BACKGROUND AND AIMS During the last 2 years, we have witnessed several waves of the COVID-19 pandemic characterized by massive infections among the general population, sudden increases in the number of hospitalizations and variable rates of complications and mortality among patients. Acute kidney injury (AKI) has been described as a common and serious complication of COVID-19. However, multiple factors that are involved in the development of this complication have been modified throughout these months, including the appearance of new variants of the virus, the modification of treatment protocols or the advancement of vaccination among the general population. In this study, we aimed to compare the rates of AKI among patients who required admission due to COVID-19 in the first and current (sixth) waves of the pandemic. METHOD Consecutive patients that required admission due to COVID-19 in a tertiary referral hospital during the first (March to May 2020) and current (December 2021) waves of the pandemic were enrolled in the study. Patient characteristics, rates of AKI incidence, 28-day mortality and in-hospital length of stay were compared between groups. Viral infection was confirmed by real-time RT-qPCR in all cases. AKI was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines using peak serum creatinine and acute dialysis criteria. Multivariate logistic regression was performed to define potential predictors of AKI. RESULTS Table 1 summarizes demographic and clinical characteristics among enrolled patients. Compared with the current wave, patients admitted during the first wave were older, had higher baseline serum creatinine and lower baseline eGFR. During the first wave, patients presented higher peak serum creatinine values and a higher incidence of in-hospital AKI. Age, male sex, hypertension, diabetes, CKD and pandemic wave were included in multivariate logistic regression analysis as potential predictors of AKI. Only past history of hypertension [OR 2.867; 95% confidence interval (95% CI) 1.279–6.424; P-value: .011] and CKD (OR 2.418; 95% CI 1.237–4.73; P-value: .01) independently predicted AKI in the sample. CONCLUSION Despite multiple changes that have occurred throughout the pandemic, including new treatment protocols, the appearance of new variants of the virus with different clinical profiles or the extensive application of vaccines, these changes have not translated into a significant decrease in the risk of AKI among patients admitted due to COVID-19, which appears to still be conditioned mainly by comorbidities of each patient, including past history of CKD.
BACKGROUND AND AIMS Increased intra-abdominal pressure (IAP) is common after kidney transplantation (KT). However, the role of potential transplant-specific predictors of this complication, such as tacrolimus-associated endothelial dysfunction, remains unclear. We aimed to describe the relationship between tacrolimus trough levels and IAP in a sample of incident KT patients. METHOD Single-centre prospective cohort of deceased-donor KTs. Anesthesia, surgical technique and immunosuppression induction therapy were the same in all cases. IAP monitoring was performed according to WSACS guidelines using the urinary bladder technique (UnoMeter Abdo-Pressure kit). IAP values were registered every 8h during the first 72 h after surgery or until reoperation. Mean IAP values during the first 7 2h (72 h-IAP) were used in this analysis. The first measured tacrolimus trough levels after transplantation were included as a potential predictor of IAP. Patients without recorded tacrolimus trough levels during the first 7 days after surgery were excluded. The study was approved by the local ethics committee. RESULTS A total of 192 patients were enrolled in the study. Table 1A summarizes relevant patient and haemodynamic variables. Subjects with more severe intra-abdominal hypertension were more commonly males, with longer dialysis vintage, higher BMI and suffered diabetes more frequently. Multivariate linear regression analysis was used to examine potential predictors of 72 h-IAP, including male sex, months on dialysis, body mass index (BMI) (Table 1B), 72 h-fluid balance and tacrolimus trough levels. Recipient age, months on dialysis, BMI and tacrolimus trough levels were independent predictors of 72 h-IAP. CONCLUSION Tacrolimus-associated endothelial dysfunction may play a role in the increase of IAP after transplantation. In contrast, accumulated fluid balance, one of the strongest predictors of IAP in the ICU setting, failed to predict IAP values in our sample. These results offer new insight both into the pathophysiology of increased IAP and into the complex mechanisms of tacrolimus-associated nephrotoxicity in the early post-transplant period.
BACKGROUND AND AIMS Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been in our daily practice for almost 2 years now. Since the beginning of the pandemic, we have aimed to study its most immediate effects on patients to find the best line of treatment or, at least, mitigate its worst outcomes. Nevertheless, we also know some long-term health consequences such as fatigue, sleep difficulties, headache, among others, but its long-term kidney effects are not entirely clear yet. The aim of this study was to describe if coronavirus disease's (COVID-19) severity increases the risk of chronic kidney disease (CKD) progression after a previous hospitalization and observe if there are any additional risk factors that could help us predict this outcome. METHOD In this study, a sample of consecutive patients who required admission due to COVID-19 during the first wave of the pandemic (from March to May of 2020) was recruited. Patients were followed for 12 months since initial admission. The composite outcome of the study included either death or CKD progression. CKD progression was defined as incremental progression to a higher KDIGO CKD stage compared to baseline pre COVID-19 renal function [(in mL/min/1.73 m2): estimated glomerular filtration rate (eGFR) ≥60; stage 3a: 45–59; stage 3b: 30–44; stage 4: 15–29; stage 5: <15], or dialysis initiation. Cardiovascular disease was defined as a history of myocardial infarction, stroke, or peripheral vascular disease. Chronic lung diseases included asthma, chronic obstructive pulmonary disease and chronic bronchitis. RESULTS The sample was composed of 93 patients, of which 14 (15.1%) died during follow-up. Of those alive 12 months after initial admission, 17 (21.5%) suffered CKD progression. No patient required renal replacement therapy. Patients that suffered the composite outcome presented a higher prevalence of cancer, tended to be slightly older and suffered from additional comorbidities more frequently (Table). In multivariate logistic regression analysis, previous history of CKD [odds ratio (OR): 1.066 (0.433–2.624); P = 0.889], severe or critical COVID-19 on admission [OR: 0.657 (0.24–1.8); P =0.414] or ICU admission [OR: 0.986 (0.082–11.898); P = 0.991] failed to predict the composite outcome. CONCLUSION Our main hypothesis was that COVID-19 sequelae should be due to an exaggerated activation of the immune system against the virus. Thus, patients that suffered severe COVID-19 should be expected to develop more long-term health consequences of the infection when compared with those with milder disease. However, we failed to prove any link between COVID-19 severity and long-term CKD progression. History of CKD or ICU admission was also unable to predict the composite outcome. Previous studies have described a relationship between COVID-19 severity and adverse renal outcomes, a relationship that we failed to observe. These discrepancies could be due to the small sample size of our study and the different definition of CKD progression applied. In addition, age could act as a potential modifier of CKD progression after admission due to COVID. More studies are required to further clarify the mechanisms and long-term renal consequences of COVID-19 and define potential lines of treatment.
Background and Aims Intra-abdominal hypertension (IAH) is common among post-surgical, critically ill and kidney transplant patients, and is associated with acute kidney injury and increased morbidity and mortality. We aimed to describe the medium-term effect of IAH on graft and patient survival after deceased-donor kidney transplantation. Method 192 consecutive patients who received a cadaveric renal allograft transplant at our hospital were included in this study. IAP was measured every 8h for at least the first 72h after surgery using the urinary bladder technique, and an average value was obtained. Patients were followed up for 24 months or until a composite outcome (defined as graft loss or recipient death) occurred. Clinical, anthropometric, and analytical data was extracted from our hospital's database. Statistical analysis was performed using IBM SPSS Statistics 22. The study was approved by the local ethics committee. Results 192 patients were included. Relevant clinical and anthropometric data are summarized in Table 1. Patients with grades II or III IAH were more frequently male, had longer dialysis vintage, received more frequently hemodialysis as renal replacement therapy and suffered delayed graft function, graft loss or death more repeatedly. In Kaplan-Meier analysis, grade II IAH or higher were associated with lower composite-outcome free survival (Log-Rank: 8.053; p = 0.018) (Figure 1). Conclusion Grade II-III IAH appear to be a risk factor for graft loss or recipient death in our sample of deceased donor kidney transplant recipients. Monitoring of intra-abdominal hypertension could provide useful information to identify patients at higher risk of post-transplant complications.
BACKGROUND AND AIMS Reaching a SCr ≥ 4 is one criterion of classification for stage 3 in the KDIGO-2012 AKI guidelines. No previous study has challenged this arbitrary cut point by comparing its performance on how patients with pure AKI (pAKI) versus acute on chronic kidney disease (AoCKD) reach that ‘magical number’, and how it affects the prognosis. METHOD Retrospective study of patients with AKI, classified according to the KDIGO-2012 guidelines. We analysed a sub-group of patients that reached a maximum SCr ≥ 4 and divided them in pAKI (basal eGFR ≥ 60) and AoCKD (≥15–≤59). We evaluated epidemiological and clinical variables, and compared the clinical outcomes needed for HD, in-hospital mortality and HD dependence at discharge. As 21 (6%) of AoCKD individuals already had a basal SCr ≥ 4.0, they were excluded in the analysis. RESULTS A total of 492 individuals met the inclusion criteria: 341 (69%) in the AoCKD group. Individuals in this group were older and had a higher Charlson's index. Table 1A summarizes the comparison of clinical characteristics, all patients in the pAKI group reached a four SCr with a rate of SCr increments ≥ 3×. We found no statistically significant difference in in-hospital mortality and the need for HD. The AoCKD group was more dependent on HD at discharge (Table 1B). Figure 1 shows the rate of SCr increments by which individuals reached > 4.0 mg/dL. CONCLUSION We found that individuals in the AoCKD group differ in their basal characteristics from the pAKI group and need lesser increments in SCr to reach the magical number of 4.0 mg/dL to be classified in stage 3. May be, one size does not fit all, and individuals with prior CKD may benefit from a lower rate of SCr increase to stratify AKI severity. We consider that a pitfall in this staging criterion consists in the small portion of patients in the AoCKD group that have a basal SCr ≥ 4.0, with a skew to AKI-KDIGO stage 3.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.