Cases reported "Renal Artery Obstruction"

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1/11. Renal thrombotic microangiopathy in patients with systemic lupus erythematosus and the antiphospholipid syndrome.

    Current studies indicate that a thrombotic microangiopathy (TMA) identifies patients with systemic lupus erythematosus (SLE) who are at high risk of progressing to end-stage renal disease. We have observed two patients with SLE and one patient with a primary antiphospholipid syndrome (APS) who developed acute renal insufficiency with thrombocytopenia. Renal biopsies showed a TMA characterized by thrombi or by cellular and mucoid intimal hyperplasia of small arteries and arterioles. No arterial or arteriolar immune-complex deposits were detected by immunofluorescent or electron microscopy. Biopsies from one SLE patient and the APS patient showed no immune-complex glomerular disease. Both had serum antiphospholipid antibodies (aPL). aPL were not detected in the serum of the other SLE patient who had an active lupus nephritis. Acute renal failure and thrombocytopenia resolved in each case following treatment by plasmapheresis or prednisone and heparin. None of the patients were initially treated with cytotoxic drugs. As more knowledge is gained, the accurate identification of renal vascular lesions in SLE or related diseases could influence renal prognosis and choice of therapy. The cases reported here provide further evidence that a TMA can cause acute renal failure independent of lupus nephritis. TMA should be distinguished from other forms of renal vascular disease, particularly a noninflammatory lupus microangiopathy, which is probably mediated by subendothelial immune-complex deposits. The absence of immunoglobulin deposits in vessels involved by a TMA indicates that microvascular thrombosis is promoted by mechanisms other than those usually attributed to immune-complex disease. Phospholipid reactive antibodies may be pathogenetic in some cases.
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2/11. adult hemolytic uremic syndrome with renal arteriolar deposition of IgM andC3.

    Two cases of idiopathic adult hemolytic uremic syndrome in which deposits of IgM and C3 were identified in renal arterioles showing fibrinoid necrosis are reported. fibrin was also identified in the lumina of the involved vessels, but there was no laboratory evidence of disseminated intravascular coagulation. In both cases, serum C3 was decreased and C4 was normal, suggesting involvement of the alternate pathway of complement activation. These two cases suggest that in some instances the adult hemolytic uremic syndrome may be immunologically mediated, and that renal vascular thrombosis is a secondary phenomenon.
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3/11. Lupus vasculopathy combined with renal infarction: unusual manifestation of lupus nephritis.

    A 30-year-old woman with a 10-year history of systemic lupus erythematosus was admitted to our hospital because of the onset of hypertension and renal dysfunction. Renal arteriogram revealed multiple renal infarctions, and cut-off or tapering-stenosis in the interlobular arteries. Renal biopsy showed concentric intimal thickening with narrowed lumen in some arterioles and deposition of IgG/IgM/complement 3 in the wall of arteriole without any active lesions or immune complex deposition in glomeruli. The present case indicates that this type of renal vascular lesion in lupus nephritis, lupus vasculopathy, may cause renal infarction and the loss of renal function without active glomerular lesions.
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4/11. Systemic and renal fibrinolytic activity in a patient with anticardiolipin syndrome and renal thrombotic microangiopathy.

    A 24-year-old white woman with a past history of recurrent venous thromboses of the lower extremities was admitted for hypertension and renal failure. She had a chronic cutaneous ulcer on the anterior side of the left leg and oral ulcers of the palatum. Laboratory tests demonstrated rapidly progressive renal failure and the presence of an anticardiolipin antibody (ELISA). thrombosis of the inferior vena cava was shown by phlebocavography. Renal biopsy revealed typical thrombotic microangiopathy. Tissue-type plasminogen activator (tPA) was visualized by immunofluorescence in endothelial cells of renal arterioles and glomeruli. Normal plasma levels of tPA, urokinase and plasminogen activator inhibitor 1 were found by ELISA, and tPA antigen levels rose after desmopressin acetate infusion. Thus, in this case, the diffuse thrombotic process was not related to defective circulating or renal fibrinolytic systems and could be promoted by the procoagulant effect of antiphospholipid antibodies.
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5/11. Reversibility of captopril-induced renal insufficiency after prolonged use in an unusual case of renovascular hypertension.

    We report a case of severe hypertension with an occluded renal artery to a solitary kidney, who developed sudden deterioration of renal function following treatment with captopril. His renal function remained impaired but stable during 2 years' treatment with captopril but returned to pre-treatment levels soon after cessation of the drug. This indicates reversibility in captopril-induced renal failure even after its prolonged use and suggests that no organic damage occurs to glomerular arterioles following chronic ACE inhibition.
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6/11. cyclosporine-induced renal macroangiopathy.

    Although nephrotoxicity secondary to cyclosporine (CsA) is common and has a predilection for arterioles, stenosis of the major renal artery or its primary branches has not yet been described as a manifestation of CsA toxicity. A case of a primary cadaveric renal transplant recipient treated with CsA who developed significant deterioration of renal function associated with angiographic evidence of high-grade stenosis of all three major branches of the renal artery that resolved completely after discontinuation of the drug is reported.
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7/11. Renovascular hypertension: a case of intimal fibroplasia with congenital anomaly of the renal artery.

    We report a case of renovascular hypertension caused by fibromuscular dysplasia (intimal fibroplasia) with congenital anomaly of the renal artery. Arteriography revealed complete occlusion from the root to the middle of the right renal artery and a collateral artery from the right lumbar artery. Histological examination showed intimal fibroplasia and three arterioles in the intima of the renal artery.
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8/11. Renal vascular lesions after chemotherapy with vinblastine, bleomycin, and cisplatin.

    A 30 year old man with metastatic embryonal carcinoma became hypertensive during vinblastine, bleomycin, and cisplatin therapy. Three months after completion of therapy, accelerated hypertension occurred (blood pressure 210/140 mm Hg). nitroprusside failed to control the hypertension, but captopril resulted in a prompt and sustained normalization of the blood pressure. The plasma renin activity was markedly elevated before therapy. Renal biopsy disclosed "onionskin" narrowing of the interlobular arteries and fibrin thrombosis of a majority of the afferent arterioles. A form of drug-induced renovascular hypertension is suggested.
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9/11. Morphologic aspects of Goldblatt hypertension in a newborn infant.

    hypertension (210 mm Hg), hyponatremia, hypochloremia, and hypokalemia were observed in an 11-day-old infant. After electrolyte repletion, blood pressure rose to 320 mm Hg in spite of administration of antihypertensive drugs. The child died of a massive cerebral hemorrhage on the 17th day of life. At autopsy, the left renal artery was partially thrombosed and the left kidney partially infarcted. The glomeruli in the preserved cortical areas were of normal size; the juxtaglomerular apparatuses markedly enlarged. The blood vessels were inconspicuous. Enlarged glomeruli, multiple ruptures in the mesangium, ectactic glomerular capillaries, and fragile capillary walls were found in the nonconstricted right kidney. Fibrinoid necrosis with occasional fibrin thrombi in the lumina was present in the arterioles. Pronounced intimal edema with fragmented cells and monocytes embedded in the intima were observed in the interlobular and larger arteries. The histologic findings in the blood vessels of the nonconstricted kidney resembled those found in the hemolytic-uremic syndrome (Gasser's syndrome).
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10/11. Malignant vascular disease of the kidney: nature of the lesions, mediators of disease progression, and the case for bilateral nephrectomy.

    A case of thrombotic microangiopathy presenting as a hemolytic uremic syndrome complicated by untreatable hypertension and ultimately requiring bilateral nephrectomy is discussed. Severe hypertension and renal failure may complicate the course of vascular diseases of the kidney, including thrombotic microangiopathy, chronic hypertension, and scleroderma. Toxins, pressure stress, and immune material may trigger the initial injury to vascular endothelium. The malignant course of these renal vascular diseases seems linked to the severity of vascular injury. Endothelial injury manifests with swelling and detachment of endothelial cells from the basement membrane, expansion of the subendothelial space, and newly formed basement membrane-like material. In arterioles, endothelial injury precedes myointimal swelling and proliferation, leading to vascular lumina narrowing or obliteration and secondary glomerular ischemia, with glomerular tuft collapse and garland-like wrinkling and thickening of the capillary wall. Endothelial cell injury is very likely the common determinant of a cascade of events that lead to irreversible renal failure. When the initial insult (toxins, mechanical stress, antibodies) is promptly removed, lesions are self-limiting and the patient usually recovers. However, a severe insult persisting for some time can lead to chronic and irreversible vascular lesions that, through renal ischemia, trigger maximal activation of the renin angiotensin system with a brisk elevation in arterial blood pressure that may combine to further vascular injury and renal ischemia. Moreover, enhanced shear stress in the severely narrowed microcirculation, through abnormal von willebrand factor processing, can also favor endothelial injury and platelet aggregation, which may further worsen the vascular lesions and sustain the microangiopathic process. Plasma manipulation, arteriolar vasodilators, and angiotensin-converting enzyme inhibitors normally control the vicious circle, but in few severe cases bilateral nephrectomy remains the last chance to save the patient's life.
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