic kidney insufficiency or failure, For the wider public and health authorities, CKD evokes kidney replacement therapy (KRT). In Spain, the prevalence of KRT is 0.13%. Thus, health authorities may consider CKD a non-issue: very few persons eventually need KRT and, for those in whom kidneys fail, the problem is “solved” by dialysis or kidney transplantation. However, KRT is the tip of the iceberg in the burden of CKD. The main burden of CKD is accelerated aging and premature death. The cut-off points for kidney function and kidney damage indexes that define CKD also mark an increased risk for all-cause premature death. CKD is the most prevalent risk factor for lethal COVID-19 and the factor that most increases the risk of death in COVID-19, after old age. Men and women undergoing KRT still have an annual mortality which is 10- o 100-fold higher than similar age peers, and life expectancy is shortened by around 40 years for young persons on dialysis and by 15 years for young persons with a functioning kidney graft. CKD is expected to become the fifth global cause of death by 2040 and the second cause of death in Spain before the end of the century, a time when 1 in 4 Spaniards will have CKD. However, by 2022, CKD will become the only top-15 global predicted cause of death that is not supported by a dedicated well-funded CIBER network research structure in Spain. Realizing the underestimation of the CKD burden of disease by health authorities, the Decade of the Kidney initiative for 2020-2030 was launched by the American Association of Kidney Patients (AAKP) and the European Kidney Health Alliance (EKHA). Leading Spanish kidney researchers grouped in the kidney collaborative research network REDINREN have now applied for the RICORS call of collaborative research in Spain with the support of the Spanish Society of Nephrology, ALCER and ONT: RICORS2040 aims to prevent the dire predictions for the global 2040 burden of CKD from becoming true.

In the skin of good-responders the expression of dermal CD31(+) endothelium remains significantly elevated within the treated lesions compared with the distant uninvolved skin, whereas a marked reduction in the perfusion intensity and SUM score was found. This indicates that clinical improvement might outrun endothelial changes.

Intradialytic hypotension is the most frequently occurring complication during hemodialysis (HD) treatments. It associates significant morbidity secondary to end-organ hypoperfusion, such as brain and heart. 1,2 During a HD session the fluid is initially removed from circulating blood volume. To compensate for the drop of blood volume, interstitial fluid is shifted from extravascular to intravascular space. This fact is known as vascular refilling (V REF ). 3 The imbalance between ultrafiltration volume (UF) and V REF leads to significant hypovolemia, which is the major cause of intradialytic hypotension. 4 An adequate fluid management could substantially improve patient outcome and is, therefore, an important challenge for the dialysis staff. 5 Modern dialysis devices include biosensors that monitor continuously and noninvasively relative blood volume (RBV) changes during HD, defined as variations in blood volume from initial baseline during treatment. [6][7][8] It is calculated from changes in hemoconcentration, correlating increases in blood density with variations in plasma volume.It has been suggested that keeping RBV between pre-established thresholds could help prevent intradialytic morbid events (IME). 6,7 However the same drop in RBV may translate to different absolute blood volumes (ABVs), depending on individual baseline volume status. 9 Additionally, IME have been observed with wide variations in RBV, ranging from just minimal changes to higher decreases up to 70%. 10 Finally, postural changes, exercise, food intake, and intravenous fluids administration may also influence the RBV level during HD. 11 It is therefore difficult to identify a uniform threshold for a critical RBV.

Immunosuppression (IS) and autoimmune disease (AD) are prevalent in patients with severe coronavirus disease 2019 (COVID-19), but their impact on its clinical course is unknown. We investigated relationships between IS, AD, and outcomes in patients hospitalized with COVID-19. Data on consecutive admissions for COVID-19 were extracted retrospectively from medical records. Patients were assigned to one of four cohorts, according to whether or not they had an AD (AD and NAD) or were immunosuppressed (IS and NIS). The primary endpoint was development of severe acute respiratory distress syndrome (ARDS); secondary endpoints included death, and a composite of mechanical ventilation (MV) or death. A total of 789 patients were included: 569 (72.1%) male, 76 (9.6%) with an AD, and 63 (8.0%) with IS. Relative to the NIS-NAD cohort, patients in the IS-AD cohort had a significantly reduced risk of severe ARDS (adjusted hazard ratio [aHR] 0.42; 95% confidence interval [CI] 0.23-0.80; p = 0.008). No significant relationships between IS or AD status and either death or the composite of MV and death were identified, although a trend towards higher mortality was identified in the IS-NAD cohort (aHR vs NIS-NAD 1.71; 95% CI 0.94-3.12; p = 0.081). Patients in this cohort also had higher median serum levels of interleukin-6 compared with IS-AD patients (98.2 vs 21.6 pg/mL; p = 0.0328) and NIS-NAD patients (29.1 pg/mL; p = 0.0057). In conclusion, among patients hospitalized with COVID-19, those receiving immunosuppressive treatment for an AD may have a reduced risk of developing severe ARDS.