Nefrologia
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Browsing Nefrologia by Subject "Acute kidney injury"
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- Acute Kidney Injury Biomarkers: from bench to clinical usePublication . Soto, K; Devarajan, P
- Association between transient acute kidney injury and morbidity and mortality after lung transplantation: a retrospective cohort study.Publication . Fidalgo, P; Ahmed, M; Myer, S; Lien, D; Weinkauf, J; Kapasi, A; Cardoso, F; Jackson, K; Bagshaw, SAcute kidney injury (AKI) is a common occurrence after lung transplantation (LTx). Whether transient AKI or early recovery is associated with improved outcome is uncertain. Our aim was to describe the incidence, factors, and outcomes associated with transient AKI after LTx. MATERIALS AND METHODS: We performed a retrospective cohort study of all adult recipients of LTx at the University of Alberta between 1990 and 2011. Our primary outcome transient AKI was defined as return of serum creatinine below Kidney Disease-Improving Global Outcome AKI stage I within 7days after LTx. Secondary outcomes included occurrence of postoperative complications, mortality, and long-term kidney function. RESULTS: Of 445 LTx patients enrolled, AKI occurred in 306 (68.8%) within the first week after LTx. Of these, transient AKI (or early recovery) occurred in 157 (51.3%). Transient AKI was associated with fewer complications including tracheostomy (17.2% vs 38.3%; P<.001), reintubation (16.4% vs 41.9%; P<.001), decreased duration of mechanical ventilation (median [interquartile range], 69 [41-142] vs 189 [63-403] hours; P<.001), and lower rates of chronic kidney disease at 3 months (28.5% vs 51.1%, P<.001) and 1 year (49.6% vs 66.7%, P=.01) compared with persistent AKI. Factors independently associated with persistent AKI were higher body mass index (per unit; odds ratio [OR], 0.91; 95% confidence interval, 0.85-0.98; P=.01), cyclosporine use (OR, 0.29; 0.12-0.67; P=.01), longer duration of mechanical ventilation (per hour [log transformed]; OR, 0.42; 0.21-0.81; P=.01), and AKI stages II to III (OR, 0.16; 0.08-0.29; P<.001). Persistent AKI was associated with higher adjusted hazard of death (hazard ratio, 1.77 [1.08-2.93]; P=.02) when compared with transient AKI (1.44 [0.93-2.19], P=.09) and no AKI (reference category), respectively. CONCLUSIONS: Transient AKI after LTx is associated with fewer complications and improved survival. Among survivors, persistent AKI portends an increased risk for long-term chronic kidney disease.
- Cystatin C as a marker of acute kidney injury in the emergency departmentPublication . Soto, K; Coelho, S; Rodrigues, B; Martins, H; Frade, F; Lopes, S; Cunha, L; Papoila, A; Devarajan, PBACKGROUND AND OBJECTIVES: The diagnosis of acute kidney injury (AKI) is usually based on changes in serum creatinine, which is a poor marker of early renal dysfunction. The discriminative and predictive abilities of serum and urinary cystatin C were examined for the prediction of AKI. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this prospective cohort study, serum and urinary cystatin C were serially measured in a heterogeneous group of patients (n = 616) presenting to a tertiary care emergency department. The primary outcome was AKI, classified according to RIFLE and AKIN criteria. The secondary outcome was an adjudication based on clinical criteria to AKI, prerenal azotemia, chronic kidney disease (CKD), and normal kidney function. RESULTS: Patients were adjudicated to have AKI in 21.1%, prerenal azotemia in 25.8%, CKD in 2.4%, and normal kidney function in 50.7%. For the diagnosis of AKI, the discriminatory ability of urinary creatinine and cystatin C was marginal. Both serum cystatin C and serum creatinine (at presentation and 6 hours later) showed high discriminatory ability for the diagnosis of AKI. However, only serum cystatin C attained a significant early predictive power (Hosmer-Lemeshow P value > 0.05). Serum cystatin C could differentiate between AKI and prerenal azotemia, but not between AKI and CKD. CONCLUSIONS: Serum cystatin C is an early, predictive biomarker of AKI, which outperforms serum creatinine in the heterogeneous emergency department setting. However, neither biomarker discriminated between AKI and CKD. Additional biomarkers continue to be needed for improved specificity in the diagnosis of community-acquired AKI.
- Letter to the editor: Acute Kidney Injury in patients referred for ECMO therapyPublication . Lima, A; Coelho, S; Freitas, PT
- Plasma NGAL for the diagnosis of AKI in patients admitted from the emergency department settingPublication . Soto, K; Papoila, A; Coelho, S; Bennett, M; Ma, Q; Rodrigues, B; Fidalgo, P; Frade, F; Devarajan, PBACKGROUND AND OBJECTIVES: The purpose of this study was to determine the accuracy of plasma neutrophil gelatinase-associated lipocalin as a marker of AKI in patients admitted from the emergency department. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this prospective cohort study, patients (n=616) admitted from the emergency department from March to November of 2008 were classified according to clinical criteria as AKI, transient azotemia, stable CKD, and normal function. Plasma neutrophil gelatinase-associated lipocalin was measured serially. A logistic regression model using clinical characteristics was fitted to the data, and a second model included discretized plasma neutrophil gelatinase-associated lipocalin. Performance of the models was evaluated by Hosmer-Lemeshow goodness-of-fit test, area under the receiver operating characteristic curve, net reclassification improvement, integrated discrimination improvement, and predictiveness curve. RESULTS: Twenty-one percent of patients were classified as AKI; the highest median levels of plasma neutrophil gelatinase-associated lipocalin were in the AKI group (146-174 ng/ml at various time points) and increased with AKI severity (207-244 ng/ml for Acute Kidney Injury Network classification stage>2). The discriminative ability of plasma neutrophil gelatinase-associated lipocalin for AKI diagnosis (area under the curve, 0.77-0.82 at various time points) improved with higher grades of severity (area under the curve, 0.85-0.89 for AKIN>2). Plasma neutrophil gelatinase-associated lipocalin discriminated AKI from normal function and transient azotemia (area under the curve, 0.85 and 0.73, respectively). Patients were classified into three grades of AKI risk according to plasma neutrophil gelatinase-associated lipocalin levels (low, moderate [i.e., the gray zone], and high). Patients with plasma neutrophil gelatinase-associated lipocalin in the high-risk category displayed a 10-fold greater risk of AKI (odds ratio, 9.8; 95% confidence interval, 5.6 to 16.9). The addition of plasma neutrophil gelatinase-associated lipocalin to the clinical model yielded a net reclassification improvement of 94.3% and an integrated discrimination improvement of 0.122. CONCLUSION: Plasma neutrophil gelatinase-associated lipocalin is an accurate biomarker for prediction of AKI in patients admitted from the emergency department. This work proposes a three-grade classification of AKI risk based on plasma neutrophil gelatinase-associated lipocalin levels.
- Severe Acute Kidney Injury and Double Tubulopathy Due to Dual Toxicity Caused by Combination Antiretroviral Therapy.Publication . Soto, K; Campos, P; Manso, RT, et al.
- Severe Systemic Lupus Erythematosus presentation in patient with alternative complement pathway mutationsPublication . Pereira, F; Cunha, L; Campos, P; Gaspar, A; Manso, RT; Soto, KSystemic lupus erythematosus (SLE) is an autoimmune disease which can involve almost any organ, making its difficult therapeutic approach. Immune complex deposition can often activate complement, accounting for many of SLE clinical manifestations and laboratory findings. We present a case of a patient who presented with acute pancreatitis and acute kidney injury as onset manifestations of SLE, later developing neurological manifestations, who was successfully treated with rituximab, plasma exchange and steroids as induction therapy. Persistently low C3 level led to a genetic analysis of the complement system components. We found three polymorphisms in the alternative pathway of complement regulators (complement factor H c2669 G>T, p.Ser890Ile and c3019 G>T, p.Val1007Leu and complement factor I c.482+6 G>T), two of which have been correlated with atypical haemolytic uraemic syndrome and dense deposit disease and also complement factor H -related protein (CFHR1 and CFHR3) mutations by deletion. This raises the question whether these polymorphisms and mutations played any role in our patient’s clinical course.
- The risk of chronic kidney disease and mortality are increased after community-acquired acute kidney injury.Publication . Soto, K; Campos, P; Pinto, I; Rodrigues, B; Frade, F; Papoila, AL; Devarajan, PWe investigated whether community-acquired acute kidney injury encountered in a tertiary hospital emergency department setting increases the risk of chronic kidney disease (CKD) and mortality, and whether plasma biomarkers could improve the prediction of those adverse outcomes. In a prospective cohort study, we enrolled 616 patients at admission to the emergency department and followed them for a median of 62.1 months. Within this cohort, 130 patients were adjudicated as having acute kidney injury, 159 transient azotemia, 15 stable CKD, and 312 normal renal function. Serum cystatin C and plasma neutrophil gelatinase-associated lipocalin (NGAL) were measured at index admission. After adjusting for clinical variables, the risk of developing CKD stage 3, as well as the risk of death, were increased in the acute kidney injury group (hazard ratio [HR], 5.7 [95% confidence interval, 3.8-8.7] and HR, 1.9 [95% confidence interval, 1.3-2.8], respectively). The addition of serum cystatin C increased the ability to predict the risk of developing CKD stage 3, and death (HR, 1.5 [1.1-2.0] and 1.6 [1.1-2.3], respectively). The addition of plasma NGAL resulted in no improvement in predicting CKD stage 3 or mortality (HR, 1.0 [0.7-1.5] and 1.2 [0.8-1.8], respectively). The risk of developing CKD stage 3 was also significantly increased in the transient azotemia group (HR, 2.4 [1.5-3.6]). Thus, an episode of community acquired acute kidney injury markedly increases the risk of CKD, and moderately increases the risk of death. Our findings highlight the importance of follow-up of patients with community acquired acute kidney injury, for potential early initiation of renal protective strategies.
- Urgent-Start Peritoneal Dialysis – a viable option? A case report and literature reviewPublication . Tavares, J; Silva, F; Lima, A; Carvalho, MJ; Cabrita, A; Rodrigues, ABackground: Many patients with end -stage renal disease start renal replacement therapy in an unplanned manner. The vast majority initiate hemodialysis by a central venous catheter, since its use is more widespread and available. This technique is associated with a high risk of infection and damage of the vascular patrimony associated with the use of central veins. Urgent -start peritoneal dialysis comes as an alternative treatment for selected patients. Case report: A 55 -year -old woman with focal segmental glomerulosclerosis presented with a rapid decline of renal function and was given renal replacement therapy counselling and opted for peritoneal dialysis. Her chosen modality was postponed for one month due to early uremic symptoms, followed by hemodialysis start through a central venous catheter. During this period a sepsis due to central venous catheter infection occurred, implying four weeks of intravenous antibiotics. Discussion and Conclusion: Although there has been an increase in the number of publications on urgent -start peritoneal dialysis, showing that this technique has comparable results either to urgent -start hemodialysis and planned -start peritoneal dialysis, there still is some resistance to the use of this modality. Given the importance of this subject, this review aims to describe and summarize the available evidence on urgent -start peritoneal dialysis outcomes. Moreover, specific barriers are addressed. Its use is encouraged in hospitals where peritoneal dialysis is available, as an opportunity to improve chronic kidney disease patient management and transition to dialysis.