Search

Kidney injury is a significant complication in end-stage liver disease (ESLD), leading to increased morbidity and mortality. While liver transplant alone (LTA) can promote kidney recovery (KR), non-recovery associates with adverse outcomes, but the underlying pathophysiology is still unclear. We studied 10 LTA recipients with or without kidney failure (KF) and measured serum levels of OPN and TIMP-1 (previously identified predictors of KR), 92 proinflammatory proteins (Olink), and urinary cell populations. Our findings revealed elevated OPN and TIMP-1 levels in KF patients, strongly correlated with tubular epithelial cells in urine. Proteomic analysis showed distinct profiles in KF, non-KF, and healthy donors, indicating an ongoing proinflammatory signature in KF. Cytokines correlated with OPN and TIMP-1 levels. We propose that high pre-LTA OPN and TIMP-1 levels are crucial for tubular regeneration and normalize with kidney recovery. Insufficient pre-LTA OPN levels may lead to persistent kidney failure. Our present data also newly indicate that kidney failure post-LTA is an active condition, in which tubular cells are persistently shed in the urine. The strict association between systemic inflammation and tubular cell loss suggests a pathogenic link that could offer therapeutic opportunities to promote kidney recovery.

Nonsteroidal anti-inflammatory drugs (NSAIDs) constitute approximately one-third of the global pharmaceutical market and are the first drugs of choice when treating fever and pain. Furthermore, among NSAIDs, the use of diclofenac sodium (DS) is preferred as it is a strong inhibitor of cyclooxygenase enzyme. However, despite its strong efficacy, DS is known for its potential to cause hepatorenal damage. Currently, to mitigate the adverse effects of certain drugs, medically effective agricultural products are often preferred as they are inexpensive, effective and safe. One such agricultural product—mandarin—is noteworthy for its high phenolic contents. The purpose of the present study was to assess the efficacy of mandarin peel ethanolic extract (MPEE) in protecting against hepatorenal damage induced by DS. Four groups (six/group) of adult male albino rats received oral administration of physiological saline (control group), DS (10 mg/kg body weight), MPEE (200 mg/kg body weight), and DS + MPEE for 7 days. Rats in the DS group showed increased serum levels of ALT, AST, ALP, BUN, CRE, and UA. Furthermore, the hepatic and renal tissue levels of MDA, TNF-α and IL-1β increased, whereas those of GSH, SOD, GP-x and IL-10 decreased (p < 0.05). Investigation of MPEE in terms of its effects on biochemical, oxidative and inflammatory parameters, it exerted protective and healing effects. Therefore, MPEE can be used to ameliorate DS-induced hepatorenal damage. [ABSTRACT FROM AUTHOR]

Diabetes and chronic liver and kidney disease are common long-term conditions worldwide. Taraxacum officinale (TOE) has many medicinal properties, due to it phytochemicals constitutions. This study investigate activities of TOE in Streptozotocin diabetes-Induced Hepatorenal toxicity. Sixty rats were randomized into groups A, B, C, D, E, and F of ten rats each (n = 10). Group normal control, group B treated with TOE, group C diabetic (DM) negative control, group D DM rats treated with TOE, group E DM rats treated with metformin (MF)], group F treated with TOE follow by STZ-diabetic). Serum lipid profile, alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), Gamma-glutamyl transferase (GGT), total proteins (TP), albumin (ALB), Urea, and creatinine, electrolyte, oxidative and antioxidant enzymes, caspase 3, inflammatory cytokines, tricarboxylic acid (TCA) cycle enzymes and mitochondrial membrane potential (ΔΨm), liver and kidney histology were investigated.Treatment with TOE ameliorated all the electrolyte disruptions in DM rats. Treatment with TOE and TOE + MF recovered caspase 3, inflammatory makers, oxidative and antioxidant enzymes in DM rats. Moreover, an increase in lipid profile, hepatic and renal functional markers, ALT, AST, ALP, GGT, TP, ALB, Urea, TCA and renal mitochondrial respiratory-chain complexes (I-IV) and ΔΨm and a decrease in creatinine clearance was recovered in DM rats by TOE and TOE + MF treatment. TOE and TOE + MF protected against hepatic and renal histological damage in DM group.Hepatorenal toxicity was effectively ameliorated by the TOE administration. TOE might be considered as a potential protective agent against hepatorenal toxicity.

The present study was conducted to evaluate the ameliorative effect of L-carnitine (LC) against possible deleterious effects of cefquinome sulfate (CS) on hematological, hepatorenal parameters and histopathological changes of some internal organs in male rat's model. Therefore, sixty mature male rats were equally assigned into four groups as following: The control group of rats was administered with two subcutaneous (SC) injections of physiological saline (vehicle of other drugs) (2 ml/kg. b.wt once daily for 5 successive days and 2ml/kg. b.wt once daily for 56 successive days), the second group was injected subcutaneously with LC (200 mg/kg b.wt. once daily for 56 successive days), the third group was administered with SC injection with CS (50 mg/kg. b. wt once daily for 5 successive days) and the fourth group was injected subcutaneously with CS concomitantly with LC by the same doses at the same treatment periods as mentioned in 2nd and 3rd groups. The obtained results showed that administration of CS induced a significant (P= 0.05) increase in WBCs count and serum levels of alanine amino transferase, alkaline phosphatase and creatinine with significant (P= 0.05) decrease in PCV value and serum levels of albumin. Moreover, CS induced histopathological changes on liver and kidney tissues. Conversely, administration of LC concomitantly with CS ameliorates all previous hematological, biochemical, and histopathological alterations induced by CS. It could be concluded that CS induces mild to moderate troubles on blood picture, hepato-renal indices and histopathological findings which could be ameliorated by L-carnitine in male albino rats. [ABSTRACT FROM AUTHOR]

DDeltamethrin (DM) is one of the most environmental and industrial pollutants that are toxic to humans, animals, fishes, and birds. The most common sources of human and animal exposure to deltamethrin (DM) are polluted water and food. This study was done to evaluate the nephrohepatic toxicity of deltamethrin. Twenty-four male rats were used. The first group was used as a control. The second and third groups were given deltamethrin orally in a dose of 1/10 % of the LD50 equal to 0.6mg\kg b w alone plus Royal Jelly (RJ) at a dose of 100 mg/kg/day for two months, respectively. Oral administration of DM-induced biochemical and histopathological alterations. DM toxicity exhibited changes in the liver and kidney function tests manifested by an increase in AST, ALT, urea, uric acid and creatinine with no changes noticed in plasma proteins when compared to the control group. Giving RJ ameliorated the hepatorenal toxicity by causing recovery in both liver and kidney functions in comparison to DM given group. Pathologically, severe degenerative and necrotic changes in livers and kidneys were present in the deltamethrin group, where it improved to moderate to mild lesions with a protective royal gel substance. This study concluded that royal gel substance has been shown to benefit in lower down the side effects and increasing the rate of improvement of injury induced by deltamethrin.

Background: Mortalities resulting from liver and kidney failure are enormous. It is however worrisome that conventional medications are rarely available for their treatment. Honey is traditionally reputed as a natural supplement for relieving disease symptoms. The therapeutic values of honey vary widely from one botanical source to the other. Aim and Objective: To evaluate the beneficial effects of Nigerian Bitter Honey (BH) on hepatorenal damage induced by Streptozotocin (STZ). Material and Methods: Forty female Wistar rats (90-110 g) were randomly grouped into five (n=8 each) as follows: Group A (2 ml/kg distilled water), Group B (50 mg/kg BH), Group C (65 mg/kg STZ), Group D (STZ + BH), and Group E (BH + STZ). Hepatorenal damage was induced in rats by a single dose of STZ (65 mg/kg body weight). Animals were sacrificed after 28 days of treatment. Blood samples were collected into sterile plain bottles. Liver and kidney tissues were harvested and processed for histopathological assessment. Liver function tests (Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT), total protein, albumin, bilirubin); kidney function tests (urea and creatinine) were carried out. Results: Bitter honey treatment (Group D) significantly (p

The current study purposed to investigate the 3-indoleacetic acid (IAA) possible adverse impacts on hematological parameters, hepatorenal function, cardiac, and skeletal muscles as well as testes of rats and histopathological alterations of respective organs and to determine the extent of reversing any adverse impacts occurred in animals after IAA withdrawal. Rats were exposed orally to 500 mg/kg BW by gastric intubation once daily for 14 days, after which one-half was sacrificed and the remaining half left for a further 14 days without IAA exposure. The exposure of rats to IAA produced anemia, leukopenia, neutrophilia, lymphopenia, and a significant increase in activities of serum transaminase, gamma-glutamyl transferase, creatine kinase-myocardial band, creatine kinase-muscle type, and levels of serum creatinine, sodium, chloride, and potassium. Furthermore, serum levels of testosterone, gonadotropins, and leptin significantly declined. The changes in most of measured parameters continued after IAA withdrawal. Histopathological alterations in different tissues supported these changes. In conclusion, subacute exposure to IAA at a high concentration could exert hematotoxicity and toxic effects on many soft organs and its withdrawal led to incomplete recovery of animals. Thus, IAA should be used cautiously as extensive use of it at high concentrations can cause harmful effects on the environment, animals and human beings. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) is a clinical syndrome caused by a multitude of hemodynamic, toxic, and structural insults to the kidney, and portends worse patient outcomes. Despite careful history taking, physical examination, and analysis of laboratory data, a void is evident in the diagnostic process and clinical monitoring of AKI. Point-of-care ultrasonography (POCUS) is a limited ultrasound study performed by the clinician at bedside as an adjunct to physical examination. Growing body of evidence points to POCUS as a powerful tool in a variety of clinical settings. Herein, we discuss how nephrologist-performed POCUS has the potential to provide answers to focused questions that we encounter in diagnosis and management of patients with AKI. From excluding hydronephrosis to providing real-time insights into hemodynamics, incorporation of POCUS helps integrate all the pieces of patient data and formulate individualized treatment plans. Future studies are needed to evaluate the impact of multi-organ POCUS on AKI-related pragmatic patient outcomes, the potential of this technique to stratify the risk and to identify patients with different levels of severity of AKI and different pathophysiological signatures. [ABSTRACT FROM AUTHOR]

The present study investigated the individual and collective effect of organochlorinated fungicide hexachlorobenzene (HCB) and manganese (Mn), a metal, on the hepatorenal function in adult rats. Rats were divided into four groups of rats comprising of control, HCB alone (15 mg/kg), Mn alone (10 mg/kg) and co-exposure group that were orally treated for 25 consecutive days. After sacrifice, hepatorenal damage and antioxidant status markers, myeloperoxidase (MPO) activity, levels of nitric oxide, total antioxidant capacity (TAC), total oxidative stress (TOS) and lipid peroxidation (LPO) were analyzed spectrophotometrically. Levels of tumor necrosis factor alpha (TNF-α), interleukin-1 β (IL-1β) and caspase-3 activity were assessed using ELISA. Results revealed that the HCB administration significantly (p < 0.05) increased the biomarkers of hepatorenal toxicity, decreased the antioxidant status and TAC, raised the levels of TOS and LPO as well as increased the levels of TNF-α, IL-1β and caspase-3 activity. Rats co-exposed to HCB and Mn showed decreased biomarkers of hepatorenal damage, increased antioxidant status and TAC with simultaneous reduction in the levels of TOS and LPO significantly (p < 0.05). Furthermore, the increased levels of TNF-α, IL-1β and caspase-3 activity were significantly (p < 0.05) reduced in the liver and kidney of rats' co-expose to HCB and Mn. Histological examination showed that damages induced by HCB were assuaged in rats co-treated with HCB and Mn. In conclusion, the results demonstrated that co-treatment of HCB and Mn in rats' alleviated HCB-induced oxidative stress, inflammation and caspase-3 activation in the liver and kidney of the rats. [ABSTRACT FROM AUTHOR]

Kidney injury is a significant complication in end-stage liver disease (ESLD), leading to increased morbidity and mortality. While liver transplant alone (LTA) can promote kidney recovery (KR), non-recovery associates with adverse outcomes, but the underlying pathophysiology is still unclear. We studied 10 LTA recipients with or without kidney failure (KF) and measured serum levels of OPN and TIMP-1 (previously identified predictors of KR), 92 proinflammatory proteins (Olink), and urinary cell populations. Our findings revealed elevated OPN and TIMP-1 levels in KF patients, strongly correlated with tubular epithelial cells in urine. Proteomic analysis showed distinct profiles in KF, non-KF, and healthy donors, indicating an ongoing proinflammatory signature in KF. Cytokines correlated with OPN and TIMP-1 levels. We propose that high pre-LTA OPN and TIMP-1 levels are crucial for tubular regeneration and normalize with kidney recovery. Insufficient pre-LTA OPN levels may lead to persistent kidney failure. Our present data also newly indicate that kidney failure post-LTA is an active condition, in which tubular cells are persistently shed in the urine. The strict association between systemic inflammation and tubular cell loss suggests a pathogenic link that could offer therapeutic opportunities to promote kidney recovery., Competing Interests: PE holds a patent for preservation or urine cells (CHA124WOEP-UP). BS is employed at Precision for Medicine, a company offering molecular biology services. JD was employed by company Eurofins Viracor. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (© 2024 Goerlich, Kim-Schulze, Kotanko, Grobe, Wang, Samans, Douglas, Enghard, Molinari, Fribourg, Cravedi and Levitsky.)

Outcomes of heart failure (HF) hospitalization are driven by the presence or absence of comorbid conditions. Cirrhosis is associated with worse outcomes in patients with HF, and both HF and cirrhosis are associated with worse renal outcomes. Using a nationally representative sample we describe inpatient outcomes of all-cause mortality and length of stay (LOS) among patients with and without cirrhosis hospitalized for decompensated with HF. We conducted a cross sectional analysis using Nationwide Inpatient Sample (2010–2014) data including patients hospitalized for decompensated HF, with or without cirrhosis. We calculated the adjusted odds of all-cause mortality, acute kidney injury (AKI), and target LOS after adjusting for potential confounders. Out of the 2,487,445 hospitalized for decompensated HF 39,950 had cirrhosis of which majority (75.1%) were non-alcoholic cirrhosis. Patients with comorbid cirrhosis were more likely to die (OR, 1.26; 95% CI, 1.11 to 1.43) and develop AKI (OR, 1.26; 95% CI, 1.16 to 1.36) as compared to those without cirrhosis. Underlying CKD was associated with a greater odds of AKI (OR, 4.99; 95% CI, 4.90 to 5.08), and the presence of cirrhosis amplified this risk (OR, 6.03; 95% CI, 5.59 to 6.51). There was approximately a 40% decrease in the relative odds of lower HF hospitalization length of stay among those with both CKD and cirrhosis, relative to those without either comorbidities. Cirrhosis in patients with hospitalizations for decompensated HF is associated with higher odds of mortality, decreased likelihood of discharge by the targeted LOS, and AKI. Among patients with HF the presence of cirrhosis increases the risk of AKI, which in turn is associated with poor clinical outcomes.

We described a case of a 73-year-old female admitted to the emergency department with acute hepatic and renal failure (hepato-renal syndrome, HRS) due to acute Budd-Chiari syndrome associated with complete portal vein thrombosis (BCS-PVT) for an unknown cause. Despite the initial therapy with anticoagulants, a sudden impairment of the renal function requiring hemodialysis was observed. The hepatic transplant was excluded for patient age and clinical conditions. Thus, the patient was successfully treated by emergent transjugular intrahepatic portosystemic shunt (TIPS) previous rheolytic thrombectomy of the PVT with AngioJet Ultra PE Thrombectomy System (Boston Scientific, Marlborough, MA, USA). After the procedure, the sudden resolution of the HRS was observed, and the patient is alive 13 months after hospital dismission with no TIPS dysfunction. In conclusion, emergent extended TIPS with the usage of rheolytic thrombectomy device in patient with acute BCS-PVT complicated by HRS is feasible by experienced operators and provide resolution of the HRS. [ABSTRACT FROM AUTHOR]

Monosodium glutamate (MSG), a commonly used flavor enhancer, has been reported to induce hepatic and renal dysfunctions. In this study, the palliative role of protocatechuic acid (PCA) in MSG-administered rats was elucidated. Adult male rats were assigned to four groups, namely control, MSG (4 g/kg), PCA (100 mg/kg), and the last group was co-administered MSG and PCA at aforementioned doses for 7 days. Results showed that MSG augmented the hepatic and renal functions markers as well as glucose, triglycerides, total cholesterol, and low-density lipoprotein levels. Moreover, marked increases in malondialdehyde levels accompanied by declines in glutathione levels and notable decreases in the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were observed in MSG-treated group. The MSG-mediated oxidative stress was further confirmed by downregulation of nuclear factor erythroid 2–related factor 2 (Nrf2) gene expression levels in both tissues. In addition, MSG enhanced the hepatorenal inflammation as witnessed by increased inflammatory cytokines (interleukin-1b and tumor necrosis factor-α) and elevated nuclear factor-κB (NF-κB) levels. Further, significant increases in Bcl-2-associated X protein (Bax) levels together with decreases in B-cell lymphoma 2 (Bcl-2) levels were observed in MSG administration. Histopathological screening supported the biochemical and molecular findings. In contrast, co-treatment of rats with PCA resulted in remarkable enhancement of the antioxidant cellular capacity, suppression of inflammatory mediators, and apoptosis. These effects are possibly endorsed for activation of Nrf-2 and suppression of NF-kB signaling pathways. Collectively, addition of PCA counteracted MSG-induced hepatorenal injuries through modulation of oxidative, inflammatory and apoptotic alterations. [ABSTRACT FROM AUTHOR]

Background: Mortalities resulting from liver and kidney failure are enormous. It is however worrisome that conventional medications are rarely available for their treatment. Honey is traditionally reputed as a natural supplement for relieving disease symptoms. The therapeutic values of honey vary widely from one botanical source to the other. Aim and Objective: To evaluate the beneficial effects of Nigerian Bitter Honey (BH) on hepatorenal damage induced by Streptozotocin (STZ). Material and Methods: Forty female Wistar rats (90-110 g) were randomly grouped into five (n=8 each) as follows: Group A (2 ml/kg distilled water), Group B (50 mg/kg BH), Group C (65 mg/kg STZ), Group D (STZ + BH), and Group E (BH + STZ). Hepatorenal damage was induced in rats by a single dose of STZ (65 mg/kg body weight). Animals were sacrificed after 28 days of treatment. Blood samples were collected into sterile plain bottles. Liver and kidney tissues were harvested and processed for histopathological assessment. Liver function tests (Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT), total protein, albumin, bilirubin); kidney function tests (urea and creatinine) were carried out. Results: Bitter honey treatment (Group D) significantly (p<0.05) reduced AST, ALT, urea, creatinine and bilirubin levels while also increasing total protein and albumin concentrations. Also, BH significantly improved the histoarchitectural integrity of the liver and the kidney of the treated and pretreated rats. Conclusion: Bitter honey demonstrated outstanding hepatoprotective and renoprotective effects. It may therefore serve as a novel natural supplement for the management of liver and kidney diseases. [ABSTRACT FROM AUTHOR]

Objective: To evaluate a novel polyherbal formulation (BSVT) containing the standardized extracts from the leaves of Boerhavia diffusa, Solidago virgaurea, Vitex negundo, and thymoquinone in CCl4 induced hepatorenal toxicity in rats. Methods: A total of 36 rats were divided into six groups including normal control, CCl4 (2 mL/kg, i.p.), CCl4 (2 mL/kg, i.p.) + Cystone® (750 mg/kgp.o.), CCl4 (2 mL/kg, i.p.) + BSVT (25 mg/ kg, p.o.), CCl4 (2 mL/kg, i.p.) + BSVT (50 mg/kg, p.o.), and CCl4 (2 mL/kg, i.p.) + BSVT (100 mg/kg,p.o.). All treatments were given for four weeks. Serum levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, cholesterol, total protein, serum urea, blood urea nitrogen and creatinine were assessed. Superoxide dismutase, malondialdehyde, and glutathione peroxidase were evaluated in tissue homogenate. The histopathological study of liver and kidney tissues was also done. Results: Aspartate transaminase, alanine transaminase, alkaline phosphatase, cholesterol, serum urea, blood urea nitrogen and creatinine were significantly elevated (P

Background and objective Hepatorenal syndrome (HRS) is a systemic disorder that affects both the kidneys and the liver. HRS refers to the occurrence of kidney failure in individuals with advanced liver cirrhosis, portal hypertension, and ascites, without any underlying kidney disease. The interplay of systemic and portal hemodynamics causes severe constriction of blood vessels in the kidneys, which defines HRS. The study aims to illuminate the demographic profiles, etiology, and outcomes of patients with HRS. Material and methods The study was designed as a prospective, cross-sectional, hospital-based observational study conducted at Dr. D.Y. Patil Medical College, Hospital, and Research Centre in Pimpri, Pune. The study period spans from September 2022 to June 2024. Before commencement, approval was obtained from the institutional ethics committee, and informed written consent was secured from all participating patients. The sample size consists of 100 patients diagnosed with HRS, selected from the general medicine outpatient department, wards, and ICU of Dr. D.Y. Patil Hospital and Research Centre. A comprehensive clinical history was recorded for all patients, focusing on the symptoms of cirrhosis and HRS, followed by a thorough examination for related signs and symptoms. Results Among the 100 patients included in this study on HRS, 25% (N=25) fell within the age range of 18-30 years, and 76% (N=76) were identified as male. Alcoholic cirrhosis accounted for 78% (N=78) of cases, with hepatitis B infection being the subsequent leading cause. The mortality rate was 12% (N=12) while the survival rate was 88% (N=88). Conclusion This study provides insights into the demographic profile, etiology, and outcomes of HRS. The results of this study contribute valuable insights into the complex nature of HRS, highlighting the importance of early detection and monitoring to optimize patient care., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Institutional Ethics Sub-Committee issued approval IESC/PGS/2022/01. Animal subjects: All authors have confirmed that this study did not involve animal subjects or tissue. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Borle et al.)

Atrazine (ATZ) is an herbicide commonly detected in groundwater. Several studies have focused on its immunological and endocrine effects on adult Xenopus laevis species. However, we investigated the impact of atrazine on the renal and hepatic biochemistry and histomorphology in adult male frogs. Forty adult male frogs were allocated to four treatment groups (control, one ATZ (0.01 µg/L), two ATZ (200 µg/L) and three ATZ (500 µg/L), 10 animals per group, for 90 days. Alanine aminotransferase (ALT) and creatinine levels increased significantly (p < 0.05) in the 200 and 500 μg/L groups but malondialdehyde only in the 500 μg/L group (p < 0.05). Histopathological observations of derangement, hypertrophy, vascular congestion and dilation, infiltration of inflammatory cells incursion, apoptosis and hepatocytes cell death were observed with atrazine exposure, mostly in the 500 μg/L group. Additionally, histochemical labelling of caspase-3 in the sinusoidal endothelium was observed in all the treated groups, indicating vascular compromise. Evaluation of renal histopathology revealed degradation and atrophy of the glomerulus, vacuolization, thick loop of Henle tubule epithelial cells devolution and dilation of the tubular lumen. Furthermore, expression of caspase-3 indicates glomerular and tubular apoptosis in atrazine-exposed animals. These findings infer that environmentally relevant atrazine doses (low or high) could induce hepatotoxicity and nephrotoxicity in adult male Xenopus laevis frogs and potentially related aquatic organisms. [ABSTRACT FROM AUTHOR]

Coconut water is used in folklore medicine for oral rehydration, treatment of childhood diarrhoea, gastroenteritis and cholera, and is also known to possess antioxidant properties. In this study, we examined the ameliorative potentials of coconut water on carbon tetrachloride (CCl4) induced toxicity in rats. Rats were randomly assigned into separate cages according to the sex of 5 groups. Groups 2–5 were intraperitoneally injected a single dose of 1 mL/kg CCl4 diluted in olive oil. Only 3, 4 and 5 were orally given 2, 4, 6 mL/kg coconut water respectively, whereas groups 1 and 2 received distilled water. Treatment with coconut water significantly (p < 0.05) increased red blood cell, packed cell volume, haemoglobin, high-density lipoprotein, glutathione, superoxide dismutase, catalase, total protein, and albumin compared to the negative control in both sexes of the rats. Furthermore, platelets, white blood cells, urea, low-density lipoprotein, triglyceride, total cholesterol, malondialdehyde, bilirubin, alkaline phosphatase, alanine and aspartate transaminases decreased significantly (p < 0.05) compared to the negative control in both male and female rats. Thus, coconut water supplementation may reverse CCl4 induced toxicity and distortions on haematological parameters, lipid profile and antioxidant enzymes, liver and kidney biomarkers in rats. [ABSTRACT FROM AUTHOR]

Outcomes of heart failure (HF) hospitalization are driven by the presence or absence of comorbid conditions. Cirrhosis is associated with worse outcomes in patients with HF, and both HF and cirrhosis are associated with worse renal outcomes. Using a nationally representative sample we describe inpatient outcomes of all-cause mortality and length of stay (LOS) among patients with and without cirrhosis hospitalized for decompensated with HF. We conducted a cross sectional analysis using Nationwide Inpatient Sample (2010-2014) data including patients hospitalized for decompensated HF, with or without cirrhosis. We calculated the adjusted odds of all-cause mortality, acute kidney injury (AKI), and target LOS after adjusting for potential confounders. Out of the 2,487,445 hospitalized for decompensated HF 39,950 had cirrhosis of which majority (75.1%) were non-alcoholic cirrhosis. Patients with comorbid cirrhosis were more likely to die (OR, 1.26; 95% CI, 1.11 to 1.43) and develop AKI (OR, 1.26; 95% CI, 1.16 to 1.36) as compared to those without cirrhosis. Underlying CKD was associated with a greater odds of AKI (OR, 4.99; 95% CI, 4.90 to 5.08), and the presence of cirrhosis amplified this risk (OR, 6.03; 95% CI, 5.59 to 6.51). There was approximately a 40% decrease in the relative odds of lower HF hospitalization length of stay among those with both CKD and cirrhosis, relative to those without either comorbidities. Cirrhosis in patients with hospitalizations for decompensated HF is associated with higher odds of mortality, decreased likelihood of discharge by the targeted LOS, and AKI. Among patients with HF the presence of cirrhosis increases the risk of AKI, which in turn is associated with poor clinical outcomes. [ABSTRACT FROM AUTHOR]

There are limited techniques available to assess the health of sea turtles as physical examination has little correlation to clinical findings, and blood reference intervals are broad and provide limited prognostic significance. Advances in the portability of ultrasound machines allow echocardiography to be increasingly used in the health assessments of wild animals. This study performed blood analysis and echocardiograms on 11 green sea turtles upon admission to a rehabilitation clinic and six animals before release. Significant differences were seen between groups, with admission animals having significantly smaller diameters of the cavum arteriosum at systole and diastole, smaller E‐waves and an increased fractional shortening. Pre‐release animals displayed significant increases in the maximum blood velocities of both the pulmonary artery and the left aorta. Significant negative correlations were seen between fractional shortening and uric acid and between the velocity time integral of the pulmonary artery and urea. The pulmonary artery velocity time integral was also significantly correlated to the E wave. Furthermore, there was asynchrony between the cavum arteriosum and the cavum pulmonale and the detection of a parasitic granuloma in the ventricular outflow tract of one animal. Overall, the results suggest that cardiac function in stranded green sea turtles is significantly impaired and that echocardiography has applications in the health assessments of green sea turtles. [ABSTRACT FROM AUTHOR]

Discerning the etiology of acute kidney injury (AKI) in cirrhotic patients remains a formidable challenge due to diverse and overlapping causes. The conventional approach of empiric albumin administration for suspected volume depletion may inadvertently lead to fluid overload. In the recent past, point-of-care ultrasonography (POCUS) has emerged as a valuable adjunct to clinical assessment, offering advantages in terms of diagnostic accuracy, rapidity, cost-effectiveness, and patient satisfaction. This review provides insights into the strategic use of POCUS in evaluating cirrhotic patients with AKI. The review distinguishes basic and advanced POCUS, emphasizing a 5-point basic POCUS protocol for efficient assessment. This protocol includes evaluations of the kidneys and urinary bladder for obstructive nephropathy, lung ultrasound for detecting extravascular lung water, inferior vena cava (IVC) ultrasound for estimating right atrial pressure, internal jugular vein ultrasound as an alternative to IVC assessment, and focused cardiac ultrasound for assessing left ventricular (LV) systolic function and identifying potential causes of a plethoric IVC. Advanced POCUS delves into additional Doppler parameters, including stroke volume and cardiac output, LV filling pressures and venous congestion assessment to diagnose or prevent iatrogenic fluid overload. POCUS, when employed judiciously, enhances the diagnostic precision in evaluating AKI in cirrhotic patients, guiding appropriate therapeutic interventions, and minimizing the risk of fluid-related complications., Competing Interests: Conflict-of-interest statement: The author has no conflicts(s) of interest to disclose in relation to this manuscript., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

This study focused to assess the efficacy of Gynura procumbens (GP) leaf extract against cisplatin (CP)-induced hepatorenal complications in Wister albino rats. Additionally, it aims to detect polyphenolic compounds using high-performance liquid chromatography with diode-array detection (HPLC-DAD). The rats were treated intraperitoneally with CP (7.5 mg/kg) to mediate hepatorenal damage. They were then treated with GP extract (75 and 150 mg/kg, P.O.) for 7 consecutive days. Although GP extract significantly ameliorated CP-mediated hepatorenal biomarkers like alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, and blood urea nitrogen (BUN) levels in a dose-dependent manner, GP extract at 150 mg/kg dose normalized hepatorenal biomarkers ALP (45.11 U/L), ALT (34 U/L), AST (29 U/L), creatinine (10.3 mg/dl) and BUN (11.19 mg/dl) while comparing to control and disease group. Similarly, though it significantly reduced CP-induced oxidative stress inducers, including nitric oxide (NO) and advanced oxidative protein products (AOPP), higher dose (150 mg/kg) exhibited better activity in reducing NO (281.54 mmol/gm tissue in liver and 52.73 mmol/gm tissue in the kidney) and AOPP (770.95 mmol/mg protein in liver and 651.90 mmol/mg protein in the kidney). Besides, it showed better enhancement in the antioxidant enzymes superoxide dismutase, and glutathione levels at a higher dose (150 mg/kg). Histopathological studies showed that CP caused collagen accumulation in the liver and kidney tissues. GP extract drained the collagen mass and acted against hepatorenal damage. Ellagic acid, gallic acid, quercetin hydrate, kaempferol, and rutin hydrate were revealed in GP extract. In-silico modelling showed good docking scores of the polyphenolic compounds with molecular targets including CYP4502E1, NF-κB, caspase-3, and TNF-α. GP could be an effective therapeutic option for management of anticancer drugs' complications like CP-induced organ damage, although clinical studies are required to establish herbal formulation., (© 2024 Wiley-VHCA AG, Zurich, Switzerland.)

Gender-affirming hormone therapy carries the potential risk for shifts in biochemical markers that may impact cardiometabolic, hematologic, hepatic, and renal health. The critical evaluation of biochemical data is an integral part of a comprehensive nutrition assessment; therefore, nutrition professionals should be aware of shifts that are expected during the course of masculinizing and feminizing hormone therapy. Changes in important biochemical values along with binary sex-specific standards for interpreting laboratory data can pose significant challenges for nutrition professionals working with transgender and gender-diverse patients who receive gender-affirming hormone therapy. Overall, research on the biochemical impact of masculinizing and feminizing hormone therapy is nascent and limited. Methodologies and outcomes measured are heterogenous across studies, introducing complexities that impede researchers from drawing definitive conclusions. In light of these limitations, this narrative review aims to describe the potential implications of masculinizing and feminizing hormone therapy regimens on biochemical measures that may influence nutrition strategies and interventions to promote optimal health., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Waters and Linsenmeyer.)

Acute kidney injury and hepatorenal syndrome (HRS) are frequent complications in patients with cirrhosis and ascites. First-line treatment is terlipressin, which reverses HRS in ~40% of patients but also lowers cardiac output (CO). We aimed to investigate whether reversing the cardio-suppressive effect of terlipressin with the β-adrenoceptor agonist dobutamine would increase CO and thereby increase the glomerular filtration rate (GFR). We randomized 25 patients with cirrhosis, ascites, and impaired renal function (2:2:1): group A received terlipressin followed by the addition of dobutamine; group B received dobutamine and terlipressin as monotherapies; and group C received placebo. Renal and cardiac functions were assessed during 8 clearance periods of 30 min, and concentrations of vasoactive hormones were measured. Dobutamine as a monotherapy increased CO (1.03 L/min, P < 0.01) but had no significant effects on GFR. Renin (P < 0.05), angiotensin II (P < 0.005), and aldosterone (P < 0.05) increased after dobutamine infusion. Terlipressin as a monotherapy improved GFR (18.9 mL·min-1·m-2, P = 0.005) and mean arterial pressure (MAP) (14 mmHg, P = 0.001) but reduced CO (-0.92 L/min, P < 0.005) and renin (P < .005). A combined treatment of dobutamine and terlipressin had a positive effect on CO (1.19 L/min, P < 0.05) and increased renin (P < 0.005), angiotensin II (P < 0.005), and aldosterone (P < 0.05), but it had no significant effects on MAP or GFR. Dobutamine reversed the cardio-suppressive effect of terlipressin in cirrhosis, ascites, and impaired renal function. However, dobutamine reduced peripheral vascular resistance, activated renin-angiotensin-aldosterone system, and did not improve GFR compared with terlipressin as a monotherapy. Therefore, dobutamine cannot be recommended in cirrhosis and ascites. NEW & NOTEWORTHY This study shows that the cardio-suppressive effects of the vasopressin receptor agonist terlipressin can be reversed by dobutamine. This is a novel observation in patients with decompensated cirrhosis. Furthermore, we show that dobutamine reduced the peripheral vascular resistance and activated the renin-angiotensin system, whereas renal function was not further improved by terlipressin alone. [ABSTRACT FROM AUTHOR]

Atrazine (ATZ) is an herbicide commonly detected in groundwater. Several studies have focused on its immunological and endocrine effects on adult Xenopus laevis species. However, we investigated the impact of atrazine on the renal and hepatic biochemistry and histomorphology in adult male frogs. Forty adult male frogs were allocated to four treatment groups (control, one ATZ (0.01 µg/L), two ATZ (200 µg/L) and three ATZ (500 µg/L), 10 animals per group, for 90 days. Alanine aminotransferase (ALT) and creatinine levels increased significantly (p < 0.05) in the 200 and 500 μg/L groups but malondialdehyde only in the 500 μg/L group (p < 0.05). Histopathological observations of derangement, hypertrophy, vascular congestion and dilation, infiltration of inflammatory cells incursion, apoptosis and hepatocytes cell death were observed with atrazine exposure, mostly in the 500 μg/L group. Additionally, histochemical labelling of caspase-3 in the sinusoidal endothelium was observed in all the treated groups, indicating vascular compromise. Evaluation of renal histopathology revealed degradation and atrophy of the glomerulus, vacuolization, thick loop of Henle tubule epithelial cells devolution and dilation of the tubular lumen. Furthermore, expression of caspase-3 indicates glomerular and tubular apoptosis in atrazine-exposed animals. These findings infer that environmentally relevant atrazine doses (low or high) could induce hepatotoxicity and nephrotoxicity in adult male Xenopus laevis frogs and potentially related aquatic organisms.

Individuals with liver disease are susceptible to pathophysiological derangements that lead to kidney dysfunction. Patients with advanced cirrhosis and acute liver failure (ALF) are at risk of developing acute kidney injury (AKI). Hepatorenal syndrome type 1 (HRS-1, also called HRS-AKI) constitutes a form of AKI unique to the state of cirrhosis and portal hypertension. Although HRS-1 is a condition primarily characterized by marked renal vasoconstriction and kidney hypoperfusion, other pathogenic processes, such as acute tubular injury and renal vein congestion, can overlap and further complicate the course of HRS-1. ALF can lead to AKI through mechanisms that involve systemic inflammation, direct drug toxicity, or bile acid-induced tubulopathy. In addition, the growing prevalence of nonalcoholic steatohepatitis is changing the spectrum of chronic kidney disease in cirrhosis. In this installment of AJKD's Core Curriculum in Nephrology, we explore the underpinnings of how cirrhosis, ALF, acute cholestasis, and post-liver transplantation can be associated with various forms of acute, subacute, or chronic kidney diseases. We navigate through the recommended therapies for each condition, including supportive care, pharmacological interventions, kidney replacement therapy, and organ transplantation. Finally, key acid-base and electrolyte disorders associated with hepatobiliary disease are also summarized., (Copyright © 2023 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

The efficacy of methotrexate (MTX) as an anticancer drug is limited by some adverse effects including hepatic and renal toxicities. The present study investigated the possible protective effect of protocatechuic acid (PCA), a phenolic phytochemical widely present in several edible vegetables and fruits, on hepatorenal toxicity associated with MTX treatment in rats. Male Wistar rats were randomly assigned to five groups (n = 10), namely control, MTX alone (20 mg/kg), PCA alone (50 mg/kg), and rats that were coadministered MTX and PCA at 25 and 50 mg/kg. The MTX was administered as a single intraperitoneal dose on the first day, whereas PCA treatment lasted 7 days. Results indicated that PCA significantly (p < 0.05) abrogated MTX-mediated elevation in indices of hepatorenal toxicity. Furthermore, PCA protected against MTX-induced decreases in glutathione level and antioxidant enzyme activities as well as the increase in reactive oxygen and nitrogen species and lipid peroxidation in the liver and kidney of the treated rats. Administration of PCA markedly abated MTX-induced increases in interleukin-1β, tumor necrosis factor alpha, and caspase 3 activity in the rats. The biochemical data on the hepatorenal protective effects of PCA were well supported by the histological data. Collectively, PCA protected against MTX-induced hepatorenal toxicity via antioxidant, anti-inflammatory, and antiapoptotic mechanisms. [ABSTRACT FROM AUTHOR]

The Thymus vulgaris (T. vulgaris) has been used in foods for the flavor, aroma, and preservation and in folk medicines. The objective of the present work was to determine the antioxidant and protective effects of T. vulgaris extract against lead (Pb)-intoxicated rats. A thirty-two male Sprague-Dawley were randomly assigned into 4 equal groups and treated for six weeks as follows: group I (GP-I), served as negative control; GP-II, -III, and -IV received either Pb acetate in drinking water (500 mg/L), T. vulgaris extract (500 mg/kg/day) by oral gavage or Pb acetate with T. vulgaris extract, respectively. Blood samples were collected at the end of the study week 6 to measure the hepatic and renal biochemical markers, complete blood count alongside the serum levels of interleukin (IL)-1β, IL-6, IL-10, tumor necrosis (TNF)-α, and interferon (IFN)-γ. Additionally, liver and kidney tissue specimens were collected for histopathology as well as to measure the antioxidant-reduced glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) alongside the lipid peroxidation marker, malonaldehyde (MDA). The results indicated that Pb toxicity increased the serum levels of IL-1β, IL-6, and TNF-α, whereas IL-10 and IFN-γ were reduced. The results showed disturbed liver and renal functions; increased serum levels of ALT, AST, ALP, total bilirubin, creatinine, and urea; and decreased total protein, albumin, and calcium. The GSH, Gpx, and CAT levels were significantly decreased in the Pb-administrated group, while MDA was increased. However, regarding the hepatorenal markers, those animals treated with T. vulgaris alone did not induce any significant changes. Moreover, the combined treatment with T. vulgaris extract together with Pb showed significant improvement in Pb-induced toxicity in all the tested parameters compared to the negative control group. We investigated the potential protective effects of the medicinal plant T. vulgaris in vivo, since there are no publications that address the potential protective effect of this leaf extract against Pb-induced hepatorenal toxicity. Our studies concluded that the T. vulgaris extract reduces Pb overload in hepatorenal tissues, and that this has a potential immunomodulatory role, antioxidant activity, and a protective effect against Pb toxicity. [ABSTRACT FROM AUTHOR]

Abstract Although cisplatin (CIS) has been associated with serious adverse effects, such as hepatotoxicity and nephrotoxicity in adult rats, there is few reports on its use in newborn rats. The aim of this study was to evaluate acute toxic effects of CIS in newborn rats. Adult and newborn Wistar rats received CIS by the i. p. route, at the dose of 5 or 10 mg/kg. After 24 h of treatment, blood, kidney, and liver were excised from the animals and parameters of renal and hepatic functions, oxidative stress markers were determined. Acute administration of CIS caused an increase of AST activity and urea levels, suggesting hepatorenal toxicity in newborn and adult rats. However, the pattern and intensity of damage was different between ages and tissues. Newborn rats showed more pronouncedly oxidative stress damage, characterized by an increase in reactive species and protein carbonyl levels, lower NPSH content and highest inhibition in δ-ALA-D and CAT activities. Besides that, it was observed a faster molecular response in protein levels involved with apoptosis and oxidative stress response; whereas in the beginning the damage was less severe in the kidney than in the liver of adult rats. Thus, the present study shows that there are body response differences between adult and newborn rats to CIS acute exposure being that newborn rats are more susceptible than adults. Highlights • Cisplatin causes hepatorenal toxicity in newborn and adult rats. • The pattern of damage was different between ages and tissues. • Newborn rats showed similar tissue alterations in oxidative stress parameters. • Newborn and adult rats showed variations in apoptotic protein levels. • Newborn rats were more sensitive than adult rats to CIS acute exposure. [ABSTRACT FROM AUTHOR]

Background: Malaria is the most prevalent infectious diseases in the world. This study aims to assess the correlation of hepatorenal dysfunction in malaria patients in pediatric age group. Materials and Methodology: This study was conducted on patients of malaria admitted in the Department of Paediatrics, PBM hospital, Bikaner (Rajasthan), during resurgence of various outbreaks of malaria in the year 2011 and 2012. The diagnosis of malaria was confirmed by examination of thick and thin smear/optimal test; malarial hepatic and renal patients were included in the study. Results: The mean age of patients with hepatic and/or renal dysfunction in malaria was 5–10 years and preponderance of males. Association between hepatic and renal dysfunction was significant as 9 (40.9%) in 22 patients with serum bilirubin >3 mg/dl had renal failure in Plasmodium falciparum (PF) and 5 (71.43%) out of 7 patients in mixed (Plasmodium vivax [PV] and PF) patients. This association was not significant in PV as 6 (10.52%) out of 57 patient with serum bilirubin >3 mg/dl had renal failure. Conclusion: The specific reason for presenting our observation is to develop awareness regarding the early complications of malaria and to prevent them prompt action can be taken. [ABSTRACT FROM AUTHOR]

Background: Cirrhosis is a significant cause of death in the U.S. and has a variety of causes, most commonly Hepatitis C and alcohol. Liver fibrosis and nodule formation result in significant complications due to portal system hypertension. There are several deadly complications emergency physicians must consider.Objective Of the Review: Provide an evidence-based update for the resuscitation of decompensating cirrhotic patients and an overview of cirrhosis complications.Discussion: Cirrhosis is a common condition in the U.S. and leads to several deadly complications. The disease develops from liver fibrosis, elevating portal pressures and modifying patient hemodynamics. Cirrhosis results in significant anatomic and physiologic modifications involving the gastrointestinal, cardiopulmonary, neurologic, renal, immunologic, and hematologic systems. The disease can be divided into compensated and decompensated states, with decompensation associated with significant morbidity and mortality. Complications include variceal hemorrhage, ascites, increased risk of bacterial infection, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, umbilical hernia, and hepatic hydrothorax. Resuscitation including airway and circulation measures is paramount in these patients, and several new techniques are offered for the approach to intubation and resuscitation for patients with severe cirrhosis.Conclusions: Decompensating cirrhotics may require extensive resuscitation, and knowledge of the evaluation and management of complications associated with cirrhosis can improve care for patients with severe liver disease. [ABSTRACT FROM AUTHOR]

Liver cirrhosis is a major cause of morbidity and mortality worldwide, mainly due to complications of portal hypertension. In this article, we review the current understanding on the pathophysiology, the diagnostic criteria and the available therapeutic options for patients with emerging hepatic syndromes in cirrhosis, namely the hepatorenal, hepato-adrenal and hepatopulmonary syndrome. The hepatorenal syndrome is a well-recognized complication of advanced cirrhosis and is usually associated with an accelerated course to death unless liver transplantation is performed. The hepatopulmonary syndrome is often missed in the evaluation of patients with cirrhosis; however, early recognition is essential for the efficient management of individual patients. The hepato-adrenal syndrome, although not fully characterized, offers an exciting field for research and potential therapeutic interventions. [ABSTRACT FROM AUTHOR]

Chronic injury to the liver from a variety of different sources can result in irreversible scarring of the liver, known as cirrhosis. Cirrhosis is a major cause of morbidity and mortality in the USA, and according to the Centers for Disease Control and Prevention was responsible for 31,903 deaths in 2010 alone. It is thus of the utmost importance to appropriately manage these patients in the inpatient and outpatient setting to improve morbidity and mortality. In this review, we address four major areas of cirrhosis management: outpatient management of portal hypertension with decompensation, hepatic encephalopathy, hepatorenal syndrome, and bleeding/coagulation issues. Outpatient management covers recommendations for health care maintenance and screening. Hepatic encephalopathy encompasses a brief review of pathophysiology, treatment in the acute setting, and long-term prevention. Hepatorenal syndrome is discussed in regards to pathophysiology and treatment in the hospital setting. Finally, a discussion of the assessment of coagulation profiles in cirrhosis and recommendations for bleeding and thrombosis complications is included. These topics are not all encompassing with regard to this complicated population, but rather an overview of a few medical problems that are commonly encountered in their care. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To assess the determinants of longterm outcome in patients with spontaneous bacterial peritonitis (SBP). METHODS: This study was conducted retrospectively. Kaplan-Meier (KM) and Cox proportional hazards survival analyses were performed. RESULTS: Altogether, 93 patients with SBP were identified, with their mean age of 57.9 ± 12.9 years, Child-Pugh score 10.4 ± 1.9 and model for end-stage liver disease (MELD) score 20.2 ± 6.8. The etiology of chronic liver disease (CLD) was alcohol-related liver disease (ARLD) (n = 58) and viral hepatitis/nonalcoholic steatohepatitis (n = 28). SBP was the index presentation of cirrhosis in 26 (28.0%) patients. Overall mortality was 80.6%; among them 81.3% were liver-related, and 33 (35.5%) died during index hospitalization. In total, 70.0% of patients who survived index hospitalization died during follow-up, with a median survival of 12.5 months. Estimated survival at 3 months, 1 year and 5 years was 54.8%, 34.4% and 15.2%, respectively. Non-ARLD etiology for CLD was an independent predictor of overall mortality (HR 3.484, 95% CI 1.802-6.757, P < 0.001) and mortality in those surviving hospitalization (HR 2.319, 95% CI 1.210-4.444, P = 0.011). Hepatorenal syndrome did not predict outcomes. Two (3.3%) patients surviving hospitalization underwent liver transplantation (LT). CONCLUSIONS: One-year survival after hospitalization with SBP remains poor (34.4%) with unacceptably low LT rates. Non-ARLD etiology for CLD is an independent predictor of both overall mortality and mortality after discharge. In view of the projected increase in non-alcoholic steatohepatitis-related CLD, screening strategies for timely CLD diagnosis are warranted. [ABSTRACT FROM AUTHOR]

High or toxic doses of acetaminophen (APAP), a mild analgesic and antipyretic drug, can cause life-threatening hepatic and renal dysfunction. This study is designed to investigate the potential protective role of quercetin to attenuate the hepatorenal toxicity induced by a high single oral dose (3 g/kg) of APAP in rats. Three main groups of Sprague-Dawley rats were used: quercetin, APAP and quercetin plus APAP-receiving animals. Corresponding control animals were also used. Interestingly, oral supplementation of quercetin (15 mg/kg/day) prior to APAP intoxication dramatically reduced APAP-induced hepatorenal toxicity as evidenced by measuring serum lipid profile, total protein, urea, creatinine, ALT, AST, ALP, G-GT and liver tissue content of TC and TG. Quercetin treatment markedly prevented the generation of TBARS and PCC with substantial improvement in terms of GSH and activities of antioxidant enzymes in both liver and kidney homogenates. The relationship between quercetin and NO levels which is still a matter of debate, was also investigated. NO levels in serum, liver and kidney tissues were significantly inhibited in quercetin pre-treated animals. Furthermore, quercetin administration significantly inhibited the reduction of liver and kidney contents of ATP parcels associated with this hepatorenal toxicity. These results suggest that the protective role of quercetin in the prevention of APAP-induced hepatorenal toxicity in rats was associated with the decrease of oxidative and nitrosative stress in hepatic and renal tissues as well as its capacity to improve the mitochondrial energy production. However, clinical studies are warranted to investigate such an effect in human subjects. [ABSTRACT FROM AUTHOR]

Objective(s): This study aimed to develop drugs from natural sources to overcome the side effects of many of synthetic drugs. Methanol extracts of both pericarp and seeds of Pleiogynium solandri were used to investigate antioxidant, hepatoprotective, and renal function protective, analgesic, and anti-inflammatory effects and to determine the chemical composition of the extract responsible for bioactivity. Materials and Methods: Methanol (70%) extracts of the seeds and pericarps of P. solandri were prepared. Hot plate method was used to test analgesic activity, carrageenan-induced paw inflammation method was used to test anti-inflammatory activity, and colorimetric methods were used to test antioxidant, hepatoprotective (by determination of serum alanine and aspartate aminotransferase activities), and renal function protective effects (by measuring uric acid and creatinine levels). Chromatographic methods and means of 1H-NMR, 13C -NMR, and UV spectra were used for isolation and identification of the responsible compounds. Results: In this study for the first time, four phenolic compounds were isolated from the pericarp of P. solandri which were identified as catechin, quercetin, quercetrin and rutin. Methanolic extract of both seeds and pericarp of P. solandri showed strong antioxidant effect, hepatoprotective, renal function protective, analgesic, and anti-inflammatory effects. However, seed extract had lower effect than pericarp in a dose dependent manner. Conclusion: This study showed that methanol extract of pericarp of P. solandri is more powerful than that of the seed regarding its antioxidant, hepato-protective; renal function protective, analgesic, and anti-inflammatory effects. The phenolic compounds isolated from the methanol extract of pericarp were responsible for bioactivity. [ABSTRACT FROM AUTHOR]

Alpha-lipoic acid (ALA) is a natural dithiol compound, with a free radical scavenger and biological antioxidant properties. The purpose of the current study was to investigate the protective effects of ALA on biochemical alteration and oxidative stress induced by acute deltamethrin intoxication in rats. Markers of liver and kidney injuries in serum of deltamethrin-intoxicated as well as ALA-pretreated rats were analyzed. Moreover, serum and (or) tissue lipid peroxidation, malondialdehyde and antioxidant markers, reduced glutathione, catalase, superoxide dismutase activity, and total antioxidant capacity were evaluated. The results showed that all parameters were altered in the intoxicated group, indicating hepatorenal oxidative damage of deltamethrin. Pre-treatment with ALA reversed the changes in most of the studied parameters in a dose-dependent manner. Histopathological and biochemical findings were parallel. It can be concluded that ALA may be a promising therapeutic option for prevention and (or) treatment of deltamethin toxicity. [ABSTRACT FROM AUTHOR]

A 62-year-old man with cirrhosis secondary to hepatitis C and chronic alcohol abuse was admitted to the intensive care unit with hematemesis and mental status changes. Physical examination showed ascites and stigmata of chronic liver disease. Blood pressure was noted as 87/42 mm Hg and laboratory studies showed a serum creatinine level of 0.8 mg/dL, an estimated glomerular filtration rate of 84 mL/min/1.73 m2 calculated using the Modification of Diet in Renal Disease Study equation, a serum sodium level of 123 mEq/L, a total serum bilirubin level of 4.3 mg/dL, and an international normalization ratio of 1.6. The patient was resuscitated with packed red blood cells and fresh-frozen plasma and bleeding was controlled. However, on the third day of admission, creatinine level increased to 1.5 mg/dL. Examination of urine sediment showed 1 to 5 bilirubin-stained granular casts per high-powered field and a few renal tubular epithelial cells. The urine sodium level was 21 mEq/L and the fractional excretion of sodium was 0.43%. [Copyright &y& Elsevier]