Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
Advanced search 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 1695 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 

Table of Contents   
Year : 2017  |  Volume : 28  |  Issue : 6  |  Page : 1397-1403
Atypical antiglomerular basement membranes disease with nephrotic-range proteinuria, mesangial proliferation, and membranoproliferative glomerulonephritis pattern of injury

1 College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia
2 College of Medicine, King Saud bin Abdulaziz University for Health Sciences; Department of Pathology and Laboratory Medicine, King Abdulaziz Medical, Riyadh, Saudi Arabia
3 College of Medicine, King Saud bin Abdulaziz University for Health Sciences; Department of Pathology and Laboratory Medicine, King Abdulaziz Medical; Department of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia
4 Department of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia

Click here for correspondence address and email

Date of Web Publication18-Dec-2017


Antiglomerular basement membrane (anti-GBM) disease is an uncommon autoimmune disease characterized by the presence of IgG autoantibodies targeting the alpha-3 chain of type IV collagen. Some of the atypical forms of the disease have been described. Herein, we describe a case of atypical anti-GBM in a 27-year-old Saudi male who presented with lower limb edema, gross hematuria, elevated serum creatinine concentration, and nephrotic-range proteinuria. All serology tests were negative, except for anti-GBM which was weakly positive. Renal biopsy showed proliferative glomerulonephritis (GN) with nodular transformation of the glomerular tufts, mesangial hypercellularity (mesangial cell proliferation), segmental endocapillary hypercellularity and three incomplete cellular crescents, and recapitulating membranoproliferative GN pattern of glomerular injury. Direct immunofluorescence microscopy demonstrated diffuse, intense linear positivity for IgG and Kappa and Lambda light chains, and compatible with anti-GBM disease. The patient was treated with cyclophosphamide and corticosteroids in addition to therapeutic plasma exchange which resulted in mild improvement in renal function over a period of six weeks. We emphasize the importance of recognition of atypical pathological and serological patterns of anti-GBM disease, which is crucial for proper and early diagnosis and possibly improved clinical outcome and we highlight the importance of clinicopathological correlation in cases with atypical clinical and pathological presentations.

How to cite this article:
AlSowailmi B, AlSowailmi G, Aloudah N, Alsaad KO, Elhassan E, Al Sayyari AA. Atypical antiglomerular basement membranes disease with nephrotic-range proteinuria, mesangial proliferation, and membranoproliferative glomerulonephritis pattern of injury. Saudi J Kidney Dis Transpl 2017;28:1397-403

How to cite this URL:
AlSowailmi B, AlSowailmi G, Aloudah N, Alsaad KO, Elhassan E, Al Sayyari AA. Atypical antiglomerular basement membranes disease with nephrotic-range proteinuria, mesangial proliferation, and membranoproliferative glomerulonephritis pattern of injury. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2020 Jul 6];28:1397-403. Available from: http://www.sjkdt.org/text.asp?2017/28/6/1397/220868

   Introduction Top

Antiglomerular basement membrane (anti-GBM) disease is uncommon autoimmune disease characterized by the presence of IgG autoantibodies targeting the alpha-3 chain of type IV collagen. This type of collagen is found in restricted basement membranes although only glomerular and alveolar basement membranes are of clinical importance.[1] The clinicopathological hallmark of anti-GBM disease is rapidly progressive, necrotizing crescentic glomerulonephritis (GN) with diffuse and intense linear immunofluorescence (IF) positivity of IgG along the GBM; when the disease also involves the alveolar basement membranes (Goodpasture’s syndrome), pulmonary hemorrhage is considered as an important clinical presentation and can be a serious complication.[2],[3] The symptoms are highly dependent on the intensity of the renal injury, and usually start with malaise and a viral-like prodrome followed by marked increase in serum creatinine (SCr), hematuria, and active urine sediment with or without pulmonary hemorrhage.[4]

The incidence of anti-GBM disease was estimated to be one to two cases per one million population,[1] and it accounts for 5% of all cases of GN.[5] As for the prevalence in the Arabian Gulf region, it is estimated to be ranging from 1.5% to 4.4% of biopsy diagnosed GN.[6] A study from Bahrain identified only one case of anti-GBM among 336 renal biopsies of glomerular disease over the course of 13 years.[7] A bimodal distribution is observed in anti-GBM; the first peak is in the third decade, in which there is male predominance while the second peak is in sixth decade, in which there is female predominance.[8] Younger men have the highest incidence of Goodpasture’s syndrome, whereas isolated renal disease is more common in the older population.[1]

Typical histopathological manifestation of anti-GBM disease is exuberant, necrotizing crescentic GN with significant damage to the glomeruli owing to alpha-3 chain of type IV collagens exposure and binding to anti-GBM antibodies. This binding starts a cascade of complement activation, release of chemokines, cytokines, and proteolytic enzymes, and T lymphocytes recruitment, which enhance B lymphocytes proliferation and autoantibodies production. These events eventually lead to damage and disruption of the endothelial lining of the GBM and subsequent extracapillary proliferation and crescents formation.[5] Cases of anti-GBM disease with atypical clinical presentations, and atypical histopathological and IF manifestations were previously reported.[9],[10],[11],[12] Herein, we report a case of atypical anti-GBM disease in a 27-year-old Saudi male who presented with lower limb edema, gross hematuria, renal function impairment, nephrotic range proteinuria, and weak serological positivity for circulating anti-GBM antibodies, associated with biopsy-proved mesangioproliferative and membranoproliferative (MPGN) patterns of glomerular injury, which are atypical morphological presentations for anti-GBM disease.

   Case Report Top

A 27-year-old smoker male was presented with intermittent headache, dizziness, lower limb edema, gross hematuria, and oliguria for three months. There was no history of fever, weight loss, hemoptysis, abdominal pain, arthralgia, or other clinical manifestations. Clinical inquiry revealed a history of the upper respiratory tract infection two weeks before symptoms. His past surgical history revealed surgical correction of transposition of the great arteries and appendectomy. The parents were consanguineous with positive family history of diabetes mellitus and hypertension. His brother had sickle cell anemia and bronchial asthma, while his sister had glucose-6-phosphate dehydrogenase deficiency.

On physical examination, the patient was alert and conscious, well hydrated, and not in respiratory distress. His vital signs were stable; heart and respiratory rates were 98 beats/min and 19 breath/min, respectively. He was afebrile with blood pressure of 145/92 mm Hg. His weight was 145 kg, height was 176 cm, and body mass index was 46.8 kg/m2. Chest, cardiovascular and abdominal examinations were unremarkable. There was no evidence of rashes, arthritis, or mucosal ulcers.

Laboratory workup revealed white blood cells of 10.10 ×109/L (reference range 4.5–11.0 × 109/L), red blood cell count (RBC) 3.38 ×1012/L (4.4–5.8 × 1012/L), hemoglobin of 95 g/L (138–172 g/L), and platelet count of 263×109/L (150–400 ×109/L). His erythrocyte sedimentation rate was 35 mm/H (0–15 mm/ H). The patient’s SCr level was 277 μmol/L (64–110 μmol/L), and the estimated glomerular filtration rate (eGFR) at 26 mL/min; however, one month before the admission the SCr level was 143 μmol/L, and eGFR was 55 mL/min. Blood urea nitrogen (BUN) level was 27.3 mmol/L (2.5–7.1 mmol/L), protein creatinine ratio was 13.73 (<0.2 g protein/g creatinine) and serum albumin was 22 g/L (34–54 g/L). Serum electrolytes were normal. Twenty-four hour urine protein was 13.4 g. Urine analysis showed dysmorphic RBC of 868/hpf and protein of 600 mg/d. Prothrombin time, partial thromboplastin time, and international normalized ratio were normal. His serum lipid profile demonstrated total cholesterol of 6.26 mmol/L (≤5 mmol/L), low-density lipoprotein of 3.93 mmol/L (≤3 mmol/L), high-density lipoprotein level of 1.27 mmol/L (<1 mmol/L), and triglycerides of 1.75 mmol/L (<2.3 mmol/ L). Liver function test was normal. Serological tests for viral hepatitis B and C, antinuclear antibody, anti-dsDNA, and cytoplasmic and perinuclear anti-neutrophil cytoplasmic antibodies (c-ANCA and p-ANCA) were all negative. Direct enzyme-linked immunoassay for circulating anti-GBM was weakly-positive (2.9 U/mL) (<1.0 U/mL).

A kidney biopsy was performed and two cores of renal cortex and medulla were obtained. Two μm thickness sections from the formalin-fixed, paraffin-embedded tissue were stained with hematoxylin and eosin, periodic acid Schiff (PAS), Masson’s Trichrome and Methenamine silver special stains. For IF study, 3 μm cryostat sections were stained with fluorescein isothiocyanate-conjugated rabbit antihuman IgG, IgM, IgA, C3, C4, C1q, Kappa and Lambda light chains, albumin, and fibrinogen (Dako, Carpinteria, CA, USA). The intensity of IF positivity was graded on a scale of 0, trace; and 1 to 3+. Electron microscopy was performed on glutaraldehyde-fixed tissue after usual processing and staining with a JOEL1230 electron microscope (Akishima, Japan).

Light microscopic examination showed 12 glomeruli which of none was globally sclerosed. The glomeruli showed diffuse nodular transformation of the glomerular tufts, moderate to marked increase in mesangial matrix and moderate to marked increase in mesangial cellularity [Figure 1]a. Segmental glomerular scarring in the form of obliteration of the glomerular capillaries and adhesion of the glomerular tufts to the Bowman’s capsule was seen in at least two glomeruli. The GBM showed moderate to marked increase in thickness, and segmental replication and remodeling on PAS and silver special stains, which was more appreciated in glomeruli with less nodular transformation [Figure 1]b. No definite disruption or discontinuity of the GBM was identified, and no spike reaction of the GBM was seen. Focal segmental glomerular endocapillary hypercellularity was seen [Figure 1]b, along with scattered pyknotic cellular debris and extra-capillary proliferation in the form of three small incomplete cellular crescents [Figure 1]c. There was no evidence of subendothelial deposits, fibrinoid necrosis, or microthrombi. Moderate acute tubular cell degenerative and regenerative changes/acute kidney injury were present along with mild interstitial inflammation; the interstitial inflammatory cell infiltrate consisted mainly of lymphocytes and scattered neutrophils. No significant tissue eosinophilia was seen and there was no evidence of multinucleated giant cell reaction or granulomas. There were minimal interstitial fibrosis and tubular atrophy. No arteriolar hyalinosis or arterial sclerosis was seen and there was no evidence of interstitial vasculitis.
Figure 1: Atypical morphological features of anti-glomerular basement membranes disease: (a) marked nodular accentuation of the glomerular tufts, and expansion of the mesangium by increased mesangial matrix and mesangial cells, (b) segmental endocapillary hypercellularity (arrowheads) and segmental replication of the glomerular basement membranes (arrows), (c) mild extracapillary proliferation forming small, incomplete cellular crescents (arrows) (a, b and c, Periodic acid Schiff ×400), (d) immunofluorescence microscopy demonstrating diffuse, intense, ribbon-like linear positivity for IgG (×400).

Click here to view

IF microscopy revealed diffuse and global, strong and intense (3+) linear staining for IgG [Figure 1]d, and Kappa and Lambda light chains along the GBM. This was associated with segmental weak nonspecific granular capillary staining for IgA (trace) and C3 (1+). There was no staining for IgM, C4, and C1q, and staining for fibrinogen and albumin was not contributory. The electron microscopy demonstrated increase in mesangial matrix and cellularity, obliteration of the glomerular tufts, and endocapillary hypercellularity. Focal minimal subepithelial dense deposits were seen, but no definite immune-type dense deposits were identified. The GBM showed areas of attenuation and discontinuity with no abnormal texture. The foot processes of the glomerular visceral epithelial cells are effaced over at least 80% of the GBM.

The patient received 150 mg of cyclophos-phamide, and 80 mg of prednisolone with the aim of gradually reducing the doses over five to six months. He also received 60 mg of furosemide and 10 mg of lisinopril daily. In addition, the patient had three sessions of 4L of therapeutic plasma exchange; however, it was stopped because negative anti-GBM titer was reached.

Over the period of observation of six weeks, the patient showed mild improvement with gradual subsiding of his lower limb edema and disappearance of the gross hematuria. The SCr level and BUN dropped mildly to 232 μmol/L and 24.5 mmol/L, respectively. Urine analysis continued to show RBC 68/hpf and protein of 600 mg/d. Unfortunately, the patient was lost to follow-up.

   Discussion Top

Anti-GBM disease is aggressive, rapidly progressive, necrotizing GN that is characterize by extensive glomerular damage and exuberant extracapillary proliferation and crescents formation. Typical acute form of anti-GBM disease lacks mesangial cell and endocapillary proliferation, and GBM changes. In this report, we present an unusual case of atypical anti-GBM disease. The presence of definite diffuse, global and strong linear IF positive staining for IgG is consistent with the diagnosis of anti-GBM disease. However, the light microscopic mesangioproliferative and MPGN with endocapillary hypercellularity patterns of glomerular injury are not those typically encountered in anti-GBM disease. Such cases of atypical anti-GBM are rarely encountered in diagnostic renal biopsy but are increasingly reported. In one study,[11] atypical anti-GBM counted approximately 8% of all cases of biopsy-proved anti-GBM disease. Nasr et al[12] described 20 patients with atypical anti-GBM nephritis, of which renal biopsies of nine patients demonstrated endocapillary proliferative GN, six biopsies showed mesangioprolferative GN, and three biopsies showed membranoproliferative GN pattern of injury; in addition, two patients had focal segmental glomerulosclerosis with mesangial hypercellularity. Compared to conventional anti-GBM disease, atypical cases do not have pulmonary involvement, have low titers or undetectable circulating anti-GBM antibodies, creatinine levels do not rise to high levels seen in typical cases, and renal biopsy demonstrates endocapillary proliferation, which can be focal and segmental, mesangioproliferative GN or MPGN GN, and atypical linear immunoglobulin IF positive staining along the GBM.[11],[12],[13] Anti-GBM disease with atypical non-IgG IF strong and linear staining of IgA, IgM and Lambda light chain were reported.[9],[12],[13],[14]

Typically, in anti-GBM disease, more than 50% of the glomeruli show fibrinoid necrosis, which might be segmental, and exuberant formation of cellular crescents, that obliterate the urinary space.[15] Similar to our case that showed only small incomplete cellular crescents only in three of 12 (25%) glomeruli, atypical anti-GBM disease with only focal and segmental glomerular fibrinoid necrosis and/or few small and incomplete crescents, or no crescents are well documented.[14],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26] Ang et al[21] reported five patients of anti-GBM disease who lacked diffuse crescentic phenotype on light microscopic examination; four of these patients exhibited mild mesangial hypercellularity, while one patient displayed unremarkable glomeruli. It is possible that this morphological heterogeneity is an outcome of nonconventional GBM epitopes, atypical IgG subclass, and involvement of T lymphocytes or complement-mediated injury.[12],[27]

Testing for anti-GBM antibody can be falsely negative in approximately 5% of cases of anti-GBM disease.[27] This might be accounted for different reasons that include: antibodies against nonconventional GBM epitopes, non-IgG anti-GBM antibodies or different subclass of IgG such as IgG4 instead of IgG1. Further-more, the anti-GBM antibodies could be of low affinities toward the standard assay or low concentrations that might be due to higher rate of clearance or lower rate of synthesis.[4] In addition, immunological sink phenomenon can provide a potential explanation of the negative or detection of low titers of anti-GBM antibodies. In this phenomenon, the autoantibodies with higher affinities are rapidly cleared from the circulations leaving only low concentrations of autoantibodies with low affinities that cannot be detected by the standard assays. Furthermore, other possible explanation of negative testing for circulating anti-GBM antibodies is that the pathogenesis of tissue injury might be mediated by T cell, complement factors or cytokines instead of antibodies.[27]

The frequency of pulmonary involvement in classic anti-GBM nephritis ranges from 34–62.[13] Our patient did not have any symptoms or signs of pulmonary involvement. In a cohort of patients with classical form of anti-GBM disease, Jennette[15] reported a mean SCr level at the time of presentation in 86 cases of 857 μmol/L and mean 24 h proteinuria in 68 cases of 1.7 g/d. Contrary to the classical, anti-GBM disease, which usually presents clinically as rapidly progressive GN with very high rise in SCr, our patient had an indolent course with proteinuria, hematuria, and mild renal impairment. Our patient’s serum SCr level at the time of diagnosis was 277 μmol/L, which was significantly lower than the usual SCr level that encountered in typical cases of anti-GBM disease and consistent with atypical clinical presentation of anti-GBM disease. Interestingly, the 24 h proteinuria was of nephrotic range (6 g/d) rather than the subnephrotic proteinuria that might be seen in typical anti-GBM disease patients.

According to Nasr et al,[12] atypical anti-GBM has better prognosis than the typical disease; in his cohort of 20 patients with atypical anti-GBM disease, the one-year survival rate for renal and patient survival rates were 85% and 93%, respectively. Better prognosis of atypical anti-GBM can be explained by the lack of pulmonary involvement, and low anti-GBM titer, which results to mild renal impairment and less aggressive GN with small numbers of crescents.[28] Our patient had low level of circulating anti-GBM antibodies, small numbers of small incomplete crescents and absence of pulmonary involvement, which all should contribute to a favorable prognosis and clinical outcome. Despite that he did not clinically and biochemically deteriorate but did not significantly improved over the short period of observed clinical management, which was unusual for atypical anti-GBM. Unfortunately as the patient was lost to follow-up and achievement of significant improvement could not be established.

In summary, we reported a case of atypical anti-GBM disease, characterized by low circulating anti-GBM antibodies titer, modest elevation in SCr, nephrotic range proteinuria and renal biopsy with histopathological features of mesangial hypercellularity, MPGN patterns of glomerular injury and paucity of cellular crescents. Recognizing the difference between the typical and atypical anti-GBM disease is essential for proper and prompt diagnosis and proper therapeutic intervention.

Funding: None.

Conflicts of interest: None declared.

   References Top

Kluth DC, Rees AJ. Anti-glomerular basement membrane disease. J Am Soc Nephrol 1999; 10:2446-53.  Back to cited text no. 1
Holdsworth S, Boyce N, Thomson NM, Atkins RC. The clinical spectrum of acute glomerulonephritis and lung haemorrhage (Goodpasture’s syndrome). Q J Med 1985;55:75-86.  Back to cited text no. 2
Cui Z, Zhao J, Jia XY, et al. Anti-glomerular basement membrane disease: Outcomes of different therapeutic regimens in a large single-center Chinese cohort study. Medicine (Baltimore) 2011;90:303-11.  Back to cited text no. 3
Troxell ML, Houghton DC. Atypical antiglomerular basement membrane disease. Clin Kidney J 2016;9:211-21.  Back to cited text no. 4
Olson SW, Arbogast CB, Baker TP, et al. Asymptomatic autoantibodies associate with future anti-glomerular basement membrane disease. J Am Soc Nephrol 2011;22:1946-52.  Back to cited text no. 5
Waness A. Pulmonary renal syndrome in the Arabian Gulf region: A case report. Int J Case Rep Imag 2012;3:29-34.  Back to cited text no. 6
Al Arrayed A, George SM, Malik AK, et al. The spectrum of glomerular diseases in the Kingdom of Bahrain: An epidemiological study based on renal biopsy interpretation. Transplant Proc 2004;36:1792-5.  Back to cited text no. 7
Pedchenko V, Bondar O, Fogo AB, et al. Molecular architecture of the Goodpasture autoantigen in anti-GBM nephritis. N Engl J Med 2010;363:343-54.  Back to cited text no. 8
Moulis G, Huart A, Guitard J, Fortenfant F, Chauveau D. IgA-mediated anti-glomerular basement membrane disease: An uncommon mechanism of Goodpasture’s syndrome. Clin Kidney J 2012;5:545-8.  Back to cited text no. 9
Balasubramaniyan T, Dhanapriya J, Dineshkumar T, et al. Atypical anti-glomerular basement membrane disease superimposed on IgA nephropathy. J Integr Nephrol Andril 2017; 4:26-8.  Back to cited text no. 10
L’Imperio V, Ajello E, Pieruzzi F, et al. Clinicopathological characteristics of typical and atypical anti-glomerular basement membrane nephritis. J Nephrol 2017;30:503-9.  Back to cited text no. 11
Nasr SH, Collins AB, Alexander MP, et al. The clinicopathologic characteristics and outcome of atypical anti-glomerular basement membrane nephritis. Kidney Int 2016;89:897-908.  Back to cited text no. 12
Wen YK, Wen KI. An unusual case of igA-mediated anti-glomerular basement membrane disease. Int Urol Nephrol 2013;45:1229-34.  Back to cited text no. 13
Coley SM, Shirazian S, Radhakrishnan J, D’Agati VD. Monoclonal igG1κ anti-glome-rular basement membrane disease: A case report. Am J Kidney Dis 2015;65:322-6.  Back to cited text no. 14
Jennette JC. Rapidly progressive crescentic glomerulonephritis. Kidney Int 2003;63:1164-77.  Back to cited text no. 15
Zimmerman SW, Varanasi UR, Hoff B. Goodpasture’s syndrome with normal renal function. Am J Med 1979;66:163-71.  Back to cited text no. 16
Carre P, Lloveras JJ, Didier Aet al. Good-pasture’s syndrome with normal renal function. Eur Respir J 1989;2:911-5.  Back to cited text no. 17
Knoll G, Rabin E, Burns BF. Antiglomerular basement membrane antibody-mediated nephritis with normal pulmonary and renal function. A case report and review of the literature. Am J Nephrol 1993;13:494-6.  Back to cited text no. 18
Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P. Goodpasture’s syndrome: Normal renal diagnostic findings. Ann Intern Med 1975;82:215-8.  Back to cited text no. 19
Bailey RR, Simpson IJ, Lynn KL, et al. Goodpasture’s syndrome with normal renal function. Clin Nephrol 1981;15:211-5.  Back to cited text no. 20
Ang C, Savige J, Dawborn J, et al. Anti-glomerular basement membrane (GBM)-antibody-mediated disease with normal renal function. Nephrol Dial Transplant 1998;13: 935-9.  Back to cited text no. 21
Cui Z, Zhao MH, Singh AK, Wang HY. Antiglomerular basement membrane disease with normal renal function. Kidney Int 2007; 72:1403-8.  Back to cited text no. 22
Sethi S, Lewin M, Lopez L, Lager D. Linear anti-glomerular basement membrane igG but no glomerular disease: Goodpasture’s syndrome restricted to the lung. Nephrol Dial Transplant 2007;22:1233-5.  Back to cited text no. 23
Fervenza FC, Terreros D, Boutaud A, et al. Recurrent goodpasture’s disease due to a monoclonal igA-kappa circulating antibody. Am J Kidney Dis 1999;34:549-55.  Back to cited text no. 24
Bazari H, Guimaraes AR, Kushner YB. Case records of the Massachusetts general hospital. Case 20-2012. A 77-year-old man with leg edema, hematuria, and acute renal failure. N Engl J Med 2012;366:2503-15.  Back to cited text no. 25
Lamriben L, Kourilsky O, Mougenot B, Ronco P, Sraer JD. Goodpasture’s syndrome with asymptomatic renal involvement. Disappearance of Antiglomerular basement membrane antibodies deposits after treatment. Nephrol Dial Transplant 1993;8:1267-9.  Back to cited text no. 26
Glassock RJ. Atypical anti-glomerular basement membrane disease: Lessons learned. Clin Kidney J 2016;9:653-6.  Back to cited text no. 27
Levy JB, Turner AN, Rees AJ, Pusey CD. Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med 2001;134:1033-42.  Back to cited text no. 28

Correspondence Address:
Abdulla A Al Sayyari
Department of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, P. O. Box 22490, Riyadh 11426
Saudi Arabia
Login to access the Email id

DOI: 10.4103/1319-2442.220868

PMID: 29265053

Rights and Permissions


  [Figure 1]


    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  

   Case Report
    Article Figures

 Article Access Statistics
    PDF Downloaded236    
    Comments [Add]    

Recommend this journal