Multiple Systemic Infarctions as a Complication of Bronchial Artery Embolization With Polyvinyl Alcohol: A Case Report

Bronchial artery embolization (BAE) is a widely used modality of treatment for massive hemoptysis which has well known complications such as chest pain, groin hematoma and transverse myelitis but systemic embolization of the material used in the procedure is very rare and was reported only four times in the literature which were all caused by the use of microspheres. Herein we report a case of a 41-year-old caucasian male who had a history of tuberculosis 10 years ago. He had BAE with polyvinyl alcohol (PVA) for the treatment of recurrent hemoptysis. After the procedure, the patient complained of severe pain on the left upper quadrant and bilateral costovertebral regions and in abdominal CT, multiple infarcts in the subcapsular area of the spleen and kidneys were observed. This is the first reported case of inadvertent systemic embolization secondary to BAE with PVA. Although the risk of systemic embolization is greater with microspheres, still potentially serious and life threatening complications may occur with PVA

Mucosa-associated lymphoid tissue lymphoma of the duodenum together with multiple intra-abdominal thromboses and hepatitis C virus infection: a case report

Mucosa associated lymphoid tissue MALT lymphoma is a low grade malignancy that arises most commonly from the gastric mucosa. Small intestinal involvement is very rare. The causative relationship between Helicobacter pylori and the gastric MALT lymphoma is a well known issue, but recently there are several data suggesting the role of hepatitis C virus (HCV) infection in the pathogenesis of lymphoma including MALT lymphoma. Herein we present a rare case of duodenal MALT lymphoma with multiple intra-abdominal thromboses together with HCV infection that was confirmed by real-time polymerase chain reaction detecting HCV-RNA within the peripheral blood mononuclear cells

Hepatitis c virus associated glomerulopathies

Hepatitis C virus (HCV) infection is a systemic disorder which is often associated with a number of extrahepatic manifestations including glomerulopathies. Patients with HCV infection were found to have a higher risk of end-stage renal disease. HCV positivity has also been linked to lower graft and patient survivals after kidney transplantation. Various histological types of renal diseases are reported in association with HCV infection including membranoproliferative glomerulonephritis (MPGN), membranous nephropathy, focal segmental glomerulosclerosis, fibrillary glomerulonephritis, immunotactoid glomerulopathy, IgA nephropathy, renal thrombotic microangiopathy, vasculitic renal involvement and interstitial nephritis. The most common type of HCV associated glomerulopathy is type. MPGN associated with type. mixed cryoglobulinemia. Clinically, typical renal manifestations in HCV-infected patients include proteinuria, microscopic hematuria, hypertension, acute nephritis and nephrotic syndrome. Three approaches may be suggested for the treatment of HCV-associated glomerulopathies and cryoglobulinemic renal disease: (1) antiviral therapy to prevent the further direct damage of HCV on kidneys and synthesis of immune-complexes; (2) B-cell depletion therapy to prevent formation of immune-complexes and cryoglobulins; and (3) nonspecific immunosuppressive therapy targeting inflammatory cells to prevent the synthesis of immune-complexes and to treat cryoglobulin associated vasculitis. In patients with moderate proteinuria and stable renal functions, anti-HCV therapy is advised to be started as pegylated interferon-a plus ribavirin. However in patients with nephrotic-range proteinuria and/or progressive kidney injury and other serious extra-renal manifestations, immunosuppressive therapy with cyclophosphamide, rituximab, steroid pulses and plasmapheresis should be administrated. (C) 2014 Baishideng Publishing Group Inc. All rights reserved

Endothelial Progenitor Cells and Kidney Diseases

Endothelial progenitor cells (EPC) are bone marrow derived or tissue-resident cells that play major roles in the maintenance of vascular integrity and repair of endothelial damage. Although EPCs may be capable of directly engrafting and regenerating the endothelium, the most important effects of EPCs seem to be depended on paracrine effects. In recent studies, specific microvesicles and mRNAs have been found to mediate the pro-angiogenic and regenerative effects of EPCs on endothelium. EPC counts have important prognostic implications in cardiovascular diseases (CVD). Uremia and inflammation are associated with lower EPC counts which probably contribute to increased CVD risks in patients with chronic kidney disease. Beneficial effects of the EPC therapies have been shown in studies performed on different models of CVD and kidney diseases such as acute and chronic kidney diseases and glomerulonephritis. However, lack of a clear definition and specific marker of EPCs is the most important problem causing difficulties in interpretation of the results of the studies investigating EPCs

Pathophysiology of Cisplatin-Induced Acute Kidney Injury

Cisplatin and other platinum derivatives are the most widely used chemotherapeutic agents to treat solid tumors including ovarian, head and neck, and testicular germ cell tumors. A known complication of cisplatin administration is acute kidney injury (AKI). The nephrotoxic effect of cisplatin is cumulative and dose-dependent and often necessitates dose reduction or withdrawal. Recurrent episodes of AKI may result in chronic kidney disease. The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. There is predominantly acute tubular necrosis and also apoptosis in the proximal tubules. There is activation of multiple proinflammatory cytokines and infiltration of inflammatory cells in the kidney. Inhibition of the proinflammatory cytokines TNF-α or IL-33 or depletion of CD4+ T cells or mast cells protects against cisplatin-induced AKI. Cisplatin also causes endothelial cell injury. An understanding of the pathogenesis of cisplatin-induced AKI is important for the development of adjunctive therapies to prevent AKI, to lessen the need for dose decrease or drug withdrawal, and to lessen patient morbidity and mortality