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Cardiovascular II 10:30 AM Saturday, February 23, 2019 Abstracts J Investig Med: first published as 10.1136/jim-2018-000974.619 on 28 January 2019. Downloaded from 669 NITRIC OXIDE SYNTHASE INHIBITION STIMULATES diagnostic information otherwise not identified in a single RENIN SYNTHESIS INDEPENDENT OF CGMP IN inspection. COLLECTING DUCT CELLS Methods used Microscopic examination of the urinary sedi- 1 1 1 1 1 2 ment (MicrExUrSed)±Sternheimer Malbin stain was under- A Curnow*, SR Gonsalez, B Visniauskas, SL Crabtree, VR Gogulamudi, EE Simon, 3Lara Morcillo Ld, 1,4MC Prieto. 1Tulane University-SOM, New Orleans, LA; 2Tulane taken in all patients with AKI stage 2 who were seen on University HSC, New Orleans, LA; 3Instituto de Biofisica Chagas Filho, Universidade Federal consultation in an inpatient nephrology service during a do Rio de Janeiro, Rio de Janeiro, Brazil; 4Tulane Hypertension and Renal Center of 6 month period. MicrExUrSed were done on the day of con- Excellence, Tulane University, New Orleans, LA sult (day 1), 48 hours later (day 3) and 96 hours later (day 5). Urinary cast scores (based on Chawla et al and Perazella 10.1136/jim-2018-000974.675 et al) were assigned to each specimen. Chawla scores (CS) 3– 4 and Perazella scores (PS) 2–3 were categorized as consistent Purpose of study Nitric oxide (NO) synthase (NOS) inhibitors with acute tubular injury (ATI), whereas CS 1–2 and PS 0–1 attenuate any stimulation of juxtaglomerular renin gene were categorized as non-diagnostic for ATI (non-ATI). Worsen- expression, regardless of the underlying challenge of the ing AKI was defined as a rise in serum creatinine renin-angiotensin system. However, the regulation of renin in (sCr) 0.3 mg/dL at either day 3 or 5. the collecting duct (CD renin) in response to NOS inhibition Summary of results At least 2 serial specimens were collected is unknown. We tested the hypothesis that NO inhibits renin in 60 patients (mean age 58, 32% women, mean sCr at day synthesis and secretion via the NO/GC/cGMP pathway in M-1 1 3.8 mg/dL). Overall, CS and PS category changed over time cells. in 16 (27%) patients, and the change was observed at day 3 Methods used Cultured cortical collecting duct (M-1) cells in almost all cases (15 of 16). On day 1, a CS and PS consis- were treated with either: 1) PBS (control); 2) NO donor tent with non-ATI was assigned to 31 (52%) patients. Among (NONOate, 1 mM); or 3) NOS inhibitor (L-NAME, 1 mM) those 31 patients, CS and PS changed from non-ATI category to assess renin synthesis and secretion using qRT-PCR and to ATI in 9 (24%) at day 3. Those 9 patients accounted for Western blot, and ELISA in extracellular media. To elucidate 32% of the total 38 with ATI score. Patients with worsening the involvement of guanylyl cyclase (GC) on renin, we quanti- AKI were more likely to change their score from non-ATI to fied intracellular cGMP levels in response to NONOate, as ATI compared to those with stable or improved AKI [relative well as renin protein with concomitant treatment of NON- risk 3.3 (CI: 1.0 to 10.9) for CS (p=0.047); 8.3 (CI: 1.1 to Oate and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), 63.1) for PS (p=0.041)]. to inhibit GC. Renin immunohistochemistry in M-1 cells and Conclusions Serial MicrExUrSed reveals diagnostic findings of kidney from eNOS-KO mice was also used. ATI otherwise not identified in a single examination, particu- Summary of results In M-1 cells, L-NAME increased renin larly in specimens of patients with worsening AKI. A repeat transcript as compared to control (2.5±0.6 vs 1.0±0.1) but MicrExUrSed within 48 hours may be warranted in cases of not NONOate (0.9±0.2). These data paralleled increased worsening AKI with unclear etiology. renin immunoexpression in eNOS-KO mouse kidneys (p<0.05). In M-1 cells, L-NAME and NONOate increased renin protein (1.0±0.01 and 1.1±0.1 vs. 0.6±0.1 au, p<0.05) and its immunoexpression. Intracellular cGMP levels increased http://jim.bmj.com/ in response to NONOate (3.5±0.5 vs. 1.5±0.2 pmol/mL; Cardiovascular II p<0.05). Concomitant treatment with NONOate and ODQ increased renin protein compared to control (0.3±0.04 vs 0.1 10:30 AM ±0.01 au, p<0.05), but not to NONOate alone. These data suggested that GC inhibition did not ameliorate this effect. Saturday, February 23, 2019 No changes in renin extracellular media were found in any group. on September 28, 2021 by guest. Protected copyright. 671 EOSINOPHILIC ENDOCARDIAL FIBROSIS CAUSING Conclusions In M-1 cells, NO inhibition stimulates CD renin HEART FAILURE synthesis independent of cGMP. Although, NO per se, does not increase renin transcript, it seems to augment intracellular E Sherman*, A Penmetsa, A Nat, K Galbraith. SUNY Upstate, Syracuse, NY renin protein, possibly by inhibiting renin secretion. 10.1136/jim-2018-000974.677 Case report Endomyocardial fibrosis is an idiopathic etiology 670 DIAGNOSTIC UTILITY OF SERIAL MICROSCOPY which progressively weakens the cardiac muscle causing EXAMINATION OF THE URINARY SEDIMENT IN ACUTE restrictive physiology. Loffler’s disease, first described in the KIDNEY INJURY 1930s, includes peripheral eosinophilia, endocardial fibrosis and small vessel vasculitis. Echocardiogram, cardiac MRI and ME Gonzalez*, J Velez. Ochsner Clinic Foundation, New Orleans, LA occasionally cardiac muscle biopsy are used to yield the diag- 10.1136/jim-2018-000974.676 nosis. Patients suffer from heart failure and treatment includes diuretics or surgical resection of the fibrosis. We present a 63- Purpose of study Urine microscopy is a clinical tool of diag- year-old male, working as an airplane mechanic, with hyper- nostic and prognostic value in acute kidney injury (AKI). tension and stage 3 kidney disease who suddenly developed However, the natural history and timing of cast formation shortness of breath and pleuritic chest pain. He was found to remains underexplored. A single inspection of a urine speci- have bilateral pleural effusions, mild peripheral eosinophilia, men during the course of AKI is a mere snapshot that marked neutrophilia and lymphocytopenia. The effusions were depends on the day of inspection. We hypothesized that longi- tapped and were transudative with two negative cytology sam- tudinal inspection of the urinary sediment provides additional ples. Other causes of dyspnea were ruled out so acute heart J Investig Med 2019;67:350–652 619 Abstracts J Investig Med: first published as 10.1136/jim-2018-000974.619 on 28 January 2019. Downloaded from failure exacerbation was diagnosed. Echocardiogram showed a is unique in that the severe degree of esophageal angioedema restrictive physiology and work up was subsequently negative lead to left atrial compression and hemodynamic compromise for autoimmune pathology. Heavy metal toxicity screen was of the patient. unremarkable. Given his degree of hypoxia and diuretic resist- ant effusions, he had a right heart catheterization which revealed severe pulmonary hypertension with PCWP of 19/20/ 18 mmHg and normal cardiac output. He also necessitated 673 WITHDRAWN bilateral pleural catheters and bleomycin pleurodesis. Cardiac MRI showed asymmetric basal septal and inferior hypertrophy, chronic RV strain, mild diffuse pericardial thickening due to possible mild pericarditis, dilated pulmonary artery and mild 674 NONCOMPACTION OR OVERREACTION? mediastinal lymphadenopathy. This prompted a left cardiac catheterization which showed stenosis in the distal LAD for B Lennep*, WF Campbell, MR McMullan, ME Hall. University of Mississippi Medical Center, which he received a DES and a cardiac biopsy demonstrated Madison, MS eosinophils and dense fibrosis in the endocardium. Stains were 10.1136/jim-2018-000974.679 negative for amyloid. He became unstable, went into ARDS, required intubation and hemodialysis. Repeat cardiac catheter- Case report A 22 year old man presented via ambulance after izations disclosed normal PA and heart filling pressures. a syncopal episode witnessed by his mother. She could not Despite paralysis and proning, he deteriorated and expired feel a pulse and began chest compressions. On ambulance ’ shortly after. Our patient likely had a subtype of Loeffler s arrival he was in sinus rhythm and hemodynamically stable. disease with mild peripheral eosinophilia but without vasculi- Echocardiography demonstrated mildly reduced left ventricular tis. Our goal is to emphasize that heart failure treatment is (LV) systolic function. Because his LV ejection fraction not identical for every patient, and an underlying etiology was >35% and there was no documented arrhythmia, he did may change management significantly. not meet criteria for a secondary prevention defibrillator (ICD). Still, our team was concerned about his syncope with reported pulselessness. A cardiac MRI was performed which demonstrated biventricular hypertrabeculation. Late gadolinium 672 A CASE OF ANGIOEDEMA LEADING TO LEFT ATRIAL enhancement (LGE) imaging (figure 1) showed extensive mid- COLLAPSE myocardial and subepicardial enhancement suggestive of fibro- M Heckle*1, L Julio1, Romero Legro I2,NGarg1. 1University of Tennessee Health Science sis. This fibrosis, along with the hypertrabeculation and Center, Memphis, TN; 2University of Tennessee, Memphis, TN physical exam finding of dysmorphic facies, suggested a diag- nosis of noncompaction cardiomyopathy. After some debate, 10.1136/jim-2018-000974.678 we elected to implant an ICD based on the high-risk LGE finding of diffuse fibrosis. A few months later, he had a long Background Angioedema secondary to angiotensin-converting- run of ventricular tachycardia with syncope. enzyme (ACE) inhibitors is a rare but well known life threaten- Noncompaction cardiomyopathy is associated with heart – http://jim.bmj.com/ ing complication, with an overall incidence of 0.1% 0.2%. This failure, arrhythmias, and sudden cardiac death.
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