Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the numeruos adverse side effects of tacrolimus (TAC), de novo thrombotic microangiopathy stands out as an infrecuente but severe complication. Renal dysfunction is the only alteration that should lead to suspicion of thrombotic microangiopathy, because the clinical features of intravascular hemolysis are not always found. The definitive diagnosis can usually be made with kidney biopsy. Patientes with TAC induced thrombotic microangiopathy usually promptly recover after treatment withdrawal or reduction in the dose of TAC and a short course of plasma therapy, but the risk of rejection increases. Switching from TAC to cyclosporine has also been tried with resolution of the hemolysis but thrombotic microangiopathy has been noted with both and this condition may later recur. We present a 29-year-old man who received a kidney-pancreas transplant for end-stage diabetic nephropathy. After initial induction with basiliximab, the immunosuppression consisted of prednisone, tacrolimus and mycophenolate mofetil. Twenty four days posttransplantation his renal function declined with a peak creatine level of 2.35 mg/dl. Laboratory studies showed thrombocytopenia and features of intravascular hemolysis. TAC associated hemolytic uremic syndrome was suspected and drug was immediately stopped and converted to sirolimus. Also he was treated with plasma infusion. The allograft biopsy showed focal glomerular and arteriolar acute thrombosis without evidence of rejection. Our experience demostrate that switching from tacrolimus to sirolimus could be an adecuate strategy for patients who develop FK506-associated de novo thrombotic microangiopathy without increase risk of acute rejection.
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PMID:[De novo hemolytic uremic syndrome in a kidney-pancreas recipient in the postoperative period]. 1521 59

Sulodexide represents a novel antithrombotic agent with multiple sites of action on blood coagulation and vascular processes. The purpose of this study was to compare sulodexide and enoxaparin on anticoagulant effects, tissue factor (TF)-induced activation of platelets, inhibition of microparticle generation and to investigate their effect on heparin-induced platelet aggregation (HIPA). Sulodexide was compared with enoxaparin at equigravimetric concentrations. When compared to enoxaparin, sulodexide produced a stronger anticoagulant effect in the prothrombin time (PT), activated partial thromboplastin time (APTT), Heptest, and thrombin time (TT) assays. In addition, sulodexide had a stronger inhibitory effect on TF-mediated microparticle generation (IC(50) = 2.8 microg/ mL), P-selectin expression (IC(50) = 4.8 microg/ml), and platelet aggregate formation (IC(50) = 8.5 microg/mL) compared to higher IC(50) values with enoxaparin. Sulodexide and enoxaparin exhibited a similar effect on heparin-induced thrombocytopenia (HIT) antibody-mediated platelet activation HIPA assays. These results suggest that sulodexide is a relatively stronger anticoagulant agent than enoxaparin. Sulodexide is subcutaneously absorbed. Its ability to inhibit TF-mediated platelet activation may contribute to the observed therapeutic effects of sulodexide in microvascular vasculopathy such as diabetic nephropathy. These results also suggest that inhibition of TF activation of platelets by sulodexide may be independent of its anticoagulant effects. These results warrant further investigation of sulodexide in additional preclinical and clinical studies.
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PMID:Comparative anticoagulant and platelet modulatory effects of enoxaparin and sulodexide. 1970 18

We report a 66-year-old man with chronic hepatitis caused by hepatitis type C virus of genotype-1b and high-viral-load combined with cryoglobulinemia and advanced diabetic nephropathy in whom we successfully achieved viral removal and eradication by DFPP (VRAD). The dose of PEG-interferon was reduced to 70 mg/week due to thrombocytopenia. Rivavirin was discontinued at day 21 due to anemia. Even with treatment of PEG-interferon alone, the condition was judged to be sustained viral remission at the end of the observation. This is a successful report of VRAD in a combined case of diabetic and HCV-related cryoglobulin-nephropathy with nephrotic syndrome. The therapeutic effect of IFN seemed to be efficiently enhanced by concomitant DFPP (VRAD therapy).
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PMID:A case of chronic hepatitis C with nephrotic diabetic nephropathy who achieved sustained viral remission by double-filtration plasmapheresis and interferon combination therapy. 2286 24

Pseudo-pulmonary embolism (PPE) superimposed on heparin-induced thrombocytopenia (HIT) is an important complication in patients undergoing hemodialysis (HD) treatment. We report the clinical profile of an HD patient with acute respiratory distress induced by PPE and HIT. A 67-year-old man with diabetic nephropathy and end-stage renal failure developed congestive heart failure. He was admitted to Kitasato University Hospital. He was introduced to HD treatment using low-molecular-weight heparin as an anticoagulant for an HD session on day 1 of admission. On day 11 after admission, he suddenly developed respiratory distress and hypoxia at 30 min after the start of the fifth HD session. The HD session was immediately discontinued, and oxygen inhalation improved his complaints and hypoxia. The platelet count decreased from 220 x 10(9)/L at the start of the HD session to 80 x 10(9)/L at the end of the HD session. We suspected HIT when blood clotting occurred in his hemodialyzer and blood circuit for HD during the HD session on day 12. Chest X-ray, electrocardiogram, echocardiography, and pulmonary microcirculation scintigraphy were normal. Serum analysis was positive for heparin-platelet factor 4 (PF4) antibody. We then diagnosed him with PPE superimposed on HIT. After the anticoagulant agent for HD was changed from low-molecular-weight heparin to nafamostat mesilate, his clinical symptoms and thrombocytopenia disappeared. PPE superimposed on HIT appeared approximately 7-10 days after the initial use of heparin for the HD session. PPE also led to acute respiratory distress, blood coagulation in the hemodialyzer and blood circuit for HD, as well as thrombocytopenia with less than a 50% decrease in platelet counts. The prognosis of PEE and HIT is good after discontinuing the use of heparin.
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PMID:[Heparin-induced thrombocytopenia with pseudo-pulmonary embolism in a patient who was newly introduced to hemodialysis treatment]. 2666 17

A 75-year-old male undergoing hemodialysis because of diabetic nephropathy was referred to our hospital complaining of high fever and swelling of the left kidney. Our initial clinical diagnosis was severe pyelonephritis. He was initially treated with intravenous antibiotics and his clinical symptoms subsequently improved but only temporarily. The high fever soon recurred, accompanied by progressive thrombocytopenia. His general condition deteriorated despite conservative treatment. He then underwent nephrectomy of the left kidney. However, the thrombocytopenia persisted and his general condition did not improve. The pathological diagnosis was malignant lymphoma (non-Hodgkin's lymphoma, diffuse large B-cell type). He received chemotherapy, but his status rapidly deteriorated and he died 1.5 months after the operation. Primary renal malignant lymphoma is very rare, because the kidney lacks lymphatic tissue.
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PMID:[A Case of Primary Renal Malignant Lymphoma Initially Managed as Severe Pyelonephritis in a Patient Undergoing Hemodialysis]. 2713 86

Hemophagocytic syndrome combines febrile hepatosplenomegaly, pancytopenia, hypofibrinemia, and hepatic dysfunction. It is characterized by bone marrow and organ infiltration of activated, nonmalignant macrophages that phagocytize blood cells. It is rare among renal transplant recipients. Here, we present the successful management of late-onset cytomegalovirusinduced hemophagocytic lymphohistiocytosis in a kidney transplant recipient after coronary artery bypass graft surgery. In 2012, our patient had end-stage kidney disease due to diabetic nephropathy and underwent related living-donor renal transplant. He was also hypertensive and hyperuricemic and had heart ischemia for which percutaneous coronary intervention for triple vessel disease was performed before transplant. In March 2017, he underwent successful aortic valve replacement and coronary artery bypass graft surgery; however, the patient had persistent thrombocytopenia. Heparin-induced thrombocytopenia was negative. His bone marrow showed hemophagocytosis possibly due to cytomegalovirus. Moreover, antiglycoprotein IIb/IIIA autoantibodies were positive. A positron emission tomography scan was negative for malignancy. He started treatment for cytomegalovirus with modifi cation of his immunosuppressive regimen (pulse steroid). Antiplatelet therapy was held and only resu med if platelet count exceeded 30000/L. Moreover, he received intravenous immunoglobulin and romiplostim treatment with partial response. Throughout treatment, he had stable kidney graft function with improving platelet count. A multi disciplinary approach is needed to treat patients with hemophagocytic syndrome, especially renal transplant recipients. Late-onset cytomegalovirus is an important cause for this syndrome.
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PMID:Successful Management of Late-Onset Cytomegalovirus-Induced Hemophagocytic Lymphohistiocytosis in Kidney Transplant Recipient After Coronary Artery Bypass Graft Surgery. 3077 56

Fluorouracil plus oxaliplatin (L-OHP) (FOLFOX) plus bevacizumab (BV) therapy is commonly administered to patients with metastatic colorectal cancer. However, few reports have described L-OHP therapy in hemodialysis patients, and the efficacy and safety remain uncertain in this population. Here, we report three cases of hemodialysis patients with colorectal cancer who received a modified FOLFOX-6 (mFOLFOX-6, or FOLFOX plus folinic acid) plus BV regimen every 3 weeks. One patient, a 65-year-old man with chronic renal failure consequent to diabetic nephropathy, underwent hemodialysis 3 times/week. He exhibited a partial response after 7 cycles of mFOLFOX-6 plus BV, with the major adverse events of Grade 1 peripheral neuropathy and Grade 2 thrombocytopenia. He died of perforation-related septic shock. A 71-year-old man previously treated with bosutinib for chronic myelocytic leukemia received 9 cycles of mFOLFOX-6 plus BV and achieved stable disease. Chemotherapy was administered every 4 weeks, and the 5-fluorouracil dose was reduced after he developed Grade 4 neutropenia. A 71-year-old woman with chronic renal failure consequent to diabetic nephropathy underwent hemodialysis 3 times a week. She received 3 cycles of mFOLFOX-6 plus BV, but exhibited disease progression and developed Grade 4 neutropenia, which necessitated a reduced 5-fluorouracil dose. After completing FOLFOX therapy, she began second-line irinotecan/5-fluorouracil/leucovorin (FOLFIRI) plus BV therapy. In two cases, bone marrow suppression increased the difficulty of L-OHP dose escalation. We conclude that mFOLFOX-6 plus BV, with appropriate dose reduction, is acceptable for patients with chronic renal failure. Further data are needed to determine the adequate chemotherapy dose.
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PMID:Modified FOLFOX-6 Plus Bevacizumab Chemotherapy for Metastatic Colorectal Cancer in Patients Receiving Hemodialysis: A Report of Three Cases and Review of the Literature. 3157 55