Renin-Angiotensin System Inhibitor is Associated with Lower Risk of Ensuing Chronic Kidney Disease after Functional Recovery from Acute Kidney Injury

Chou, Yu‐Hsiang; Huang, Tao‐Min; Pan, Szu-Yu; Chang, Chin‐Hao; Lai, Chun-Fu; Wu, Vin‐Cent; Wu, Ming-Shiou; Wu, Kwan‐Dun; Chu, Tzong‐Shinn; Lin, Shuei‐Liong

doi:10.1038/srep46518

Cited by 50 publications

(50 citation statements)

References 65 publications

(87 reference statements)

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“…Moreover, we have demonstrated that C20 suppressed renin expression under normal levels of calcium and phosphorus in vivo, which further indicated the beneficial role of C20 on renal protection. The down-regulation of renin expression markedly ameliorated the renal and cardiomyocyte injury [39,42].…”

Section: Discussionmentioning

confidence: 99%

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Riligustilide Attenuated Renal Injury by the Blockade of Renin

Kong

Han

et al. 2018

Cell Physiol Biochem

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Background/Aims: Nephropathy related with renin can be alleviated with ACE-inhibitors or AT1R blockers, whereas they might be ineffective after long-term administration because of a feedback production of enhanced renin. Therefore, it is urgent to develop a new category of anti-nephropathy medicine directly targeting renin. Riligustilide (C20), originally isolated from the Chinese herb Ligusticumporteri, a rhizome, was confirmed effective against many diseases. Methods: The therapeutic effect of C20 on renal injury and its underlying mechanism were investigated in three different nephrotic models, which were spontaneously hypertension rats (SHR) model, diabetic nephropathy in BTBR ob/ob mice model and 5/6-nephrectomized (5/6NX) rats model. Results: The intensity of kidney fibrosis was extensively decreased in the C20-treated rats compared to the vehicle animals. C20 significantly alleviated renal injury much more in 5/6 NX rats than in vehicle group. The rats in 5/6 NX without administrated C20 developed albuminuria earlier with more severe symptoms. Additionally, our findings showed that C20 down-regulated the renin expression and relocation of CREB-CBP complex in vivo and in vitro. Conclusion: C20 plays importantly reno-protective roles most likely through the relocation of CREB-CBP complex.

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Section: Discussionmentioning

confidence: 99%

“…Therefore, increased oxygen consumption and work burden in hypertrophic nephrons (Fig. 1, F) can give rise to activated renin signaling system and result eventually in glomerulosclerosis and tubulointerstitial fibrosis [39]. It has been shown that the degree of renal injury is positive association with the activity of renin [36].…”

Section: Discussionmentioning

confidence: 99%

Riligustilide Attenuated Renal Injury by the Blockade of Renin

Kong

Han

et al. 2018

Cell Physiol Biochem

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“…In Taiwan, Lai et al reported the median interval between the onset of AKI and the composite endpoints ‘stage 3 CKD or death’ was 685 days in an analysis of 634 critically ill patients with AKI not requiring dialysis. In our recent study, 39.7% patients with renal functional recovery from cardiac surgery‐associated AKI (CSA‐AKI) developed ensuing CKD during median follow‐up period of 2.99 years …”

Section: Epidemiology Of Aki‐ckd Continuummentioning

confidence: 99%

“…In our recent study, 39.7% patients with renal functional recovery from cardiac surgery-associated AKI (CSA-AKI) developed ensuing CKD during median follow-up period of 2.99 years. 35…”

Section: Epidemiology Of Aki-ckd Continuummentioning

confidence: 99%

“…56 Our recent clinical study, which is the first one to evaluate the effect of RAS inhibitor administered post-operatively, further demonstrates lower rate of ensuing CKD (users vs non-users, 26.6 vs 42.2%) and longer median CKD-free survival time (users vs non-users, 1079 vs 520 days) in users of RAS inhibitor, started and continued after clinical renal recovery after CSA-AKI. 35 Therefore, RAS inhibitors, usually avoided during the acute phase of AKI events, are potential to be a powerful and safe agent to improve survival and renal outcome for patients recovering from AKI who are often neglected (Fig. 1).…”

Section: Clinical Study Of Ras Inhibitor In Aki-ckd Continuummentioning

confidence: 99%

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Role of renin‐angiotensin system in acute kidney injury‐chronic kidney disease transition

2018

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Acute kidney injury (AKI) can increase the risk of developing incident chronic kidney disease (CKD). The severity, frequency and duration of AKI are crucial predictors of poor renal outcome. A repair process after AKI can be adaptive and kidney recovers completely after a mild injury. However, severe injury will lead to a maladaptive repair, which frequently progresses to nephron loss, vascular rarefaction, chronic inflammation and fibrosis. Although different mechanisms underlying AKI‐CKD transition have been extensively discussed, no definite intervention has been proved effective to block or to retard the transition until recently. In CKD, renin‐angiotensin system (RAS) inhibitor has been proved effective to slow down disease progression. Furthermore, RAS needs to be highlighted again in AKI‐CKD transition because recent animal studies have shown the activation of intra‐renal RAS after AKI, and RAS blockade can reduce the ensuing CKD and mortality. In patients with the complete renal recovery after AKI, administration of RAS inhibitor is associated with reduced risk of subsequent CKD as well. In this article, we will demonstrate the role of RAS in AKI‐CKD transition comprehensively. We will then emphasize the promising effect of RAS inhibitor on CKD prevention in patients recovering from AKI based on evidence from the bench to clinical research. All of these discussions will contribute to the establishment of reliable monitoring and therapeutic strategies for patients with functional recovery from AKI who can be most easily ignored.

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Post–Acute Kidney Injury Proteinuria and Subsequent Kidney Disease Progression

et al. 2020

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IMPORTANCE Among patients who had acute kidney injury (AKI) during hospitalization, there is a need to improve risk prediction such that those at highest risk for subsequent loss of kidney function are identified for appropriate follow-up.OBJECTIVE To evaluate the association of post-AKI proteinuria with increased risk of future loss of renal function. DESIGN, SETTING, AND PARTICIPANTSThe Assessment, Serial Evaluation, and Subsequent Sequelae in Acute Kidney Injury (ASSESS-AKI) Study was a multicenter prospective cohort study including 4 clinical centers in North America included 1538 patients enrolled 3 months after hospital discharge between December 2009 and February 2015.EXPOSURES Urine albumin-to-creatinine ratio (ACR) quantified 3 months after hospital discharge.MAIN OUTCOMES AND MEASURES Kidney disease progression defined as halving of estimated glomerular filtration rate (eGFR) or end-stage renal disease. RESULTSOf the 1538 participants, 769 (50%) had AKI durring hospitalization. The baseline study visit took place at a mean (SD) 91 ( 23) days after discharge. The mean (SD) age was 65 (13) years; the median eGFR was 68 mL/min/1.73 m 2 ; and the median urine ACR was 15 mg/g. Overall, 547 (37%) study participants were women and 195 (13%) were black. After a median follow-up of 4.7 years, 138 (9%) participants had kidney disease progression. Higher post-AKI urine ACR level was associated with increased risk of kidney disease progression (hazard ratio [HR], 1.53 for each doubling; 95% CI, 1.45-1.62), and urine ACR measurement was a strong discriminator for future kidney disease progression (C statistic, 0.82). The performance of urine ACR was stronger in patients who had had AKI than in those who had not (C statistic, 0.70). A comprehensive model of clinical risk factors (eGFR, blood pressure, and demographics) including ACR provided better discrimination for predicting kidney disease progression after hospital discharge among those who had had AKI (C statistic, 0.85) vs those who had not (C statistic, 0.76). In the entire matched cohort, after taking into account urine ACR, eGFR, demographics, and traditional chronic kidney risk factors determined 3 months after discharge, AKI (HR, 1.46; 95% CI, 0.51-4.13 for AKI vs non-AKI) or severity of AKI (HR, 1.54; 95% CI, 0.50-4.72 for AKI stage 1 vs non-AKI; HR, 0.56; 95% CI, 0.07-4.84 for AKI stage 2 vs non-AKI; HR, 2.24; 95% CI, 0.33-15.29 for AKI stage 3 vs non-AKI) was not independently associated with more rapid kidney disease progression.CONCLUSIONS AND RELEVANCE Proteinuria level is a valuable risk-stratification tool in the post-AKI period. These results suggest there should be more widespread and routine quantification of proteinuria after hospitalized AKI.

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Renin-Angiotensin System Inhibitor is Associated with Lower Risk of Ensuing Chronic Kidney Disease after Functional Recovery from Acute Kidney Injury

Cited by 50 publications

References 65 publications

Riligustilide Attenuated Renal Injury by the Blockade of Renin

Riligustilide Attenuated Renal Injury by the Blockade of Renin

Role of renin‐angiotensin system in acute kidney injury‐chronic kidney disease transition

Post–Acute Kidney Injury Proteinuria and Subsequent Kidney Disease Progression

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