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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2011  |  Volume : 22  |  Issue : 3  |  Page : 531-533
Successful hybrid procedure in flash pulmonary edema

Institute of Cardiovascular Diseases, Madras Medical Mission, 4A, Dr. J. J. Nagar, Mogappair, Chennai, India

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Date of Web Publication7-May-2011


A 70-year-old lady with recurrent flash pulmonary edema and acute coronary syndrome was detected to have bilateral renal artery disease and uncontrolled hypertension. Her right kidney size was 9.3 Χ 3.2 cm [glomerular filtration rate (GFR) 32.65 mL/min], left kidney size was 6.8 Χ 2.9 cm (GFR 12.78 mL/min), with a total GFR of 45.43 mL/min. Angiogram showed significant bilateral atherosclerotic renal artery stenosis and 90% right coronary artery lesion. She underwent successful percutaneous transluminal angioplasty of right renal artery lesion. Her serum creatinine of 1.6 mg/dL (GFR 45.43 mL/min) came down to 1.3 mg/dL (GFR 63 mL/min) post procedure and her blood pressure was controlled. She then underwent percutaneous transluminal coronary angioplasty of right coronary artery lesion. Renal artery stenosis is an important cause of uncontrolled hypertension and progression to chronic kidney disease. An early intervention and prompt revascularization prevents recurrent flash pulmonary edema and end stage kidney failure.

How to cite this article:
George T, Latchumanadhas K, Abraham G, Devapriya S, Ezhilan J, Mullasari AS. Successful hybrid procedure in flash pulmonary edema. Saudi J Kidney Dis Transpl 2011;22:531-3

How to cite this URL:
George T, Latchumanadhas K, Abraham G, Devapriya S, Ezhilan J, Mullasari AS. Successful hybrid procedure in flash pulmonary edema. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 Oct 3];22:531-3. Available from: https://www.sjkdt.org/text.asp?2011/22/3/531/80492

   Introduction Top

Renal artery stenosis (RAS) is a progressive disease and leads to poorly controlled hyper-tension and chronic kidney disease (CKD) due to hypertensive or ischemic nephropathy. It is imperative to perform early catheter based interventions in patients with hemodynamically significant RAS (cross-sectional area reduced to >75%) as it may be difficult to cross near occluded renal arteries by percutaneous methods. [1] Progression of RAS depends on high-grade >60% diametric stenosis, systolic blood pressure (SBP) >160 mmHg and whether the patient has diabetes mellitus. [2] Literature review shows that it is still unclear which group of patients benefits most with this treatment.

   Case Report Top

A 70-year-old lady was referred to our hospital with recurrent episodes of angina at rest. Two days back, she was admitted elsewhere with acute left ventricular failure (LVF) and flash pulmonary edema, due to uncontrolled hypertension despite administering nifedepine retard 20 mg twice daily, telmisartan 20 mg once daily, clonidine 100 μg thrice daily and carvedilol 6.25 mg once daily.

Blood pressure (BP) at admission was 210/110 mmHg, with no postural variation. There was no peripheral arterial or renal bruit. Respiratory system examination revealed bilateral basal crepitations. Cardiovascular systemic examination was normal.

Investigations showed Hb of 10.2 g/dL, blood urea of 95 mg/dL and serum creatinine of 3.0 mg/dL. Urine showed trace proteinuria, and 2- 3 RBCs/HPF and granular casts. Her fasting blood sugar (FBS) was 137 mg/dL. ECG revealed sinus rhythm with ST depression in V 1 - V 3 , L1 and aVL. Two-dimensional echocardiogram study showed apical hypokinesia with adequate left ventricular (LV) function with ejection fraction (EF) 50%.

Ultrasonography showed contracted and diseased left kidney (6.8 × 2.9 cm). Right kidney was mildly diseased (9.3 × 3.2 cm). Technetium renal perfusion scan showed total glomerular filtration rate (GFR) of 45.43 mL/min. Relative renal function of left kidney was 12.78 mL/min and that of right kidney was 32.65 mL/min. Left kidney was small and showed very poor tracer concentration. Right kidney showed mildly reduced tracer concentration.

She was subjected to a coronary and a renal angiogram, which showed critical stenosis of proximal right coronary artery (90%). Selective renal angiogram confirmed bilateral RAS. She underwent a successful percutaneous transluminal renal angioplasty (PTRA) of right renal artery at the same sitting. The lesion was pre-dilated with 3.5 × 15 mm Tracker balloon at 10 atm. Then, a Genesis stent (5.0 × 15 mm) was deployed at 12 atm. Final angiogram showed no residual stenosis, with good antegrade flow.

Patient had an uneventful further hospital stay and was discharged with a blood urea of 90 mg/dL and a serum creatinine of 1.6 mg/dL.

Post procedure, her hypertension was well controlled with carvedilol 6.25 mg twice daily and telmisartan 20 mg once daily. She underwent repeat renal perfusion scan at discharge. Total GFR was 63 mL/min (lower limit of GFR for age: 73 mL/min). Relative renal function of left kidney was 3 mL/min (5%) and that of right kidney was 60 mL/min (95%). Patient underwent successful percutaneous transluminal coronary angioplasty (PTCA) and stenting to right coronary artery lesion after 2 months. Blood urea was 31 mg/dL and serum creatinine was 1.3 mg/dL.

   Discussion Top

The benefit of PTRA or stent placement, when compared to medical management or surgical revascularization, in reducing cardiovascular mortality, BP control or improving renal function is still not conclusively proved. [3] Prospectively identifying the patients whose renal function or BP control will improve after intervention for RAS is difficult. Twenty to forty percent of patients do not show improvement in either hypertension or renal function. Patients with age >65 years, pulse pressure >70 mmHg, non-dipper BP, proteinuria >1 g/day, creatinine clearance <40 mL/min and evidence of peripheral or coronary artery disease are unlikely to benefit. [4] Independent predictors of improvement in renal function are baseline elevation in serum creatinine level (>1.5 mg/dL) and LV dysfunction. Similarly, female gender, a higher baseline mean arterial BP and preserved parenchymal thickness are predictors of improved BP control. [5]

Chances for renal salvage are increased in patients with unexplained renal failure or renal failure induced by angiotensin receptor blockers (ARB)/angiotensin-converting enzyme (ACE)-inhibitors, loss of renal mass over time as documented by Magnetic Resonance Imaging (MRI) or duplex ultrasound and established progression of RAS. Studies have shown that improvement is more in patients having renal length of >7-9 cm, serum creatinine levels < 4 g/dL, filling of distal collateral bed by collaterals on angiogram, visualization of excretory pyelogram and intact glomeruli on renal biopsy. [6]

The success rates for renal artery stenting are in the order of 98%. Hypertension was cured in 20% of patients while renal function improved in 30% and stabilized in 30% patients. [7] Restenosis rates of 8.3% are being reported following renal stenting. [8]

Our patient had bilateral RAS with uncontrolled hypertension and had presented with recurrent flash pulmonary edema and non-ST elevation myocardial infarction. She had a non-functioning left kidney and a functioning right kidney for which PTRA was done. The treatment options available were: conservatively manage her renal failure and undertake a PTCA of her right coronary artery lesion or treat her RAS with a PTRA and after improvement of renal functions, proceed with a PTCA of her right coronary artery lesion. We decided to go ahead with the latter option as there is a risk of worsening of renal failure due to contrast study.

She was pre-treated with saline infusion and N-acetyl cysteine to prevent contrast-induced renal injury. We also used an iso-osmolar contrast-iohexol (visipaque) to reduce the renal toxicity. Following catheter-based intervention of her viable right kidney, her renal parameters settled to near normal values with improvement of GFR of the treated kidney as well as overall GFR. In addition, her hypertension also got well controlled. Thereafter, she could undergo a successful intervention for her coronary artery disease with considerably less risk factors.

Our strategy helped in salvaging her functional right kidney and improved overall GFR. Thereafter, her right coronary artery lesion could be successfully treated without increasing morbidity and mortality. In addition to the cost benefit to the patient, this mode of therapy improved the quality of her life as well. Hence, we advocate such hybrid procedures at optimal time with active involvement of cardiologists and nephrologists.

   References Top

1.Kennedy DJ, Colyer WR, Brewster PS, et al. Renal insufficiency as a predictor of adverse events and mortality after renal artery stent placement. Am J Kidney Dis 2003:42;926-35.  Back to cited text no. 1
2.Caps MT, Perissinotto C, Zierler RE, et al. Prospective study of atherosclerotic progresssion in the renal artery. Circ 1998;98:2866-72.  Back to cited text no. 2
3.Rundback JH, Sacks D, Kent KC, et al. Guidelines for the reporting of renal artery revascularization. J Vasc Interv Radiol 2002; 13:959-74.  Back to cited text no. 3
4.Radermaker J, Chavan A, Bleck J, et al. Use of Doppler Ultrasonography to predict the outcome of therapy for renal artery stenosis. N Engl J Med 2001;344:410-7.  Back to cited text no. 4
5.Zeller T, Frank U, Muller C, et al. Predictors of improved renal function after percutaneous stent supported angioplasty of severe atherosclerotic ostial renal artery stenosis. Circulation 2003; 108:2244.  Back to cited text no. 5
6.Safian RD, Textor SC. Renal artery stenosis. N Engl J Med 2001;344:431-42.  Back to cited text no. 6
7.Leertouwer TC, Gussenhoven EJ, Bosch JL, et al. Stent placement for renal artery stenosis - where do we stand? A meta-analysis. Radiology 2000;216:78-85.  Back to cited text no. 7
8.Campo A, Boero R, Stratta P, Quarello F. Selective stenting and the course of athero-sclerotic renovascular nephropathy. J Nephrol 2002;15:525-9.  Back to cited text no. 8

Correspondence Address:
Georgi Abraham
Senior Consultant Nephrology, Madras Medical Mission, 4A, Dr. J. J. Nagar, Mogappair, Chennai 600 037
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Source of Support: None, Conflict of Interest: None

PMID: 21566313

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