Extended Mortality and Chronic Kidney Disease After Septic Acute Kidney Injury

2018 ◽  
Vol 35 (6) ◽  
pp. 527-535 ◽  
Author(s):  
Horng-Ruey Chua ◽  
Weng-Kin Wong ◽  
Venetia Huiling Ong ◽  
Dipika Agrawal ◽  
Anantharaman Vathsala ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Simplified Acute Physiology Score ◽  
Cardiac Events ◽  
Ckd Progression ◽  
Septic Acute Kidney Injury ◽  
Adverse Cardiac Events ◽  
Kidney Disease Progression

Purpose: To evaluate 1-year mortality in patients with septic acute kidney injury (AKI) and to determine association between initial AKI recovery patterns ( reversal within 5 days, beyond 5 days but recovery, or nonrecovery) and chronic kidney disease (CKD) progression. Methods: Prospective observational study, with retrospective evaluation of initial nonconsenters, of critically ill patients with septic AKI. Results: We studied 207 patients (age, mean [SD]: 64 [16] years, 39% males), of which 56 (27%), 18 (9%), and 9 (4%) died in intensive care unit (ICU), post-ICU in hospital, and posthospitalization, respectively. Infections (including pneumonia) and major adverse cardiac events accounted for 64% and 12% of deaths, respectively. Factors independently associated with 1-year mortality include older age, ischemic heart disease, higher Simplified Acute Physiology Score II, central nervous system or musculoskeletal primary infections, higher daily fluid balance (FB), and frusemide administration during ICU stay (all P < .05). Among 63 patients receiving renal replacement therapy (RRT), hospital mortality was higher with cumulative median FB >8 L versus ≤8 L at RRT initiation (57% vs 24%; P = .009); there was trend for less ICU- and RRT-free days at day 28 in patients with higher FB pre-RRT ( P = NS). Chronic kidney disease progression over 1 year developed in 21%, 30%, and 79% of 105 initial survivors with AKI reversal, recovery, and nonrecovery, respectively ( P < .001). Acute kidney injury nonrecovery during hospitalization independently predicted CKD progression ( P = .001). Conclusions: Patients with septic AKI had 40% 1-year mortality, mainly associated with infections. High FB and frusemide administration were modifiable risk factors. Risk of CKD progression is high especially with initial AKI nonrecovery.

scholarly journals HMOX1 and Acute Kidney Injury in Sickle Cell Anemia

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 686-686
Author(s):  
Santosh L. Saraf ◽  
Maya Viner ◽  
Ariel Rischall ◽  
Binal Shah ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Risk Factor ◽  
Kidney Disease ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Kidney Injury ◽  
Ckd Progression ◽  
Kdigo Guidelines

Abstract Acute kidney injury (AKI) is associated with tubulointerstitial fibrosis and nephron loss and may lead to an increased risk for subsequently developing chronic kidney disease (CKD). In adults with sickle cell anemia (SCA), high rates of CKD have been consistently observed, although the incidence and risk factors for AKI are less clear. We evaluated the incidence of AKI, defined according to Kidney Disease Improving Global Outcomes (KDIGO) guidelines as a rise in serum creatinine by ≥0.3mg/dL within 48 hours or ≥1.5 times baseline within seven days, in 158 of 299 adult SCA patients enrolled in a longitudinal cohort from the University of Illinois at Chicago. These patients were selected based on the availability of genotyping for α-thalassemia, BCL11A rs1427407, APOL1 G1/G2, and the HMOX1 rs743811 and GT-repeat variants. Median values and interquartile range (IQR) are provided. With a median follow up time of 66 months (IQR, 51-74 months), 137 AKI events were observed in 63 (40%) SCA patients. AKI was most commonly observed in the following settings: acute chest syndrome (25%), an uncomplicated vaso-occlusive crisis (VOC)(24%), a VOC with pre-renal azotemia determined by a fractional excretion of sodium &lt;1% or BUN-to-creatinine ratio &gt;20:1 (14%), or a VOC with increased hemolysis, defined as an increase in serum LDH or indirect bilirubin level &gt;1.5 times over the baseline value at the time of enrollment (12%). Compared to individuals who did not develop AKI, SCA adults who developed an AKI event were older (AKI: median and IQR age of 35 (26-46) years, no AKI: 28 (23 - 26) years; P=0.01) and had a lower estimated glomerular filtration rate (eGFR) (AKI: median and IQR eGFR of 123 (88-150) mL/min/1.73m2, no AKI: 141 (118-154) mL/min/1.73m2; P=0.02) by the Kruskal-Wallis test at the time of enrollment. We evaluated the association of a panel of candidate gene variants with the risk of developing an AKI event. These included loci related to the degree of hemolysis (α-thalassemia, BCL11A rs1427407), to chronic kidney disease (APOL1 G1/G2 risk variants), and to heme metabolism (HMOX1) . Using a logistic regression model that adjusted for age and eGFR at the time of enrollment, the risk of an AKI event was associated with older age (10-year OR 2.6, 95%CI 1.4-4.8, P=0.002), HMOX1 rs743811 (OR 3.1, 95%CI 1.1-8.7, P=0.03), and long HMOX1 GT-repeats, defined as &gt;25 repeats (OR 2.5, 95%CI 1.01-6.1, P=0.04). Next, we assessed whether AKI is associated with a more rapid decline in eGFR and with CKD progression, defined as a 50% reduction in eGFR, on longitudinal follow up. Using a mixed effects model that adjusted for age and eGFR at the time of enrollment, the rate of eGFR decline was significantly greater in those with an AKI event (β = -0.51) vs. no AKI event (β = -0.16) (P=0.03). With a median follow up time of 66 months (IQR, 51-74 months), CKD progression was observed in 21% (13/61) of SCA patients with an AKI event versus 9% (8/88) without an AKI event. After adjusting for age and eGFR at the time of enrollment, the severity of an AKI event according to KDIGO guidelines (stage 1 if serum creatinine rises 1.5-1.9 times baseline, stage 2 if the rise is 2.0-2.9 times baseline, and stage 3 if the rise is ≥3 times baseline or ≥4.0 mg/dL or requires renal replacement therapy) was a risk factor for CKD progression (unadjusted HR 1.6, 95%CI 1.1-2.3, P=0.02; age- and eGFR-adjusted HR 1.6, 95%CI 1.1-2.5, P=0.03). In conclusion, AKI is commonly observed in adults with sickle cell anemia and is associated with increasing age and the HMOX1 GT-repeat and rs743811 polymorphisms. Furthermore, AKI may be associated with a steeper decline in kidney function and more severe AKI events may be a risk factor for subsequent CKD progression in SCA. Future studies understanding the mechanisms, consequences of AKI on long-term kidney function, and therapies to prevent AKI in SCA are warranted. Disclosures Gordeuk: Emmaus Life Sciences: Consultancy.

scholarly journals Low-dose hydralazine prevents fibrosis in a murine model of acute kidney injury–to–chronic kidney disease progression

2017 ◽  
Vol 91 (1) ◽  
pp. 157-176 ◽  
Author(s):  
Björn Tampe ◽  
Ulrike Steinle ◽  
Désirée Tampe ◽  
Julienne L. Carstens ◽  
Peter Korsten ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Disease Progression ◽  
Murine Model ◽  
Low Dose ◽  
Kidney Injury ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression

scholarly journals Vitamin D Deficiency Aggravates Chronic Kidney Disease Progression after Ischemic Acute Kidney Injury

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107228 ◽  
Author(s):  
Janaína Garcia Gonçalves ◽  
Ana Carolina de Bragança ◽  
Daniele Canale ◽  
Maria Heloisa Massola Shimizu ◽  
Talita Rojas Sanches ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Disease Progression ◽  
Vitamin D Deficiency ◽  
Kidney Injury ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression ◽  
Ischemic Acute Kidney Injury

scholarly journals P0547THE DELETION OF AKT1 ATTENUATES RENAL FIBROSIS AND TUBULAR EPITHELIAL-MESENCHYMAL TRANSITION DURING ACUTE KIDNEY INJURY TO CHRONIC KIDNEY DISEASE PROGRESSION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Byung Min Ye ◽  
Il Young Kim ◽  
Min Jeong Kim ◽  
Soo Bong Lee ◽  
Dong Won Lee ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Epithelial Mesenchymal Transition ◽  
Kidney Injury ◽  
Wild Type ◽  
Ckd Progression ◽  
Mesenchymal Transition ◽  
Tgf Β1

Abstract Background and Aims Acute kidney injury (AKI) is an underestimated, yet important risk factor for the development of chronic kidney disease (CKD), which is characterized by the tubulointerstitial fibrosis and tubular epithelial-mesenchymal transition (EMT). Akt has been reported to be involved in renal fibrosis and EMT. Thus, we investigated the role of Akt1, one of the three Akt isoforms, in the murine model of AKI to CKD progression. Method We subjected the wild type and Akt1−/− mice to unilateral ischemia-reperfusion injury (UIRI). UIRI was induced by clamping the left renal artery for 30 min followed by reperfusion. After 6 weeks of UIRI, the renal fibrosis and EMT were assessed by histology, immunohistochemistry, and western blot. Results After 6 weeks after UIRI, we found that Akt1, not Akt2 or Akt3, was activated in UIRI-kidney. The tubulointerstitial fibrosis was significantly alleviated in Akt1−/− mice compared with the wild type (WT) mice. Besides, the deletion of Akt1 decreased the expression of the vimentin and α-SMA and increased the expression of E-cadherin, indicating the suppression of tubular EMT. However, there was no difference in the activity of TGF-β1/Smad signalling, which is the potent inducer of renal fibrosis and EMT, between WT mice and Akt1−/− mice. The deletion of Akt1 also increased the GSK-3β activity and decreased the expression of β-catenin, Snail, and twist1. Conclusion Our findings demonstrate that the deletion of Akt1 attenuates the renal fibrosis and tubular EMT independently of TGF-β1/Smad signalling during the AKI to CKD progression. Akt1 may be the therapeutic target against the AKI to CKD progression.

scholarly journals N-Acetylcysteine for Preventing of Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Cardiac Surgery: A Metaanalysis

2018 ◽  
Vol 21 (6) ◽  
pp. E513-E521 ◽  
Author(s):  
Guiyuan He ◽  
Qi Li ◽  
Wenxin Li ◽  
Li Wang ◽  
Jun Yang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Disease ◽  
Intravenous Infusion ◽  
Kidney Injury ◽  
Cochrane Library ◽  
Cardiac Events ◽  
Primary Analysis ◽  
Clinical Trial Registry

Objective: The aim of this study was to determine whether N-acetylcysteine (NAC) has an effect on acute kidney injury (AKI) in chronic kidney disease patients undergoing cardiac surgery. Methods: We reviewed literature through PubMed, Medline through PubMed and OVID, The Cochrane Library, Wan Fang Database, China Biology Medicine Database, Chinese Periodical Database, China Knowledge Resource Integrated Database, and Chinese Clinical Trial Registry (1980 to July 10, 2018). Two investigators independently collected the data and assessed the quality of each study. RevMan 5.3 was used for the present metaanalysis. Results: A total of 5 RCTs (N = 678 participants) were included in the primary analysis. Pooled analysis showed that intravenous infusion of NAC significantly reduced the incidence of AKI (RR = 0.77, 95% = 0.63 to 0.94, P < .01) and that NAC could decrease the adverse cardiac events (RR = 0.83, 95% = 0.70 to 0.97, P < .05), but that it may increase the length of stay in the ICU (mean difference [MD] = 2.1, 95% CI = 1.61 to 2.60, P < .01). There were no statistically significant differences between the 2 groups in the requirement for renal replacement therapy(RRT) (RR = 1.33, 95% = 0.63 to 2.81, P = .45) and all-cause mortality (RR = 0.51, 95% = 0.25 to 1.06, P = .07). Conclusion: Our study shows that intravenous infusion of NAC could prevent postoperative AKI in preexisting-renal-failure patients undergoing cardiac surgery.

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