In Japan, amyloidosis is a rare cause of renal failure and of renal transplantation. We treated a patient who underwent a renal transplantation because of chronic renal failure caused by secondary amyloidosis with a good result. The patient was a 50-year-old woman who was diagnosed with secondary amyloidosis and an amyloid kidney. She underwent living donor renal transplantation after about 7 years of hemodialysis. During the 3-year posttransplantation period, she maintained good allograft function with a serum creatinine level about 1.2 mg/dL. Because of amyloidosis is a systemic disease, amyloid kidney patients often experience fatal complications, so the indications for renal transplantation in amyloid patients are still controversial. But if the patient's general condition is good, renal transplantation can be an effective therapy for patients with kidney failure caused by amyloidosis.
"RTx should be performed, at earliest time possible after onset of maintenance dialysis prior to development of severe cardiac disease. The outcome appears to be best in patients without cardiac involvement on echocardiography [5, 6]. "
[Show abstract][Hide abstract] ABSTRACT: Although end-stage renal disease (ESRD) related to AA amyloidosis nephropathy secondary to tuberculosis is most common in our country, there are limited data concerning patient and graft outcome after renal transplantation (RTx). To the best of our knowledge, this is the first report of RTx in ESRD patient with secondary amyloidosis due to tuberculosis from India. A 30-year-old female with past history of pulmonary tuberculosis 3 years back was admitted with complaint of gradually progressive pedal oedema and nausea for 3 months. Renal biopsy was suggestive of secondary renal amyloidosis with vascular involvement and chronic tubulointerstitial involvement. She was transplanted with kidney from her 28-year-old brother with 3/6 human leukocyte antigen match. She had immediate good graft function without any perioperative complications (cardiovascular, infections, rejection and delayed graft function). She was discharged with serum creatinine of 0.8 mg/dL. Her last serum creatinine level was 0.9 mg/dL with cyclosporine level of 100 mg/dL at 9-month followup without any medical or surgical complication. The quality of life also improved after transplantation. With careful selection, ESRD patients with secondary amyloidosis due to tuberculosis are eligible for RTx with favorable outcome and improved quality of life.
[Show abstract][Hide abstract] ABSTRACT: Chemokines are small molecular weight proteins primarily known to drive migration of immune cell populations. In both acute and chronic liver injury, hepatic chemokine expression is induced resulting in inflammatory cell infiltration, angiogenesis, and cell activation and survival. During acute injury, massive parenchymal cell death due to apoptosis and/or necrosis leads to chemokine production by hepatocytes, cholangiocytes, Kupffer cells, hepatic stellate cells, and sinusoidal endothelial cells. The specific chemokine profile expressed during injury is dependent on both the type and course of injury. Hepatotoxicity by acetaminophen for example leads to cellular necrosis and activation of Toll-like receptors while the inciting insult in ischemia reperfusion injury produces reactive oxygen species and subsequent production of pro-inflammatory chemokines. Chemokine expression by these cells generates a chemoattractant gradient promoting infiltration by monocytes/macrophages, NK cells, NKT cells, neutrophils, B cells, and T cells whose activity are highly regulated by the specific chemokine profiles within the liver. Additionally, resident hepatic cells express chemokine receptors both in the normal and injured liver. While the role of these receptors in normal liver has not been well described, during injury, receptor up-regulation, and chemokine engagement leads to cellular survival, proliferation, apoptosis, fibrogenesis, and expression of additional chemokines and growth factors. Hepatic-derived chemokines can therefore function in both paracrine and autocrine fashions further expanding their role in liver disease. More recently it has been appreciated that chemokines can have diverging effects depending on their temporal expression pattern and the type of injury. A better understanding of chemokine/chemokine receptor axes will therefore pave the way for development of novel targeted therapies for the treatment of liver disease.
Frontiers in Physiology 06/2012; 3:213. DOI:10.3389/fphys.2012.00213 · 3.53 Impact Factor
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