Clinical features and outcomes of acute kidney injury among patients with acute hepatitis A

Choi, Hee Kyoung; Song, Young Goo; Han, Sang Hoon; Ku, Nam Su; Jeong, Su Jin; Baek, Ji Hyeon; Kim, Hyewon; Kim, Sun Bean; Kim, Chang Oh; Kim, June Myung; Choi, Jun Yong

doi:10.1016/j.jcv.2011.07.013

Cited by 22 publications

(13 citation statements)

References 28 publications

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“…Choi et al (27) conducted a retrospective case-control study of 30 acute kidney injury (AKI) patients with hepatitis A. These data indicated that total bilirubin is an independent risk factor for AKI with hepatitis.…”

Section: Systematic Review Of Clinical Studiesmentioning

confidence: 99%

Circulating bilirubin and defense against kidney disease and cardiovascular mortality: mechanisms contributing to protection in clinical investigations

Boon

Bulmer

Coombes

et al. 2014

American Journal of Physiology-Renal Physiology

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Unconjugated bilirubin is an endogenous circulating antioxidant, bound to albumin, and therefore is retained in the vascular compartment. Bilirubin has well-documented neurotoxic effects in infants; however, current evidence indicates mildly elevated bilirubin is associated with protection from cardiovascular disease and all-cause mortality in adults. Recent clinical studies show mildly elevated bilirubin is associated with protection from kidney damage and dysfunction, in addition to cardiovascular events and all-cause mortality in patients undergoing hemodialysis. This is the first review to examine the clinical evidence and summarize the potential mechanisms of action that link bilirubin to protection from kidney damage, subsequent kidney failure, and dialysis-related mortality. With this understanding, it is hoped that new therapies will be developed to prevent renal dysfunction and mortality from cardiovascular disease in at-risk individuals.

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Section: Systematic Review Of Clinical Studiesmentioning

confidence: 99%

Circulating bilirubin and defense against kidney disease and cardiovascular mortality: mechanisms contributing to protection in clinical investigations

Boon

Bulmer

Coombes

et al. 2014

American Journal of Physiology-Renal Physiology

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“…Disruption of mitochondrial homeostasis is linked to AKI caused by many renal stressors/toxicants [ 21 ]. It is well known that chronic or acute severe liver injury/liver failure (e.g., cirrhosis, cholestasis, alcoholic or viral hepatitis, I/R injury and LT) causes AKI but whether mitochondrial homeostasis is disrupted in these cases remains unclear [ 61 – 66 ].…”

Section: Discussionmentioning

confidence: 99%

Disrupted Renal Mitochondrial Homeostasis after Liver Transplantation in Rats

et al. 2015

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BackgroundSuppressed mitochondrial biogenesis (MB) contributes to acute kidney injury (AKI) after many insults. AKI occurs frequently after liver transplantation (LT) and increases mortality. This study investigated whether disrupted mitochondrial homeostasis plays a role in AKI after LT.MethodsLivers were explanted from Lewis rats and implanted after 18 h cold storage. Kidney and blood were collected 18 h after LT.ResultsIn the kidney, oxidative phosphorylation (OXPHOS) proteins ATP synthase-β and NADH dehydrogenase-3 decreased 44% and 81%, respectively, with marked reduction in associated mRNAs. Renal PGC-1α, the major regulator of MB, decreased 57% with lower mRNA and increased acetylation, indicating inhibited synthesis and suppressed activation. Mitochondrial transcription factor-A, which controls mtDNA replication and transcription, protein and mRNA decreased 66% and 68%, respectively, which was associated with 64% decreases in mtDNA. Mitochondrial fission proteins Drp-1 and Fis-1 and mitochondrial fusion protein mitofusin-1 all decreased markedly. In contrast, PTEN-induced putative kinase 1 and microtubule-associated protein 1A/1B-light chain 3 increased markedly after LT, indicating enhanced mitophagy. Concurrently, 18- and 13-fold increases in neutrophil gelatinase-associated lipocalin and cleaved caspase-3 occurred in renal tissue. Both serum creatinine and blood urea nitrogen increased >2 fold. Mild to moderate histological changes were observed in the kidney, including loss of brush border, vacuolization of tubular cells in the cortex, cast formation and necrosis in some proximal tubular cells. Finally, myeloperoxidase and ED-1 also increased, indicating inflammation.ConclusionSuppression of MB, inhibition of mitochondrial fission/fusion and enhancement of mitophagy occur in the kidneys of recipients of liver grafts after long cold storage, which may contribute to the occurrence of AKI and increased mortality after LT.

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“…That is why one of cutoff levels of bilirbuin in our study is 1.2 mg/dl. However, not all studies supported the same conclusion [14,22,[35][36][37][38][39][40][41][42]. For example, Targher et al [22], did an observational study with 2,678 patients and they found that total bilirubin was inversely associated with eGFR in both non-diabetic (r = -0.17; p<0.0001) and diabetic patients (r = -0.14; p<0.05).…”

Section: Plos Onementioning

confidence: 99%

“…bacterial peritonitis [36], and heart failure [42]. On the contrary, in patients with nonfulminant hepatitis A, lower levels of bilirubin are associated with fewer [37]. In the vent of hepatopathy, total bilirubin level is no longer associated with the protective effects from cardiovascular disease.…”

Section: Plos Onementioning

confidence: 99%

Severe hyperbilirubinemia is associated with higher risk of contrast-related acute kidney injury following contrast-enhanced computed tomography

Cheng

et al. 2020

PLoS ONE

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Introduction Contrast-induced acute kidney injury (CI-AKI) is associated with high risks of morbidity and mortality. Hyperbilirubinemia might have some renal protection but with no clear cutoff value for protection. Related studies are typically on limited numbers of patients and only in conditions of vascular intervention. Methods We performed this study to elucidate CI-AKI in patients after contrast-enhanced computed tomography (CCT). The outcomes were CI-AKI, dialysis and mortality. Patients were divided to three groups based on their serum levels of total bilirubin: �1.2 mg/dl, 1.3-2.0 mg/dl, and >2.0 mg/dl. Results We enrolled a total of 9,496 patients who had received CCT. Patients with serum total bilirubin >2.0 mg/dl were associated with CI-AKI. Those undergoing dialysis had the highest incidence of PC-AKI (p<0.001). No difference was found between the two groups of total bilirubin �1.2 and 1.3-2.0 mg/dl. Patients with total bilirubin >2mg/dl were associated with CI-AKI (OR = 1.89, 1.53-2.33 of 95% CI), dialysis (OR = 1.40, 1.01-1.95 of 95% CI) and mortality (OR = 1.63, 1.38-1.93 of 95% CI) after adjusting for laboratory data and all comorbidities (i.e., cerebrovascular disease, coronary artery disease, peripheral arterial disease, and acute myocardial infarction, diabetes mellitus, hypertension, gastrointestinal bleeding, cirrhosis, peritonitis, ascites, hepatoma, shock lung and colon cancer). We concluded that total bilirubin level >2 mg/dl is an independent risk factor for CI-AKI, dialysis and mortality after CCT. These patients also had high risks for cirrhosis or hepatoma.

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Clinical features and outcomes of acute kidney injury among patients with acute hepatitis A

Cited by 22 publications

References 28 publications

Circulating bilirubin and defense against kidney disease and cardiovascular mortality: mechanisms contributing to protection in clinical investigations

Circulating bilirubin and defense against kidney disease and cardiovascular mortality: mechanisms contributing to protection in clinical investigations

Disrupted Renal Mitochondrial Homeostasis after Liver Transplantation in Rats

Severe hyperbilirubinemia is associated with higher risk of contrast-related acute kidney injury following contrast-enhanced computed tomography

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