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class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2x77t6qr"><div class="c-clientmarkup">Urinary Biochemistry in the Diagnosis of Acute Kidney Injury</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ALima%2C%20Camila">Lima, Camila</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2018<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Acute kidney injury (AKI) is a common complication, impacting short- and long-term patient outcomes. Although the application of the classification systems for AKI has improved diagnosis, early clinical recognition of AKI is still challenging, as increments in serum creatinine may be late and low urine output is not always present. The role of urinary biochemistry has remained unclear, especially in critically ill patients. Differentiating between a transient and persistent acute kidney injury is of great need in clinical practice, and despite studies questioning their application in clinical practice, biochemistry indices continue to be used while we wait for a novel early injury biomarker. An ideal marker would provide more detailed information about the type, intensity, and location of the injury. In this review, we will discuss factors affecting the fractional excretion of sodium (FeNa) and fractional excretion of urea (FeU). We believe that the frequent assessment of urinary biochemistry and microscopy can be useful in evaluating the likelihood of AKI reversibility. The availability of early injury biomarkers could help guide clinical interventions.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2x77t6qr"><img src="/cms-assets/749d27a1f7c398bfcb9938829951b911342964982a6511213b635e2bbde5124d" alt="Cover page: Urinary Biochemistry in the Diagnosis of Acute Kidney Injury"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/6mm4x8t6"><div class="c-clientmarkup">Comprehensive Assessment of Kidney Health in Acute Kidney Injury: Can It Be Achieved?</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ALima%2C%20Camila">Lima, Camila</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2019<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Acute kidney injury (AKI) is a frequent event in hospitalized patients, with an incidence that continues to rise, reaching as high as 70-80% in intensive care settings. The need for dialysis and progression to end-stage kidney disease (ESKD) after an episode of AKI is relatively low, from 5 to 20%. However, it is now recognized that patients with AKI may have very different kidney outcomes, varying from complete recovery, incipient chronic kidney disease (CKD), to progression to ESKD. Recent studies have shown that even mild AKI episodes can be associated with a 90% increased risk of developing CKD during long-term follow-up. There is a significant need to focus our efforts on factors that could mitigate the progression of kidney dysfunction and ultimately improve outcomes from AKI. The first step toward this goal encompasses a better understanding of tubular and glomerular alterations during and following an AKI episode. Our current approach, based solely on glomerular filtration rate (GFR), is flawed, since the loss of kidney function does not correspond to the degree of decline in estimated GFR (eGFR), and eGFR does not reflect tubular function. Changes in tubular concentration, reabsorptive and secretory capacity are recognized in AKI; however, they have not been incorporated in clinical assessments of overall kidney function. Here we review a few candidates to assess glomerular filtration/permeability, tubular dysfunction, and injury and how we expect these markers to alter during the development and recovery phase of AKI.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/6mm4x8t6"><img src="/cms-assets/0af614527bc7173a1ea41de4b5bda621b29c2b8b6d31cb1d41e9c623fe2294ec" alt="Cover page: Comprehensive Assessment of Kidney Health in Acute Kidney Injury: Can It Be Achieved?"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2dg1663g"><div class="c-clientmarkup">Predictive Modeling of Factors Influencing Adherence to SGLT-2 Inhibitors in Ambulatory Care: Insights from Prescription Claims Data Analysis.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AKhartabil%2C%20Nadia">Khartabil, Nadia</a>; </li><li><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMorello%2C%20Candis">Morello, Candis</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2024<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are novel oral anti-hyperglycemic drugs that demonstrate cardiovascular and metabolic benefits for patients with type 2 diabetes (T2D), heart failure (HF), and chronic kidney disease (CKD). There is limited knowledge of real-world data to predict adherence to SGLT-2i in an ambulatory setting. The study aims to predict SGLT-2i adherence in patients with T2D and/or HF and/or CKD by building a prediction model using electronic prescription claims data presented within EPIC datasets. This is a retrospective study of 174 adult patients prescribed SGLT-2i at UC San Diego Health ambulatory pharmacies between 1 January 2020 to 30 April 2021. Adherence was measured by the proportion of days covered (PDC). R packages were used to identify regression and non-linear regression predictive models to predict adherence. Age, gender, race/ethnicity, hemoglobin A1c, and insurance plan were included in the model. Diabetes control based on hemoglobin A1c (HbA1c) and the glomerular filtration rate (GFR) was also evaluated using Welch t-test with a p-value of 0.05. The best predictive model for measuring adherence was the simple decision tree. It had the highest area under the curve (AUC) of 74% and accuracy of 82%. The model accounted for 21 variables with the main node predictors, including glycated hemoglobin, age, gender, and insurance plan payment amount. The adherence rate was inversely proportional to HbA1c and directly proportional to the plan payment amount. As for secondary outcomes, HbA1c values from baseline till 90 days post-treatment duration were consistently higher in the non-compliant group: 7.4% vs. 9.6%, p < 0.001 for the PDC ≥ 0.80 and PDC < 0.80, respectively. Baseline eGFR was 55.18 mL/min/1.73m2 vs. 54.23 mL/min/m2 at 90 days. The mean eGFR at the end of the study (minimum of 90 days of treatment) was statistically different between the groups: 53.1 vs. 59.6 mL/min/1.73 m2, p < 0.001 for the PDC ≥ 0.80 and PDC < 0.80, respectively. Adherence predictive models will help clinicians to tailor regimens based on non-adherence risk scores.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2dg1663g"><img src="/cms-assets/0b997bd26608625a832f331760aa64c1e7786ed16ec6d495a299bd73f278e9ac" alt="Cover page: Predictive Modeling of Factors Influencing Adherence to SGLT-2 Inhibitors in Ambulatory Care: Insights from Prescription Claims Data Analysis."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2k52532p"><div class="c-clientmarkup">Regional Citrate Anticoagulation for Continuous Kidney Replacement Therapy With Calcium-Containing Solutions: A Cohort Study.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ARhee%2C%20Harin">Rhee, Harin</a>; </li><li><a href="/search/?q=author%3ABerenger%2C%20Brendan">Berenger, Brendan</a>; </li><li><a href="/search/?q=author%3AMehta%2C%20Ravindra%20L">Mehta, Ravindra L</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2021<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Objective</h3>Regional citrate anticoagulation (RCA) is the preferred anticoagulation method for continuous kidney replacement therapy (CKRT) recommended by KDIGO. Limited availability of calcium-free solutions often imposes challenges to the implementation of RCA for CKRT (RCA-CKRT). The principal purpose of this study was to characterize the outcomes of RCA-CKRT using calcium-containing solutions.<h3>Study design</h3>Retrospective cohort study.<h3>Setting & participants</h3>We evaluated the safety and efficacy of RCA-CKRT with calcium-containing dialysate and replacement fluid used for 128 patients. A total of 571 filters and 1,227 days of CKRT were analyzed.<h3>Exposures</h3>Liver disease, sepsis in the absence of liver disease, and sepsis with liver disease.<h3>Outcomes</h3>Filter life and metabolic complications per 100 CKRT days.<h3>Analytical approach</h3>Linear mixed-effects model and generalized linear mixed-effects models.<h3>Results</h3>The majority of patients were male (91; 71.1%), 32 (25%) had liver disease, and 29 (22.7%) had sepsis without liver disease. Median filter life was 50.0 (interquartile range, 22.0-118.0) hours, with a maximum of 322 hours, and was significantly lower (33.5 [interquartile range, 17.5-60.5] h) in patients with liver disease. Calcium-containing replacement solutions were used in 41.6% of all CKRT hours and reduced intravenous calcium requirements by 31.7%. Hypocalcemia (ionized calcium<0.85mmol/L) and hypercalcemia (total calcium>10.6mg/dL) were observed in 6.0 and 6.7 per 100 CKRT days, respectively. Citrate accumulation was observed in 13.3% of all patients and was associated with metabolic acidosis in 3.9%, which was not significantly different in patients with liver disease (9.3%; P = 0.2).<h3>Limitations</h3>Lack of control groups that used calcium-free dialysate and replacement solutions with RCA-CKRT. Possible overestimation of filter life from incomplete data on cause of filter failure.<h3>Conclusions</h3>Our study suggests that RCA-CKRT with calcium-containing solutions is feasible and safe in critically ill patients, including those with sepsis and liver disease.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2k52532p"><img src="/cms-assets/85fa66f8040aadf8f82772688aa43a81b3d719e6fe92166dcdcfe08f2c16d1c7" alt="Cover page: Regional Citrate Anticoagulation for Continuous Kidney Replacement Therapy With Calcium-Containing Solutions: A Cohort Study."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/0vc567rk"><div class="c-clientmarkup">A randomized trial of albumin infusion to prevent intradialytic hypotension in hospitalized hypoalbuminemic patients</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li><a href="/search/?q=author%3AKarl%2C%20Bethany">Karl, Bethany</a>; </li><li><a href="/search/?q=author%3ALee%2C%20Euyhyun">Lee, Euyhyun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMehta%2C%20Ravindra%20L">Mehta, Ravindra L</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2021<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Intradialytic hypotension (IDH) is a frequent complication of intermittent hemodialysis (IHD), occurring from 15 to 50% of ambulatory sessions, and is more frequent among hospitalized patients with hypoalbuminemia. IDH limits adequate fluid removal and increases the risk for vascular access thrombosis, early hemodialysis (HD) termination, and mortality. Albumin infusion before and during therapy has been used for treating IDH with the varying results. We evaluated the efficacy of albumin infusion in preventing IDH during IHD in hypoalbuminemic inpatients.<h3>Methods</h3>A randomized, crossover trial was performed in 65 AKI or ESKD patients with hypoalbuminemia (albumin < 3 g/dl) who required HD during hospitalization. Patients were randomized to receive 100 ml of either 0.9%sodium chloride or 25% albumin intravenously at the initiation of each dialysis. These two solutions were alternated for up to six sessions. Patients' vital signs and ultrafiltration removal rate were recorded every 15 to 30 min during dialysis. IDH was assessed by different definitions reported in the literature. All symptoms associated with a noted hypotensive event as well as interventions during the dialysis were recorded.<h3>Results</h3>Sixty-five patients were submitted to 249 sessions; the mean age was 58 ([Formula: see text] 12), and 46 (70%) were male with a mean weight of 76 ([Formula: see text] 18) kg. The presence of IDH was lower during albumin sessions based on all definitions. The hypotension risk was significantly decreased based on the Kidney Disease Outcomes Quality Initiative definition; (15% with NS vs. 7% with albumin, p = 0.002). The lowest intradialytic SBP was significantly worse in patients who received 0.9% sodium chloride than albumin (NS 83 vs. albumin 90 mmHg, p = 0.035). Overall ultrafiltration rate was significantly higher in the albumin therapies [NS - 8.25 ml/kg/h (- 11.18 5.80) vs. 8.27 ml/kg/h (- 12.22 to 5.53) with albumin, p = 0.011].<h3>Conclusion</h3>In hypoalbuminemic patients who need HD, albumin administration before the dialysis results in fewer episodes of hypotension and improves fluid removal. Albumin infusion may be of benefit to improve the safety of HD and achievement of fluid balance in these high-risk patients. ClinicalTrials.gov Identifier: NCT04522635.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/0vc567rk"><img src="/cms-assets/8f8e843a00f210dfb3db4364f0e69fb5ba6eb8545834386c87a5c78a83ea33a7" alt="Cover page: A randomized trial of albumin infusion to prevent intradialytic hypotension in hospitalized hypoalbuminemic patients"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/4mr6089t"><div class="c-clientmarkup">Role of proenkephalin in the diagnosis of severe and subclinical acute kidney injury during the perioperative period of liver transplantation</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ALima%2C%20Camila">Lima, Camila</a>; </li><li><a href="/search/?q=author%3AGorab%2C%20Daniella%20Lacerda">Gorab, Daniella Lacerda</a>; </li><li><a href="/search/?q=author%3AFernandes%2C%20Carol%20Ribeiro">Fernandes, Carol Ribeiro</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2022<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">In recent decades, clinical research on early biomarkers of renal injury has been frequent and intensive, with proenkephalin (PENK) being indicated as a promising filtration biomarker (BM). From a cohort of 57 patients, blood samples were collected preoperatively and 48 h after liver transplantation (LT). The following BMs were analyzed: PENK, cystatin-C (CYS-C), and serum creatinine (Scr). Diagnosis of AKI was based on the KDIGO criteria. Of the 57 patients undergoing LT, 50 (88%) developed acute kidney injury (AKI) and were categorized as follows: no-AKI/mild-AKI - 21 (36.8%) and severe-AKI 36 (63.2%). During the preoperative period, only PENK was significantly higher in patients with severe AKI, with an AUC of 0.69 (CI 0.54-0.83), a cutoff of 55.30 pmol/l, a sensitivity of 0.86, a specificity of 0.52, and an accuracy of 0.75. In addition, subclinical AKI was determined preoperatively in 32 patients. Forty-eight hours after LT, PENK maintained its performance in determining severe AKI, with an AUC of 0.83 (CI 0.72-0.94), a cutoff of 119.05 pmol/l, a sensitivity of 0.81, a specificity of 0.90, and an accuracy of 0.84. PENK detected AKI 48 h earlier than serum creatinine. In a multivariate linear regression analysis, PENK was an independent predictor of severe AKI. This small study suggests that the filtration biomarker PENK shows promise for detecting AKI in patients undergoing LT, revealing greater accuracy and an earlier rise in patients with severe AKI. The combination of kidney functional and filtration BMs may aid in the management and prevention of AKI progression.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/4mr6089t"><img src="/cms-assets/b5d7c6cdc3f39513fd15186937bfa25f2b5ebea21840d8541ca391df557b0551" alt="Cover page: Role of proenkephalin in the diagnosis of severe and subclinical acute kidney injury during the perioperative period of liver transplantation"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8wz4451q"><div class="c-clientmarkup">Acute kidney injury developed in the intensive care unit: a population-based prospective cohort study in the Brazilian Amazon.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMelo%2C%20Fernando">Melo, Fernando</a>; </li><li><a href="/search/?q=author%3ABurdmann%2C%20Emmanuel">Burdmann, Emmanuel</a>; </li><li><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li><a href="/search/?q=author%3AMehta%2C%20Ravindra">Mehta, Ravindra</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AZanetta%2C%20Dirce">Zanetta, Dirce</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2024<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">The Brazilian Amazon is a vast area with limited health care resources. To assess the epidemiology of critically ill acute kidney injury (AKI) patients in this area, a prospective cohort study of 1029 adult patients of the three intensive care units (ICUs) of Rio Branco city, the capital of Acre state, were evaluated from February 2014 to February 2016. The incidence of AKI was 53.3%. Risk factors for AKI included higher age, nonsurgical patients, admission to the ICU from the ward, higher Acute Physiology and Chronic Health Evaluation (APACHE) II scores at ICU admission, and positive fluid balance > 1500 ml/24 hours in the days before AKI development in the ICU, with aOR of 1.3 (95% CI 1.03-1.23), 1.47 (95% CI 1.07-2.03), 1.96 (95% CI 1.40-2.74), 1.05 (95% CI 1.03-1.08) for each unit increase, and 1.62 (95% CI 1.16-2.26), respectively. AKI was associated with higher ICU mortality (aOR 2.03, 95% CI 1.29-3.18). AKI mortality was independently associated with higher age, nonsurgical patients, sepsis at ICU admission, presence of shock or use of vasoactive drugs, mechanical ventilation and mean positive fluid balance in the ICU > 1500 ml/24 hours, both during ICU follow-up, with aOR 1.27 (95% CI 1.14-1.43) for each 10-year increase, 1.64 (95% CI 1.07-2.52), 2.35 (95% CI 1.14-4.83), 1.88 (95% CI 1.03-3.44), 6.73 (95% CI 4.08-11.09), 2.31 (95% CI 1.52-3.53), respectively. Adjusted hazard ratios for AKI mortality 30 and 31-180 days after ICU discharge were 3.13 (95% CI 1.84-5.31) and 1.69 (95% CI 0.99-2.90), respectively. AKI incidence was strikingly high among critically ill patients in the Brazilian Amazon. The AKI etiology, risk factors and outcomes were similar to those described in high-income countries, but mortality rates were higher.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8wz4451q"><img src="/cms-assets/2c2e092b02e9b17b905bb88f69232700362b40a84c862e0a574b8b608bf14bd8" alt="Cover page: Acute kidney injury developed in the intensive care unit: a population-based prospective cohort study in the Brazilian Amazon."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/62r5387w"><div class="c-clientmarkup">Risk of de novo proteinuria following hospitalization with acute kidney injury</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ABonde%2C%20Saniya%20S">Bonde, Saniya S</a>; </li><li><a href="/search/?q=author%3AZaman%2C%20Warda">Zaman, Warda</a>; </li><li><a href="/search/?q=author%3ACuomo%2C%20Raphael">Cuomo, Raphael</a>; </li><li><a href="/search/?q=author%3AMalhotra%2C%20Rakesh">Malhotra, Rakesh</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2023<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Acute Kidney Injury (AKI) incidence has continued to rise and is recognized as a major risk factor for kidney disease progression and cardiovascular complications. Early recognition of factors associated with post-AKI complications is fundamental to stratifying patients that could benefit from closer follow-up and management after an episode of AKI. Recent studies have shown that proteinuria is a prevalent sequela after AKI and a strong predictor of complications post-AKI. This study aims to evaluate the frequency and timing of the development of de-novo proteinuria after an AKI episode in patients with known kidney function and no prior history of proteinuria.<h3>Methods</h3>We retrospectively analyzed data from adult AKI patients with pre- and post-kidney function information between Jan 2014 and March 2019. The presence of proteinuria determined before and after index AKI encounter was based on ICD-10 code and/or urine dipstick and UPCR during the follow-up period.<h3>Results</h3>Of 9697 admissions with AKI diagnoses between Jan 2014 and March 2019, 2120 eligible patients with at least one assessment of Scr and proteinuria before AKI index admission were included in the analysis. The median age was 64 (IQR 54-75) years, and 57% were male. 58% (n-1712) patients had stage 1 AKI, 19% (n = 567) stage 2 AKI, and 22% (n = 650) developed stage 3 AKI. De novo proteinúria was found in 62% (n = 472) of patients and was already present by 90 days post-AKI in 59% (209/354). After adjusting for age and comorbidities, severe AKI (stage 2/3 AKI) and diabetes, were independently associated with increased risk for De novo proteinuria.<h3>Conclusion</h3>Severe AKI is an independent risk factor for subsequent de novo proteinuria post-hospitalization. Further prospective studies are needed to determine whether strategies to detect AKI patients at risk of proteinuria and early therapeutics to modify proteinuria can delay the progression of kidney disease.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/62r5387w"><img src="/cms-assets/aca7ddca1c6daacc266c59da59ba898531cbed4592f8a4e403b22e11dbe02755" alt="Cover page: Risk of de novo proteinuria following hospitalization with acute kidney injury"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/56k0b4c8"><div class="c-clientmarkup">Chromogranin A pathway: from pathogenic molecule to renal disease.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMir%2C%20Saiful">Mir, Saiful</a>; </li><li><a href="/search/?q=author%3ACheung%2C%20Wai">Cheung, Wai</a>; </li><li><a href="/search/?q=author%3AWan%2C%20Ji">Wan, Ji</a>; </li><li><a href="/search/?q=author%3AOConnor%2C%20Daniel">OConnor, Daniel</a>; </li><li><a href="/search/?q=author%3AWebster%2C%20Nicholas">Webster, Nicholas</a>; </li><li><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li><a href="/search/?q=author%3AVaingankar%2C%20Sucheta">Vaingankar, Sucheta</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ABiswas%2C%20Nilima">Biswas, Nilima</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2020<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">BACKGROUND: Chromogranin A (CHGA) is an index granin protein critical for biogenesis and exocytotic release of catecholamine storage granules. It is elevated in plasma of patients with sympathetic over-activity and kidney dysfunction. Several CHGA polymorphisms are associated with hypertensive kidney disease. Previously, we unraveled the molecular mechanism by which CHGA expression is regulated in African Americans carrying a genetic variation associated with hypertensive chronic kidney disease (CKD). METHOD: Experimental CKD mouse model were created by 5/6th nephrectomy (Npx) using wild-type and Chga-/- knockout mouse strains to delineate the role of CHGA in CKD. RESULT: Wild-type-Npx mice expressing Chga developed exacerbated azotemia and fibrosis as compared with their knockout-Npx counterparts. Gene expression profiling revealed downregulation of mitochondrial respiratory complexes genes consistent with maladaptive mitochondria in wild-type-Npx mice, contrasted to knockout-Npx. In healthy individuals, an inverse relationship between circulating CHGA levels and glomerular function was observed. In vitro, mesangial cells treated with CHGA-triggered nitric oxide release by a signaling mechanism involving scavenger receptor SR-A. The CHGA-treated and untreated mesangial cells displayed differential expression of cytokine, chemokine, complement, acute phase inflammatory and apoptotic pathway genes. Thus, build-up of plasma CHGA because of kidney injury served as an insult to the mesangial cells resulting in expression of genes promoting inflammation, fibrosis, and progression of CKD. CONCLUSION: These findings improve understanding of the role of elevated CHGA in the progression of CKD and reveal novel pathways that could be exploited for therapeutic strategies in hypertensive kidney disease.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/56k0b4c8"><img src="/cms-assets/f4482c5a732d5c47ac017676dd134a6ae92c8948867674db9f7c872d32b0a92a" alt="Cover page: Chromogranin A pathway: from pathogenic molecule to renal disease."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2xg8h01t"><div class="c-clientmarkup">Use of Estimating Equations for Dosing Antimicrobials in Patients with Acute Kidney Injury Not Receiving Renal Replacement Therapy</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AAwdishu%2C%20Linda">Awdishu, Linda</a>; </li><li><a href="/search/?q=author%3AConnor%2C%20Ana%20Isabel">Connor, Ana Isabel</a>; </li><li><a href="/search/?q=author%3ABouchard%2C%20Jos%C3%A9e">Bouchard, Josée</a>; </li><li><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li><a href="/search/?q=author%3AChertow%2C%20Glenn%20M">Chertow, Glenn M</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMehta%2C%20Ravindra%20L">Mehta, Ravindra L</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (<!-- -->2018<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Acute kidney injury (AKI) can potentially lead to the accumulation of antimicrobial drugs with significant renal clearance. Drug dosing adjustments are commonly made using the Cockcroft-Gault estimate of creatinine clearance (CLcr). The Modified Jelliffe equation is significantly better at estimating kidney function than the Cockcroft-Gault equation in the setting of AKI. The objective of this study is to assess the degree of antimicrobial dosing discordance using different glomerular filtration rate (GFR) estimating equations. This is a retrospective evaluation of antimicrobial dosing using different estimating equations for kidney function in AKI and comparison to Cockcroft-Gault estimation as a reference. Considering the Cockcroft-Gault estimate as the criterion standard, antimicrobials were appropriately adjusted at most 80.7% of the time. On average, kidney function changed by 30 mL/min over the course of an AKI episode. The median clearance at the peak serum creatinine was 27.4 (9.3⁻66.3) mL/min for Cockcroft Gault, 19.8 (9.8⁻47.0) mL/min/1.73 m² for MDRD and 20.5 (4.9⁻49.6) mL/min for the Modified Jelliffe equations. The discordance rate for antimicrobial dosing ranged from a minimum of 8.6% to a maximum of 16.4%. In the event of discordance, the dose administered was supra-therapeutic 100% of the time using the Modified Jelliffe equation. Use of estimating equations other than the Cockcroft Gault equation may significantly alter dosing of antimicrobials in AKI.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2xg8h01t"><img src="/cms-assets/29bddf0ad58c96aca3f7e81f4a87dbcb0e30d6f4c97ad8845fc999f902dec7ec" alt="Cover page: Use of Estimating Equations for Dosing Antimicrobials in Patients with Acute Kidney Injury Not Receiving Renal Replacement Therapy"/></a></div></section><nav class="c-pagination"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" class="c-pagination__item">4</a></li></ul></nav></section></main></form></div><div><div 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Publishing","slug":"publishing","type":"page","url":"/publishing"}],"social":{"facebook":null,"twitter":null,"rss":"/rss/unit/root"},"breadcrumb":[{"name":"eScholarship","id":"root","url":"/"}]},"campuses":[{"id":"","name":"eScholarship at..."},{"id":"ucb","name":"UC Berkeley"},{"id":"ucd","name":"UC Davis"},{"id":"uci","name":"UC Irvine"},{"id":"ucla","name":"UCLA"},{"id":"ucm","name":"UC Merced"},{"id":"ucr","name":"UC Riverside"},{"id":"ucsd","name":"UC San Diego"},{"id":"ucsf","name":"UCSF"},{"id":"ucsb","name":"UC Santa Barbara"},{"id":"ucsc","name":"UC Santa Cruz"},{"id":"ucop","name":"UC Office of the President"},{"id":"lbnl","name":"Lawrence Berkeley National Laboratory"},{"id":"anrcs","name":"UC Agriculture & Natural Resources"}],"query":{"q":"author:Macedo, Etienne","sort":"rel","rows":"10","info_start":"0","start":"0","filters":{}},"count":37,"info_count":0,"infoResults":[],"searchResults":[{"id":"qt2x77t6qr","title":"Urinary Biochemistry in the Diagnosis of Acute Kidney Injury","abstract":"Acute kidney injury (AKI) is a common complication, impacting short- and long-term patient outcomes. Although the application of the classification systems for AKI has improved diagnosis, early clinical recognition of AKI is still challenging, as increments in serum creatinine may be late and low urine output is not always present. The role of urinary biochemistry has remained unclear, especially in critically ill patients. Differentiating between a transient and persistent acute kidney injury is of great need in clinical practice, and despite studies questioning their application in clinical practice, biochemistry indices continue to be used while we wait for a novel early injury biomarker. An ideal marker would provide more detailed information about the type, intensity, and location of the injury. In this review, we will discuss factors affecting the fractional excretion of sodium (FeNa) and fractional excretion of urea (FeU). We believe that the frequent assessment of urinary biochemistry and microscopy can be useful in evaluating the likelihood of AKI reversibility. The availability of early injury biomarkers could help guide clinical interventions.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Lima, Camila","fname":"Camila","lname":"Lima"},{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo","ORCID_id":"0000-0002-3669-6519"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":168,"asset_id":"749d27a1f7c398bfcb9938829951b911342964982a6511213b635e2bbde5124d","timestamp":1667313279,"image_type":"png"},"pub_year":2018,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt6mm4x8t6","title":"Comprehensive Assessment of Kidney Health in Acute Kidney Injury: Can It Be Achieved?","abstract":"Acute kidney injury (AKI) is a frequent event in hospitalized patients, with an incidence that continues to rise, reaching as high as 70-80% in intensive care settings. The need for dialysis and progression to end-stage kidney disease (ESKD) after an episode of AKI is relatively low, from 5 to 20%. However, it is now recognized that patients with AKI may have very different kidney outcomes, varying from complete recovery, incipient chronic kidney disease (CKD), to progression to ESKD. Recent studies have shown that even mild AKI episodes can be associated with a 90% increased risk of developing CKD during long-term follow-up. There is a significant need to focus our efforts on factors that could mitigate the progression of kidney dysfunction and ultimately improve outcomes from AKI. The first step toward this goal encompasses a better understanding of tubular and glomerular alterations during and following an AKI episode. Our current approach, based solely on glomerular filtration rate (GFR), is flawed, since the loss of kidney function does not correspond to the degree of decline in estimated GFR (eGFR), and eGFR does not reflect tubular function. Changes in tubular concentration, reabsorptive and secretory capacity are recognized in AKI; however, they have not been incorporated in clinical assessments of overall kidney function. Here we review a few candidates to assess glomerular filtration/permeability, tubular dysfunction, and injury and how we expect these markers to alter during the development and recovery phase of AKI.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo","ORCID_id":"0000-0002-3669-6519"},{"name":"Lima, Camila","fname":"Camila","lname":"Lima"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":162,"asset_id":"0af614527bc7173a1ea41de4b5bda621b29c2b8b6d31cb1d41e9c623fe2294ec","timestamp":1688555089,"image_type":"png"},"pub_year":2019,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt2dg1663g","title":"Predictive Modeling of Factors Influencing Adherence to SGLT-2 Inhibitors in Ambulatory Care: Insights from Prescription Claims Data Analysis.","abstract":"Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are novel oral anti-hyperglycemic drugs that demonstrate cardiovascular and metabolic benefits for patients with type 2 diabetes (T2D), heart failure (HF), and chronic kidney disease (CKD). There is limited knowledge of real-world data to predict adherence to SGLT-2i in an ambulatory setting. The study aims to predict SGLT-2i adherence in patients with T2D and/or HF and/or CKD by building a prediction model using electronic prescription claims data presented within EPIC datasets. This is a retrospective study of 174 adult patients prescribed SGLT-2i at UC San Diego Health ambulatory pharmacies between 1 January 2020 to 30 April 2021. Adherence was measured by the proportion of days covered (PDC). R packages were used to identify regression and non-linear regression predictive models to predict adherence. Age, gender, race/ethnicity, hemoglobin A1c, and insurance plan were included in the model. Diabetes control based on hemoglobin A1c (HbA1c) and the glomerular filtration rate (GFR) was also evaluated using Welch t-test with a p-value of 0.05. The best predictive model for measuring adherence was the simple decision tree. It had the highest area under the curve (AUC) of 74% and accuracy of 82%. The model accounted for 21 variables with the main node predictors, including glycated hemoglobin, age, gender, and insurance plan payment amount. The adherence rate was inversely proportional to HbA1c and directly proportional to the plan payment amount. As for secondary outcomes, HbA1c values from baseline till 90 days post-treatment duration were consistently higher in the non-compliant group: 7.4% vs. 9.6%, p < 0.001 for the PDC \u2265 0.80 and PDC < 0.80, respectively. Baseline eGFR was 55.18 mL/min/1.73m2 vs. 54.23 mL/min/m2 at 90 days. The mean eGFR at the end of the study (minimum of 90 days of treatment) was statistically different between the groups: 53.1 vs. 59.6 mL/min/1.73 m2, p < 0.001 for the PDC \u2265 0.80 and PDC < 0.80, respectively. Adherence predictive models will help clinicians to tailor regimens based on non-adherence risk scores.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Khartabil, Nadia","fname":"Nadia","lname":"Khartabil"},{"name":"Macedo, Etienne","fname":"Etienne","lname":"Macedo"},{"name":"Morello, Candis","email":"cmmorello@ucsd.edu","fname":"Candis","lname":"Morello"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":177,"asset_id":"0b997bd26608625a832f331760aa64c1e7786ed16ec6d495a299bd73f278e9ac","timestamp":1715462873,"image_type":"png"},"pub_year":2024,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt2k52532p","title":"Regional Citrate Anticoagulation for Continuous Kidney Replacement Therapy With Calcium-Containing Solutions: A Cohort Study.","abstract":"<h4>Objective</h4>Regional citrate anticoagulation (RCA) is the preferred anticoagulation method for continuous kidney replacement therapy (CKRT) recommended by KDIGO. Limited availability of calcium-free solutions often imposes challenges to the implementation of RCA for CKRT (RCA-CKRT). The principal purpose of this study was to characterize the outcomes of RCA-CKRT using calcium-containing solutions.<h4>Study design</h4>Retrospective cohort study.<h4>Setting & participants</h4>We evaluated the safety and efficacy of RCA-CKRT with calcium-containing dialysate and replacement fluid used for 128 patients. A total of 571 filters and 1,227 days of CKRT were analyzed.<h4>Exposures</h4>Liver disease, sepsis in the absence of liver disease, and sepsis with liver disease.<h4>Outcomes</h4>Filter life and metabolic complications per 100 CKRT days.<h4>Analytical approach</h4>Linear mixed-effects model and generalized linear mixed-effects models.<h4>Results</h4>The majority of patients were male (91; 71.1%), 32 (25%) had liver disease, and 29 (22.7%) had sepsis without liver disease. Median filter life was 50.0 (interquartile range, 22.0-118.0) hours, with a maximum of 322 hours, and was significantly lower (33.5 [interquartile range, 17.5-60.5] h) in patients with liver disease. Calcium-containing replacement solutions were used in 41.6% of all CKRT hours and reduced intravenous calcium requirements by 31.7%. Hypocalcemia (ionized calcium<0.85mmol/L) and hypercalcemia (total calcium>10.6mg/dL) were observed in 6.0 and 6.7 per 100 CKRT days, respectively. Citrate accumulation was observed in 13.3% of all patients and was associated with metabolic acidosis in 3.9%, which was not significantly different in patients with liver disease (9.3%; P = 0.2).<h4>Limitations</h4>Lack of control groups that used calcium-free dialysate and replacement solutions with RCA-CKRT. Possible overestimation of filter life from incomplete data on cause of filter failure.<h4>Conclusions</h4>Our study suggests that RCA-CKRT with calcium-containing solutions is feasible and safe in critically ill patients, including those with sepsis and liver disease.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Rhee, Harin","fname":"Harin","lname":"Rhee"},{"name":"Berenger, Brendan","email":"bnberenger@ucsd.edu","fname":"Brendan","lname":"Berenger"},{"name":"Mehta, Ravindra L","email":"rmehta@ucsd.edu","fname":"Ravindra L","lname":"Mehta","ORCID_id":"0000-0002-0908-2968"},{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo","ORCID_id":"0000-0002-3669-6519"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":149,"asset_id":"85fa66f8040aadf8f82772688aa43a81b3d719e6fe92166dcdcfe08f2c16d1c7","timestamp":1687303264,"image_type":"png"},"pub_year":2021,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt0vc567rk","title":"A randomized trial of albumin infusion to prevent intradialytic hypotension in hospitalized hypoalbuminemic patients","abstract":"<h4>Background</h4>Intradialytic hypotension (IDH) is a frequent complication of intermittent hemodialysis (IHD), occurring from 15 to 50% of ambulatory sessions, and is more frequent among hospitalized patients with hypoalbuminemia. IDH limits adequate fluid removal and increases the risk for vascular access thrombosis, early hemodialysis (HD) termination, and mortality. Albumin infusion before and during therapy has been used for treating IDH with the varying results. We evaluated the efficacy of albumin infusion in preventing IDH during IHD in hypoalbuminemic inpatients.<h4>Methods</h4>A randomized, crossover trial was performed in 65 AKI or ESKD patients with hypoalbuminemia (albumin\u2009<\u20093 g/dl) who required HD during hospitalization. Patients were randomized to receive 100 ml of either 0.9%sodium chloride or 25% albumin intravenously at the initiation of each dialysis. These two solutions were alternated for up to six sessions. Patients' vital signs and ultrafiltration removal rate were recorded every 15 to 30 min during dialysis. IDH was assessed by different definitions reported in the literature. All symptoms associated with a noted hypotensive event as well as interventions during the dialysis were recorded.<h4>Results</h4>Sixty-five patients were submitted to 249 sessions; the mean age was 58 ([Formula: see text]\u200912), and 46 (70%) were male with a mean weight of 76 ([Formula: see text]\u200918) kg. The presence of IDH was lower during albumin sessions based on all definitions. The hypotension risk was significantly decreased based on the Kidney Disease Outcomes Quality Initiative definition; (15% with NS vs. 7% with albumin, p\u2009=\u20090.002). The lowest intradialytic SBP was significantly worse in patients who received 0.9% sodium chloride than albumin (NS 83 vs. albumin 90 mmHg, p\u2009=\u20090.035). Overall ultrafiltration rate was significantly higher in the albumin therapies [NS\u2009-\u20098.25 ml/kg/h (-\u200911.18 5.80) vs. 8.27 ml/kg/h (-\u200912.22 to 5.53) with albumin, p\u2009=\u20090.011].<h4>Conclusion</h4>In hypoalbuminemic patients who need HD, albumin administration before the dialysis results in fewer episodes of hypotension and improves fluid removal. Albumin infusion may be of benefit to improve the safety of HD and achievement of fluid balance in these high-risk patients. ClinicalTrials.gov Identifier: NCT04522635.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo","ORCID_id":"0000-0002-3669-6519"},{"name":"Karl, Bethany","email":"bkarl@ucsd.edu","fname":"Bethany","lname":"Karl"},{"name":"Lee, Euyhyun","fname":"Euyhyun","lname":"Lee"},{"name":"Mehta, Ravindra L","fname":"Ravindra L","lname":"Mehta"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":175,"asset_id":"8f8e843a00f210dfb3db4364f0e69fb5ba6eb8545834386c87a5c78a83ea33a7","timestamp":1664805703,"image_type":"png"},"pub_year":2021,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt4mr6089t","title":"Role of proenkephalin in the diagnosis of severe and subclinical acute kidney injury during the perioperative period of liver transplantation","abstract":"In recent decades, clinical research on early biomarkers of renal injury has been frequent and intensive, with proenkephalin (PENK) being indicated as a promising filtration biomarker (BM). From a cohort of 57 patients, blood samples were collected preoperatively and 48 h after liver transplantation (LT). The following BMs were analyzed: PENK, cystatin-C (CYS-C), and serum creatinine (Scr). Diagnosis of AKI was based on the KDIGO criteria. Of the 57 patients undergoing LT, 50 (88%) developed acute kidney injury (AKI) and were categorized as follows: no-AKI/mild-AKI - 21 (36.8%) and severe-AKI 36 (63.2%). During the preoperative period, only PENK was significantly higher in patients with severe AKI, with an AUC of 0.69 (CI 0.54-0.83), a cutoff of 55.30 pmol/l, a sensitivity of 0.86, a specificity of 0.52, and an accuracy of 0.75. In addition, subclinical AKI was determined preoperatively in 32 patients. Forty-eight hours after LT, PENK maintained its performance in determining severe AKI, with an AUC of 0.83 (CI 0.72-0.94), a cutoff of 119.05 pmol/l, a sensitivity of 0.81, a specificity of 0.90, and an accuracy of 0.84. PENK detected AKI 48 h earlier than serum creatinine. In a multivariate linear regression analysis, PENK was an independent predictor of severe AKI. This small study suggests that the filtration biomarker PENK shows promise for detecting AKI in patients undergoing LT, revealing greater accuracy and an earlier rise in patients with severe AKI. The combination of kidney functional and filtration BMs may aid in the management and prevention of AKI progression.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Lima, Camila","fname":"Camila","lname":"Lima"},{"name":"Gorab, Daniella Lacerda","fname":"Daniella Lacerda","lname":"Gorab"},{"name":"Fernandes, Carol Ribeiro","fname":"Carol Ribeiro","lname":"Fernandes"},{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo","ORCID_id":"0000-0002-3669-6519"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":171,"asset_id":"b5d7c6cdc3f39513fd15186937bfa25f2b5ebea21840d8541ca391df557b0551","timestamp":1667313158,"image_type":"jpeg"},"pub_year":2022,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt8wz4451q","title":"Acute kidney injury developed in the intensive care unit: a population-based prospective cohort study in the Brazilian Amazon.","abstract":"The Brazilian Amazon is a vast area with limited health care resources. To assess the epidemiology of critically ill acute kidney injury (AKI) patients in this area, a prospective cohort study of 1029 adult patients of the three intensive care units (ICUs) of Rio Branco city, the capital of Acre state, were evaluated from February 2014 to February 2016. The incidence of AKI was 53.3%. Risk factors for AKI included higher age, nonsurgical patients, admission to the ICU from the ward, higher Acute Physiology and Chronic Health Evaluation (APACHE) II scores at ICU admission, and positive fluid balance\u2009>\u20091500 ml/24 hours in the days before AKI development in the ICU, with aOR of 1.3 (95% CI 1.03-1.23), 1.47 (95% CI 1.07-2.03), 1.96 (95% CI 1.40-2.74), 1.05 (95% CI 1.03-1.08) for each unit increase, and 1.62 (95% CI 1.16-2.26), respectively. AKI was associated with higher ICU mortality (aOR 2.03, 95% CI 1.29-3.18). AKI mortality was independently associated with higher age, nonsurgical patients, sepsis at ICU admission, presence of shock or use of vasoactive drugs, mechanical ventilation and mean positive fluid balance in the ICU\u2009>\u20091500 ml/24 hours, both during ICU follow-up, with aOR 1.27 (95% CI 1.14-1.43) for each 10-year increase, 1.64 (95% CI 1.07-2.52), 2.35 (95% CI 1.14-4.83), 1.88 (95% CI 1.03-3.44), 6.73 (95% CI 4.08-11.09), 2.31 (95% CI 1.52-3.53), respectively. Adjusted hazard ratios for AKI mortality 30 and 31-180 days after ICU discharge were 3.13 (95% CI 1.84-5.31) and 1.69 (95% CI 0.99-2.90), respectively. AKI incidence was strikingly high among critically ill patients in the Brazilian Amazon. The AKI etiology, risk factors and outcomes were similar to those described in high-income countries, but mortality rates were higher.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Melo, Fernando","fname":"Fernando","lname":"Melo"},{"name":"Burdmann, Emmanuel","fname":"Emmanuel","lname":"Burdmann"},{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo"},{"name":"Mehta, Ravindra","fname":"Ravindra","lname":"Mehta"},{"name":"Zanetta, Dirce","fname":"Dirce","lname":"Zanetta"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":156,"asset_id":"2c2e092b02e9b17b905bb88f69232700362b40a84c862e0a574b8b608bf14bd8","timestamp":1731359759,"image_type":"png"},"pub_year":2024,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt62r5387w","title":"Risk of de novo proteinuria following hospitalization with acute kidney injury","abstract":"<h4>Background</h4>Acute Kidney Injury (AKI) incidence has continued to rise and is recognized as a major risk factor for kidney disease progression and cardiovascular complications. Early recognition of factors associated with post-AKI complications is fundamental to stratifying patients that could benefit from closer follow-up and management after an episode of AKI. Recent studies have shown that proteinuria is a prevalent sequela after AKI and a strong predictor of complications post-AKI. This study aims to evaluate the frequency and timing of the development of de-novo proteinuria after an AKI episode in patients with known kidney function and no prior history of proteinuria.<h4>Methods</h4>We retrospectively analyzed data from adult AKI patients with pre- and post-kidney function information between Jan 2014 and March 2019. The presence of proteinuria determined before and after index AKI encounter was based on ICD-10 code and/or urine dipstick and UPCR during the follow-up period.<h4>Results</h4>Of 9697 admissions with AKI diagnoses between Jan 2014 and March 2019, 2120 eligible patients with at least one assessment of Scr and proteinuria before AKI index admission were included in the analysis. The median age was 64 (IQR 54-75) years, and 57% were male. 58% (n-1712) patients had stage 1 AKI, 19% (n\u2009=\u2009567) stage 2 AKI, and 22% (n\u2009=\u2009650) developed stage 3 AKI. De novo protein\u00FAria was found in 62% (n\u2009=\u2009472) of patients and was already present by 90 days post-AKI in 59% (209/354). After adjusting for age and comorbidities, severe AKI (stage 2/3 AKI) and diabetes, were independently associated with increased risk for De novo proteinuria.<h4>Conclusion</h4>Severe AKI is an independent risk factor for subsequent de novo proteinuria post-hospitalization. Further prospective studies are needed to determine whether strategies to detect AKI patients at risk of proteinuria and early therapeutics to modify proteinuria can delay the progression of kidney disease.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Bonde, Saniya S","fname":"Saniya S","lname":"Bonde"},{"name":"Zaman, Warda","fname":"Warda","lname":"Zaman"},{"name":"Cuomo, Raphael","email":"racuomo@ucsd.edu","fname":"Raphael","lname":"Cuomo","ORCID_id":"0000-0002-8179-0619"},{"name":"Malhotra, Rakesh","fname":"Rakesh","lname":"Malhotra"},{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo","ORCID_id":"0000-0002-3669-6519"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":174,"asset_id":"aca7ddca1c6daacc266c59da59ba898531cbed4592f8a4e403b22e11dbe02755","timestamp":1689768311,"image_type":"png"},"pub_year":2023,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt56k0b4c8","title":"Chromogranin A pathway: from pathogenic molecule to renal disease.","abstract":"BACKGROUND: Chromogranin A (CHGA) is an index granin protein critical for biogenesis and exocytotic release of catecholamine storage granules. It is elevated in plasma of patients with sympathetic over-activity and kidney dysfunction. Several CHGA polymorphisms are associated with hypertensive kidney disease. Previously, we unraveled the molecular mechanism by which CHGA expression is regulated in African Americans carrying a genetic variation associated with hypertensive chronic kidney disease (CKD). METHOD: Experimental CKD mouse model were created by 5/6th nephrectomy (Npx) using wild-type and Chga-/- knockout mouse strains to delineate the role of CHGA in CKD. RESULT: Wild-type-Npx mice expressing Chga developed exacerbated azotemia and fibrosis as compared with their knockout-Npx counterparts. Gene expression profiling revealed downregulation of mitochondrial respiratory complexes genes consistent with maladaptive mitochondria in wild-type-Npx mice, contrasted to knockout-Npx. In healthy individuals, an inverse relationship between circulating CHGA levels and glomerular function was observed. In vitro, mesangial cells treated with CHGA-triggered nitric oxide release by a signaling mechanism involving scavenger receptor SR-A. The CHGA-treated and untreated mesangial cells displayed differential expression of cytokine, chemokine, complement, acute phase inflammatory and apoptotic pathway genes. Thus, build-up of plasma CHGA because of kidney injury served as an insult to the mesangial cells resulting in expression of genes promoting inflammation, fibrosis, and progression of CKD. CONCLUSION: These findings improve understanding of the role of elevated CHGA in the progression of CKD and reveal novel pathways that could be exploited for therapeutic strategies in hypertensive kidney disease.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Mir, Saiful","fname":"Saiful","lname":"Mir"},{"name":"Cheung, Wai","fname":"Wai","lname":"Cheung"},{"name":"Wan, Ji","fname":"Ji","lname":"Wan"},{"name":"OConnor, Daniel","fname":"Daniel","lname":"OConnor"},{"name":"Webster, Nicholas","email":"nwebster@ucsd.edu","fname":"Nicholas","lname":"Webster"},{"name":"Macedo, Etienne","email":"emmacedo@ucsd.edu","fname":"Etienne","lname":"Macedo"},{"name":"Vaingankar, Sucheta","email":"svaingankar@ucsd.edu","fname":"Sucheta","lname":"Vaingankar"},{"name":"Biswas, Nilima","email":"nbiswas@ucsd.edu","fname":"Nilima","lname":"Biswas"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":149,"asset_id":"f4482c5a732d5c47ac017676dd134a6ae92c8948867674db9f7c872d32b0a92a","timestamp":1698017850,"image_type":"png"},"pub_year":2020,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}},{"id":"qt2xg8h01t","title":"Use of Estimating Equations for Dosing Antimicrobials in Patients with Acute Kidney Injury Not Receiving Renal Replacement Therapy","abstract":"Acute kidney injury (AKI) can potentially lead to the accumulation of antimicrobial drugs with significant renal clearance. Drug dosing adjustments are commonly made using the Cockcroft-Gault estimate of creatinine clearance (CLcr). The Modified Jelliffe equation is significantly better at estimating kidney function than the Cockcroft-Gault equation in the setting of AKI. The objective of this study is to assess the degree of antimicrobial dosing discordance using different glomerular filtration rate (GFR) estimating equations. This is a retrospective evaluation of antimicrobial dosing using different estimating equations for kidney function in AKI and comparison to Cockcroft-Gault estimation as a reference. Considering the Cockcroft-Gault estimate as the criterion standard, antimicrobials were appropriately adjusted at most 80.7% of the time. On average, kidney function changed by 30 mL/min over the course of an AKI episode. The median clearance at the peak serum creatinine was 27.4 (9.3\u207B66.3) mL/min for Cockcroft Gault, 19.8 (9.8\u207B47.0) mL/min/1.73 m\u00B2 for MDRD and 20.5 (4.9\u207B49.6) mL/min for the Modified Jelliffe equations. The discordance rate for antimicrobial dosing ranged from a minimum of 8.6% to a maximum of 16.4%. In the event of discordance, the dose administered was supra-therapeutic 100% of the time using the Modified Jelliffe equation. Use of estimating equations other than the Cockcroft Gault equation may significantly alter dosing of antimicrobials in AKI.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Awdishu, Linda","fname":"Linda","lname":"Awdishu"},{"name":"Connor, Ana Isabel","fname":"Ana Isabel","lname":"Connor"},{"name":"Bouchard, Jos\u00E9e","fname":"Jos\u00E9e","lname":"Bouchard"},{"name":"Macedo, Etienne","fname":"Etienne","lname":"Macedo"},{"name":"Chertow, Glenn M","fname":"Glenn M","lname":"Chertow"},{"name":"Mehta, Ravindra L","fname":"Ravindra L","lname":"Mehta"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":203,"asset_id":"29bddf0ad58c96aca3f7e81f4a87dbcb0e30d6f4c97ad8845fc999f902dec7ec","timestamp":1590001025,"image_type":"png"},"pub_year":2018,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Diego Previously Published Works","link_path":"ucsd_postprints"}}],"facets":[{"display":"Type of Work","fieldName":"type_of_work","facets":[{"value":"article","count":37,"displayName":"Article"},{"value":"monograph","count":0,"displayName":"Book"},{"value":"dissertation","count":0,"displayName":"Theses"},{"value":"multimedia","count":0,"displayName":"Multimedia"}]},{"display":"Peer Review","fieldName":"peer_reviewed","facets":[{"value":"1","count":37,"displayName":"Peer-reviewed only"}]},{"display":"Supplemental Material","fieldName":"supp_file_types","facets":[{"value":"video","count":0,"displayName":"Video"},{"value":"audio","count":0,"displayName":"Audio"},{"value":"images","count":0,"displayName":"Images"},{"value":"zip","count":0,"displayName":"Zip"},{"value":"other files","count":0,"displayName":"Other files"}]},{"display":"Publication Year","fieldName":"pub_year","range":{"pub_year_start":null,"pub_year_end":null}},{"display":"Campus","fieldName":"campuses","facets":[{"value":"ucb","count":0,"displayName":"UC Berkeley"},{"value":"ucd","count":0,"displayName":"UC Davis"},{"value":"uci","count":0,"displayName":"UC Irvine"},{"value":"ucla","count":0,"displayName":"UCLA"},{"value":"ucm","count":0,"displayName":"UC Merced"},{"value":"ucr","count":0,"displayName":"UC Riverside"},{"value":"ucsd","count":37,"displayName":"UC San Diego"},{"value":"ucsf","count":2,"displayName":"UCSF"},{"value":"ucsb","count":0,"displayName":"UC Santa Barbara"},{"value":"ucsc","count":0,"displayName":"UC Santa Cruz"},{"value":"ucop","count":1,"displayName":"UC Office of the President"},{"value":"lbnl","count":0,"displayName":"Lawrence Berkeley National Laboratory"},{"value":"anrcs","count":0,"displayName":"UC Agriculture & Natural Resources"}]},{"display":"Department","fieldName":"departments","facets":[{"value":"rgpo","count":1,"displayName":"Research Grants Program Office"},{"value":"ucsdsom","count":34,"displayName":"School of Medicine"},{"value":"sspps","count":5,"displayName":"Skaggs School of Pharmacy and Pharmaceutical Sciences (SSPPS)"}]},{"display":"Journal","fieldName":"journals","facets":[]},{"display":"Discipline","fieldName":"disciplines","facets":[]},{"display":"Reuse License","fieldName":"rights","facets":[{"value":"CC BY","count":1,"displayName":"BY - Attribution required"},{"value":"CC BY-NC-ND","count":1,"displayName":"BY-NC-ND - Attribution; NonCommercial use; No derivatives"}]}]};</script> <script src="/js/vendors~app-bundle-7424603c338d723fd773.js"></script> <script src="/js/app-bundle-8362e6d7829414ab4baa.js"></script> </body> </html>