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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five of 182 recipients of allogeneic bone marrow transplants performed between 2/84 and 6/90 developed seizures while receiving cyclosporine and methylprednisolone to prevent acute graft-versus-host disease. All received a radiation-free regimen of busulfan and cyclophosphamide as preparative therapy. Two patients received HLA-mismatched allografts; and three patients received marrow from HLA-identical sibling donors. Two patients had received extensive intrathecal therapy prior to transplantation. All patients were receiving standard prophylactic doses of CsA and MP at the time of onset (median 31 days posttransplantation) of seizures. Three patients had mild-to-moderate hypertension and varying degrees of morphologic evidence of microangiopathic hemolytic anemia. None had unusually low magnesium levels. Cyclosporine levels were not in the toxic range. Cranial magnetic resonance imaging and computed tomography (CT) showed bilateral abnormalities primarily in the posterior temporal, occipital, and parietal lobes. These abnormalities were shown to be transient on sequential MRI exams in two patients. Seizures as well as radiologic abnormalities resolved on stopping CsA and did not recur in 2 patients who subsequently received CsA in lower doses. These findings confirm and expand previous observations of CsA-associated seizures and demonstrate that they occur in allogeneic bone marrow transplant recipients following a radiation-free preparative regimen of busulfan and cyclophosphamide.
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PMID:Cyclosporine-associated seizures in bone marrow transplant recipients given busulfan and cyclophosphamide preparative therapy. 187 5

One hundred and sixty eight adult patients with B-cell non-Hodgkin's lymphoma (NHL) and other hematologic malignancies who underwent autologous or allogeneic bone marrow transplantation (BMT) were investigated for the subsequent development of hemolytic-uremic syndrome (HUS). All patients were conditioned with cyclophosphamide and total body irradiation. When examined at 3-month intervals for the first year post-BMT, all patients had uniform measurements of hematocrit (Hct) and serum creatinine. Sixteen patients who initially exhibited Hct and creatinine values that were normal range for the BMT populations developed a sudden decrease in Hct and increase in creatinine between 3 and 11 months post-BMT and fulfilled the clinical and laboratory criteria for HUS. None of these patients had known active cytomegalovirus infection, graft-versus-host disease, or cyclosporine administration. The degree of decrease in Hct and creatinine elevation ranged from solely laboratory abnormalities to a clinically significant syndrome. Twelve of the 16 patients developed acute clinical complications of congestive heart failure, hypertension (HTN), or peripheral edema. Twelve patients required red blood cell support, whereas only four patients required platelet transfusions. Both hemolytic anemia and thrombocytopenia have resolved in virtually all cases. At a mean follow up of 18 months postdiagnosis, creatinine elevations have persisted along with HTN. All patients have survived without life-threatening long-term sequelae. With the increasing use of BMT as a curative modality for patients with hematologic malignancies, it becomes important to prospectively monitor patients for the development of HUS and its potential long-term impact on renal function.
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PMID:Hemolytic-uremic syndrome following bone marrow transplantation in adults for hematologic malignancies. 201 7

Thrombotic thrombocytopenic purpura (TTP) is a syndrome that occurs mainly in adults with multiorgan microvascular thrombosis consisting of thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal involvement, and fever. The female to male ratio is 3:2, and peak incidence occurs in the 3rd decade of life. Clinical signs are the consequence of hyaline thrombosis and occlusion of capillaries and arterioles. Renal ailment manifests itself in hematuria and proteinuria with azotemia and even overt renal failure. In severe disease, azotemia is typical of hemolytic uremic syndrome (HUS). TTP was first described in 1925 by Moschcowitz. The clinical picture of TTP consists of a prodromal phase, a viruslike disease occurring in up to 40% of patients. 60% have neurologic disturbances, 90% have purpura initially, and fever occurs in all. Anemia is often severe with hemoglobin values of 7-9 gm/dl, renal involvement in 90%, and renal failure in 40-80% of patients. Clinical variants include the acute and fulminant variety mortality, the chronic form, and the relapsing form. Predisposing factors and triggering agents are autosomal recessive inherited traits in acute idiopathic TTP, systemic diseases, tumor antigens, pregnancy and puerperium, viruses (endotoxins for HUS), and possibly oral contraceptives and hypertension. Therapy includes corticosteroids (prednisone 100-400 mg/day); heparin for postpartum HUS; and antiplatelet agents (Dextran 70, aspirin, and dipyridamole in high doses). The infusion of PGI2 is controversial; splenectomy is also questionable; and vincristine, azathioprine, and cyclophosphamide have unproven efficacy. Fresh-frozen plasma exchange is the method of choice as it produces survival in 90%. Others are iv immunoglobulins, vitamin E, and dialysis and renal transplant. Platelet transfusions are contraindicated because of sudden death and decreased survival.
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PMID:Thrombotic thrombocytopenic purpura and related disorders. 210 74

A case of microangiopathic hemolytic anemia (MHA) associated with the immunosuppressive agent, cyclosporine, is reported herein. The patient manifested anemia with red blood cell fragmentation, hypertension, thrombocytopenia, elevation of serum LDH levels and glomerular capillary thromboses within a few days of his transplantation. Extensive treatments with urokinase and heparin proved ineffective and graftectomy was performed 7 days after his transplantation. Immunofluorescent staining failed to show immunoglobulin (IgG or IgM) or complement (C3) deposition within the glomeruli, which discriminated MHA from acute humoral-vascular rejection.
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PMID:Cyclosporine-associated microangiopathic hemolytic anemia in a renal transplant recipient. 265 53

Of 140 patients with "scleroderma renal crisis" encountered during a 33-year period, 15 of 131 (11%) whose blood pressures were recorded were normotensive during this complication. In comparison with 116 patients with hypertension, the normotensive patients significantly more often had microangiopathic hemolytic anemia (90% versus 38%) and thrombocytopenia (83% versus 21%). Pulmonary hemorrhage occurred in 6 normotensive patients. More normotensive patients had received high doses of corticosteroids (prednisone greater than or equal to 30 mg/day) during the 2 months immediately preceding renal crisis (64% versus 16%). A role for corticosteroids in precipitating renal crisis is suggested. The 12-month survival was significantly reduced in the normotensive patients (13% versus 35%).
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PMID:Normotensive renal failure in systemic sclerosis. 277 21

A patient with scleroderma renal crisis is described. At presentation he had severe hypertension, deteriorating renal function, microangiopathic haemolytic anaemia, and elevated levels of renin, aldosterone and noradrenaline. Enalapril controlled blood pressure, stabilized renal function, lowered aldosterone and noradrenaline levels, and improved peripheral circulation. It appears that converting-enzyme inhibitors can favourably alter the outlook of this otherwise fatal disorder.
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PMID:Successful treatment of scleroderma renal crisis with enalapril. 281 41

Intracranial hypertension with papilledema occurred in two patients receiving danazol therapy for either cyclic neutropenia or immune hemolytic anemia. Results of clinical, laboratory, and neuroradiologic studies showed no apparent cause for the condition in Case 1 and the papilledema resolved one month after discontinuing danazol. Carotid angiography in Case 2 demonstrated cerebral venous sinus thrombosis; the papilledema showed gradual improvement after cessation of danazol. An additional seven cases of pseudotumor cerebri presumed secondary to danazol therapy have been reported to the Food and Drug Administration. The papilledema resolved in all seven cases soon after discontinuing danazol. A drug-induced complication should be suspected, and alternative therapy sought, in patients who develop intracranial hypertension associated with administration of danazol.
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PMID:Pseudotumor cerebri induced by danazol. 291 2

Secondary hemolytic uremic syndrome (HUS) is uncommon. When it occurs, it is usually in association with pregnancy, malignancy, severe hypertension, drugs, or collagen vascular diseases. It has rarely been reported in patients with glomerular disease. Two such patients with secondary HUS are described. A 17-month-old girl with hematuria and the nephrotic syndrome, negative antistreptolycin O (ASO) titer, and low serum levels of C3 and C4 developed oliguria, progressive azotemia, thrombocytopenia, and microangiopathic hemolytic anemia. A kidney biopsy showed fibrin in glomerular capillaries and cresentic membranoproliferative glomerulonephritis. A 22-year-old man with a 16-year history of relapsing minimal change nephrotic syndrome had been in remission for 5 years when he experienced nephrotic syndrome relapse and developed thrombocytopenia, microangiopathic hemolytic anemia, and renal failure. A kidney biopsy revealed foot process fusion and obstruction of glomerular capillaries with fibrin and platelets. These cases illustrate that HUS can occur in association with other glomerular diseases and should be considered when thrombocytopenia and hemolytic anemia occur in a nephritic or nephrotic patient.
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PMID:Hemolytic uremic syndrome associated with glomerular disease. 291 69

CSA toxicity includes renal impairment, microangiopathic hemolytic anemia (MAHA), thrombocytopenia (T), and consumptive coagulopathy (CC). We report five BMT patients who developed CSA-associated hematological toxicity. All were conditioned with Ara-C, Cyclophosphamide, Methylprednisolone, TBI, and in two cases busulfan. IV CSA was started the day after marrow infusion and, when practicable, changed to the enteral route. Five patients developed MAHA and T resulting in significantly increased transfusion requirements. All patients had renal impairment and red cell fragmentation. In all patients fragmentation was noted before renal impairment. All developed disproportionate increases in BUN relative to serum creatinine consistent with decreased renal perfusion. Hypertension followed renal impairment in four cases and occurred at the same time as the renal impairment in one case. Two developed CC, prolongation in APTT, and marked decreases in plasma fibrinogen. All patients improved on reduction of the CSA dose. BMT recipients receiving CSA at variable doses may develop evidence of a TTP-like syndrome and/or CC.
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PMID:Coagulation defects in cyclosporine A treated allogeneic bone marrow transplant patients. 304 63

After treatment with mitomycin C, a patient developed pulmonary hypertension with interstitial infiltrates, microangiopathic hemolytic anemia, systemic hypertension, and renal failure with the nephrotic syndrome. Open lung biopsy documented intracapillary fibrin thrombi in the pulmonary vasculature. Renal biopsy documented glomerular and arteriolar changes that were most consistent with a thrombotic-thrombocytopenic-like process. Treatment with corticosteroids, fresh-frozen plasma, and total plasma exchange was ineffective. The patient died six months after the onset. When mitomycin-C therapy is given, the clinician should be aware of the pulmonary, renal, and microangiopathic changes that can be associated with such therapy.
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PMID:Pulmonary hypertension, hemolytic anemia, and renal failure. A mitomycin-associated syndrome. 308 8


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