Journal of Renal and Hepatic Disorders
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Direct-Acting-Antivirals Anti-hepatitis C Virus in Renal Transplant Patients: Relevance of Pharmacologic Interaction
Get PDFRenal transplantation in patients affected by hepatitis C virus (HCV) infection has been a serious problem because of the use of immunosuppressants. HCV virus may be more aggressive in both the liver and the kidney. Several posttransplantation pathologies are known to be ascribed to the HCV virus. Virus eradication has been historically attempted with interferon (IFN) and ribavirin with poor results. In addition, IFN given posttransplantation may cause severe acute rejection. The introduction of direct antiviral agents (DAA) has revolutionized the treatment, and now it is possible to treat renal transplant patients with these agents leading to a HCV-free status in 3 months without the use of IFN. The major problem caused by these agents is their interference with the immunosuppressive agents. The pharmacokinetics of DAA and immunosuppressants often meet the same metabolic pathways and use the same cytochromes or proteic complexes. In some cases, this may lead to high or low immunosuppressant levels with the risk of rejection. In other cases, the DAAs are interested and they may be increase or decrease in a dangerous way. Therefore, a strict monitoring is always recommended
Cholemic Nephropathy: Hyperbilirubinemia and its Impact on Renal Function
Get PDFCholemic nephropathy represents a spectrum of renal injury, from proximal tubulopathy to intrarenal bile cast formation, found in patients with severe liver dysfunction. It is caused by hyperbilirubinemia, usually in jaundiced patients. Acute kidney injury is one of the most important complications in patients with end-stage liver disease. The relationship between liver disease and renal impairment, especially the effect of hyperbilirubinemia on renal tissue and renal function, has not been fully elucidated. These considerations deem necessary for nephrologists, when performing a clinical evaluation of patients with liver diseases, for the implementation of an integrated medical approach. This review focuses on the current knowledge on cholemic nephropathy with emphasis on the role of hyperbilirubinemia on renal impairment. The treatment strategies and outcome are also discussed
Hepatitis C Virus Infection and Renal Disorders
Get PDFHepatitis C virus (HCV) infection is frequently associated with extrahepatic disorders, among which renal diseases are frequent. This article highlights the most frequent HCV-associated renal disorders, the impact of HCV infection on chronic renal disease and renal transplantation, and the role of current direct-acting antiviral therapies. HCV is associated with membranoproliferative glomerulonephritis, acceleration of end-stage renal diseases in patients with glomerulopathies, and a higher risk of death in patients affected by chronic kidney disease. Before the introduction of direct-acting antiviral drugs as treatment modality, renal transplantation was a challenging clinical problem because the drugs available until 2011 obtained a poor sustained virologic response, had several side effects, and caused acute rejection when used after transplantation. The knowledge of the viral structure and its replication allowed the discovery of new classes of direct-acting antiviral drugs that revolutionized this scenario. These new drugs are comparatively more effective and safer. Accumulating evidence suggests that it is possible to cure HCV-related glomerulonephritis, and obtain a sustained virologic response in patients with renal failure, or on dialysis, before commencing transplantation. Finally, it became possible to transplant HCV-positive kidneys into HCV-positive or HCV-negative recipients
ADAM and ADAMTS Proteases in Hepatic Disorders
Get PDFProteolysis is an irreversible post-translational modification that regulates protein function and signal transduction. This includes remodelling of the extracellular matrix, release of membrane-bound cytokines and receptor ectodomains, as well as the initiation of intracellular signalling cues. Members of the adamalysin protease subfamily, in particular the ADAM (a disintegrin and metalloprotease) and ADAMTS (the ADAM containing thrombospondin motif) families, are involved in these processes. This review presents an overview of how ADAM and ADAMTS proteins are involved in liver physiology and pathophysiology
The Role of Stearoyl-coenzyme A Desaturase 1 in Liver Development, Function, and Pathogenesis
Get PDFStearoyl-coenzyme A desaturase 1 (SCD1) is a microsomal enzyme that controls fatty acid metabolism and is highly expressed in hepatocytes. SCD1 may play a key role in liver development and hepatic lipid homeostasis through promoting monounsaturated protein acylation and converting lipotoxic saturated fatty acids into monounsaturated fatty acids. Imbalanced activity of SCD1 has been implicated in fatty liver induction, inflammation and stress. In this review, the role of SCD1 in hepatic development, function and pathogenesis is discussed. Additionally, emerging novel therapeutic agents targeting SCD1 for the treatment of liver disorders are presented
Wasting Away with Cirrhosis: A Review of Hepatic Sarcopenia
Get PDFThe complications of decompensated cirrhosis are well documented and include variceal bleeding, fluid retention, and hepatic encephalopathy. A less well recognized complication of cirrhosis is muscle wasting or sarcopenia. It is now recognized to have a significant impact on patient survival, especially in patients who are awaiting liver transplantation. An understanding of the pathophysiology of muscle protein homeostasis has led to several proposed mechanisms of sarcopenia and the potential to reverse muscle loss. This review discusses the potential mechanisms of sarcopenia and highlights the possible future means of reversing sarcopenia
Imaging of Renal Angiomyolipomatosis
Get PDFAngiomyolipoma is a type of benign renal tumor. It is sporadic and isolated in 80% of cases. The remaining 20% is associated with tuberous sclerosis complex or pulmonary lymphangioleiomyomatosis. Generally, angiomyolipomas manifest themselves as angiomyolipomatosis, in which the angiomyolipomas are larger, bilateral, and widespread. Understanding whether angiomyolipomas are present in the context of angiomyolipomatosis is of considerable importance because it might be associated with malignant lesions. This article provides an overview of the radiological features of renal angiomyolipomatosis under different imaging techniques such as ultrasound, computed tomography, and magnetic resonance
Single Nucleotide Polymorphisms of Cytotoxic T-lymphocyte Antigen 4 (CTLA-4) and Susceptibility to Chronic Viral Hepatitis B and C Infections
Get PDFThe cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene is a negative regulator of T-lymphocyte activation and proliferation. Single nucleotide polymorphisms (SNPs) occurring on the CTLA-4 gene can modify the ability to control the proliferation of T-lymphocytes, thereby impacting the clearance of hepatitis B (HBV) and hepatitis C (HCV) virus infections. The −319C/T and +49A/G SNPs of CTLA-4 gene have been associated with autoimmune disorders and liver infections. Studies show that the +49G allele confers susceptibility to HBV and HCV infections in chronic disease (without cirrhosis), associates with the risk of chronic HCV infection in males, confers protective effect against the development of hepatocellular carcinoma, and favors viral elimination. Furthermore, the +49G allele alone or in haplotype with the −319C favors chronic infection with genotype 3 HCV, has an inverse association with HCV genotype 1, and decreases viral load in chronic hepatitis C associated with sustained virological response (SVR). These findings support an important role of the SNPs of CTLA-4 gene in viral hepatitis; however, the mechanisms by which they influence immune response against viral infections are not fully understood. This review gives an overview of the current understanding of the association between CTLA4 SNPs and HBV/HCV infections
Role of JAK3 in the Pathogenesis of Oxidative Stress-Induced Kidney Fibrosis
Get PDFThe Janus kinase (JAK) tyrosine kinase family and JAK/STAT signal transduction pathway may act in kidney fibrogenesis. JAK3 expression was investigated in in vitro and in vivo models of kidney fibrosis involving oxidative stress. There was a marked down-regulation of JAK3 mRNA in rat kidney tubular epithelial cells (NRK52E) and fibroblasts (NRK49F) exposed to 1.0 mM H2O2 for 18–20 h compared with controls, which correlated with increased apoptosis and decreased mitosis in both cell lines. However, JAK3 protein levels were not significantly different in control and H2O2-treated epithelial and fibroblast cultures. JAK3 activation (phospho-tyrosine) increased in NRK52E cells and decreased in NRK49F cells with oxidative stress. STAT3 phosphorylation decreased in both cell lines with oxidative stress compared with controls. JAK3 protein expression and localisation were investigated in kidneys using the unilateral ureteral obstruction (UUO) model (0–7 days, rats) of kidney fibrosis that involves oxidative stress. JAK3 protein expression did not differ between UUO and controls; however, JAK3 localisation increased temporally with UUO, with strong epithelial expression in mitotic cells compared with controls. Apoptotic tubular epithelium showed minimal JAK3. In summary, in vitro, decreased kidney JAK3 mRNA after oxidative stress was not seen translationally. Differences in the activation of the JAK3/STAT3 pathway may have different consequences for renal fibrosis. In vivo, changes in JAK3 protein localisation, and especially its colocalisation with mitotic cells, indicate that JAK3 protein may contribute to renal tubular epithelial cell proliferation after oxidative stress
Potassium Profiling in Hemodialysis
Get PDFCardiac dysrhythmia and sudden death account for a large proportion of cardiac mortality in dialysis patients. Risk factors for sudden death that are specific to dialysis patients include fluid and electrolyte imbalances during hemodialysis, particularly those of potassium. The risk of arrhythmia may be related to changes in serum K+ concentration during dialysis, and thus close attention should be paid to the dialysate K+ concentration and the serum–dialysate concentration gradient. Potassium profiling is a technique where the dialysate K+ concentration is gradually reduced to keep the gradient between blood and dialysate at a non-fluctuating low level. We provide a review of studies that compare constant potassium concentration in dialysate to gradual reduction in dialysate potassium concentration. These studies illustrate that adequate and more gradual potassium removal can be achieved with potassium profiling techniques, while having lower cardiac irritability