Dear Label_Name,

Greetings! I hope you are well.

I am writing on behalf of an international publishing house, Science and Education Publishing, USA (http://www.sciepub.com).

Science and Education Publishing (SciEP) is a multidisciplinary open access publisher of Journals covering the fields of Science, Technology and Medicine. All SciEP publications are subject to high-quality peer review, editorial and production processes and are freely available online.

Welcome to the April, 2013 edition of SciEP newsletter, providing monthly summaries of articles on science & education related topics of interest to scientist and professionals. The mission of our journals is to provide an open access forum for publishing new findings on issues pertinent to scientific and academic field. We also invite you to submit original research papers, review articles, short reports, or case studies are considered for publication in our Multidisciplinary Journals.

American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

American Journal of Medical and Biological Research
DOI: 10.12691/ajmbr-1-1-2

The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
DOI: 10.12691/ajmsm-1-1-1

Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
DOI: 10.12691/ajidm-1-1-2

The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

We have released issues of some journals on February 2013.
American Journal of Public Health Research
American Journal of Medical Sciences and Medicine
American Journal of Medical and Biological Research
American Journal of Pharmacological Sciences
American Journal of Clinical Medicine Research
American Journal of Nursing Research
American Journal of Cancer Prevention
American Journal of Medicine Studies
American Journal of Infectious Diseases and Microbiology
American Journal of Cardiovascular Disease Research
American Journal of Biomedical Research
American Journal of Mechanical Engineering
American Journal of Microbiological Research
Journal of Preventive Medicine
American Journal of Food and Nutrition
American Journal of Hypertension Research
American Journal of Sports Science and Medicine
Journal of Cancer Research and Treatment
American Journal of Zoological Research
Journal of Biomedical Engineering and Technology
American Journal of Microbiological Research
Biomedical Science and Engineering

We are pleased to announce that submissions are now being accepted for peer review for all the journals across all our subject areas in SciEP.

Please submit your manuscript via our online submission system:
http://www.sciepub.com/author/signin

To unsubscribe from our mailing list, please click on the following link: unsubscribe

I am looking forward to hearing from you.

Kind regards,

David Rain
Email:join@sciepub.com
Science and Education Publishing (http://www.sciepub.com)

Pickering Syndrome precipitated by Angiotensin Converting Enzyme Inhibitor

Pramod Theetha Kariyanna*, Apoorva Jayarangaiah, Robert Adrah, Abhishek Sharma, Debabrata Sen

Department of Internal Medicine, State university of New York (SUNY)- Downstate Medical center, Brooklyn, New York, U.S.A.

Abstract: Pickering syndrome is an under recognised cardio-renal syndrome where life threatening flash pulmonary edema develops in the setting of diastolic dysfunction of the heart. Renal artery stenosis induced activation of sympathetic nervous system and renin-angiotensin-aldosterone system result in fluid retention; such fluid retention in the setting of diastolic dysfunction results in flash pulmonary edema. Most patients who present with pickering syndrome have normal coronary circulation and left ventricular systolic function. We here present a case of pickering syndrome that was precipitated by initiation of angiotensin converting enzyme inhibitor therapy in a patient with undiagnosed unilateral renal artery stenosis. The incidence of flash pulmonary edema decreases on revascularization of renal artery stenosis. Underlying renal artery stenosis should be suspected in a patient with recurrent flash pulmonary edema as such patients merit from revascularization of renal artery stenosis. To the best of our knowledge we are the first to report angiotensin converting enzyme inhibitors as a precipitator of pickering syndrome.

Keywords: pickering syndrome, renal artery stenosis, diastolic dysfunction of heart, angiotensin converting enzyme inhibitors, renal artery revascularization

Citation: Pramod Theetha Kariyanna, Apoorva Jayarangaiah, Robert Adrah, Abhishek Sharma, Debabrata Sen, Pickering Syndrome precipitated by Angiotensin Converting Enzyme Inhibitor. American Journal of Medical Case Reports, 4 (1). 31-34. January 2016. doi:10.12691/ajmcr-4-1-9

1. Introduction

Pickering syndrome is a less know cardio-renal syndrome where patients with renal artery stenosis (RAS) who have an underlying diastolic dysfunction develop flash pulmonary edema (FPE) upon slightest fluid overload [1]. Owing to their renal and cardio-protective properties angiotensin converting enzyme inhibitors (ACEI) are commonly used medications in patients with chronic renal failure and heart failure [2,3,4]. Bilateral RAS is an absolute contraindication for initiation of ACEI. Due to the blockade of angiotensin II induced efferent arteriolar vasoconstriction a slight fall in glomerular filtration rate (GFR) is expected to happen upon initiation of ACEI therapy [5]. Such a decrease in GFR can result in activation of sympathetic nervous system and renin-angiotensin-aldosterone system resulting in salt and water retention and this may precipitate pickering syndrome.

2. Case Presentation

An 80-year-old-woman with past medical history of hypertension, hyperlipidemia, non-ST segment elevation myocardial infarction (NSTEMI) 24days ago presented with anuria, nausea/vomiting and weight gain for four days. She underwent percutaneous coronary intervention with drug eluting stent implantation 24 days ago and subsequently discharged on aspirin (81 mg once a day, orally), clopidogrel (75 mg once a day, orally), metoprolol (50 mg once daily, orally), atorvastatin (80 mg once daily, orally), furosemide (40 mg once daily, orally) and quinapril (10 mg twice daily, orally). At the time of presentation physical examination revealed a blood pressure of 178/99 mm of Hg, jugular venous distention, grade II edema till knees and rales in bilateral posterior lung fields.

Blood urea nitrogen (BUN) and serum creatinine 24 days prior to presentation were 30 mg/dl and 0.8 mg/dl respectively; the calculated glomerular filtration rate (GFR) was > 60 ml/min/1.73 sq. ms. She presented with frank renal failure with BUN of 91 mg/dl, serum creatinine of 8.6 mg per dl and GFR of 5 ml/min/1.73 sq. ms (Figure 1 and Figure 2) Transthoracic echocardiography obtained 24 days prior revealed left atrial dilation, left ventricular ejection fraction of 55%, grade 1 diastolic dysfunction, mild fibro-calcific changes of the aortic root and mild mitral annular calcification. Chest radiography revealed diffuse bilateral infiltrates (Figure 3), which along physical examination indicated biventricular failure. Furosemide and quinapril were discontinued and patient was emergently hemodialyzed. Duplex ultrasound revealed right renal artery stenosis (RAS) (Figure 4). Patient was managed for flash pulmonary edema with diuresis. Serum creatinine levels eventually returned to baseline.

Figure 1. Serum creatinine trend in the patient. Blue arrow indicates serum creatinine levels 24 days prior to presentation (0.8 mg/dl) during which ACEI therapy was initiated. Red arrow indicates serum creatinine (8.6 mg/dl) at presentation and green arrow indicates return of serum creatinine (day 24) after ACEI therapy was discontinued at presentation. X- axis represents days, Y-axis represents serum creatinine level

Figure 2. Glomerular filtration rate trends in the patient. Blue arrow indicates a GFR of > 60 ml/min/1.73 sq. ms, 24 days prior to presentation, during which ACEI therapy was initiated. Red arrow indicates a low GFR of of 5 ml/min/1.73 sq. ms at presentation and green arrow represents return of GFR to normal levels upon discontinuation of ACEI in the patient. X- axis represents days, Y-axis represents serum creatinine level

Figure 3. Chest radiography of the patient consistent with bilateral pulmonary edema

Figure 4. Duplex of right renal artery showing significantly reduced flow (20 cms per second), a finding consistent with renal artery stenosis

3. Discussion

Atherosclerotic renovascular disease accounts for 90% of RAS [6]. RAS is usually asymptomatic but may present with hypertension, renal dysfunction, athero-embolism, proteinuria, and CHF [7]. Hypertension secondary to RAS usually presents in younger individuals with no family history of hypertension, difficult to control hypertension, renal impairment with mild proteinuria and > 1.5 cms difference in kidney function on ultrasonography. Patient with RAS tend to have reversible early deterioration of renal function upon initiation of angiotensin converting enzyme inhibitors (ACEI) [8,9].

In patients who underwent cardiac catheterization for suspected coronary artery disease (CAD), the prevalence of significant RAS (RAS >50%) was found to be 8% [1]. In patient with heart failure, McDowall and colleagues had reported prevalence of RAS to be as high as 34%; however they had excluded patients whose serum creatinine rose previously upon initiation of captopril therapy [10]. Heart failure patients with renal dysfunction have poor clinical outcomes, though it is not clear if the renal dysfunction can be attributed to RAS or if the RAS has contribution in the poor outcomes [11].

Various patho-physiological mechanisms are attributed in development of FPE in patients with bilateral RAS: i) Activation of renin-angiotensin-aldosterone system (RAAS) results in significant sodium and fluid retention [12], ii) decreased renal blood flow and subsequent renal ischemia stimulated sympathetic nervous system and RAAS [13], iii) diastolic dysfunction of heart that ensues as a result of hypertension [14], iv) pulmonary capillary stress failure and increased pulmonary capillary permeability [15], v) absence of pressure natriuresis [16]. The relative lower prevalence of FPE in patients with unilateral RAS as compared to patients with bilateral RAS may partially be attributed to pressure natriuresis is the functionally normal kidney [1].

Fluid overload and diastolic dysfunction appears to play an important role in development of FPE. Two-thirds of a patient's FPE have normal ventricular function [12]. Persistent hypertension results in left ventricular hypertrophy and diastolic dysfunction. Sympathetic activation increases arterial stiffening, and for such an increase in the after load the left ventricle normally compensated by increasing the left ventricular end diastolic volume. This compensation is curtailed by stiff left ventricle in diastolic dysfunction [18,19,20,21]. Sympathetic activation induced tachycardia decreases diastolic left ventricular filling [22]. Underlying ischemic heart disease and decrease diastolic duration impairs normal cardiac perfusion [23]. Left ventricular systolic dysfunction, elevated left ventricular end diastolic pressure and excessive sympathetic activation results in FPE [1,22]. Endothelial dysfunction secondary to elevated neurohumoral mediators such as angiotensin II, endothelin-1 and catecholamines with decreased synthesis of nitric oxide in endothelium is contributory; FPE ensues at intracapillary pressure of 20-25 mm Hg [24]. Following development of FPE, left ventricular function worsens resulting in significant fall in renal perfusion which further triggers activation of the vicious cycle.

Most patients with pickering syndrome present with unprovoked dyspnea secondary to FPE, Pickering et al reported FPE prevalence of 2.3 times prior to presentation [25]. Messerli et al in their case series reported that 93% of patients had recurrent FPE and the remaining 7% a single event prior to diagnosis. Normal left ventricular function and absence of flow limiting coronary artery lesions in the patient population may result in a “false sense of security” for absence of cardiac pathology [1].

Though renal angiogram is the gold standard for diagnosis of RAS, renal duplex scan is an alternate as it is rapid and non-invasive [26]. FPE in patients should be managed as an hypertensive emergency, diuresis to induce sodium and water loss. Antihypertensive medications including ACEI are useful in relieving FPE but they may decrease renal perfusion hence may worsen pulmonary edema [1]. The American College of Cardiology/ American Heart Association recommend percutaneous revascularization in patients who have hemodynamically significant RAS and recurrent, unexplained CHF or pulmonary edema [27]. Failure of pressure natriuresis is contributory in development of pickering syndrome. Hence renal revascularization is beneficial [28,29]. Renal artery stenting is superior to balloon angioplasty for RAS revascularization [27,30,31].

The case of pickering syndrome we present here was precipitated by ACEI in a patient with asymptomatic unilateral RAS and mild diastolic and systolic heart failure.

4. Conclusion

Pickering syndrome, a cardio-renal syndrome is increasingly being reported. Physicians should be mindful of precipitating FPE in patients with asymptomatic RAS in setting of diastolic dysfunction. Disease free coronaries and normal ejection fraction should not mislead the management; the possibility of underlying RAS should be investigated. ACEI may precipitate pickering syndrome in patients with undiagnosed RAS. A renal duplex can help establishing diagnosis of RAS in such patients, who can benefit from renal artery revascularization. To the best of our knowledge we are the first to report angiotensin converting enzymes as a precipitator of pickering syndrome.

References

[1]   | Messerli FH, Bangalore S, Makani H, Rimoldi SF, Allemann Y, White CJ, Textor S, Sleight P. Flash pulmonary oedema and bilateral renal artery stenosis: the Pickering syndrome. Eur Heart J. 2011 Sep;32(18):2231-5.
[2]   | Juggi JS1, Koenig-Berard E, Van Gilst WH, Cardioprotection by angiotensin-converting enzyme (ACE) inhibitors, Can J Cardiol. 1993 May; 9(4):336-52.
[3]   | Gerstein H, Cardiovascular and Metabolic Benefits of ACE Inhibition,: moving beyond blood pressure reduction, Diabetes Care. 2000 Jul;23(7):882-3.
[4]   | Taal M, Brenner B, Renoprotective benefits of RAS inhibition: From ACEI to angiotensin II antagonists, Kidney International (2000) 57, 1803-1817.

[5]  
Schoolwerth A, Sica D, Ballermann B, Wilcox C, Renal Considerations in Angiotensin Converting Enzyme Inhibitor Therapy, A Statement for Healthcare Professionals From the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association, Circulation, 2001; 104: 1985-1991.

[6]   | Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med. 2001 Feb 8; 344(6):431-42.
[7]   | Scoble JE. Renal artery stenosis as a cause of renal impairment: implications for treatment of hypertension and congestive heart failure. J R Soc Med. 1999 Oct;92(10):505-10.
[8]   | Simon N, Franklin SS, Bleifer KH, Maxwell MH. Clinical characteristics of renovascular hypertension. JAMA. 1972 May 29;220(9):1209-18.
[9]   | Vashist A, Heller EN, Brown EJ Jr, Alhaddad IA. Renal artery stenosis: a cardiovascular perspective. Am Heart J. 2002 Apr;143(4):559-64.
[10]   | MacDowall P, Kalra PA, O'Donoghue DJ, Waldek S, Mamtora H, Brown K. Risk of morbidity from renovascular disease in elderly patients with congestive cardiac failure. Lancet. 1998 Jul 4;352(9121):13-6.
[11]   | de Silva R, Nikitin NP, Bhandari S, Nicholson A, Clark AL, Cleland JG. Atherosclerotic renovascular disease in chronic heart failure: should we intervene? Eur Heart J. 2005 Aug;26(16):1596-605
[12]   | Rundback JH, Murphy TP, Cooper C, Weintraub JL, Chronic renal ischemia: pathophysiologic mechanisms of cardiovascular and renal disease, J Vasc Interv Radiol. 2002 Nov; 13(11):1085-92.
[13]   | Ritz E, Amann K, Fliser D. The sympathetic nervous system and the kidney: its importance in renal diseases. Blood Press Suppl. 1998; 3:14-9.
[14]   | Mandinov L, Eberli FR, Seiler C, Hess OM. Diastolic heart failure, 813-825, 1 March 2000
[15]   | Rimoldi SF, Yuzefpolskaya M, Allemann Y, Messerli F. Flash pulmonary edema. Prog Cardiovasc Dis. 2009 Nov-Dec; 52(3): 249-59.
[16]   | Gavras H, Brunner HB, Vaughan ED, Laragh JH, Angiotensin-sodium interaction in blood pressure maintenance of renal hypertensive and normotensive rats. Science. 1973; 180: 1369-1371.
[17]   | Messina LM, Zelenock GB, Yao KA, Stanley JC, Renal revascularization for recurrent pulmonary edema in patients with poorly controlled hypertension and renal insufficiency: a distinct subgroup of patients with arteriosclerotic renal artery occlusive disease. J Vasc Surg. 1992;15:73-80.
[18]   | Avolio AP, Deng FQ, Li WQ, Luo YF, Huang ZD, Xing LF, O'Rourke MF. Effects of aging on arterial distensibility in populations with high and low prevalence of hypertension: comparison between urban and rural communities in China. Circulation. 1985 Feb;71(2):202-10.
[19]   | Laurent S. Arterial wall hypertrophy and stiffness in essential hypertensive patients. Hypertension. 1995 Aug;26(2):355-62.
[20]   | Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB, Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults, J Am Coll Cardiol. 1996 Sep; 28(3):751.
[21]   | Grisk O, Rettig R. Interactions between the sympathetic nervous system and the kidneys in arterial hypertension. Cardiovasc Res. 2004 Feb 1;61(2):238-46.
[22]   | Kawaguchi M, Hay I, Fetics B, Kass DA. Combined ventricular systolic and arterial stiffening in patients with heart failure and preserved ejection fraction: implications for systolic and diastolic reserve limitations. Circulation. 2003 Feb 11;107(5):714-20.
[23]   | Ramanathan T, Skinner H. Coronary blood flow. Contin Educ Anaesth Crit Care Pain (2005) 5 (2): 61-64.
[24]   | Rimoldi SF, Yuzefpolskaya M, Allemannemail Y, Messerli F, Flash Pulmonary Edema, November–December, 2009, Volume 52, Issue 3, Pages 249-259.

[25]  
ThomasG. Pickering, RichardB. Devereux, GaryD. James, MichaelF. Silane, Lawrence Herman, JulioE. Sotelo, ThomasA. Sos, JohnH. Laragh, RECURRENT PULMONARY OEDEMA IN HYPERTENSION DUE TO BILATERAL RENAL ARTERY STENOSIS: TREATMENT BY ANGIOPLASTY OR SURGICAL REVASCULARISATION, Volume 332, No. 8610, p551-552, 3 September 1988.

[26]   | Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB. The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis. Ann Intern Med. 1995 Jun 1;122(11):833-8.

[27]  
Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, Hiratzka LF, Murphy WR, Olin JW, Puschett JB, Rosenfield KA, Sacks D, Stanley JC, Taylor LM Jr, White CJ, White J, White RA, Antman EM, Smith SC Jr, Adams CD, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B; American Association for Vascular Surgery; Society for Vascular Surgery; Society for Cardiovascular Angiography and Interventions; Society for Vascular Medicine and Biology; Society of Interventional Radiology; ACC/AHA Task Force on Practice Guidelines; American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; Vascular Disease Foundation. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the

[28]   | Bloch MJ, Trost DW, Pickering TG, Sos TA, August P, Prevention of recurrent pulmonary edema in patients with bilateral renovascular disease through renal artery stent placement. Am J Hypertens 1999;12:1-7.
[29]   | Wierema TK, Yaqoob MM, Renal artery stenosis in chronic renal failure: caution is advised for percutaneous revascularization. Eur J Intern Med 2008;19:276-279.
[30]   | Gray BH. Intervention for renal artery stenosis: endovascular and surgical roles. J Hypertens Suppl. 2005 Oct;23(3):S23-9.
[31]   | Mackrell PJ, Langan EM III., Sullivan TM, Gray BH, Taylor SM, Cull DL, Snyder BA, Youkey JR, Carsten CGIII, Management of renal artery stenosis: effects of a shift from surgical to percutaneous therapy on indications and outcomes. Ann Vasc Surg 2003;17:54-59.