Critically ill patients with COVID-19-associated acute kidney injury treated with kidney replacement therapy: Comparison between the first and second pandemic waves in São Paulo, Brazil.

INTRODUCTION: This study aimed to compare the characteristics and outcomes of critically ill patients with COVID-19-associated acute kidney injury (AKI) who were treated with kidney replacement therapy (KRT) in the first and second waves of the pandemic in the megalopolis of Sao Paulo, Brazil. METHODS: A multicenter retrospective study was conducted in 10 intensive care units (ICUs). Patients aged ≥18 years, and treated with KRT due to COVID-19-associated AKI were included. We compared demographic, laboratory and clinical data, KRT parameters and patient outcomes in the first and second COVID-19 waves. RESULTS: We assessed 656 patients (327 in the first wave and 329 in the second one). Second-wave patients were admitted later (7.1±5.0 vs. 5.6±3.9 days after the onset of symptoms, p<0.001), were younger (61.4±13.7 vs. 63.8±13.6 years, p = 0.023), had a lower frequency of diabetes (37.1% vs. 47.1%, p = 0.009) and obesity (29.5% vs. 40.0%, p = 0.007), had a greater need for vasopressors (93.3% vs. 84.6%, p<0.001) and mechanical ventilation (95.7% vs. 87.8%, p<0.001), and had higher lethality (84.8% vs. 72.7%, p<0.001) than first-wave patients. KRT quality markers were independently associated with a reduction in the OR for death in both pandemic waves. CONCLUSIONS: In the Sao Paulo megalopolis, the lethality of critically ill patients with COVID-19-associated AKI treated with KRT was higher in the second wave of the pandemic, despite these patients being younger and having fewer comorbidities. Potential factors related to this poor outcome were difficulties in health care access, lack of intra-hospital resources, delay vaccination and virus variants.

The Effect of Long-Term Cholecalciferol Supplementation on Vascular Calcification in Chronic Kidney Disease Patients With Hypovitaminosis D.

OBJECTIVE: The role of vitamin D supplementation on vascular calcification (VC) in patients with chronic kidney disease (CKD) is controversial. The objective of this study was to evaluate the effects of long-term cholecalciferol supplementation on VC in nondialysis patients with CKD stages 3-4 with hypovitaminosis D. DESIGN AND METHODS: Eighty patients aged 18-85 years with creatinine clearance between 15 and 60 mL/min/1.73 m2 and serum 25(OH)D level < 30 ng/mL were enrolled in a 18-month prospective study. Individuals with vitamin D insufficiency (25-hydroxyvitamin D [25(OH)D] level between 16 and 29 ng/mL) were included in a randomized, double-blind, two-arm study to receive cholecalciferol or placebo. Patients with vitamin D deficiency [25(OH)D < 15 ng/mL] were included in an observational study and mandatorily received cholecalciferol. The coronary artery calcium score was obtained by multislice computed tomography at baseline and the 18th month. RESULTS: During the study, VC did not change in the treated insufficient group (418 [81-611] to 364 [232-817] AU, P = 0.25) but increased in the placebo group (118 [37-421] to 199 [49-490] AU, P = 0.01). The calcium score change was inversely correlated with 25(OH)D change (r = -0.45; P = 0.037) in the treated insufficient group but not in the placebo group. Renal function did not change in the insufficient, treated, and placebo groups. In multivariate analysis, there was no difference in VC progression between the treated and placebo insufficient groups (interaction P = 0.92). In the deficient group, VC progressed (265 [84-733] to 333 [157-745] AU; P = 0.006) and renal function declined (33 [26-43] to 23 [17-49] mL/min/1.73 m2; P = 0.04). The calcium score change was inversely correlated with cholecalciferol cumulative doses (r = -0.41; P = 0.048) and kidney function change (r = -0.43; P = 0.033) but not with 25(OH)D change (r = -0.08; P = 0.69). CONCLUSION: Vitamin D supplementation did not attenuate VC progression in CKD patients with hypovitaminosis D. CONCLUSION: Vitamin D supplementation did not attenuate VC progression in CKD patients with hypovitaminosis D.

Severe hypovitaminosis D in chronic kidney disease: association with blood pressure and coronary artery calcification.

Hypovitaminosis D occurs early in the course of chronic kidney disease (CKD), and its association with cardiovascular morbidity and mortality is well known. In this study, we aimed to evaluate whether the degree of hypovitaminosis D may differently affect blood pressure (BP) and coronary artery calcification (CAC) in nondialyzed CKD patients. This study included 80 CKD patients with a creatinine clearance between 15 and 60 ml/min/1.73 m(2) and serum 25 hydroxivitamin D [25(OH)D] level <30 ng/ml. Patients underwent 24-h ambulatory BP monitoring, evaluation of CAC (multi-slice computed tomography), and laboratory evaluation. Two groups, based on the degree of hypovitaminosis D, were defined according to the median 25(OH)D value. Patients with severe hypovitaminosis D [25(OH)D <17.2 ng/ml; S-group) exhibited a higher systolic BP at all time periods (24-h, nighttime, daytime) when compared to patients with mild hypovitaminosis D [25(OH)D >17.2 ng/ml; M-group]. No differences were found between the S and M-group in terms of diastolic BP and the presence of coronary calcification. In the multiple linear regression analysis, severe hypovitaminosis D was a predictor of 24-h, daytime and nighttime BP after controlling for a number of confounders. The severity of hypovitaminosis D was associated with increased BP in nondialyzed CKD patients. The degree of hypovitaminosis D was not related to CAC, which was equally elevated in both the severe and mild hypovitaminosis D groups.

Cholecalciferol supplementation in chronic kidney disease: restoration of vitamin D status and impact on parathyroid hormone.

BACKGROUND/AIMS: Hypovitaminosis D is highly prevalent among patients with chronic kidney disease (CKD) and has been associated with poor outcome. We aimed to test the effect of a protocol of cholecalciferol supplementation on the restoration of vitamin D status and on parathyroid hormone (PTH) levels in patients with CKD. METHODS: This was a prospective interventional study of 6 months. Forty-five CKD patients (stages 3 and 4) with 25-hydroxyvitamin D deficiency [25(OH)D <15 ng/ml] were included. Patients received a weekly dose of 50,000 IU of cholecalciferol during 3 months, and 50,000 IU/month thereafter for those who had achieved 25(OH)D ≥30 ng/ml. RESULTS: At 3 months, 78% of the patients restored their vitamin D status. At 6 months, only 43% of those patients maintained adequate vitamin D status. PTH decreased at 3 months (p = 0.02) but returned to baseline levels after 6 months. Fibroblast growth factor 23 increased at 3 months (p = 0.001) and returned to initial levels at 6 months. No changes were found in serum 1,25(OH)(2)D, ionized calcium and phosphorus. CONCLUSIONS: A weekly dose of 50,000 IU of cholecalciferol for 3 months restored the vitamin D status of most patients and led to a reduction in PTH. The monthly dose of 50,000 IU appears not to be sufficient to maintain the levels of 25(OH)D.