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Introduction: Acute kidney injury (AKI) is common in coronavirus disease 2019 (COVID-19). It is unknown if hospital-acquired AKI (HA-AKI) and community-acquired AKI (CA-AKI) convey a distinct prognosis. Methods: The study aim was to evaluate the incidence and risk factors associated with both CA-AKI and HA-AKI. Consecutive patients hospitalized at a reference center for COVID-19 were included in this prospective cohort study. Results: We registered 349 (30%) AKI episodes in 1,170 hospitalized patients, 224 (19%) corresponded to CA-AKI, and 125 (11%) to HA-AKI. Compared to patients with HA-AKI, subjects with CA-AKI were older (61 years [IQR 49–70] vs. 50 years [IQR 43–61]), had more comorbidities (hypertension [44 vs. 26%], CKD [10 vs. 3%]), higher Charlson Comorbidity Index (2 points [IQR 1–4] vs. 1 point [IQR 0–2]), and presented to the emergency department with more severe disease. Mortality rates were not different between CA-AKI and HA-AKI (119 [53%] vs. 63 [50%], p = 0.66). In multivariate analysis, CA-AKI was strongly associated to a history of CKD (OR 4.17, 95% CI 1.53–11.3), hypertension (OR 1.55, 95% CI 1.01–2.36), Charlson Comorbidity Index (OR 1.16, 95% CI 1.02–1.32), and SOFA score (OR 2.19, 95% CI 1.87–2.57). HA-AKI was associated with the requirement for mechanical ventilation (OR 68.2, 95% CI 37.1–126), elevated troponin I (OR 1.95, 95% CI 1.01–3.83), and glucose levels at admission (OR 1.05, 95% CI 1.02–1.08). Discussion/Conclusions: CA-AKI and HA-AKI portend an adverse prognosis in CO­VID-19. Nevertheless, CA-AKI was associated with a higher comorbidity burden (including CKD and hypertension), while HA-AKI occurred in younger patients by the time severe multiorgan disease developed.

Background . There is controversy regarding the association between hypovitaminosis D and COVID-19 outcomes. Aim of the study . We assessed the association between 25-hydroxyvitamin D levels and COVID-19 outcomes in hospitalized subjects with severe SARS-CoV-2 infection. Methods . Retrospective cohort study. Serum 25-hydroxyvitamin D levels of subjects with severe COVID-19 pneumonia were measured at hospital admission, between March 17th, 2020, and March 1st, 2021. Results . Out of 2,908 patients, 571 (19.6%) had vitamin D deficiency (defined as a serum 25-hydroxyvitamin D level

El hiperparatiroidismo secundario grave relacionado con la enfermedad renal crónica avanzada es una complicación acompañada de morbimortalidad cuyo diagnóstico y tratamiento son complejos. La interpretación de las mediciones de la hormona paratiroidea molécula intacta y las opciones terapéuticas con calcimiméticos, vitamina D, paratiroidectomía o maniobras mixtas se presentan en un algoritmo clínico para los pacientes con enfermedad renal crónica avanzada sin diálisis y para aquellos bajo tratamiento sustitutivo de la función renal.

Vitamin D deficiency is common in peritoneal dialysis (PD) patients, so its supplementation has been advocated as potentially beneficial.Double-blind, placebo-controlled, randomized clinical trial. Subjects on PD treated with high calcium peritoneal dialysate (Ca 3.5 mEq/l) and serum levels of 25-hydroxi vitamin D (25D) 20 ng/ml were randomized to receive cholecalciferol (4800 IU/daily) or placebo for 16 weeks. The outcome measures were the effects on the osteogenic biomarkers osteoprotegerin (primary endpoint), intact fibroblast growth factor-23 (iFGF23), osteocalcin, osteopontin, iPTH, 1,25-dyhydroxivitamin D (1,25D), and interleukin-6.Fifty-eight subjects were randomly assigned. Baseline characteristics were similar in both groups. Cholecalciferol supplemented subjects had a significant increase in serum 25D (from 11.4 ± 5.0 to 28.3 ± 10.3 ng/ml), 1,25D and iFGF23 compared with placebo group. iFGF23 levels increased an average of 10,875 pg/ml per month (95% CI 11,778-88,414) in the cholecalciferol group and was unchanged in the placebo group (2829 pg/ml, 95% CI - 2181 to 14,972). Extremely high iFGF23 levels ( 30,000 pg/ml) were observed in 74% of subjects receiving cholecalciferol although iFGF23 returned to baseline values after 32 weeks of withdrawal. The observed changes in iFGF23 correlated with 1,25D levels and were not modified by other variables. No difference was observed between groups in osteoprotegerin or other osteogenic biomarkers levels.Cholecalciferol supplementation increases serum 25D levels in subjects on PD exposed to high calcium dialysate, yet it induces an exponential increase of iFGF23 in most patients, which disappear after withdrawal of supplementation and may be a major concern for this maneuver.

Free calcium is the gold standard for diagnosis of calcium disorders, although calcium assessment is routinely performed by albumin-adjusted calcium. Our objective was to develop a novel-specific correction equation for free calcium employing serum total calcium and other analytes.Retrospective single-center cohort study. A new equation for free calcium assessment was formulated from data of hospitalized patients (n = 3481, measurements = 7157) and tested in a validation cohort (n = 3218, measurements = 6911). All measurements were performed simultaneously from the same blood draw.Total COThe novel equation proposed for prediction of free calcium could be useful when free calcium is not available. The conventional formulas misclassify many patients, in particular when phosphate or bicarbonate disturbances are present.

AIM Severe hypocalcaemia following parathyroidectomy for secondary or tertiary hyperparathyroidism (SHPT/THPT) is scarcely studied. We aimed to describe and identify risk factors for early and persistent hypocalcaemia after parathyroidectomy. METHODS Retrospective pair-matched cohort study. We assessed 87 dialysis patients with SHPT (n = 73) or THPT (n = 14) paired with 146 subjects with primary hyperparathyroidism (PHPT) who underwent parathyroidectomy and were followed for 12 months. Early severe hypocalcaemia was defined as a free Ca ≤0.8 mmol/L [3.2 mg/dl] or corrected Ca ≤1.87 mmol/L [7.5 mg/dl] within 48 h. After parathyroidectomy and persistent hypocalcaemia, as an elemental Ca intake >3.0 g/day to achieve corrected Ca >2 mmol/L [8.0 mg/dl]. RESULTS Early severe hypocalcaemia occurred in 77% (67/87) versus 6.8% (10/146) of subjects with SHPT/THPT and PHPT, respectively (p

Background and Aims The FGF23-lowering effect of different phosphate-sources (vegetable versus animal) in low-phosphorus diets are scarcely known. In this trial, we assess the effect on intact FGF23 (iFGF23) of two low-phosphorus diets, animal versus mixed (vegetable + animal), in dialysis patients. Method A randomized, two-center, open-label, clinical trial was performed. Subjects on stable dialysis for >6 months with P>4.5 mg/dL were randomized into a mixed-based (3 ounces equivalent of animal protein + 3 ounces equivalent of legumes) vs. animal-based (6 ounce equivalent of animal protein) low phosphorus diet with equivalent nutrients (phosphorus Results 556 subjects were screened, only 57 subjects (37 hemodialysis[HD] and 18 peritoneal dialysis[PD]) were randomized. Age, sex, phosphate-binders use, and other baseline characteristics were similar between groups. Baseline iFGF23 levels were 7394 (IQR 2379-16629) and 6859 (1543-17521) ng/mL in mixed-based and animal-based groups respectively (p=0.62). Both groups had a significant decrease in iFGF23 after 12 weeks of intervention (iFGF23 change: -285 [IQR -3002 to 227] ng/mL, p Conclusion Dietary phosphorus restriction for 12 weeks with animal-based or mixed-based phosphorus sources similarly decreases iFGF23 concentration in HD or PD patients.

Introduction: Patients with acute respiratory distress syndrome (ARDS) secondary to COVID-19 frequently develop severe acute kidney injury (AKI). Although continuous renal replacement therapy is the standard of care for critically ill patients, prolonged intermittent renal replacement therapy (PIRRT) may be a feasible option. We aimed to describe the tolerability and security of PIRRT treatments in COVID-19 patients with ARDS who required mechanical ventilation and developed severe AKI. Methods: We prospectively analyzed patients who underwent PIRRT treatments at a COVID-19 reference hospital in Mexico City. Intradialytic hypotension was defined as a systolic blood pressure decrease of ≥20 mm Hg or an increase of 100% in vasopressor dose. Results: We identified 136 AKI cases (60.7%) in 224 patients admitted to the intensive care unit. Among them, 21 (15%) underwent PIRRT (130 sessions) due to stage 3 AKI. The median age of the cohort was 49 (range 36–73) years, 17 (81%) were male, 7 (33%) had diabetes, and the median time between symptoms onset and PIRRT initiation was 12 (interquartile range [IQR] 7–14) days. The median of PIRRT procedures for each patient was 5 (IQR 4–9) sessions. In 108 (83%) PIRRT sessions, the total ultrafiltration goal was achieved. In 84 (65%) PIRRT procedures, there was a median increase in norepinephrine dose of +0.031 mcg/kg/min during PIRRT (IQR 0.00 to +0.07). Intradialytic hypotensive events occurred in 56 (43%) procedures. Fifteen (12%) PIRRT treatments were discontinued due to severe hypotension. Vasopressor treatment at PIRRT session onset (OR 6.2, 95% CI 1.4–28.0, p: 0.02) and a pre-PIRRT lactate ≥3.0 mmol/L (OR 4.63, 95% CI 1.3–12.8, p: 0.003) were independently and significantly associated with the risk of hypotension during PIRRT. During follow-up, 11 patients (52%) recovered from AKI and respiratory failure and 9 (43%) died. Several adaptations to our PIRRT protocol during the COVID-19 outbreak are presented. Conclusions: PIRRT was feasible in the majority of COVID-19 patients with ARDS and severe AKI, despite frequent transitory intradialytic hypotensive episodes. PIRRT may represent an acceptable alternative of renal replacement therapy during the COVID-19 outbreak.

We report a case of capillary leak that developed during treatment of antibody-mediated rejection in a kidney transplant recipient. A 53-year-old female transplant recipient experienced an increase in serum creatinine from 1.1 to 1.8 mg/dL. Antibody-mediated rejection was diagnosed by graft biopsy. She was treated with five plasmapheresis sessions (on alternate days with albumin replacement), five doses of immunoglobulin (5 g/dose at 100 mg/kg), a single dose of rituximab (500 mg), and four doses of bortezomib on days 1, 4, 7, and 10 (1.72 mg/dose at 1.3 mg/m2 body surface area). During treatment, edema, slight diarrhea, pancytopenia, hypoalbuminemia, peripheral neuropathy, and postural hypotension were noted. Despite control of liquids, she presented with edema progressing to an increase of more than 10 kg body weight. Prerenal acute graft dysfunction associated with hypotension was diagnosed on day 12, heart failure or other infectious complications being discounted. On day 13, daily hemodialysis was prescribed, and a stable volume status was reached after five hemodialysis sessions. On day 20, the patient recovered diuresis and the edema and diarrhea abated, but she remained on chronic hemodialysis. After excluding other causes of distributive shock, the diagnosis of capillary leak syndrome was based on the presence of hypotension, generalized edema, and hypoalbuminemia in the absence of significant proteinuria. The concomitant presence of diarrhea, peripheral neuropathy, and pancytopenia, suggest a possible causal role for bortezomib. Awareness by clinicians of capillary leak syndrome associated with bortezomib-based treatment of AMR is paramount, despite its rarity.

Controversy exists with regard to the causal role of hyperuricemia in chronic kidney disease. Vascular stiffness may be the link that explains the relation between hyperuricemia and kidney disease. Hyperuricemia is associated with a number of effects on the vascular endothelium and vascular smooth muscle cells, including an increase in oxidative stress, production of vasoconstrictors, and changes on the structural properties of the large artery wall. Observational evidence in large epidemiological cross-sectional studies suggests that there is an independent association between uric acid and arterial stiffness. The limited evidence from cohort studies or clinical trials does not support treatment of hyperuricemia to reduce vascular stiffness in order to prevent kidney disease. Nevertheless, vascular stiffness may be a valid, reproducible, and useful surrogate endpoint. At this point there seems to be sufficient evidence to warrant larger clinical trials to determine whether lowering uric acid concentrations would be useful for prevention or treatment of vascular stiffness and, subsequently, of cardiovascular and kidney diseases. Video Journal Club ‘Cappuccino with Claudio Ronco' at http://www.karger.com/?doi=452726.

Ramirez-Sandoval, Juan C., Maria F. Castilla-Peón, José Gotés-Palazuelos, Juan C. Vázquez-García, Michael P. Wagner, Carlos A. Merelo-Arias, Olynka Vega-Vega, Rodolfo Rincón-Pedrero, and Ricardo Correa-Rotter. Bicarbonate values for healthy residents living in cities above 1500 m of altitude: a theoretical model and systematic review. High Alt Med Biol. 17:85-92, 2016.-Plasma bicarbonate (HCO3(-)) concentration is the main value used to assess the metabolic component of the acid-base status. There is limited information regarding plasma HCO3(-) values adjusted for altitude for people living in cities at high altitude defined as 1500 m (4921 ft) or more above sea level. Our aim was to estimate the plasma HCO3(-) concentration in residents of cities at these altitudes using a theoretical model and compare these values with HCO3(-) values found on a systematic review, and with those venous CO2 values obtained in a sample of 633 healthy individuals living at an altitude of 2240 m (7350 ft). We calculated the PCO2 using linear regression models and calculated plasma HCO3(-) according to the Henderson-Hasselbalch equation. Results show that HCO3(-) concentration falls as the altitude of the cities increase. For each 1000 m of altitude above sea level, HCO3(-) decreases to 0.55 and 1.5 mEq/L in subjects living at sea level with acute exposure to altitude and in subjects acclimatized to altitude, respectively. Estimated HCO3(-) values from the theoretical model were not different to HCO3(-) values found in publications of a systematic review or with venous total CO2 measurements in our sample. Altitude has to be taken into consideration in the calculation of HCO3(-) concentrations in cities above 1500 m to avoid an overdiagnosis of acid-base disorders in a given individual.

Hyperuricemia may be a major contributor to the development or progression of chronic kidney disease (CKD). Although there is no clear cutoff uric acid (UA) value associated to the risk for kidney damage, it appears to be an increased risk as UA rises. Lifestyle interventions such as exercise, weight reduction, low consumption of purine-rich meat, or avoiding high fructose intake are recommended for all hyperuricemic patients. Lowering urate drugs such as allopurinol or febuxostat may be an option as a renoprotective agent; yet, randomized clinical trials evaluating the safety and efficacy of these drugs are limited to a small number of single-center studies. Several ongoing clinical trials aim to evaluate the safety and efficacy of these drugs. As of today, there is insufficient evidence to recommend the widespread use of UA-lowering therapy to prevent or slow down the progression of CKD. The purpose of this review is to summarize the evidence and future perspectives about the treatment of hyperuricemia in the prevention and progression of CKD.

Hyperuricemia may be a major contributor to the development or progression of chronic kidney disease (CKD). Although there is no clear cutoff uric acid (UA) value associated to the risk for kidney damage, it appears to be an increased risk as UA rises. Lifestyle interventions such as exercise, weight reduction, low consumption of purine-rich meat, or avoiding high fructose intake are recommended for all hyperuricemic patients. Lowering urate drugs such as allopurinol or febuxostat may be an option as a renoprotective agent; yet, randomized clinical trials evaluating the safety and efficacy of these drugs are limited to a small number of single-center studies. Several ongoing clinical trials aim to evaluate the safety and efficacy of these drugs. As of today, there is insufficient evidence to recommend the widespread use of UA-lowering therapy to prevent or slow down the progression of CKD. The purpose of this review is to summarize the evidence and future perspectives about the treatment of hyperuricemia in the prevention and progression of CKD.

The use of colistin for multi-drug resistant (MDR) infections has led to an increase of colistin-associated acute kidney injury (AKI). Nevertheless, information on long-term renal prognosis is scarce. We aimed to determine the predictors of chronic kidney disease (CKD) in survivors of MDR-infections with colistin-associated AKI.A retrospective cohort of patients with colistin-associated AKI was compared with controls (survivors of severe infections who developed AKI matched by age, sex, diabetes, vancomycin exposure, and baseline kidney function). The primary outcome was the development of CKD after 6months of follow-up.From 2011 to 2015, 122 patients with MDR infections received colistin. Among 72 survivors, 29 (40%) had colistin-associated AKI. After 6months, 22 of them (75%) progressed to CKD (G3 in 21/22) compared with 16 (27%) in 58 controls (P0.001). Independent predictors of progression to CKD were colistin use [odds ratio (OR): 8.86; 95% CI: 2.8-27.8] and age (OR: 1.04, 95% CI: 1.01-1.07). In patients exposed to colistin, a total dose of colistin5g was an independent predictor of progression to CKD (OR: 14.1, 95% CI: 2.6-75.7).Colistin-associated AKI had a substantial risk for the latter development CKD, and consequently, these patients should be tightly monitored.

Aim To evaluate the performance of urinary neutrophil gelatinase-associated lipocalin (uNGAL), kidney injury molecule, interleukin-18 and heat shock protein 72 for differential diagnosis between causes of acute kidney injury in kidney transplant recipients, especially immunological rejection. Patients and Methods We measured these biomarkers in 67 kidney transplant recipients with acute kidney injury according to the RIFLE criteria. Results There were no statistical differences in biomarkers between kidney transplant recipients with immunological rejection (n = 20), pre-renal causes (n = 20) and other AKI causes (n = 27). Only the uNGAL level relative to urinary creatinine (uNGAL/uCr) for immunological rejection was different in comparison with others (P

Background Vascular calcification is strongly associated with cardiovascular disease and mortality. However, some factors related to vascular calcification in patients with end-stage renal disease receiving peritoneal dialysis (PD) remain unknown. This study aimed to evaluate the associations of osteoprotegerin (OPG), osteopontin (OPN), osteocalcin (OCN), fibroblast growth factor 23 (FGF-23), magnesium, and phosphate clearance with vascular calcification in PD subjects, assessed by plain radiographs. Methods Simple vascular calcification scores (SVCS) obtained from plain X-rays of the pelvis and hands, and the Kauppila Index (KI) from lateral lumbar X-rays were assessed in 76 adults receiving PD for ≥ 6 months (43 women, median age 39 years, median time on PD 1.4 years). Levels of OPG, OPN, OCN, and FGF-23 were determined by luminometry. Results Serum OPG levels were higher in subjects with vascular calcification ( n = 22 with SVCS > 3; n = 19 with KI > 7) compared with those with less calcification ( p < 0.001). Spearman's correlation coefficients between OPG and SVCS and KI were r = 0.49 and r = 0.51, respectively (both p < 0.001). Subjects with vascular calcification had significantly lower renal phosphate clearance. Multiple regression analysis showed that vascular calcification assessed by SVCS was associated with age ( r = 0.2, p = 0.042), diabetes mellitus ( r = 2.4, p < 0.001), body mass index (BMI) ( r = 0.09, p = 0.037), and OPG ( r = 0.22, p = 0.001). Vascular calcification assessed by KI was associated with age ( r = 0.16, p < 0.001), time on PD ( r = 0.54, p = 0.001) and OPG ( r = 0.08, p = 0.04). Osteocalcin, OPN, FGF-23, and magnesium were not associated with vascular calcification. Conclusions Higher levels of OPG were consistently associated with vascular calcification in subjects on PD.

A change in the epidemiology of disease has occurred across the world. There has been a marked increase in the incidence and prevalence of chronic non-communicable disease including CKD in most countries. Rates of CKD in parts of the world outside the United States may be affected by factors related to lower socioeconomic status, racial heritage, and ethnicity. These factors interact in complex manners to modify the risk of developing CKD, especially in disadvantaged communities. Conditions that predispose to CKD such as hypertension, diabetes mellitus, or obesity can be more prevalent in these communities, caused by differences in predisposing genetic backgrounds, prenatal and perinatal care and experiences, including low birthweights, inadequate diets, infectious diseases, or exposure to toxins. ESRD incidence tends to rise in communities with social deprivation, and provision of RRT depends mostly on extent of national health-care expenditures and economic strength. Strategies to provide renal care for all including preventive care, early referral, timely dialysis initiation, and equalizing opportunities for kidney transplantation can be achieved through a concerted effort between nephrologists, governments, patients, charitable organizations, and industry.

To evaluate the performance of urinary neutrophil gelatinase-associated lipocalin (uNGAL), kidney injury molecule, interleukin-18 and heat shock protein 72 for differential diagnosis between causes of acute kidney injury in kidney transplant recipients, especially immunological rejection.We measured these biomarkers in 67 kidney transplant recipients with acute kidney injury according to the RIFLE criteria.There were no statistical differences in biomarkers between kidney transplant recipients with immunological rejection (n = 20), pre-renal causes (n = 20) and other AKI causes (n = 27). Only the uNGAL level relative to urinary creatinine (uNGAL/uCr) for immunological rejection was different in comparison with others (P0.001); a cut-off of 59 μg/g of uNGAL/uCr had a sensitivity and specificity of 60% and 58% respectively (area under the curve in receiver-operating characteristic curve, 0.65). The other biomarkers were not useful in differentiating the causes of acute kidney injury.The biomarkers tested are not useful in identifying immunological rejection as cause of acute kidney injury in kidney transplant recipients.

Inadequate predialysis nephrological care may be strongly associated with morbidity and mortality during the first months of dialysis. Careful planning before dialysis initiation should prevent hospitalizations for the management of untreated acute or chronic complications of advanced uremia and should allow the use of a functioning permanent access at the beginning of dialysis. Preparation for dialysis must include the following: (1) identification of CKD patients who may require dialysis (eGFR

Establish the prognostic value for graft loss of urinary neutrophil gelatinase-associated lipocalin (uNGAL), kidney injury molecule-1 (uKIM-1), interleukin-18 (uIL-18), and heat shock protein 72 (uHsp72) in kidney transplant recipients (KTR) with acute kidney injury (AKI).Biomarkers were measured in 67 KTR with AKI caused by different entities.After 1 year, 11 KTR with graft loss had higher uNGAL compared to KTR without loss (p 0.001). There were no differences for uKIM-1, uIL-18 and uHsp-72. uNGAL200 ng/mL had 84% sensitivity and 86% specificity for graft loss (ROC AUC: 0.89, 95% CI: 0.81-0.97). uNGAL may be useful to predict graft loss after AKI.