scholarly journals Hepatorenal Syndrome

2021 ◽  
Author(s):  
Arshpal Gill ◽  
Ra’ed Nassar ◽  
Ruby Sangha ◽  
Mohammed Abureesh ◽  
Dhineshreddy Gurala ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Blood Flow ◽  
Mortality Rate ◽  
Kidney Injury ◽  
Type I ◽  
Tubular Necrosis ◽  
Cirrhotic Patients

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.

scholarly journals Monitorization of NGAL, Creatinine and Renal Blood Flow in the Follow-up of Acute Kidney Injury in Intensive Care

2021 ◽  
Author(s):  
Mehmet Süleyman Sabaz ◽  
Halil Çetingök ◽  
Gökhan Sertcakacılar ◽  
Yusuf Ziya Yener ◽  
Erdal Atiç ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Blood Flow ◽  
Intensive Care ◽  
Renal Blood Flow ◽  
Early Stage ◽  
Kidney Injury ◽  
Serial Measurement ◽  
Neutrophil Gelatinase Associated Lipocalin

Objectıve: Acute Kidney Injury (AKI) and subsequent renal failure are the leading causes of morbidity and mortality in the intensive care unit (ICU). In this study, it was planned to compare Neutrophil Gelatinase-associated Lipocalin (NGAL) and creatinine values in patients diagnosed with AKI and to determine the effect of renal dose dopamine use on renal blood flow, development of chronic renal failure (CRF) and mortality. Materıals and methods: This prospective study was planned with 35 patients developed AKI in the ICU of Bakırköy Dr. Sadi Konuk Training and Research Hospital. The patients were randomized into 2 groups as 18 patients who received dopamine treatment with the recommendation of the cardiology clinic and 17 patients who did not receive dopamine treatment. Urea, creatinine and NGAL plasma levels were compared between groups. Results: There was no difference between the groups in terms of age, gender and AKI stage. The 0th, 24th hour results and 24-hour changes of urea, creatinine and NGAL values of dopamine patient, who took dopamine, were found to be similar to those of patients who did not take dopamine. A significant positive correlation was found between the 24-hour change in creatinine value and the 24-hour change in NGAL (r=0.374; p<0.05). There was no significant change in the diameter and flow of renal arteries between measurements in patients who received dopamine. The rates of patients who regain normal kidney functions, develop CRF or develop mortality between the two groups were found to be similar. Conclusıon: Treatment results of AKI developing in ICU are not satisfactory. Low-dose dopamine treatment has no effect on patient outcomes in these patients. NGAL is a biomarker that has the ability to show renal damage at an early stage. Serial measurement of NGAL concentration during ICU stay may benefit the clinician in early diagnosis and follow-up of AKI.

scholarly journals Acute Kidney Injury Epidemiology in pediatrics

2019 ◽  
Vol 41 (2) ◽  
pp. 275-283 ◽  
Author(s):  
Thais Lira Cleto-Yamane ◽  
Conrado Lysandro Rodrigues Gomes ◽  
Jose Hermogenes Rocco Suassuna ◽  
Paulo Koch Nogueira
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Regional Differences ◽  
Kidney Injury ◽  
Developed Countries ◽  
Mesh Term ◽  
Renal Diseases ◽  
Tubular Necrosis ◽  
Related Mortality

Abstract We performed a search in the MEDLINE database using the MeSH term: "Acute Kidney Injury", selecting the subtopic "Epidemiology", and applying age and year of publication filters. We also searched for the terms: "acute renal failure" and "epidemiology" "acute tubular necrosis" and "epidemiology" in the title and summary fields with the same filters. In a second search, we searched in the LILACS database, with the terms: "acute renal injury", or "acute renal failure" or "acute kidney injury" and the age filter. All abstracts were evaluated by the authors and the articles considered most relevant, were examined in their entirety. Acute Kidney Injury (AKI) -related mortality ranged from 3-63% in the studies included in this review. AKI etiology has marked regional differences, with sepsis being the main cause in developed countries. In developing countries, primary renal diseases and hypovolemia are still a common cause of AKI.

scholarly journals Evaluation of the Biomarkers HMGB1 and IL-6 as Predictors of Mortality in Cirrhotic Patients with Acute Kidney Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Célio Geraldo de Oliveira Gomes ◽  
Marcus Vinicius Melo de Andrade ◽  
Ludmila Resende Guedes ◽  
Henrique Carvalho Rocha ◽  
Roberto Gardone Guimarães ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Multivariate Analysis ◽  
Mortality Rate ◽  
Prospective Observational Study ◽  
Laboratory Data ◽  
Kidney Injury ◽  
Mortality Rates ◽  
Cirrhotic Patients ◽  
The Mean ◽  
The One

Background. Acute kidney injury (AKI) affects from 20% to 50% of cirrhotic patients, and the one-month mortality rate is 60%. The main cause of AKI is bacterial infection, which worsens circulatory dysfunction through the release of HMGB1 and IL-6. Objectives. To evaluate HMGB1 and IL-6 as biomarkers of morbidity/mortality. Methods. Prospective, observational study of 25 hospitalised cirrhotic patients with AKI. Clinical and laboratory data were collected at the time of diagnosis of AKI, including serum HMGB1 and IL-6. Results. The mean age was 55 years; 70% were male. Infections accounted for 13 cases. The 30-day and three-month mortality rates were 17.4% and 30.4%, respectively. HMGB1 levels were lower in survivors than in nonsurvivors at 30 days (1174.2 pg/mL versus 3338.5 pg/mL, p=0.035), but not at three months (1540 pg/mL versus 2352 pg/mL, p=0.243). Serum IL-6 levels were 43.3 pg/mL versus 153.3 pg/mL (p=0.061) at 30 days and 35.8 pg/mL versus 87.9 pg/mL (p=0.071) at three months, respectively. The area under the ROC curve for HMGB1 was 0.842 and 0.657, and that for IL-6 was 0.803 and 0.743 for discriminating nonsurvivors at 30 days and three months, respectively. In multivariate analysis, no biomarker was independently associated with mortality. Conclusion. HMGB1 levels were associated with decreased survival in cirrhotics. Larger studies are needed to confirm our results.

Acute Kidney Injury Before and After Liver Transplant

2018 ◽  
Vol 34 (9) ◽  
pp. 687-695 ◽  
Author(s):  
Jeffrey DellaVolpe ◽  
Ali Al-Khafaji
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Liver Disease ◽  
Liver Transplant ◽  
Acute Tubular Necrosis ◽  
Graft Failure ◽  
Kidney Injury ◽  
Tubular Necrosis ◽  
Before And After

The development of acute kidney injury in the setting of liver disease is a significant event both before and after liver transplant. Whether acute kidney injury is the cause of or merely associated with worse outcomes, the development of renal failure is significant from a prognostic as well as from a diagnostic and therapeutic standpoint. Although not every etiology is reversible, there are number of etiologies that are correctable, to include hypovolemia, nephrotoxic medications, and acute tubular necrosis. In the post-liver transplant period, renal failure is associated with graft failure as well as worse outcomes overall. Prompt recognition, workup, and intervention can significantly impact outcomes and survival both before and after liver transplant.

scholarly journals A Case of Severe Acute Kidney Injury Exacerbated by Canagliflozin in a Patient with Type 2 Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Kimya Hassani-Ardakania ◽  
Mark L. Lipman ◽  
Denny Laporta ◽  
Oriana Hoi Yun Yu
Keyword(s):  
Type 2 Diabetes ◽  
Acute Kidney Injury ◽  
Case Reports ◽  
Kidney Injury ◽  
The Elderly ◽  
Tubular Necrosis ◽  
History Of ◽  
Elevated Creatinine ◽  
Third Line

Background. Sodium glucose cotransport (SGLT)-2 inhibitors are the newest class of antihyperglycemic agents used as second- or third-line treatment in the management of type 2 diabetes. Although the use of SGLT-2 inhibitors has not been shown to cause nephrotoxicity, there have been case reports of SGLT-2 inhibitor use being associated with acute kidney injury. Case Presentation. A 72-year-old woman with a history of type 2 diabetes and no known chronic renal insufficiency presented to the emergency room with a 3-day history of nausea, vomiting, and increased somnolence. She was found to have potassium level of 7.4 (normal: 3.5-5.5) mmol/L and a markedly elevated creatinine level at 1154 (normal: 45-95) μmol/L. Imaging of the abdomen and pelvis did not reveal any findings of obstruction. Urine microscopy showed many granular casts. In the absence of other causes for her clinical presentation, the patient was diagnosed with acute kidney injury secondary to ischemic acute tubular necrosis, with canagliflozin use likely an important contributing factor. Conclusions. Physicians should inform patients to stop the use of SGLT-2 inhibitors when patients are unable to maintain hydration or during acute illness. Use of SGLT-2 inhibitors in managing type 2 diabetes should be done with caution among more vulnerable populations, including individuals with cognitive impairment and the elderly.

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 ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Impairment ◽  
Kidney Injury ◽  
Urinary Ngal ◽  
University Hospitals ◽  
Early Management ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Tubular Necrosis ◽  
Improve Risk Stratification ◽  
Cirrhotic Patients

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.

scholarly journals The Role of Urinary N-Acetyl-β-d-glucosaminidase in Cirrhotic Patients with Acute Kidney Injury: Multicenter, Prospective Cohort Study

2021 ◽  
Vol 10 (19) ◽  
pp. 4328
Author(s):  
Jeong-Ju Yoo ◽  
Jung Hyun Kwon ◽  
Young Seok Kim ◽  
Soon Woo Nam ◽  
Ji Won Park ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Significant Risk ◽  
Kidney Injury ◽  
Significant Risk Factor ◽  
Meld Score ◽  
Tubular Necrosis ◽  
Class B ◽  
Cirrhotic Patients ◽  
Multicenter Prospective Cohort Study ◽  
Parenchymal Injury

Background and Aims: Currently, it is difficult to predict the reversibility of renal function and to discriminate renal parenchymal injury in cirrhotic patients with acute kidney injury (AKI). The aim of this study is to evaluate whether urine N-acetyl-β-d-Glucosaminidase (NAG) can predict the survival and response to terlipressin in cirrhotic patients with AKI. Methods: Two hundred sixty-two cirrhotic consecutive patients who developed AKI were prospectively enrolled from 11 tertiary medical centers in Korea between 2016 to 2019. AKI was defined as an increase in serum Cr (SCr) of 0.3 mg/dL or a 50% increase in baseline SCr. Patients diagnosed with hepatorenal syndrome (HRS-AKI) were treated with terlipressin plus albumin. Results: The patients were 58.8 ± 12.9 years old on average and were predominantly male (72.5%). The mean MELD score was 25.3 ± 9.1. When classified according to the AKI phenotype, there were 119 pre-renal, 52 acute tubular necrosis, 18 miscellaneous, and 73 HRS-AKI patients. However, the urine NAG was not effective at discriminating AKI phenotypes, except for HRS-AKI. The baseline urine NAG increased as the baseline AKI stage increased (p < 0.001). In addition, within the same AKI stage, the urine NAG values were significantly lower in the AKI-resolved group than in the unresolved group. The urine NAG level was significantly lower in living patients compared with those who died or who underwent a liver transplant within 3 months (p = 0.005). In the multivariate analysis, the increased urine NAG was a significant risk factor for the 3-month transplant-free survival (TFS) rate, especially in patients with Child–Pugh class ≤ B or MELD < 24. The urine NAG did not predict the response to terlipressin treatment in patients with HRS. Conclusions: Urine NAG is strongly associated with the severity of AKI in patients with liver cirrhosis and is useful for predicting the 3-month TFS.

scholarly journals Effects of fluid and norepinephrine resuscitation in a sheep model of endotoxin shock and acute kidney injury

2019 ◽  
Vol 127 (3) ◽  
pp. 788-797 ◽  
Author(s):  
Gonzalo Ferrara ◽  
Vanina Siham Kanoore Edul ◽  
Juan Francisco Caminos Eguillor ◽  
María Guillermina Buscetti ◽  
Héctor Saúl Canales ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Renal Failure ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Kidney Injury ◽  
Endotoxin Shock ◽  
Systemic Hemodynamics ◽  
Mean Blood Pressure ◽  
Severe Renal Failure

The pathophysiology of renal failure in septic shock is complex. Although microvascular dysfunction has been proposed as a mechanism, there are controversial findings about the characteristics of microvascular redistribution and the effects of resuscitation. Our hypothesis was that the normalization of systemic hemodynamics with fluids and norepinephrine fails to improve acute kidney injury. To test this hypothesis, we assessed systemic and renal hemodynamics and oxygen metabolism in 24 anesthetized and mechanically ventilated sheep. Renal cortical microcirculation was evaluated by SDF-videomicroscopy. Shock ( n = 12) was induced by intravenous administration of endotoxin. After 60 min of shock, 30 mL/kg of saline solution was infused and norepinephrine was titrated to reach a mean blood pressure of 70 mmHg for 2 h. These animals were compared with a sham group ( n = 12). After endotoxin administration, mean blood pressure, cardiac index, and systemic O2 transport and consumption decreased ( P < 0.05 for all). Resuscitation improved these variables. Endotoxin shock also reduced renal blood flow and O2 transport and consumption (205[157–293] vs. 131 [99–185], 28.4[19.0–38.2] vs. 15.8[13.5–23.2], and 5.4[4.0–8.8] vs. 3.7[3.3–4.5] mL·min−1·100 g−1, respectively); cortical perfused capillary density (23.8[23.5–25.9] vs. 17.5[15.1–19.0] mm/mm2); and creatinine clearance (62.4[39.2–99.4] vs. 10.7[4.4–23.5] mL/min). After 2 h of resuscitation, these variables did not improve (174[91–186], 20.5[10.8–22.7], and 3.8[1.9–4.8] mL·min−1·100 g−1, 19.9[18.6–22.1] mm/mm2, and 5.9[1.0–11.9] mL/min). In conclusion, endotoxin shock induced severe renal failure associated with decreased renal flow, O2 transport and consumption, and cortical microcirculation. Normalization of systemic hemodynamics with fluids and norepinephrine failed to improve renal perfusion, oxygenation, and function. NEW & NOTEWORTHY This experimental model of endotoxin shock induced severe renal failure, which was associated with abnormalities in renal regional blood flow, microcirculation, and oxygenation. Derangements included the compromise of peritubular microvascular perfusion. Improvements in systemic hemodynamics through fluids and norepinephrine were unable to correct these abnormalities.

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