Cases reported "Renal Artery Obstruction"

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1/33. University of Miami Division of Clinical pharmacology Therapeutic Rounds: ischemic renal disease.

    Ischemic renal disease (IRD) is defined as a significant reduction in glomerular filtration rate and/or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. IRD is an important cause of chronic renal failure and end-stage renal disease (ESRD), and many patients with a presumed diagnosis of hypertensive nephrosclerosis may actually have undiagnosed ischemic nephropathy as the cause of their ESRD. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function or a delay in progression to ESRD. There are six typical clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin-converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed on poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. It is important for the clinician to identify IRD, because IRD represents a potentially reversible cause of chronic renal failure in a hypertensive patient.
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2/33. renal artery stenosis: a complication of needle puncture for manometry. Case of subintimal dissection with spontaneous resolution.

    After aortorenal bypass for renovascular hypertension secondary to atherosclerosis of the renal artery of a solitary left kidney a high-grade stenosing lesion developed distal to the site of insertion of a Dacron graft. In the immediate postoperative period the blood pressure was restored to normal, but one week later hypertension recurred. An arteriogram disclosed an area of stenosis 1 cm distal to the site of insertion of the graft in the renal artery. During the next year, serial arteriograms were made, renal function remained normal, and hypertension gradually abated. One year after the discovery of the postbypass stenosis, an arteriogram showed disappearance of the constricting lesion. The postoperative stenosis was, in all probability, caused by subintimal dissection secondary to needle puncture for strain gauge manometry.
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3/33. renal artery dissection: a complication of catheter arteriography.

    renal artery dissection is a rare complication of catheter arteriography. Predisposing factors include atherosclerosis and fibromuscular dysplasia. Optimum management requires aortographic documentation of the extent of vascular obstruction. Dissections causing incomplete obstruction of blood flow can be treated with systemic anticoagulation to prevent downstream thrombosis and should be followed with serial isotope blood flow studies and LDH measurements. dissection causing complete vascular obstruction usually requires immediate surgery, although spontaneous reestablishment of flow may occur. The 3 patients discussed illustrate a spectrum of findings, including the acute development of renovascular hypertension.
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4/33. renal artery stenosis and aneurysmatic dilatation of arteria carotis interna in tuberous sclerosis complex.

    hypertension in children with neurocutaneous disorders (phacomatoses) is a well-recognized complication of these diseases and the cause of hypertension is fairly specific within each group. In patients with neurofibromatosis, hypertension is mainly caused by renovascular disease, whereas in tuberous sclerosis (TSC) reasons for hypertension are renoparenchymal lesions, such as angiomyolipoma or cysts. We report on a girl with TSC and hypertension due to unilateral renal artery stenosis associated with aneurysmatic changes of internal carotid artery. This unusual combination of symptoms in our patient supports the importance of thorough and complete investigation of hypertension in children with phacomatoses.
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5/33. A late complication of spousal kidney donation.

    An 83-year-old female who had previously (32 years ago) donated a kidney to her husband presented with loin pain, confusion and oliguria. Acute renal failure and pulmonary edema necessitated emergency hemodialysis. The history and findings were thought to be consistent with acute renal artery occlusion on a background of atherosclerosis and severe renal artery stenosis. We present this case, not to imply that renal donation is a hazardous procedure, but rather as an illustration of a complication of donor nephrectomy that in a very large series has proved to be extremely rare. This case illustrates the point that even very rare events become more likely as the period of follow-up increases.
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6/33. Renovascular hypertension from renal artery compression by congenital bands.

    renal artery compression by fibromuscular bands containing sympathetic nerves and ganglia was encountered in 3 of 75 patients with renovascular hypertension. The hypertension was successfully managed by resection of the bands. The absence of mortality and morbidity dictates that the "stenotic" area of the renal artery be explored, especially in children and adults with minimal angiographic evidence of visceral atherosclerosis, before proceeding with a bypass graft to the renal artery.
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7/33. Successfully treated "accelerated" renovascular hypertension with intravascular stenting.

    A 76-year-old man developed progressive renal dysfunction with refractory hypertension. Bilateral renal artery stenosis due to atherosclerosis was revealed. Both the hypertension and renal dysfunction were improved by percutaneous transluminal renal angioplasty with stenting. Based on the rapidly progressive elevation of plasma renin activity and the improvement of both renal dysfunction and hypertension after stenting, this was considered a case of "accelerated" renovascular hypertension. There have been an increasing number of patients with bilateral renal artery stenosis due to atherosclerosis. The present case reminds us that a rapid progression of renal dysfunction suggests, in addition to besides rapidly progressive glomerulonephritis with crescent formation, bilateral renal artery stenosis, the incidence of which is on the rise. In the present case, angioplasty with stenting was effective for blood pressure control and preservation of renal function.
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8/33. renal artery stenosis and nephrotic syndrome: a rare combination in an infant.

    We describe an uncommon pediatric finding of unilateral renal artery stenosis, which presented as nephrotic syndrome, hypertension, failure to thrive, and hyponatremia. The child was a previously well 8-month-old male who looked well but had mild periorbital edema with severe hypertension. After 3 days of captopril therapy, the nephrotic-range proteinuria significantly improved. However, the hypertension persisted. Renal imaging revealed a small left kidney with reduced parenchymal uptake and no significant excretion. A renal angiogram demonstrated left renal artery stenosis with increased left renal vein renin activity. The hypertension resolved within 24 h of a left nephrectomy, but non-nephrotic-range proteinuria persisted for 8 months post operatively. pathology of the left kidney was consistent with fibromuscular dysplasia. Although a few glomeruli (1%) had changes consistent with focal segmental glomerulosclerosis, such a few abnormal glomeruli were unlikely to account for the nephrotic syndrome. hypertension-induced changes in the unaffected right kidney probably caused the nephrotic-range proteinuria.
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9/33. Severe arteriosclerosis in the kidney of a cocaine addict.

    cocaine abuse has been associated with sudden cardiac death with coronary artery thrombosis with or without underlying vessel disease. Additional vascular beds thus far implicated in cocaine-associated arteriopathy include thoracic and abdominal aorta, and pulmonary, cerebral, and placental vessels; abnormalities include vasospasm, thrombosis, and accelerated atherosclerosis. We report the case of an adult male cocaine user with severe arteriosclerosis of renal vessels, and suggest that cocaine may also affect the renal vasculature.
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10/33. Mast cell chymase in the ischemic kidney of severe unilateral renovascular hypertension.

    Chymase degrades angiotensin I (AI) to form angiotensin ii (AII), probably constituting a bypass of the renin-angiotensin cascade. Chymase activity increases in some vascular diseases. In the kidney, an increase in chymase activity was reported in an animal model of ischemic kidney of renovascular hypertension (RVH); however, no such evidence has been provided in humans. We treated a 64-year-old patient with severe unilateral RVH and atherosclerosis, for whom removal of the ischemic kidney was the only option. Using immunohistochemical staining, we investigated chymase activity in the removed kidney and associated artery and vein. An increase in chymase activity, together with mast cells infiltrating the interstitium, was observed where interstitial fibrosis was seen. In the renal artery, where severe atherosclerosis was seen, and also in the vein, mast cell infiltration in the adventitia was accompanied by chymase. The captopril test showed an increase in serum aldosterone level, with a concomitant increase in plasma renin activity and decrease in blood pressure. Because the decrease in blood pressure implies a decrease in circulatory AII levels, it is plausible that in this patient, chymase had a role in AII formation in the adrenal gland to stimulate aldosterone secretion. Thus, by means of captopril, AI levels increased, and chymase may have produced AII in loci tissues, which, in turn, stimulated aldosterone secretion. This is the first report of an increase in chymase activity in the interstitium of an ischemic kidney and renal artery and vein in a patient with RVH and atherosclerosis.
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