Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HUS is a well-known entity primarily associated with bacterial infection and is characterized by a classic triad of anemia, thrombocytopenia, and kidney injury. Its atypical form has been associated with calcineurin inhibitors and has been extensively discussed in renal transplantation. We present a case of tacrolimus-associated HUS in a pediatric heart transplant recipient, which we believe to be previously unreported in the literature.
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PMID:Tacrolimus-associated hemolytic uremic syndrome in a pediatric heart transplant recipient. 2737 45

Renal transplant recipients infected with hepatitis C virus (HCV) have a high risk of progressing to cirrhosis, end-stage liver diseases, and hepatocellular carcinoma. It is also considered as an independent risk for graft loss and is correlated with proteinuria, transplant glomerulopathy, HCV-associated glomerulonephritis, and chronic rejection. Previous therapy involving interferon alfa and ribavirin led to treatment complications, including toxicity, anemia, sepsis, and drug-drug interactions with calcineurin inhibitors, as well as reduced tolerability and efficacy. New direct-acting antiviral drugs simplify and shorten the treatment along with increasing tolerability and efficacy. Nevertheless, limited data and no specific regimen with direct-acting antiviral drugs have been described in the literature for renal transplant recipients with chronic HCV. We describe here the case of a 52-year-old Chinese man who diagnosed with chronic renal failure in 1997 and underwent renal transplantation the same year. In 2012, he was diagnosed with renal graft failure and again underwent hemodialysis. The patient then underwent his second renal transplantation and was administered an immunosuppressive cyclosporine-based regimen in 2015. During hemodialysis, he acquired asymptomatic genotype 1b HCV infection. Serologic test results reflecting liver cirrhosis were all negative, and ultrasound showed no abnormalities in the liver. The patient later required oral sofosbuvir monotherapy for 12 weeks after the second kidney transplantation. Curing HCV in renal transplant recipients is necessary. Although our treatment did not successfully result in a sustained virologic response, it suggests that genotype 1b HCV may have a poor response to a sofosbuvir monotherapy regimen. Specific and effective regimens for renal transplant recipients with HCV infection need to be confirmed in the future.
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PMID:Sofosbuvir Monotherapy for Asymptomatic and Noncirrhotic Hepatitis C Infection in a Renal Retransplantation Recipient: A Case Report. 2793 61

A 57-year-old woman was admitted to our hospital because of a high fever, anemia, and hyperferritinemia. Since a bone marrow examination revealed hemophagocytosis, she was diagnosed with hemophagocytic syndrome (HPS). During treatment of HPS, a heliotrope rash and Gottron's sign appeared with elevated levels of serum aldolase. She also developed heart failure. She was diagnosed with dermatomyositis (DM) and associated myocarditis. Although the administration of glucocorticoids, calcineurin inhibitors, intravenous immunoglobulins, and etoposide ameliorated the clinical findings of DM and cytopenia, the fever and hyperferritinemia remained. The addition of infliximab to glucocorticoids and tacrolimus improved the fever and hyperferritinemia and enabled a reduction in the dose of prednisolone without relapse of the diseases.
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PMID:Hemophagocytic Syndrome Complicated with Dermatomyositis Controlled Successfully with Infliximab and Conventional Therapies. 2919 3

Hyperchloremic metabolic acidosis of renal origin results from a defect in renal tubular acidification mechanism, and this tubular dysfunction can consist of an altered tubular proton secretion or bicarbonate reabsorption capability. Studies have documented that all forms of renal tubular acidosis (RTA), type I to IV, are documented in kidney transplant patients. Among RTA pathophysiologic mechanisms have been described the renal mass reduction, hyperkalemia, hyperparathyroidism, graft rejection, immunologic diseases, and some drugs such as renin-angiotensin-aldosterone blockers, and calcineurin inhibitors. RTA can lead to serious complications as is the case of muscle protein catabolism, muscle protein synthesis inhibition, renal osteodystrophy, renal damage progression, and anemia promotion. RTA should be treated by suppressing its etiologic factor (if it is possible), avoiding hyperkalemia, and/or supplying bicarbonate or a precursor (citrate). In conclusion: Hyperchloremic metabolic acidosis of renal origin is a relatively frequent complication in kidney transplantation patients, which can be harmful, and should be adequately treated in order to avoid its renal and systemic adverse effects.
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PMID:Hyperchloremic metabolic acidosis in the kidney transplant patient. 3092 3

Transplant-associated thrombotic microangiopathy (TA-TMA) is a rare complication of hematopoietic stem cell transplantation (HSCT) with variable presentations. TA-TMA has often been described as a diagnosis of exclusion but a renal biopsy is rarely pursued to confirm the diagnosis, an essential step for our patient with renally limited TMA. We report a case report from the onconephrology clinic and review the literature associated with TA-TMA as it relates to diagnosis and treatment. A 45-year-old woman with acute myeloid leukemia and stage 3 chronic kidney disease underwent a matched unrelated donor allogenic HSCT. Postoperatively, she developed gastrointestinal graft versus host disease (GvHD) and was treated with tacrolimus, sirolimus, budesonide, and beclomethasone. Following discharge, she developed uncontrolled hypertension and required losartan, amlodipine, carvedilol, clonidine patch, and hydralazine as needed. On day 180 post-transplant, she developed lower extremity edema and acute kidney injury (AKI) with creatinine increasing to 2 mg/dL. On day 480 post-transplant, she developed worsening thrombocytopenia, anemia, new hematuria, left flank pain, and worsening renal function with creatinine peaking to 6 mg/dL. Peripheral smear revealed no schistocytes, lactate dehydrogenase of 265 mg/dL, and urinalysis with 100 mg/dL protein. ADAMTS 13 activity was normal (92%) and no inhibitor was detected. She became anuric and was started on hemodialysis. Renal biopsy revealed glomerular changes consistent with TA-TMA. During HSCT, systemic vascular endothelial injury triggers microangiopathic hemolytic anemia, platelet consumption, injury of glomerular endothelial cells and fibrin occluded renal capillaries. Thus, TA-TMA should be considered in HSCT patients with elevated LDH, proteinuria, hypertension, and AKI. However, a diagnosis is difficult to confirm without a renal biopsy. Treatment involves discontinuing potentially toxic agents such as calcineurin inhibitors and sirolimus, prescribing adequate antimicrobial treatment, and using renal replacement therapy if needed. A renal biopsy early in the course of disease not only confirms the diagnosis, but may limit the extent of disease.
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PMID:Thrombotic Microangiopathy With Granulomatosis Interstitial Nephritis in an Allogenic Bone Marrow Transplant Patient: A Case Report and Review of the Literature. 3230 Mar 93


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