Renal Function and Blood Pressure in Patients Receiving Long-Term, Low-Dose Cyclosporine Therapy for Idiopathic Autoimmune Uveitis

Deray, Gilbert; Benhmida, Mohamed; Hoang, P. Le; Maksud, Philippe; Aupetit, B.; Baumelou, A; Jacobs, C

doi:10.7326/0003-4819-117-7-578

Cited by 77 publications

(33 citation statements)

References 27 publications

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“…Several researchers suggested that free radicals play an important part in CsA toxicity [1, 11, 12, 13]. The experimental data that lazaroid afforded renal protection against CsA toxicity through its antioxidant capacity has supported this hypothesis [1].…”

Section: Discussionsupporting

confidence: 49%

“…The data of some experimental studies suggest a possible role of free radicals in CsA toxicity [1, 11, 12, 13]. It has been established that CsA-induced functional and structural deterioration of the kidney was accompanied by renal lipid peroxidation and that concurrent administration of an antioxidant, lazaroid, afforded renal protection and attenuated renal injury [1].…”

Section: Introductionmentioning

confidence: 99%

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Impaired Antioxidant Defense System in the Kidney Tissues from Rabbits Treated with Cyclosporine

Durak

Karabacak²,

Büyükkoçak

et al. 1998

Nephron

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Enzymatic antioxidant defense system and antioxidant defense potential (AOP) were studied in kidney tissue from rabbits treated with cyclosporine (CsA, 25 mg/kg/day), antioxidant vitamins (E, 100 mg/kg/day plus C, 200 mg/kg/day), and CsA plus antioxidant vitamins, and in kidney tissue from control animals. Although no change was observed in superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were found decreased in kidney tissue exposed to CsA for 10 days compared with control tissue. The level of thiobarbituric acid-reagent substances (TBARS) was higher and antioxidant defense potential (AOP) lower in the CsA-treated group compared with the other groups. Histopathological examination reveals important subcellular damage in the renal tissue from the animals treated with CsA. Antioxidant vitamin therapy caused full improvement in the enzyme activities, TBARS levels and AOP, but the subcellular damage was partly ameliorated in the CsA plus vitamin group. Results suggest that CsA impairs the antioxidant defense system and reduces the antioxidant defense potential in the renal tissue. Antioxidant vitamin treatment protects the tissue in part against toxic effects of the drug.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

Impaired Antioxidant Defense System in the Kidney Tissues from Rabbits Treated with Cyclosporine

Durak

Karabacak²,

Büyükkoçak

et al. 1998

Nephron

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“…43, 44, 45, 46]. Even nontransplanted patients receiving cyclosporin A because of chronic rheumatoid arthritis or uveitis [47, 48]may develop hyertension. The entire spectrum from simple hypertension to malignant hypertension or HUS/thrombotic thrombocytopenic microangiopathy may be induced by cyclosporin A [49, 50].…”

Section: What Are the Mechanisms Leading To Hypertension In The Graftmentioning

confidence: 99%

Hypertension in the Transplanted Patient

Zeier

Mandelbaum

Ritz

1998

Nephron

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Hypertension is a common finding after renal transplantation, and it has a variety of underlying mechanisms. One reason is the type of immunosuppressive therapy, with a higher prevalence of hypertension in cyclosporine-treated patients. Cyclosporine interferes with several humoral and neural systems which are involved in blood pressure regulation such as the renin-angiotensin system, endothelins, nitric oxide, prostaglandins and the sympathetic nervous system. Other pathomechanisms for posttransplant hypertension are uncontrolled renin secretion of the native kidneys, polycythemia, recurrence of renal disease in the graft and renal failure. Renal transplant artery stenosis is a potentially treatable cause of post-transplant hypertension and several techniques such MRT angiography, Doppler sonography and conventional angiography are available. The diagnosis and treatment of hypertension are of high importance in general for the transplanted patient, and especially for the long-term prognosis of graft function.

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“…Alternate /3-blockers have been used. 97 Some investigators have used angiotensin converting enzyme inhibitors with diuretics with success. 111 Contrary to some expectations, we find that diuretic therapy poses relatively few problems.…”

mentioning

confidence: 99%

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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Renal Function and Blood Pressure in Patients Receiving Long-Term, Low-Dose Cyclosporine Therapy for Idiopathic Autoimmune Uveitis

Abstract: In patients with healthy native kidneys, long-term cyclosporine therapy, even at a low dose (5 mg/kg per day), is nephrotoxic and is associated with a high incidence of hypertension.

Cited by 77 publications

References 27 publications

Impaired Antioxidant Defense System in the Kidney Tissues from Rabbits Treated with Cyclosporine

Impaired Antioxidant Defense System in the Kidney Tissues from Rabbits Treated with Cyclosporine

Hypertension in the Transplanted Patient

De novo hypertension after liver transplantation.

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