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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2017  |  Volume : 28  |  Issue : 3  |  Page : 615-620
Postinfectious glomerulonephritis with a broken heart: A case report study

1 King Abdulaziz Cardiac Center, Riyadh, Saudi Arabia
2 Department of Medicine, King Abdulaziz Medical City, Riyadh, Saudi Arabia

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Date of Web Publication18-May-2017

How to cite this article:
Omer H, Ali A, Aljizeeri A, Uthman E. Postinfectious glomerulonephritis with a broken heart: A case report study. Saudi J Kidney Dis Transpl 2017;28:615-20

How to cite this URL:
Omer H, Ali A, Aljizeeri A, Uthman E. Postinfectious glomerulonephritis with a broken heart: A case report study. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2020 Oct 21];28:615-20. Available from: https://www.sjkdt.org/text.asp?2017/28/3/615/206470

   Introduction Top

Takotsubo cardiomyopathy (TCM), also called stress cardiomyopathy, apical ballooning syndrome or broken heart syndrome, has been increasingly reported from various places in the world. Its incidence is reported to have increased from 46.3/million hospital discharges in 2007 to 203/million hospital discharges in 2012.[1] TCM is not as benign as once thought, with cardiogenic shock and ventricular fibrillation occurring in 4.2% and 1.5% of patients, respectively.[2] Risk factors associated with TCM include smoking, alcohol abuse, anxiety states, and hyperlipidemia.[3] Ninety percent of sufferers from this condi- tion[1],[3],[4] are females. Older women are five times more likely to develop this condition than younger women.[3] The mean age of sufferers is 67 years.[1],[4]

The most common symptoms at presentation are chest pain that can mimic acute coronary syndrome and dyspnea.[2] ST segment elevation is seen in four of every five cases. Although TCM often has similar clinical presentations as acute coronary syndrome, there are many differences (apart from having normal coronary arteries on coronary angio- gram in the former). These differences include the fact that patients with TCM have more neurologic or psychiatric disorders, lower mean left ventricular ejection fraction,[4] and lower troponin level.[2]

Comparing 2007–2012, cardiac arrests in cases of TCM increased from 0.3% to 1.1%, cardiogenic shock from 2.9% to 4.5%, and in- hospital mortality remained unchanged (1.3% and 1.4%) with higher mortality observed in men (odds ratio = 3.0).[1]

It has been postulated that a sudden and rapid rise in epinephrine/norepinephrine may be responsible for the development of this condition. Norepinephrine concentration was found to be raised in three-quarters of the patients.[2] It has been suggested that epine- phrine causes spasm of coronary microvascu- lature and direct toxicity of cardiocytes resulting in TCM.[5],[6],[7]

Another theory put forward to explain Takotsubo cardiomyopathy phenomenon is that it results from alterations in “the coupling of myocardial blood flow to cardiac work.”[8]

Postinfectious glomerulonephritis (PIGN) is an immune-mediated glomerulonephritis caused by no renal bacterial infections. In the past, most cases occurred in childhood and followed streptococcal upper respiratory tract or skin infections and hence were called “poststreptococcal glomerulonephritis.” The past three decades have witnessed a major shift in epidemiology and outcome. In developed countries in the modern era, a significant proportion of cases afflict adults, particularly the elderly or immunocompromised.

PIGN in adults has different pathogenesis and natural history than in children. Its incidence in adults is estimated to be 2 and 0.3 cases/100,000 person-years in developing and developed countries, respectively. This compares to 24.3 and 6 cases/100,000 person- years in children.[9],[10]

To the best of our knowledge, there has been no previous case reported of TCM triggered by PIGN.

   Case Report Top

This is a 24-year-old female who presented to the emergency room (ER) with a four days history of fever, abdominal pain, vomiting, and diarrhea. She had no chest pain or shortness of breath. She has been previously well and, in fact, had normal pregnancy and delivery of a healthy baby only six months previously. Her blood pressure (BP) was normal throughout her pregnancy, and no proteinuria was noted at any stage of her pregnancy. [Table 1] shows her admission vital signs.
Table 1: Comparison of patient parameters on admission and discharge.

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During the ER stay, quick assessment and management were initiated. In view of her vomiting, IV fluid was started then an abdominal CT scan was arranged. Suddenly, she developed severe pulmonary edema, desatu- ration and had to be intubated and admitted to the ICU with the diagnosis of acute heart failure requiring mechanical ventilation. Urgent echocardiography was done; a significant drop in her ejection fraction reached 25% with mildly dilated left ventricle and large size apical, septal, anteroseptal, anterior, inferior, posterior, and lateral wall motion abnormality [Figure 1] and [Figure 2].
Figure 1: Parasternal short-axis view of the left ventricle showing mildly dilated left ventricle with reduced function and wall motion abnormalities.

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Figure 2: Apical 4 chamber view of the left ventricle showing mildly dilated left ventricle with reduced function and wall motion abnormalities.

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Cardiac magnetic resonance imaging finding

Cardiac MRI was performed 6 days after the initial presentation and demonstrated mildly dilated LV with mildly reduced left ventricular systolic function. However, the tissue characterization after contrast administration showed no evidence of myocardial damage (no delayed enhancement); this rules out the possibility of coronary artery disease or myocarditis as possible etiologies for the wall motion and LV systolic dysfunction [Figure 3].
Figure 3: Long- (upper row) and short-axis (lower row) delayed myocardial enhancement images demonstrating the absence of myocardial damage (delayed enhancement).

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Coronary angiogram finding

She underwent an urgent coronary angio- gram, which was completely normal. She was labeled as having nonischemic dilated cardio- myopathy [Figure 4].
Figure 4: Coronary angiogram showing normal right and left coronary arteries.

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Renal assessment

On admission, routine urinalysis, urinary red 3lood cells (RBCs), proteinuria, protein crea- tinine ratio, and 24-h urine protein were requested [Table 2].Her estimated glomerulai filtration rate (eGFR) on admission was 112 mL/min and remained in that range until discharge. She had normal hemoglobin, white blood cells, platelets, INR, prothrombin time, blood film. All microbiological cultures were negative. She remained in the ICU for two days after which she was transferred to the coronary care unit at which time her BP, pulse, temperature, and oxygen saturation returned to normal.

The patient herself denied any systemic symptoms, drug or herbal intake, arthritis, mouth ulcers, previous throat infection, or change in her urine color or volume. She has been well until admission without any shortness of breath even on strenuous exercise. Significantly, she had a routine checkup two weeks before this admission when she was noted to be asymptomatic with normal examination; however, a routine urinalysis at that time revealed the presence of protein 100 mg/dL and RBCs 14/hpf.

Her eGFR at the time of the routine checkup was 124 mL/min, C3 was 0.078 g/L (normal range 0.9–1.8 g/L), and C4 was 0.282 (normal range 0.1–0.4 g/L). Antistreptolysin O titer was raised at 998 iu/L. HBV, HCV, cryoglobulin, ANA, anti-DS DNA antibody, P-ANCA, C-ANCA, and anti-GBM antibody were all negative.

Percutaneous renal biopsy showed severe diffuse proliferative exudative PIGN with the crescent formation and no interstitial fibrosis, tubular atrophy, arteriolar hyalinosis, or arterial sclerosis.

Immunofluorescence revealed diffuse and global coarse granular deposits at the subepi- thelial aspect of the glomerular capillaries for C3 (3+). This was associated with dispersed coarse granular deposits at the same ultra- structural location for IgG (2+), C1q (2+), and Kappa (2+) and Lambda (2+) light chains. Focal segmental mesangial staining for IgG was also noted. There was no staining for IgM, IgA, and C4. Staining for fibrinogen and albumin was not contributory.

A repeat echocardiogram, 10 days after admission, showed a remarkable improvement in the ejection fraction to 55% with a left ventricle which was normal in size and function with no regional wall motion abnormalities [Figure 5] and [Figure 6].
Figure 5: Apical 4 chamber view of the left ventricle showing normal size left ventricle with normal function and no wall motion abnormalities.

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Figure 6: Parasternal short-axis view of the left ventricle showing normal size left ventricle with normal function and no wall motion abnormalities.

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At discharge, there was also an improvement in her BP, pulse rate, proteinuria, RBC excretion, C3 level, troponin 1, and brain natriuretic peptide [Table 1].

   Discussion Top

In view of the features at presentation, the clinical and investigative findings and the natural history of her cardiac features in this patient, TCM is the most likely diagnosis.[11] TCM is also called stress cardiomyopathy, apical ballooning syndrome, or broken heart syndrome).

TCM has been increasingly described worldwide. It is now agreed that it is more likely to be associated with an organic trigger than a psychological trigger (36.0% and 27.7% respectively) with 28.5% having an undetermined trigger.[2] In patients presenting with TCM resulting from emotional trigger, the anxiety score is significantly higher compared to controls presenting with acute coronary syndrome. However, the depression score was similar in both groups.[12]

The echo findings are typically of wall- motion abnormalities, including hypokinesis in the apical and mid left ventricular segments segment. This left ventricular dysfunction is reversible.[13] Remarkable improvement in LV function is to be expected within days or weeks.[4]

In our case, the echo findings and their reversibility is typical of this condition. As far as, we know this is the first case, in which it was associated with postinfectious glome- rulonephritis.

The renal clinical features as well as the low C3 and the renal biopsy features in this patient are undeniably consistent with PIGN. One recent paper, the authors compared the clinical and pathological features in two groups with PIGN patients; one with codominance between C3 and immunoglobulins, and the other group which met the proposed diagnostic criteria for C3 glomerulonephritis (for C3GN). They found no clinical or pathological differences between the two groups.

Our case falls within the group with codo- minance between C3 and immunoglobulin. In adults, it is more likely to be associated with prior skin or upper respiratory tract infection and be due to staphylococcal that infection streptococcal infections. It also has worse renal prognosis in adults than in children.[14],[15]

The prognosis of postinfectious glomerulo- nephritis in adults is worse than it is in children with 8–54% of patients develop persistent renal dysfunction and 4%-33% progress to end-stage renal disease. Our patient is likely to have much better prognosis as she does not suffer from diabetes, is only 24 years of age, and has normal renal function at presentation. All these four factors have been shown be associated with better prognosis.[14],[15],[16]

   Acknowledgment Top

We are grateful and thankful to Prof. Abdulla A. Al-Sayyari for his help during drafting, critical reading, and revision of this manuscript.

Conflict of interest: None declared.

   References Top

Khera R, Vyas A, Light-McGroary KA, Zahr F, Horwitz P, Girotra S. Trends in hospita- lization for takotsubo cardiomyopathy in the United States, 2007-2012. Am Heart J. 2016; 172:53-3.  Back to cited text no. 1
Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: A systematic review. Eur Heart J 2006;27:1523-9.  Back to cited text no. 2
Deshmukh A, Kumar G, Pant S, Rihal C, Murugiah K, Mehta JL. Prevalence of takotsubo cardiomyopathy in the United States. Am Heart J 2012;164:66–71.e1.  Back to cited text no. 3
Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of takotsubo (Stress) cardiomyopathy. N Engl J Med 2015;373:929-38.  Back to cited text no. 4
Sherif K, Sehli S, Jenkins LA. Takotsubo cardiomyopathy after administration of norepinephrine. Proc (Bayl Univ Med Cent) 2016;29:166-7.  Back to cited text no. 5
Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539-48.  Back to cited text no. 6
Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (takotsubo) cardio- myopathy - A novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008;5:22-9.  Back to cited text no. 7
Ohanyan V, Yin L, Bardakjian R, et al. Cate- cholamine induced takotsubo cardiomyo- pathy: The role of coronary metabolic blood flow regulation in apical ballooning. FASEB J 2016;30 1 Suppl:948.9.  Back to cited text no. 8
Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis 2005;5:685-94.  Back to cited text no. 9
Nasr SH, Markowitz GS, Stokes MB, Said SM, Valeri AM, D’Agati VD. Acute post- infectious glomerulonephritis in the modern era: Experience with 86 adults and review of the literature. Medicine (Baltimore) 2008;87: 21-32.  Back to cited text no. 10
Singh K, Carson K, Usmani Z, Sawhney G, Shah R, Horowitz J. Systematic review and meta-analysis of incidence and correlates of recurrence of takotsubo cardiomyopathy. Int J Cardiol 2014;174:696-701.  Back to cited text no. 11
Goh AC, Wong S, Zaroff JG, Shafaee N, Lundstrom RJ. Comparing anxiety and depression in patients with takotsubo stress cardiomyopathy to those with acute coronary syndrome. J Cardiopulm Rehabil Prev 2016; 36:106-11.  Back to cited text no. 12
Yoshinaga K, Tomiyama Y, Sakakibara M, Takeuchi K, Tamaki N. Relatively high prevalence of takotsubo cardiomyopathy (Stress-induced cardiomyopathy) in the Japanese population - Contribution of cardiac imaging in the identification of takotsubo cardiomyopathy and its differentiation from acute coronary syndrome. Curr Cardiovasc Imaging Rep 2015;8:1-8.  Back to cited text no. 13
Nasr SH, Radhakrishnan J, D’Agati VD. Bacterial infection-related glomerulonephritis in adults. Kidney Int 2013;83:792-803.  Back to cited text no. 14
Nasr SH, Fidler ME, Valeri AM, et al. Postinfectious glomerulonephritis in the elderly. J Am Soc Nephrol 2011;22:187-95.  Back to cited text no. 15
Luo C, Tang Z, Chen D, Liu Z. Long-term prognosis for Chinese adult patients with acute postinfectious glomerulonephritis. Clin Nephrol 2011;76:186-94.  Back to cited text no. 16

Correspondence Address:
Elmonttasir Uthman
Department of Medicine, King Abdulaziz Medical City, P. O. Box 22490, Riyadh 11426
Saudi Arabia
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DOI: 10.4103/1319-2442.206470

PMID: 28540901

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