We present a rare case of pulmonary-renal syndrome secondary to recurrent MRSA spondylodiscitis. The mechanism of involvement of each organ system is unique. The organs, lung and kidneys, have been affected by different pathologic processes that were induced, we think, by the chronic MRSA infection

Al-dliw, Majdi

Khitan, Zeid

Megri, Mohammed

Shweihat, Yousef

English

Marshall University

Marshall UniversityMarshall Digital ScholarInternal Medicine Faculty Research2017MRSA induced pulmonary-renal syndromeMohammed MegriMarshall University, megri@live.marshall.eduMajdi Al-dliwMarshall UniversityYousef ShweihatMarshall University, shweihat@marshall.eduZeid KhitanMarshall University, zkhitan@marshall.eduFollow this and additional works at: https://mds.marshall.edu/int_medPart of the Internal Medicine Commons, Nephrology Commons, and the PulmonologyCommonsThis Article is brought to you for free and open access by the Faculty Research at Marshall Digital Scholar. It has been accepted for inclusion in InternalMedicine by an authorized administrator of Marshall Digital Scholar. For more information, please contact zhangj@marshall.edu,beachgr@marshall.edu.Recommended CitationMegri M, Al-dliw M, Shweihat Y, Khitan Z. MRSA induced pulmonary-renal syndrome. Respiratory Medicine Case Reports.2017;20:42-44.Case reportMRSA induced pulmonary-renal syndromeMohammed Megri a, *, Majdi Al-dliw a, Yousef Shweihat b, Zeid Khitan ca Marshall University, USAb Critical Care Medicine, Pulmonary, Interventional Pulmonary, Marshall University, USAc Nephrology, Marshall university, USAa r t i c l e i n f oArticle history:Received 20 July 2016Received in revised form5 November 2016Accepted 7 November 2016Keywords:ANCAMRSAVasculitidesPulmonary-renal syndromeDiffuse alveolar hemorrhage1. IntroductionIt is no secret that the link between infection and vasculitis iswell established even though the exact mechanism is still understudy [1]. Infection, in addition to other factors, has been counted totrigger Vasculitis. The causal relationship has been documentedonly in few cases like Polyarthritis Nodosa (PNA)/Hepatitis B virus(HBV) and Cryoglobulinemia/Hepatitis C virus (HCV) cases [1].There has also been an established link between Methicillin-Resistant-Staphylococcus aureus (MRSA) and Microscopic Poly-angitis with perinuclear anti-neutrophils-cytoplasmic-antibody (P-ANCA) [2]. In addition, post MRSA infection IgA glomerulonephritis[2] is well described.We present a rare case of pulmonary-renal syndrome secondaryto recurrent MRSA spondylodiscitis. The mechanism of involve-ment of each organ system is unique. The organs, lung and kidneys,have been affected by different pathologic processes that wereinduced, we think, by the chronic MRSA infection.2. Case reportOur patient is 37-years-old white morbid obese female. Sheoriginally presented with MRSA spondylodiscitis at L3-L4 vertebrallevel and bilateral Psoas muscle abscesses. She was treated for 6weeks with IV antibiotics with apparent resolution of symptoms.Two months after finishing her antibiotic regimen, the patientpresented with worsening lower back pain for one-week duration.She has a previous history of IV drug abuse up until the episode ofthe initial infection but denies any recent abuse.Her vitals were normal on ambient air. Leukocytosis of 11.9 anda chronic stable anemia with hemoglobin of 8.2 was noted on herinitial blood count. Her creatinine and blood urea nitrogen werenormal. Blood cultures were negative. Magnetic resonance imaging(MRI) of the spine (Fig. 1) showed persistent Spondylodiscitis at L3-4. Therewas persistent enhancement of the adjacent psoas muscleswith associated phlegmon along the epidural space at L3-5 level.She was immediately re-started on Vancomycin. Surgical Drainageof the possible abscess was carried out in conjunction with spinestabilization. Culture of tissue obtained showed MRSA. Oralrifampin was added soon after the surgery. On the 9th day postadmission patient developed gross hematuria and her renal func-tion started to deteriorate. Urine studies suggested an intrinsicrenal etiology with moderate proteinuria. The gross hematuriaprevented urine microscopy from revealing casts or ruling theirpresence out. This was accompanied by hydronephrosis onabdominal imaging. Cystoscopy revealed clots in the ureters andbilateral ureteric bypass stents were inserted. Kidney functioncontinued to deteriorate and she required hemodialysis. Initialwork up for her hematuria and proteinuria was negative includingnegative P-ANCA, C-ANCA. Within 2 days of her cystoscopy shestarted to complain of progressive worsening dyspnea associatedwith oxygen desaturation. Her HGB further dropped by 2 g. Chest x-ray (Fig. 2) preformed and showed bilateral interstitial opacitiessuggestive of pulmonary edema. Patient continued to worsendespite repeated daily dialysis and had to be intubated for wors-ening respiratory distress. Lung protective ventilation was insti-tuted immediately after intubation. Bronchoscopic alveolar lavage(BAL) was preformed and confirmed the suspicion of diffuse alve-olar hemorrhage (DAH) with increasing blood content of thesequential aliquots from both right middle lobe and lingular seg-ments. Pulmonary renal syndrome was considered and plasmaexchange therapy (PLEX) with high dose steroids initiated. Vanco-mycin and rifampin were continued. Workup for pulmonary renal* Corresponding author.E-mail address: drmmegri@gmail.com (M. Megri).Contents lists available at ScienceDirectRespiratory Medicine Case Reportsjournal homepage: www.elsevier .com/locate /rmcrhttp://dx.doi.org/10.1016/j.rmcr.2016.11.0042213-0071/© 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Respiratory Medicine Case Reports 20 (2017) 42e44syndrome revealed elevated C-ANCA levels that were previouslynormal. Patient showed dramatic improvement and she wasweaned off the mechanical ventilation after the 4th session of PLEX(day 7 of mechanical ventilation). Renal biopsy was performed andshowed features of acute tubular necrosis and immune complexdeposits consistent with active staphylococcus infection-associatedglomerulonephritis [11] (Figs. 3 and 4). Unfortunately her course ofstay in the hospital worsened after weaning her steroids down andpatient was admitted once more to intensive care unit (ICU) withworsening hypoxia and she was intubated. Repeat Bronchoscopyrevealed recurrence diffuse alveolar hemorrhage. Steroids wereinitiated again with significant improvement. She was successfullyextubated in 6 days and was eventually discharged home on oralsteroids. No other immunosuppressive agents were used due to theinfection status of the patient.3. DiscussionVasculitides are often serious and even fatal diseases thatrequire rapid recognition [4]. They are defined by the presence ofinflammatory leukocytes in vessel walls with reactive damage tomural structures. Both loss of vessel integrity leading to bleeding,and compromise of the lumen may result in downstream tissueischemia and necrosis [3]. We can classify vasculitis according tothe involved vessels location, type, size and ANCA positive ornegative vasculitis [5]. Vasculitis may occur as a primary process ormay be secondary to another underlying disease like infection. Theexact pathogenic mechanisms underlying these diseases areunknown.The ANCA associated vasculitis (AAV) include three groups ofvasculitides; Microscopic polyangitis (MPA), granulomatosis withpolyangitis (Wegener's)(GPA), and eosinophilic granulomatosiswith polyangitis (Churg-Strauss) (EGPA) [5].There are many bacterial and viral infections associated withdifferent types of vasculitis. MRSA associated with microscopicpolyangitis with P-ANCA is reported [2], as well as post MRSAinfection IgA glomerulonephritis [2]. MRSA carriage or infectionhas been associated with cases of C-ANCA vasculitis (Wegenergranulomatosis) [12e14]. We have not identified a case with thesynchronous evolution of MRSA induced glomerulonephritis andDAH. Our case is unique given the development MRSA inducedvasculitis and Pulmonary-renal syndrome. It makes it more uniquethat the occurrence of pulmonary renal syndrome was caused by 2different mechanisms. In this case, glomerulonephritis representspost-infectious rather than pauci-immune mediated injury. This isevident by the mesangial hypercellularity as well as glomerularcomplement 3, and IgA deposition along with the classic sub-epithelial humps as shown in (Figs. 5 and 6) [10]. Although the DAHwas not biopsy proven to be secondary to a vasculitis problem, webelieve this was the case based on the rapid improvement withplasma exchange and use of steroids. The recurrence of the alveolarhemorrhagewhile patient was still on antibiotics and after weaningthe steroids makes it more likely that the DAH was inflammationinduced. The presence of C-ANCA antibodies and the response toPLEX and steroids are strong indicators of active vasculitis [7e9].Fig. 1. MRI lumbar.Fig. 2. Chest X ray.Fig. 3. Mild mesangial granular standing for C3. Fig. 4. Glomerulus with mesangial hypercellularity. H&E.M. Megri et al. / Respiratory Medicine Case Reports 20 (2017) 42e44 43The use of PLEX in AAV induced nephritis can lead to 24% reductionin the development of ESRD comparing to the conventional treat-ment with prednisone and cyclophosphamide [6e8]. The Use ofPLEX in AAV associated alveolar hemorrhage and pulmonary renalsyndrome can be life saving [14], Other possible etiologies to thepulmonary-renal syndrome are possible, but very unlikely in thiscase. Drug induced renal injury is a well-known entity. They areunlikely the cause of the pulmonary renal syndrome based on therenal biopsy findings. In addition, none of her medications areknown to induce ANCA vasculitis. The patient did not have anyother infection or known disease or drug exposure that wouldexplain the alveolar hemorrhage. She is not known to have activerheumatologic disease and there was no sign of active heart failureto cause a bland hemorrhage. The lack of volume overload(repeated dialysis) or ARDS/diffuse alveolar damage evidenced bythe rapid improvement in respiratory parameters make the di-agnoses of ANCA associated DAH the only available clinical expla-nation. Our case has significant implications. It is the first todescribe DAH related to immunologic response to MRSA infection.It also stresses the fact that multiple diseases can present due to thesame etiology but with different mechanisms. Treatment of infec-tion alone sometimes is not sufficient. Treating the derangedimmunologic response to chronic infection is as important inimproving patient outcomes. we hope our case will spark the in-terests of the readers and help spread the knowledge of the mul-tiple effects of chronic bacterial infections.References[1] http://rheumatology.oxfordjournals.org/content/early/2009/03/03/rheumatology.kep026.full.[2] A. Koyama, M. Kobayashi, N. Yamaguchi, K. Yamagata, K. Takano, M. Nakajima,F. Irie, M. Goto, M. Igarashi, T. Iitsuka, et al., Glomerulonephritis associatedwith MRSA infection: a possible role of bacterial superantigen, Kidney Int. 47(1995) 207e216.[3] Vasculitis-Definition from the Merriam-Webster online dictionary.[4] J.C. Jennette, R.J. Falk, P.A. Bacon, et al., 2012 revised international chapel hillconsensus conference nomenclature of vasculitides, Arthritis Rheum. 65(2013) 1.[5] J.C. Jennette, R.J. Falk, K. Andrassy, et al., Nomenclature of systemic vasculit-ides. Proposal of an international consensus conference, Arthritis Rheum. 37(1994) 187.[6] A.S. Bomback, G.B. Appel, ANCA-associated GNdto PLEX or not to PLEX? Nat.Rev. Nephrol. 9 (2013) 436e438.[7] H. Gallagher, J.T. Kwan, D.R. Jayne, Pulmonary renal syndrome: a 4-year,single-center experience, Am. J. Kidney Dis. 39 (1) (2002) 427.[8] A. Koyama, M. Kobayashi, N. Yamaguchi, K. Yamagata, K. Takano, M. Nakajima,F. Irie, M. Goto, M. Igarashi, T. Iitsuka, et al., Glomerulonephritis associatedwith MRSA infection: a possible role of bacterial superantigen, Kidney Int. 47(1995) 207e216. Medline.[9] A. Koyama, S. Sharmin, H. Sakurai, Y. Shimizu, K. Hirayama, J. Usui, M. Nagata,K. Yoh, K. Yamagata, K. Muro, M. Kobayashi, K. Ohtani, Ta Shimizu, To Shimizu,Staphylococcus aureus cell envelope antigen is a new candidate for the in-duction of IgA nephropathy, Kidney Int. 66 (2004) 121e132.[10] Samih H. Nasr, Vivette D. D'Agati, IgA-dominant postinfectious glomerulo-nephritis: a new twist on an old disease, Nephron Clin. Pract. 119.1 (2011)c18ec26.[11] Samih H. Nasr, et al., Postinfectious glomerulonephritis in the elderly, J. Am.Soc. Nephrol. 22.1 (2011) 187e195.[12] Jose Cardenas-Garcia, et al., Wegener's granulomatosis in a middle-agedwoman presenting with dyspnea, rash, hemoptysis and recurrent eye com-plaints: a case report, J. Med. Case Rep. 6.1 (2012) 1.[13] Philip J. Klemmer, et al., Plasmapheresis therapy for diffuse alveolar hemor-rhage in patients with small-vessel vasculitis, Am. J. Kidney Dis. 42.6 (2003)1149e1153.[14] K. Zycinska, et al., Co-trimoxazole and prevention of relapses of PR3-ANCApositive vasculitis with pulmonary involvement, Eur. J. Med. Res. 14.4(2009) 1.Fig. 5. Segmental granular glomerular IgA.Fig. 6. Subepithelial humps.M. Megri et al. / Respiratory Medicine Case Reports 20 (2017) 42e4444

MRSA induced pulmonary-renal syndrome

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MRSA induced pulmonary-renal syndrome

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