Bilateral Renal Artery Stenosis Research Articles

Critical Bilateral Renal Arterial Stenosis Presenting as Cardio‐Renal Syndrome: Isolated Ultrafiltration Preceding Percutaneous Transluminal Revascularization

Critical Bilateral Renal Arterial Stenosis Presenting as Cardio‐Renal Syndrome: Isolated Ultrafiltration Preceding Percutaneous Transluminal Revascularization

Enalapril induced reversible acute renal failure detected by 99mTc-DMSA renal scan in a patient with bilateral renal artery stenosis: a case report

The authors report and discuss a case of bilateral renal artery stenosis in a hypertensive 9 year-old girl that was first suspected with 99mTechnetium-dimercaptosuccinic acid renal scintigraphy. The scintigraphy showed signs of acute renal failure while the patient was on enalapril for controlling her hypertension. Bilateral renal artery stenosis was confirmed with computed tomography angiography. Hypertension resolved after bilateral renal artery angioplasty.

Atherosclerotic Peripheral Vascular Disease Symposium II

The primary goal of this American Heart Association renal intervention writing group was to discuss current controversies related to renal interventions and to recommend important areas of clinical research and advocacy initiatives in this peripheral arterial bed. The 4 areas covered in this section include (1) management of asymptomatic renal artery disease, (2) treatment of ischemic nephropathy, (3) prevention and treatment of atheroembolism in renal artery interventions, and (4) treatment of renal in-stent restenosis (ISR). Atherosclerotic renal artery disease is an often unrecognized contributor to refractory hypertension, renal insufficiency, and increased risk of cardiovascular death.1,2 Renal artery disease is associated with increased cardiovascular events (myocardial infarction, stroke, and death), and when associated with symptomatic coronary artery disease, it independently doubles the risk of death.3 Additionally, the presence of bilateral renal artery stenoses is associated with a reduced 4-year survival rate when compared with unilateral disease (47% versus 59%, P <0.001).3 Hypertension, renal insufficiency, and multisystem atherosclerosis are common entities, and the independent occurrence of these conditions is frequent. Thus, the physician must distinguish between association and causation in the evaluation of patients with atherosclerotic renal artery disease and critically appraise the potential for clinical improvement in selecting patients for renal artery intervention. In contrast to other regional manifestations of atherosclerosis, it is impractical to classify patients with atherosclerotic renal artery disease into symptomatic or asymptomatic categories. Two of the cardinal manifestations of renal artery disease, hypertension and renal insufficiency, are frequently “silent” with regard to clinical manifestations until end-organ damage or uremia occurs. Thus, the majority of patients may be deemed asymptomatic. A more appropriate classification of patients with atherosclerotic renal artery disease may be to classify them in relation to potential clinical consequences. We propose the following classification scheme in patients with renal artery disease:

Posterior reversible encephalopathy syndrome revealing Takayasu’s arteritis

Posterior reversible encephalopathy syndrome is a rare neuroradiologic condition associated with headache, seizures, altered sensorium, visual disturbances, and characteristic lesions on neuroimaging predominantly affecting the posterior regions of the brain. We report a 10-years-8-months-old girl who presented with headache, multiple seizures, and altered sensorium. Her blood pressure was 130/100 mmHg and left brachial pulse was not palpable. CT scan brain showed typical non-enhancing hypodensities in bilateral parieto-occiptal lobes. Prompt treatment of the hypertension led to rapid reversal of neurological symptoms. CT aortogram revealed aortoarteritis with bilateral renal artery stenosis.

Apical Hypertrophic Cardiomyopathy Combined with Bilateral Renal Artery Stenosis in Leriche Syndrome: A Rare Coexistence

We describe the case of a 60-year-old male hypertensive patient who was admitted to our department with intermittent claudication. An echocardiography evaluation detected apical hypertrophy without an intracavity pressure gradient. Transthoracic echocardiography has been the first-line imaging method for patients with suspected hypertrophic cardiomyopathy (HCM), but the method's shortcomings in evaluating the apex are well known. Thus, images from the patient's magnetic resonance imaging and angiography examinations confirmed the classic features of apical HCM. In addition, a 3-dimensional computed tomography evaluation disclosed Leriche syndrome concurrent with severe bilateral stenosis of the renal arteries. Apical HCM combined with severe renal artery stenosis is very rare and has not previously been reported with Leriche syndrome.

Segmental Neurofibromatosis Type 1 (NF1) Associated with Cobb Syndrome: Case Report

We present a 3-month-old girl who showed segmental NF1 and Cobb syndrome. She has a cutaneous vascular malformation located on the middle T (4)-T (6) region superimposed on a giant cutaneous café-au-lait spot. Magnetic resonance arteriography (MRA) revealed bilateral renal artery stenosis, extensive hypertrophy of the spinal epidural venous plexus, coarctation and tubular hypoplasia of the aortic arch and proximal portion of descending aorta. To the best of our knowledge the association of both neurocutaneous disorders has not being previously described.

Malignant hypertension in a child with phakomatosis pigmentovascularis type II b

Phakomatosis pigmentovascularis (PPV) is a rare congenital syndrome characterized predominantly by cutaneous vascular malformations and pigmentary naevi. The most frequently reported form, Type II b, is associated with systemic involvement. Sturge-Weber Syndrome (SWS) with concomitant glaucoma, Klippel-Trenaunay Syndrome (KTS) and naevus of Ota have been frequently described, but there have only been two case reports with asymptomatic renal anomalies. We report the first case of PPV associated with SWS and naevus of Ota presenting with malignant hypertension secondary to bilateral renal artery stenosis. This case raises the possibility that the phakomatoses are not distinct entities but a spectrum of overlapping neurocutaneous, vascular and renal features.

What Should the Physician Do When Creatinine Increases After Starting an Angiotensin‐Converting Enzyme Inhibitor or an Angiotensin Receptor Blocker?

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are generally well tolerated and are used extensively in the treatment of hypertension and heart failure and in patients with renal disease for the reduction of proteinuria.1–3 A common clinical problem arises when these renin-angiotensin system–blocking drugs are started and the serum creatinine becomes elevated above the patient’s baseline level. This may cause concern and may lead to stopping the ACE inhibitor or ARB. Here, we offer our clinical approach to this problem. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II by inhibiting the ACE inhibitor enzyme complex, while ARBs inhibit the binding of angiotensin to its AT1 receptor. Angiotensin II constricts both the afferent and efferent arterioles, but it preferentially increases efferent arteriole resistance. When an ACE inhibitor or ARB is used, there is a decrease in resistance at the efferent (postglomerular) arteriole; this lowers intraglomerular pressure and reduces the glomerular filtration rate (GFR).4 In patients with chronic kidney disease (CKD) and heart failure, the GFR is often even more dependent on an angiotensin II–induced increases in resistance at the efferent arteriole. Patients with heart failure and CKD and patients who are volume-depleted often due to over enthusiastic diuresis may be more susceptible to these hemodynamic effects.5 Both the serum creatinine and potassium levels should be checked from 3 days to a 1 week after an ACE inhibitor is started, particularly in patients who might be considered susceptible to the hemodynamic effects of an ACE inhibitor or an ARB. The rise in serum creatinine values usually begins a few days after beginning therapy with an ACE inhibitor or an ARB, as angiotensin II levels are rapidly reduced or blocked from binding.6 This results in efferent arteriolar dilatation and decreased effective GFR. So what is an acceptable increase in creatinine level? An increase in creatinine concentration of about 25%–30% above baseline is acceptable (eg, creatinine level of 1.2 mg/dL increasing to 1.5 mg/dL). Frequently, creatinine levels will return to baseline or below if blood pressure is lowered, despite the continued use of a renin-angiotensin-aldosterone system inhibitor. A larger rise in creatinine level is likely to occur in patients with bilateral renovascular disease, CKD, and heart failure. What should be done when a creatinine increase exceeds this threshold after a recent medication adjustment? If a decrease in systolic pressure >20 mm Hg has occurred and the ACE inhibitor or ARB was recently added to a diuretic or the dose of ACE inhibitor ARB was increased, the ACE inhibitor or ARB dosage should be reduced or stopped and therapy restarted at a lower dosage later. If the diuretic dosage was recently changed, particularly if the patient lost weight as a result, it may be prudent to temporarily withhold the diuretic and restart at a lesser dose. These are empiric approaches, but the key is to distinguish a large pharmacodynamic effect due to renin-angiotensin system blockade from subtle or overt volume depletion from the diuretic. In our experience, the volume depletion may be so subtle that neither orthostasis in blood pressure nor a detectable increase in heart rate is evident. The important issue in patients with marginally or overtly impaired renal function is to check the creatinine level. In a minority of cases in our experience, substantial increases in creatinine values may be from bilateral renal artery stenosis. Like blood pressure, the biochemical changes induced with medication may be substantial while patients remain clinically asymptomatic.

Renal failure associated with colonoscopy-what is the link?

In January 2006, a 75-year-old woman presented to her primary care physician with severe arterial hypertension and acute renal failure (ARF). She had been hypertensive for 25 years associated with stage 3 chronic kidney disease (serum creatinine 75 μmol/l and estimated GFR 45 ml/ mn/1.73 m2 in October 2005). Her medical history was remarkable for a colic cancer treated by partial colectomy in 2002. A control colonoscopy was done in November 2005; the preparation was done with a sodium phosphate bowel purgative. Her medications included enalapril, hydrochlorothiazide, amlodipine, atenolol and aspirin. The serum creatinine was 340 μmol/l. All immunological exams were negative, and hormonal assays failed to reveal any hormonal cause for hypertension. A bilateral renal arterial stenosis was excluded by a renal angiography. In April 2006, the renal function was still impaired (serum creatinine 410 μmol/l) and the patient was referred to the nephrology unit. Clinical examination was normal, there was no proteinuria and urine sediment analysis was negative. A kidney biopsy was performed (Figure 1). What is the cause of her renal failure? The diagnosis: Acute phosphate nephropathy complicated of chronic renal failure. The kidney biopsy showed, besides mild vascular lesions related to hypertension (Figure 1A), numerous intratubular crystal deposits in the kidney parenchyma (Figure 1A–C). They were stained by Von Kossa (Figure 2), confirming the calcium phosphate nature of the deposits. So ARF was related to nephrocalcinosis, which was related to the ingestion of sodium phosphate purgative. In December 2007, the renal function was still severely impaired with an estimated GFR of 11 ml/min/1.73 m2.

Repair of a pararenal abdominal aortic aneurysm with bilateral renal artery stenosis using a rapid infusion pump for renal perfusion: Report Of a case

A 73-year-old man with a history of hypertension and drug-induced hepatitis underwent surgical treatment of an enlarging pararenal abdominal aortic aneurysm (PRAAA) with bilateral renal artery stenosis, found on enhanced computed tomography (CT). His preoperative renal function was normal. We divided the right renal artery and used a 6-mm expanded polytetrafluoroethylene (ePTFE) tube graft for the anastomosis. Renal artery perfusion was achieved by a rapid infusion pump set at 200 ml/min. The left renal artery was reconstructed and perfused in the same way. The abdominal aorta was cross-clamped just distal to the superior mesenteric artery and a Y-graft was anastomosed. The ePTFE grafts were connected to the Y-graft and bilateral renal artery circulation was re-established. The renal ischemic time was 1 h 25 min and the urine output during reconstruction was 80 ml. Postoperatively, his serum blood urea nitrogen and serum creatinine levels increased slightly, but normalized within 3 days. This case report shows that this method of renal artery perfusion could prove useful for complex renal artery reconstructions.

No way in &amp; no way out: a case of renal failure due to both pre- and post-renal obstruction

A 46-year–old lady presented to the renal physicians in 2002 with a biopsy diagnosis of Langerhans cell histiocytosis (LCH). Initial presentation had been with maxillary and retro-orbital disease. A CT scan of the thorax/abdomen/pelvis in 2002 had shown extensive irregular soft tissue around and extending into the sinuses of both kidneys (Figure 1), with renal calyceal but not pelvic dilatation, as well as disseminated involvement including bone, mediastinum and lungs. Her serum creatinine was normal and a MAG3 renogram showed no evidence of functional obstruction. She had no symptoms other than occasional loin discomfort. Three years later she developed worsening hypertension, a rising serum creatinine and pulmonary oedema. MR angiography showed bilateral tight renal artery stenosis. It again showed the unusual pattern of strikingly dilated calyces but collapsed renal pelves. Dynamic renography and antegrade pyelography (Figure 2) indicated obstruction at the level of the renal pelvis bilaterally. Consequently, percutaneous nephrostomies were placed, but there was no improvement in renal function.

Nephrotic range proteinuria associated with unilateral renal artery stenosis

Sir, Mild proteinuria is often present in patients with renal artery stenosis (RAS) [1]. However, heavy proteinuria is an uncommon finding in this setting, and many of the reported cases are due to bilateral RAS [2]. A 62-year-old Caucasian male was referred to our nephrology service for worsening kidney function. He had a history of coronary artery disease, chronic kidney disease (baseline serum creatinine level of 2–3 mg/dl), and hypertension. For the past few months prior to admission, he had presented with progressive deterioration in kidney function associated with refractory hypertension. At the time of admission, he had bilateral lower extremity edema with a creatinine of 4.4 mg/dl, proteinuria of 15 g/24 h, and was treated with six antihypertensive medications. Further investigations including immunologic studies and renal ultrasound were normal, except for a plasma renin activity of 11 ng/ml/h (normal: 1–3.8) and an aldosterone level of 35 ng/dl (normal: 1–14). A carbon dioxide angiogram revealed severe ostial right RAS with normal left renal artery. A stent was placed at the site of stenosis with subsequent improvement in renal perfusion. Over the next 2 weeks, the kidney function returned to its baseline (creatinine 3.1 mg/dl), blood pressure was better controlled (needing only one antihypertensive agent), and proteinuria decreased to 2.3 g/24 h. Although mild-to-moderate proteinuria is commonly seen in patients with RAS, massive proteinuria or nephrotic syndrome is considered a rare presentation in this setting. The pathophysiology of this phenomenon is poorly understood, and the main suggested mechanisms are thought to be hormonal and hemodynamic disturbances. The ischemia induced by renal hypoperfusion can result in an increased secretion of renin from the affected kidney. Activation of the renin-angiotensin-aldosterone system (RAAS) is associated with a number of physiologic and pathophysiologic consequences [3]. The role of RAAS in the development of proteinuria was first observed in experimental animals [4] and was then confirmed in human studies. In a study on 96 patients with renal artery occlusion, Rossignol et al. found that the degree of proteinuria was independently related to the active renin level, which reflects plasma angiotensin II concentration. Angiotensin II constricts the efferent arterioles in the unaffected kidney leading to increased intraglomerular pressure [5]. It also acts directly on the endothelial cells resulting in widening of the intra-endothelial gaps and an increase in glomerular capillary permeability [5]. Our patient also showed a high plasma renin activity, likely secondary to RAS. Although biopsy was not done, the significant reduction in the amount of proteinuria over a short period of time supports the hypothesis that the renal hypoperfusion, with A. Wadhwa A. Kazory (&) Division of Nephrology, Hypertension, and Renal Transplantation, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610-0224, USA e-mail: amir.kazory@medicine.ufl.edu

Bilateral tardus-parvus waveform in kidneys secondary to mid-aortic syndrome in a hypertensive child

A 10-year-old girl who presented with hypertension and anelevated renin level underwent a renal US examination thatdemonstrated abnormal Doppler waveforms in bothkidneys, characterized by the tardus-parvus pattern withprolonged acceleration time, decreased peak systolic veloc-ity and elevated diastolic flow (Fig. 1). The child wasfurther evaluated with conventional angiography thatdemonstrated marked narrowing of the abdominal aortastarting just below the level of the superior mesentericartery (Fig. 2, short arrows) consistent with mid-aorticsyndrome. In addition, narrowing of the superior mesentericartery was seen (Fig. 2, long arrow) as well as mildnarrowing of both proximal bilateral renal arteries.Although hypertension is typically essential (primary) inolder children and adolescents, in approximately 10% ofchildrenitisduetounderlyingrenovasculardisease[1]. Whentardus-parvus waveforms are present in bilateral kidneys,however, aortic coarctation or mid-aortic syndrome should beconsidered in addition to bilateral renal artery stenosis [1, 2].References

An Unusual Cause of Young Hypertension

AbstractA 16‐year‐old male was evaluated for hypertension. On clinical examination, he had features suggestive of type 1 neurofibromatosis (NF1). Further, he had feeble pulse over both lower limbs, with arterial bruit over the abdomen. A magnetic resonance angiogram revealed constriction of the abdominal aorta with bilateral renal artery stenosis. This type of vascular lesion in NF1 is a rare entity. It may be progressive and requires timely intervention to control hypertension and prevent ischemic nephropathy.

Failure and Success of Percutaneous Angioplasty in a Hypertensive Child with Bilateral Renal Artery Stenosis

We describe the clinical course of a 5-year-old girl with severe arterial hypertension that was uncontrollable with antihypertensive medication. Renal angiography revealed bilateral renal artery stenoses. Because percutaneous transluminal renal angioplasty (PTRA) failed to dilate the stenotic lesions, a renal artery bypass grafting in both renal arteries was performed. The patient remained normotensive for 7 months, and after that the arterial pressure increased again. Digital subtraction angiography demonstrated stenosis at the peripheral and central anastomosis of the vein graft that was used for revascularization of the left kidney. PTRA was decided on and successful patency was achieved. The patient has now been normotensive for a period of 5 years.

Ischemic nephropathy in an elderly patient

Congestive heart failure often occurs in patients with bilateral renal artery stenosis. Recently, Jacobson and Breyer, and Jacobson introduced the term "ischemic nephropathy", which implies critical bilateral involvement or global ischemia. Ischemic nephropathy is not only a cause of hypertension but also an important cause of end-stage renal disease. However, the aging kidney often show that the renal artery does not demonstrate stenosis of the main trunks, but stenosis of an atherosclerotic branch. We present a case of multiple atherosclerotic peripheral renal arteries, which might have caused ischemic nephropathy in an elderly hypertensive patient with advanced atherosclerosis.

Fibromuscular dysplasia of renal arteries.

This case reports a young child having uncontrolled hypertension, resulting from bilateral renal artery stenosis due to fibromuscular dysplasia presenting with abdominal pain, headache and visual disturbance. Diagnostic features and management is discussed.

Abstract 1785: Renal Artery Angioplasty Improves Diastolic Cardiac Function In Patients With heart failure Possessing Renal Artery Stenosis.

Background: Renal artery stenosis (RAS) often plays an important role not only in malignant hypertension but also in sudden development of heart failure (HF) so called ‘flash pulmonary edema’ or chronic HF refractory to medical treatment. One of the possible mechanisms whereby RAS affects these unique conditions of HF is suppression of LV compliance through the complex interaction between neurohormonal systems originating from the reduction of renal blood flow. Renal artery angioplasty is expected to be an effective treatment for restoring renal blood flow in patients with RAS. The aim of the present study was whether the angioplasty can improve the impaired neurohormonal systems and diastolic cardiac function in patients with RAS. Methods: A prospective analysis was performed in 18 HF patients with RAS (age: 72±6, 3 females, NYHA I/II/III: 5/9/4) who underwent renal artery angioplasty between 2005 and 2007. Four patients with significant bilateral RAS and 3 patients with unilateral RAS in the vessel supplying a functional solitary kidney were included. We monitored the changes of biochemical and neurohormonal markers and blood pressure. Cardiac function was evaluated by tissue Doppler echocardiogram before and 3 months after the procedure. Results: Technical success was achieved in all interventions. The results are shown in table . Systolic arterial blood pressure significantly decreased by renal angioplasty. B-type natriuretic peptide (BNP) was significantly reduced 3 months after the angioplasty, whereas the change of sCr or angiotensinII was not statistically significant. Myocardial early diastolic velocity (Em), a parameter of diastolic LV function, was significantly improved compared with that measured before the procedure. Conclusions: In patients with either overt or latent HF possessing RAS, renal artery angioplasty not only decreases arterial blood pressure but also improves diastolic cardiac function in parallel with the reduction of BNP level.

Reno-vascular hypertension in childhood: a nationwide survey

Renovascular disease accounts for 8-10% of all cases of paediatric hypertension, whereas, in adults, its incidence is approximately 1%. The Turkish Paediatric Hypertension Group aimed to create the first registry database for childhood renovascular hypertension in Turkey. Twenty of the 28 paediatric nephrology centres in Turkey responded to the survey and reported 45 patients (27 girls, 18 boys) with renovascular hypertension between 1990 and 2005. The age at presentation ranged from 20 days to 17 years. The mean blood pressure at the diagnosis was 169/110 mmHg. Chief complaints of symptomatic patients were headache (38%), seizure (18%), epistaxis (4%), growth retardation (4%), cognitive dysfunction (4%), polyuria (2%), palpitation (2%), and hemiplegia (2%). Renovascular hypertension was found incidentally in 11 children. The diagnosis of renovascular hypertension was established with conventional angiography in 39 patients, MR angiography in three, CT angiography in two, and captopril diethylene triamine penta-acetic acid (DTPA) scintigraphy in one patient. Twenty-one children had bilateral renal artery stenosis and 24 had unilateral renal artery stenosis. Of these, 14 (31%) had fibromuscular dysplasia; 12 (27%) Takayasu's arteritis; six (13%) neurofibromatosis; two (5%) Williams syndrome; one (2%) Kawasaki disease; one (2%) mid-aortic syndrome; one (2%) extrinsic compression to the renal artery, and eight (18%) unspecified bilateral renal artery stenosis. Hypertension was controlled with antihypertensive drugs in 17 patients. Percutaneous transluminal angioplasty (PTRA) or surgery had to be performed in 28 patients: PTRA in 16 patients, PTRA + surgery in one patient and surgery in 11 patients (four nephrectomies). The importance of vasculitic disease, especially Takayasu's arteritis, should not be underestimated in children with renovascular hypertension.

Recovery of acute renal failure following bilateral renal artery angioplasty and stenting

Atherosclerotic renovascular disease commonly coexists with chronic kidney disease, and its optimal management remains unsettled. In this case report, we describe a 75-year-old woman with chronic kidney disease and critical atherosclerotic bilateral renal artery stenosis, who presented with a hypertensive emergency and developed acute renal failure following antihypertensive treatment. Bilateral percutaneous transluminal renal angioplasties (PTRA) with stent placement were performed and resulted in immediate recovery of renal function. The existing literature on this impressive response to PTRA is reviewed and discussed.