Vascular Lesions as Manifestations of Cyclosporin Nephrotoxicity

Moody, Heather; Matz, L. R.; Hurst, P.

doi:10.1016/s0140-6736(86)91210-9

Cited by 14 publications

(4 citation statements)

References 6 publications

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“…CSA stimulates release of endothelin, as do other stimuli, including radiocontrast. 48 - 73 Experimental studies indicate that the acute fall in GFR during intravenous administration of CSA can be inhibited by endothelin antibody.…”

Section: Abnormalities Of Vasomotor Regulationmentioning

confidence: 99%

“…It appears not. The kidney is particularly sensitive to this process and demonstrates increased involvement, with both microvascular thrombosis 53 ' 71 ' 73 and persistent vasoconstriction, despite changes in other vascular beds. It is of interest that a fall in systemic vascular resistance and normalization of arterial pressures did not have parallel events in the kidney in the patient described in this article (Table 1).…”

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confidence: 99%

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De novo hypertension after liver transplantation.

Textor

1993

Hypertension

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Hypertension develops in most patients after transplantation when immunosuppression is based on cyclosporine and prednisone. The pathogenesis appears to be multifactorial but involves rapidly rising vasoconstrictor tone in renal and systemic vascular beds. Much of this tone reflects abnormal vascular function, characterized by impaired prostacyclin and EDRF effects, in conjunction with increased vasoconstriction due to endothelin and possibly other factors. Effective management of the transplant recipient depends on preventing excessive vasoconstriction, usually with calcium channel blocking agents.

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Section: Abnormalities Of Vasomotor Regulationmentioning

confidence: 99%

mentioning

confidence: 99%

De novo hypertension after liver transplantation.

Textor

1993

Hypertension

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“…The pathogenesis and etiology of TMA is still unclear, but pregnancy, infections (bacterial, fungal, viral, and amebic), vascular collagen diseases, malignancies, receipt of chemotherapy, use of medical drugs, and cocaine abuse have all been reported to be possible triggering conditions [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30], although most cases in adults occur without a known precipitating event or associated disease.…”

Section: Discussionmentioning

confidence: 99%

Thrombotic Microangiopathy in Patients With Acquired Immunodeficiency Syndrome Before and During the Era of Introduction of Highly Active Antiretroviral Therapy

&NA;

2002

Infectious Diseases in Clinical Practice

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The incidence of thrombotic microangiopathy (TMA) was retrospectively evaluated in a cohort of 1223 patients with acquired immunodeficiency syndrome (AIDS) who were observed from January 1985 through December 1996 (before the era of highly active antiretroviral therapy [HAART]), and the incidence was prospectively assessed for 347 patients with AIDS during the period of January 1997 through December 2000 (during the HAART era). Seventeen cases were reported in the former cohort (1.4%). The increased risk of developing TMA was statistically significant in patients with cryptosporidiosis or AIDS-related cancer but not in those with other diseases. In the 1997-2000 cohort, no cases were observed during follow-up. TMA is associated with conditions observed in the advanced phases of human immunodeficiency virus infection. The disappearance of TMA during the HAART era may be explained by the lower percentage of patients with long-lasting CD4 + T cell depletion, advanced AIDS, or cryptosporidiosis or who have undergone multiple courses of chemotherapy for treatment of cancer. Thrombotic microangiopathy (TMA) is a clinical syndrome characterized by microangiopathic hemolytic anemia, thrombocytopenia, microvascular thrombosis, and multiple organ dysfunction. In the clinical spectrum of TMA, thrombotic thrombocytopenic purpura (TTP) is associated with up to 5 symptoms, including fever, neurological abnormalities, anemia, thrombocytopenia, and renal failure, all of which (except cerebral involvement) also occur in patients with hemolytic uremic syndrome (HUS) [1, 2].

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“…Gratifying results of alternate therapy with CyA and PSL in the management of chronic GVHD reported recently (7) may be attrib utable to the elevated blood levels of the two drugs. High plasma concentrations of CyA and the occurrence of MHA were associated with overdosage of CyA (1,(8)(9)(10) or combined use of steroids in massive doses in most instances (5, ll, 12), while similar phenomena occurring from a combination of CyA and PSL used in standard doses are exceedingly rare. Blood levels of CyA, on most occasions, are determined by the RIA method and measurements thus obtained are said to correlate with those by high performance liquid chromato graphy (HPLC) (13).…”

Section: Case Reportmentioning

confidence: 99%

Microangiopathic Hemolytic Anemia in a Graft-versus-Host Disease Patient Treated with Cyclosporine A and Prednisolone.

et al. 1992

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A 38-year-old male patient with chronic myelocytic leukemia in the first chronic phase underwent bone marrow transplantation (BMT) from an HLA identical sibling. He developed chronic graft-versus-host disease and his condition gradually deteriorated. Fourteen months after BMT, acute progressive anemia, thrombocytopenia, reticulocytosis, increased serum lactic dehydrogenase and increased serum bilirubin were revealed following treatment with cyclosporine A (240 mg/day i.v.), prednisolone (60 mg/day i.v.) and azathioprine (lOO mg/day p.o.). Red blood cell fragmentations were also found microscopically. At that time, the serum cyclosporine A trough level was 1,300ng/ml by the polyclonal antibody RIA method. These symptoms were resolved by discontinuation of cyclosporine A and administrations of aspirin, cilostazol, and dipyridamole as anti-platelet agents. We consider this phenomenon to be micro angiopathic hemolytic anemia due to a serum high cyclosporine A level which resulted from the concomitant use of cyclosporine A with prednisolone.(Internal Medicine 31: [434][435][436][437] 1992)

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Vascular Lesions as Manifestations of Cyclosporin Nephrotoxicity

Cited by 14 publications

References 6 publications

De novo hypertension after liver transplantation.

De novo hypertension after liver transplantation.

Thrombotic Microangiopathy in Patients With Acquired Immunodeficiency Syndrome Before and During the Era of Introduction of Highly Active Antiretroviral Therapy

Microangiopathic Hemolytic Anemia in a Graft-versus-Host Disease Patient Treated with Cyclosporine A and Prednisolone.

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