scholarly journals Urinary Biomarkers of Acute Kidney Injury in Patients with Liver Cirrhosis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Anass Ahmed Qasem ◽  
Salama Elsayed Farag ◽  
Emad Hamed ◽  
Mohamed Emara ◽  
Ahmed Bihery ◽  
...  

Acute kidney injury (AKI) is a common complication in cirrhotic patients. Serum creatinine is a poor biomarker for detection of renal impairment in cirrhotic patients. This study aimed to evaluate urinary neutrophil gelatinase-associated lipocalin (NGAL) and urinary interleukin-18 (IL-18) as early biomarkers of acute kidney injury in cirrhotic patients. 160 patients with cirrhosis admitted to the Liver Units at Zagazig University Hospitals were classified into three groups: (I) nonascitic patients, (II) ascitic patients without renal impairment, and (III) ascitic patients with renal impairment. Patients with renal impairment were further divided into four subgroups: [A] prerenal azotemia, [B] chronic kidney disease (CKD), [C] hepatorenal syndrome (HRS), and [D] acute tubular necrosis (ATN). Significant elevation of both urinary NGAL and urinary IL-18 in cirrhotic patients with renal impairment especially in patients with ATN was observed. Urinary NGAL and urinary IL-18 have the ability to differentiate between AKI types in patients with cirrhosis. This could improve risk stratification for patients admitted to the hospital with cirrhosis, perhaps leading to early ICU admission, transplant evaluation, and prompt initiation of HRS therapy and early management of AKI.

2021 ◽  
Author(s):  
Arshpal Gill ◽  
Ra’ed Nassar ◽  
Ruby Sangha ◽  
Mohammed Abureesh ◽  
Dhineshreddy Gurala ◽  
...  

Hepatorenal Syndrome (HRS) is an important condition for clinicians to be aware of in the presence of cirrhosis. In simple terms, HRS is defined as a relative rise in creatinine and relative drop in serum glomerular filtration rate (GFR) alongside renal plasma flow (RPF) in the absence of other competing etiologies of acute kidney injury (AKI) in patients with hepatic cirrhosis. It represents the end stage complication of decompensated cirrhosis in the presence of severe portal hypertension, in the absence of prerenal azotemia, acute tubular necrosis or others. It is a diagnosis of exclusion. The recognition of HRS is of paramount importance for clinicians as it carries a high mortality rate and is an indication for transplantation. Recent advances in understanding the pathophysiology of the disease improved treatment approaches, but the overall prognosis remains poor, with Type I HRS having an average survival under 2 weeks. Generally speaking, AKI and renal failure in cirrhotic patients carry a very high mortality rate, with up to 60% mortality rate for patients with renal failure and cirrhosis and 86.6% of overall mortality rates of patients admitted to the intensive care unit. Of the various etiologies of renal failure in cirrhosis, HRS carries a poor prognosis among cirrhotic patients with acute kidney injury. HRS continues to pose a diagnostic challenge. AKI can be either pre-renal, intrarenal or postrenal. Prerenal causes include hypovolemia, infection, use of vasodilators and functional due to decreased blood flow to the kidney, intra-renal such as glomerulopathy, acute tubular necrosis and post-renal such as obstruction. Patients with cirrhosis are susceptible to developing renal impairment. HRS may be classified as Type 1 or rapidly progressive disease, and Type 2 or slowly progressive disease. There are other types of HRS, but this chapter will focus on Type 1 HRS and Type 2 HRS. HRS is considered a functional etiology of acute kidney injury as there is an apparent lack of nephrological parenchymal damage. It is one several possibilities for acute kidney injury in patients with both acute and chronic liver disease. Acute kidney injury (AKI) is one of the most severe complications that could occur with cirrhosis. Up to 50% of hospitalized patients with cirrhosis can suffer from acute kidney injury, and as mentioned earlier an AKI in the presence of cirrhosis in a hospitalized patient has been associated with nearly a 3.5-fold increase in mortality. The definition of HRS will be discussed in this chapter, but it is characterized specifically as a form of acute kidney injury that occurs in patients with advanced liver cirrhosis which results in a reduction in renal blood flow, unresponsive to fluids this occurs in the setting of portal hypertension and splanchnic vasodilation. This chapter will discuss the incidence of HRS, recognizing HRS, focusing mainly on HRS Type I and Type II, recognizing competing etiologies of renal impairment in cirrhotic patients, and the management HRS.


2017 ◽  
Vol 2 (4) ◽  
pp. 47-52
Author(s):  
SV V Aborin ◽  
DV V Pechkurov ◽  
LI I Zakharova

In this study, we evaluated the diagnostic and prognostic value of the neutrophil gelatinase-associated lipocalin-2 (NGAL) level in urine as an early marker of renal dysfunction in preterm infants with very low and extremely low body weight. Aim - evaluation of diagnostic and prognostic significance of the urinary NGAL level as an early biomarker of acute kidney injury (AKI) in preterm infants. Materials and methods. The study included 104 premature babies, 78 of which formed the main group (AKI), and 26 babies - the comparison group (non-AKI). The main criterion for acute kidney injury in neonates according to neonatal classification AKIN (2011) is creatinine level > 1.5 mg/dL at the age of not earlier than 48 hours after birth. Results. The study identified a statistically significant correlation in the level of NGAL in the urine of children from the main and comparison groups. Conclusion. Biomarkers of kidney damage can give more accurate information than creatinine for the early diagnosis of AKI in children. In a comprehensive assessment of a child, it is necessary to take note of the indicators of renal function (creatinine, GFR) and biomarkers of injury (NGAL). This approach will allow performing the diagnostics and therapy of early AKI in children based on structural and functional criteria.


2020 ◽  
Vol 26 (7) ◽  
pp. 1643-1649
Author(s):  
Elliyeh Ghadrdan ◽  
Sholeh Ebrahimpour ◽  
Sanambar Sadighi ◽  
Samira Chaibakhsh ◽  
Zahra Jahangard-Rafsanjani

Introduction Cisplatin-associated acute kidney injury (AKI) is the major limitation to the use of cisplatin-based chemotherapy regimens. Serum creatinine as a traditional marker did not increase in a timely enough fashion in AKI patients. Therefore, recently, the novel markers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were considered for early detection of AKI. The aim of this study was to compare the sensitivity and specificity of urinary NGAL and KIM-1 with serum creatinine in cisplatin related AKI. Methods Patients ≥18 years with solid tumors who received cisplatin-based chemotherapy were included. Urine samples were collected 0, 6 and 24 h after cisplatin infusion and the urinary NGAL, KIM-1, and creatinine concentrations were evaluated. NGAL and KIM-1 concentrations were adjusted based on urine creatinine to eliminate hydration effects. Serum creatinine levels were assessed at the base and 72 h after cisplatin administration. Results Seven out of the 35 recruited patients (20%) suffered from AKI defined by Acute Kidney Injury Network criteria. In AKI patients, the ratio of urinary KIM-1–creatinine at 24 h compared to baseline (24 h/baseline) and NGAL–creatinine 24 h/baseline were significantly higher than those of non-AKI group ( p = 0.037 and 0.047 respectively). The area under the receiver-operating characteristic curve for KIM-1–creatinine 24 h/baseline and NGAL–creatinine 24 h/baseline were 0.78 (0.59–0.96, p = 0.032) and 0.77 (0.57–0.97, p = 0.036) respectively. Conclusions Our findings showed that the changes in urinary NGAL–creatinine and KIM-1–creatinine ratios, 24 h after cisplatin administration can be utilized to predict AKI in cisplatin recipients.


2019 ◽  
Vol 49 (3) ◽  
pp. 189-192 ◽  
Author(s):  
Tamer R Fouad ◽  
Eman Abdelsameea ◽  
Maha Elsabaawy ◽  
M. Ashraf Eljaky ◽  
Soha Zaki El-shenawy ◽  
...  

Cirrhotic patients with ascites are at high risk of developing spontaneous bacterial peritonitis (SBP). After exclusion of patients with acute kidney injury (AKI) or other infections, urinary neutrophil gelatinase-associated lipocalin (NGAL) levels were compared between two matched groups of Egyptian cirrhotic patients with ascites, mostly secondary to hepatitis C infection (98%). Group 1 had SBP (n = 41) and group 2 did not (n = 45). By univariate analysis, urinary-NGAL, high total bilirubin, serum creatinine, international normalised ratio and the Model of End-Stage Liver Disease (MELD) score and low platelet count were all significantly correlated with the presence of SBP, but only urinary-NGAL could independently predict development of SBP ( P = 0.001). Urinary-NGAL at a cut-off value of 1225 pg/mL, showed a sensitivity of 95% and a specificity of 76%, and is therefore a most useful tool.


2018 ◽  
Vol 17 (4) ◽  
pp. 624-630 ◽  
Author(s):  
Hassan S. Hamdy ◽  
Ahmed El-Ray ◽  
Mohamed Salaheldin ◽  
Mohammad Lasheen ◽  
Mohamed Aboul-Ezz ◽  
...  

2020 ◽  
Vol 175 (1) ◽  
pp. 75-86 ◽  
Author(s):  
Sandra M Sancho-Martínez ◽  
Víctor Blanco-Gozalo ◽  
Yaremi Quiros ◽  
Laura Prieto-García ◽  
María J Montero-Gómez ◽  
...  

Abstract Neutrophil gelatinase-associated lipocalin (NGAL) is a secreted low-molecular weight iron-siderophore-binding protein. NGAL overexpression in injured tubular epithelia partly explains its utility as a sensitive and early urinary biomarker of acute kidney injury (AKI). Herein, we extend mechanistic insights into the source and kinetics of urinary NGAL excretion in experimental AKI. Three models of experimental AKI were undertaken in adult male Wistar rats; renal ischemia-reperfusion injury (IRI) and gentamicin (G) and cisplatin (Cisp) nephrotoxicity. Alongside standard histological and biochemical assessment of AKI, urinary NGAL excretion rate, plasma NGAL concentration, and renal NGAL mRNA/protein expression were assessed. In situ renal perfusion studies were undertaken to discriminate direct shedding of NGAL to the urine from addition of NGAL to the urine secondary to alterations in the tubular handling of glomerular filtrate-derived protein. Renal NGAL expression and urinary excretion increased in experimental AKI. In acute studies in both the IRI and G models, direct renal perfusion with Kreb’s buffer eliminated urinary NGAL excretion. Addition of exogenous NGAL to the Kreb’s buffer circuit, reestablishment of perfusion with systemic blood or reperfusion with renal vein effluent restored high levels of urinary NGAL excretion. Urinary NGAL excretion in AKI arises in large proportion from reduced reabsorption from the glomerular filtrate. Hence, subclinical cellular dysfunction could increase urinary NGAL, particularly in concert with elevations in circulating prerenal NGAL and/or pharmacological inhibition of tubular reabsorption. More granular interpretation of urinary NGAL measurements could optimize the scope of its clinical utility as a biomarker of AKI.


Author(s):  
Saban Elitok ◽  
Prasad Devarajan ◽  
Rinaldo Bellomo ◽  
Berend Isermann ◽  
Michael Haase ◽  
...  

Abstract Background Acute kidney injury (AKI) subtypes combining kidney functional parameters and injury biomarkers may have prognostic value. We aimed to determine whether neutrophil gelatinase-associated lipocalin (NGAL)/hepcidin-25 ratio (urinary concentrations of NGAL divided by that of hepcidin-25) defined subtypes are of prognostic relevance in cardiac surgery patients. Methods We studied 198 higher-risk cardiac surgery patients. We allocated patients to four groups: Kidney Disease Improving Global Outcomes (KDIGO)-AKI-negative and NGAL/hepcidin-25 ratio-negative (no AKI), KDIGO AKI-negative and NGAL/hepcidin-25 ratio-positive (subclinical AKI), KDIGO AKI-positive and NGAL/hepcidin-25 ratio-negative (clinical AKI), KDIGO AKI-positive and NGAL/hepcidin-25 ratio-positive (combined AKI). Outcomes included in-hospital mortality (primary) and long-term mortality (secondary). Results We identified 127 (61.6%) patients with no AKI, 13 (6.6%) with subclinical, 40 (20.2%) with clinical and 18 (9.1%) with combined AKI. Subclinical AKI patients had a 23-fold greater in-hospital mortality than no AKI patients. For combined AKI vs. no AKI or clinical AKI, findings were stronger (odds ratios (ORs): 126 and 39, respectively). After adjusting for EuroScore, volume of intraoperative packed red blood cells, and aortic cross-clamp time, subclinical and combined AKI remained associated with greater in-hospital mortality than no AKI and clinical AKI (adjusted ORs: 28.118, 95% CI 1.465–539.703; 3.737, 95% CI 1.746–7.998). Cox proportional hazard models found a significant association of biomarker-informed AKI subtypes with long-term survival compared with no AKI (adjusted ORs: pooled subclinical and clinical AKI: 1.885, 95% CI 1.003–3.542; combined AKI: 1.792, 95% CI 1.367–2.350). Conclusions In the presence or absence of KDIGO clinical criteria for AKI, the urinary NGAL/hepcidin-25-ratio appears to detect prognostically relevant AKI subtypes. Trial registration number NCT00672334, clinicaltrials.gov, date of registration: 6th May 2008, https://clinicaltrials.gov/ct2/show/NCT00672334. Graphic abstract Definition of AKI subtypes: subclinical AKI (KDIGO negative AND Ratio-positive), clinical AKI (KDIGO positive AND Ratio-negative) and combined AKI (KDIGO positive AND Ratio-positive) with urinary NGAL/hepcidin-25 ratio-positive cut-off at 85% specificity for in-hospital death. AKI, acute kidney injury. AUC, area under the curve. NGAL, neutrophil gelatinase-associated lipocalin. KDIGO, Kidney Disease Improving Global Outcomes Initiative AKI definition.


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