Takaysu Glomerulonephritis
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Takayasu Arteritis and GN/RVH
![Case Discussions
Beka Aberra [MD]
Renal Fellow Year 1](https://image.slidesharecdn.com/takaysugn-220221133358/85/Takaysu-Glomerulonephritis-1-320.jpg)
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Takaysu Glomerulonephritis
- 1. Case Discussions Beka Aberra [MD] Renal Fellow Year 1
- 2. Outline • Objectives • Case Summaries • Takayasu arteritis and RVH • Takayasu arteritis and Glomerulopathy • Reference
- 3. Objectives • Discuss on takayasu arteritis and renovascular hypertension control • Discuss on the possible link of takayasu arteritis and glomerular diseases
- 4. A 17 Year-old female presented with constitutional symptoms of fatigue, loss of appetite and low grade intermittent fever of 02 months, with left side pleuritic chest pain, cough with expectorations for which antibiotics taken to no avail. 03 weeks prior to admission developed generalized body swelling from face to legs, decrement in urine output with bilateral flank pain for which she took antibiotics, prednisolone 80 mg/03 days and Lasix 80mg Iv Tid but had become anuric for a week. She had blurring of vision with diplopia with balance issues of 01 month. She had asymmetric (Left<Right) upper extremity in length, muscle bulk and power with relative numbness and weakness on activities. Upon admission, his temperature was 36.5°C, blood pressure 190/90 mm Hg (right arm) and 170/94 mm Hg (left arm), and pulse 70 beats per minute with regular rhythm. Auscultation of the chest, lungs and abdomen was normal. Her peripheral arteries (Left brachial faint and Left radial absent) with trace pedal edema of the lower extremities. Skin rashes were not detected. There is a 3cm discrepancy of her arms Right 24, Left 21 cm. Neurological findings were bidirectional nystagmus, vertical nystagmus and horizontal nystagmus (fast to the right with rotatory component) pronounced in the right gaze. Case Summary #1
- 6. Case Summary #1 CBC Hgb 8.8 MCV 78.2; ESR 150 CRP 16 (0-10) Creatinine Pattern 1.93>3.8>6.8>10.1>7.13>1.41>4.35>1.2 UAA Specific Gravity 1.03 Protein +2/ Blood +1 RBC 7-8/Hpf WBC 8-10/Hpf 24hr Urine protein 350 mg in 1100ml. Bilateral upper extremity arterial Doppler showed left subclavian artery stenosis. Renal Doppler Unremarkable bilaterally; Abd Us: Moderate Ascites and normal kidneys. Pleural Fluid cytology showed lymphocytosis with small mature lymphocytes in hemorrhagic background. GXpert TB –ve. ECHO: Mild concentric LVH with EF 40%; Grade 4 LVDD with mild PHTN and mild pericardial effusion. Pulsed with Methylprednisolone 500 mg Iv/03 days and took Cyclophosphamide 750 mg Iv Stat On Prednisolone 50 mg po/day; CPT-PPI-DVT Prophylaxis; amlodipine 10mg po/day; carvedilol 12.5 mg po bid.
- 10. Introduction Takayasu Arteritis • Initially described in 1761, TA, often termed pulseless disease, is one of several inflammatory disorders involving the renal vasculature causing RVH. • TA usually presents between the ages of 25 and 41 years but, like FMD, can present in childhood. It most often presents as RVH and should be considered in any child or young adult with hypertension and/or asymmetric peripheral pulses or bruits. Concomitant inflammatory aortic coarctation may be present. • Renal complication in TA is conventionally divided into two categories: renovascular disease and glomerular disease. Renal artery stenosis can occur as a consequence of arterial wall thickening due to atherosclerosis secondary to prolonged inflammation. Decreased blood supply into the kidney sometimes results in RASS activation, leading to uncontrollable hypertension.
- 11. Introduction • The pathophysiology of TA is unclear. Theories include autoimmunity and hypersensitivity response to a variety of proposed antigens, including heat shock protein and M. tuberculosis. Histologically, granulomatous inflammation involves all layers of the vessel wall during the active phase of disease, followed by fibrotic stenosis. • Classically described as a triphasic disease: (i) ‘ pre-pulseless ’ phase with systemic symptoms; fever, night sweats, malaise, and weight loss. (ii) a vascular inflammatory phase; Inflammatory markers are often elevated during this phase (iii) a quiescent occlusive phase.
- 12. Introduction • Diagnostic criteria are still somewhat controversial. The diagnosis requires arteriographic narrowing of the aorta, its branches, or large arteries not attributable to atherosclerosis, middle aortic syndrome, or FMD. One distinguishing angiographic feature of TA is the presence of inflammatory thickening or edema of the vascular wall seen on magnetic resonance angiography (MRA), computed tomographic angiography (CTA), or duplex or positron emission tomography. • Treatment is controversial but generally starts with corticosteroids or other immunomodulatory therapy during the inflammatory phase of disease followed by medical or interventional treatment to reduce organ ischemic injury. Criterion Definition Age at disease one ≤40 years Development of symptoms or findings related to Takayasu arteritis at age ≤40 years Claudication of extremities Development and worsening of fatigue and discomfort in muscles of one or more extremities while in use, especially the upper extremities Decreased brachial artery pressure Decreased pulsation of one or both brachial arteries Blood pressure difference >10 mmHg Difference of >10 mmHg in systolic blood pressure between arms Bruit over subclavian arteries or aorta Bruit audible on auscultation over one or both subclavian arteries or abdominal aorta Arteriogram abnormality Arteriographic narrowing or occlusion of the entire aorta, its primary branches, or large arteries in the proximal upper or lower extremities, not due to arteriosclerosis, fibromuscular dysplasia, or similar causes; changes usually foci or segmental
- 13. Renovascular Hypertension 1 Clip 1 Kidney 1 Clip 2 Kidney
- 16. Glomerulopathy • Information of the glomerulonephropathies associated with TA is limited. Most of the glomerulonephropathies associated with TA show the histological feature of mesangial proliferation, such as membranoproliferative glomerulonephritis, immunoglobulin A (IgA) nephropathy, focal segmental glomerulosclerosis and crescentic glomerulonephritis. • Membranous glomerulonephropathy (MG) is a non-mesangial proliferative glomerulonephropathy, and its association with TA is extremely rare.
- 17. Glomerulopathy • Mesangial proliferative glomerulonephropathy is the predominant histological feature among them. de Pablo et al. performed retrospective pathological kidney investigation in 25 autopsy cases of TA. • Their study showed that 10 out of 25 cases (40%) had diffuse mesangial proliferative glomerulonephritis, while 4 (16 %) cases had other forms of glomerulonephritis (focal segmental glomerulosclerosis, global and focal glomerulosclerosis, segmental necrotizing glomerulonephritis and amyloidosis). • To date, only two case reports have described MG associated with TA . Notably, the patients in these reports were also complicated by SLE or lupus-like glomerulonephropathy Complication of TA by SLE is also rare, only approximately 20 cases having been reported. • The patients with both TA and SLE reported by Kitazawa et al. showed intramembranous microspheres and epithelial cytoplasmic processes on the GBM, the findings of so-called podocytic infolding glomerulopathy (PIG). PIG is a relatively new disease entity proposed in 2008 and sometimes associated with lupus nephritis class V.
- 18. Discussion • Patients with TA and renal biopsy-confirmed glomerular disease were investigated retrospectively. None of them had renal artery stenosis or occlusive changes. Results: Six patients with glomerulopathy, accounting for 3.75% of the 6/160 TA patients admitted to our hospital at the same period, were analyzed. All of them were females with a mean age of 35.5 ± 10.0 years. Four cases presented with lower extremity edema. Laboratory tests showed that 1 was nephrotic syndrome, 3 nephrotic range proteinuria, and 2 mild renal dysfunction. • Renal pathology revealed mild immunoglobulin A nephropathy in 2 cases, mild mesangial proliferative glomerulonephritis (GN), membranoproliferative GN, minimal change disease, and fibrillary GN in 1 case respectively. • Five cases received glucocorticoids and cyclophosphamide therapy. Proteinuria and microscopic hematuria disappeared in 2 to 4 weeks after Rx initiation of therapy in three cases. The patient with membranoproliferative GN also reached complete remission/6 months.
- 20. Fig. 1. Microscopic Findings. a Periodic acid-Schiff staining. ×200. The glomeruli are hypertrophic, but thickening of the GBM is not apparent. A mild increase in mesangial matrix is occasionally noted, but mesangial cell proliferation is not obvious. b. Periodic acid methenamine silver staining, ×200. c Magnified view of b, ×400. Spike formation or bubble-like appearance on the capillary walls is not apparent. d Electron microscopic findings. Irregular thickening of the GBM with diffuse sub epithelial immune deposits (arrowheads) is observed along the entire capillary wall. Projection of the GBM (arrows) is noted between adjacent immune deposits, compatible with stage II MG. Intramembranous and sub endothelial immune deposits are not apparent.
- 21. Fig. 2. Immunofluorescence. Diffuse, granular patterns of IgG deposits are observed along the capillaries. Staining intensity of IgG1 and IgG4 is predominant, whereas IgG2 shows weak intensity. Deposition of IgG3 was negative (not shown).
- 22. Fig. 3. Clinical course. Percutaneous angioplasty for left subclavian artery stenosis was performed 5 years previously. Proteinuria was detected 4 months before admission. Kidney biopsy showed stage II MG and three-dimensional CT angiography confirmed the presence of TA. Oral PSL was initiated at a dose of 40 mg daily. CRP was normalized 7 days after the initiation of PSL therapy. Proteinuria decreased gradually. Three month later, proteinuria became <0.15 g/gCr. Eighteen months later, nephrotic syndrome and TA remain remitted with 5 mg PSL daily. During the clinical course, CRP increased twice due to colds. UP/UCr = Urinary protein to creatinine ratio.
- 23. Conclusion TA may induce glomerular disease as a part of its histological spectrum. Apart from ischemic glomerular disease, glomerular disease should be suspected when TA patients have microscopic hematuria or proteinuria, that may be therapeutically responsive to glucocorticoids and immunosuppressive agent in relative early phase. Mesangial proliferative glomerulonephropathy is more common than a non- mesangial MG, but it could be manifested with TA. Since information is extremely limited, further reports are needed to shed light on glomerular disease associated with TA.
- 24. References
- 25. Thank You!!!
Editor's Notes
- PSV Peak Systolic Velocity A renal/aortic ratio greater than 3.5 predicts renal artery stenosis (RAS) greater than 60% with a sensitivity of 84% to 91% and a specificity of 95% to 97%.
- Takayasu arteritis is named in honor of Japanese ophthalmologist Mikito Takayasu, who first reported a case of the disease in 1905. His patient was a 21-year-old woman with retinal vessel changes and decreased pulses in branches of the aortic arch. In April 1908, Dr. Mikito Takayasu (Fig. 1), a professor of ophthalmology at the current Kanazawa University, at the 12th Annual Meeting of Japanese Ophthalmology Society held in Fukuoka, reported a case of a 22-year-old woman. He described ‘a case of peculiar changes in the central retinal vessels’.2 He saw the female patient for the first time in May 1905. She had felt lowering and blurring of her vision since September 1904. She sometimes developed redness of conjuctiva. While the symptoms transiently improved by medication, they recurred in March 1905 and she visited Dr. Takayasu. She did not have a history of severe medical or gynecological diseases. While he described that she looked as if she suffered from tuberculosis (TB), he and his colleagues in the Department of Internal Medicine did not find any evidence of infection, including TB or syphilis. Her pupils were slightly dilated and the light reflex was damaged. He found eminent abnormalities in retinal vessels. Retinal vessels branched 2–3 mm away from the optic disc and the branches formed anastomosis with one another to create circularity around the disc. The branches branched further radially and the peripheral portions were narrow. The distal parts of the branches made aneurysms, anastomosis with other branches to form circularity, or terminated in a blind end. The optic disc was severely congested and hemorrhage was found around the disc. While these abnormalities were mainly found in arteries, veins anastomosed with arteries and venous blood flowed into the lesions. While he found these abnormalities in the oculus dexter, similar findings were reported in the oculus sinister. She was admitted and took medications. During the first admission, she was found to have cataracts and underwent an operation. However, her vision did not improve. She stopped visiting the hospital for several years after discharge. She revisited Dr. Takayasu's clinic in February 1908. She developed retinal detachment and her left pupil was remarkably dilated. Dr. Takayasu had no choice but to tell her that there was no effective treatment. He described that the anastomosis and aneurysmal changes should be the primary findings and that the others should be the secondary findings. After his presentation at the Congress, Dr. Yoshiakira Ohnishi, a professor at Kyushu University, mentioned another female case resembling the case presented by Dr. Takayasu. He described that he could not sense her pulse at the bilateral radial arteries. This case report by Dr. Takayasu was published in June in the same year in the Journal of the Juzen Medical Society in Kanazawa University (Fig. 2). In this manuscript, he presented an image of the arteries that he beautifully hand-sketched himself (Fig. 3). While it is often regarded that it was Dr. Takayasu who first reported a patient with TAK, there are other prior potential case reports of patients with TAK. Giovanni Battista Morgagni, an Italian anatomist, described a 40-year-old woman suffering from pulseless disease.3 In 1830, Rokushu Yamamoto described a 45-year-old man suffering from fever.4 After 1 year, the patient became pulseless in the right radial artery and had a very weak pulse in the left radial artery. The patient developed pulseless disease in both carotid arteries and died 11 years after the first visit. He described two other cases reported by another doctor. In 1856, Savory5 reported a 22-year-old woman presenting with pulseless disease in both upper extremities and left neck. The patient lost her vision. However, whether these cases truly suffered from TAK is uncertain. Numano4 suspected the case reported by Savory should be explained by other diseases since the patient had a corneal ulcer leading to invasion of scalp and brain. Dr. Minoru Nakajima in 1921 compared his cases with previous reports and proposed that they should be regarded as one disease. He characterized this disease by the following four criteria: (i) affecting bilateral eyes in young women; (ii) arteriovenous anastomosis around the optic disc and microaneurysm formation in retinal vessels; (iii) lowering of vision complicated with cataract; and (iv) unpalpable radial artery. He proposed to call this disease ‘Takayasu disease’. After his proposal, Japanese ophtalmologists paid attention to this disease and many cases were reported. In 1946, Frövig6 proposed that the diseases presenting pulselessness should be called ‘aortic arch syndrome’. In 1948, Drs Kentaro Shimizu and Keiji Sano, brain surgeons at the University of Tokyo, proposed to give an alias name of ‘pulseless disease’. In 1951, this disease was reported by these doctors outside of Japan for the first time, by reviewing a total of 25 cases.7 Since 1951, there have been case reports from a number of foreign countries. In 1952, Caccamise and Whitman8 reported the primary occidental case report. In 1962, Judge et al.9 described ‘Takayasu's arteritis’. In Japan, many doctors proposed acronyms of TAK. Drs Maekawa and Kakei called it ‘occlusive coagulant aortic syndrome’.10 Dr. Nasu11 called it ‘obstructive productive arteritis’. In 1965, Riehl et al.12 analyzed this disease from pathological and immunological aspects and proposed the concept that this disease is an autoimmune disease. Since 1990 when the American College of Rheumatology published a classification criteria of TAK13 and described ‘Takayasu arteritis’, the name of TAK prevailed worldwide. Although both ‘Takayasu arteritis’ and ‘Takayasu's arteritis’ are used, in the Online Mendelian Inheritance in Man (OMIM) it is registered as ‘Takayasu arteritis’ and this expression is more commonly used. The case report by Dr. Takayasu is quite suggestive. His report tells us that we should carefully examine and observe patients to find characteristics of the patients. Even if we saw just one case, there is a possibility that many patients exist with the same symptoms. It is impressive that Dr. Takayasu described the first patient as being similar to patients with TB. In fact, there are studies pointing out the overlapping of TB and TAK.14, 15 Geographical prevalence of TAK is similar to that of TB. Although there are many conflicting studies in terms of epidemiology and immunology,16 there is a possibility that exposure to TB triggers the immune reaction to TAK. In fact, my group showed that the susceptibility variant is located in the IL12B region17 and this variant has previously been reported in relation to mycobacterium infection.
- Takayasu’s arteritis (TA) is an autoimmune disease that accompanies the active inflammation of relatively large-sized vessels like the aorta and its primary branches. Kimura et al. demonstrated the association of HLA-B52 and HLA-B39.2 with TA in the Japanese population. Major histocompatibility class I chain-related A, Th17 cells, NK cells or inflammatory cytokines like VEGF and IL-6 have been clarified to be involved in the pathogenesis of TA, however, the exact pathogenesis remains to be elucidated. In half of cases, identification of arterial stenosis is preceded by a prodromal illness characterized by fever, night sweats, malaise, and weight loss. Inflammatory markers are often elevated during this phase. After this active inflammatory phase, vascular stenosis can lead to sequelae including RVH, kidney dysfunction, stroke, cerebral hemorrhage, myocardial infarction, or CHF, depending on sites of involvement.
- The American College of Rheumatology has established classification criteria for Takayasu arteritis, which were primarily designed to distinguish this disorder from other forms of vasculitis. These criteria have a sensitivity and specificity of 90.5 and 97.8 percent, respectively
- Fig. 41.2 Pathogenesis of renovascular hypertension in one-kidney versus two-kidney model. (A) In unilateral stenosis with two kidneys, opposing forces between the stenotic kidney, which has reduced perfusion pressures, and the nonstenotic contralateral kidney, which has increased perfusion pressures, result in laboratory and clinical features of angiotensin-dependent hypertension. (B) In unilateral stenosis with a solitary functioning kidney or in a patient with bilateral critical renal artery stenosis, reduced perfusion pressure to the stenotic kidney in the absence of a normal kidney excreting sodium leads to sodium and volume retention, ultimately associated with hypertension without persistent activation of the RAS.
- Fig. 41.8 Evaluation and management of renovascular disease. The intensity of imaging and revascularization depends on both the level of kidney function and the blood pressure (BP), in addition to the comorbid disease risks for the individual patient. The overall goal should focus on stable kidney function and BP levels. As with any other vascular disease, monitoring for disease progression and recurrence is an important element of long-term management. ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CTA, computed tomographic angiography; F/U, follow-up; MRA, magnetic resonance angiography; PTRA, percutaneous transluminal renal angioplasty; RAAS, renin-angiotensin-aldosterone system.
- A 54-year-old man with hyperlipidemia developed chance proteinuria during routine medical checkup. Within the next 4 months, edema in his lower limbs worsened with progression of hypoalbuminemia and increment in urinary protein excretion. He was referred to the nephrology department of our facility for the evaluation of proteinuria. Five years previously, he felt discomfort and coldness in his left hand and noted difficulty in detecting the peripheral pulse of the left radial artery. Further medical evaluation revealed left subclavian artery stenosis and he underwent percutaneous angioplasty with stent placement. This episode suggests the possibility of TA, however, the diagnosis was not made at that time. Upon admission, his temperature was 36.8°C, blood pressure 130/81 mm Hg (right arm) and 128/83 mm Hg (left arm), and pulse 70 beats per minute with regular rhythm. Auscultation of the chest, lungs and abdomen was normal. Vascular bruit was audible on his neck bilaterally. The peripheral arteries (brachial, radial, popliteal and dorsal pedal) were palpable without laterality. Edema of the lower extremities was moderate. Skin rashes were not detected. Neurological findings were unremarkable. Laboratory data was as follows: WBC 13,300/μl, Hb 14.7 g/dl, platelets 36.2 × 104/μl, BUN 7 mg/dl, creatinine 0.6 mg/dl, total protein 6.1 g/dl (α-1 4.7%, α-2 15.5%, β 15.7%, γ 22.7% without monoclonal peak), albumin 1.85 g/dl, LDL-cholesterol 160 mg/dl, fasting plasma glucose 96 mg/dl, hemoglobin A1c 5.4%, C-reactive protein (CRP) 1.23 mg/dl (normal 0.00–0.25), erythrocyte sedimentation rate 34 mm/h, immunoglobulin G (IgG) 870 mg/dl, IgA 110 mg/dl, immunoglobulin M (IgM) 35 mg/dl, C3 178.6 mg/dl (normal 65.0–135.0), and C4 46.1 mg/dl (normal 13.0–35.0). Serology for antistreptolysin-O, hepatitis B, hepatitis C, anti-nuclear antibody, anti-double-stranded DNA antibody, and MPO and PR3 anti-neutrophil cytoplasmic antibody was negative. Cryoglobulin was not detected. Plasma renin activity was 2.6 ng/ml/h (normal 0.3–5.4 ng/ml/h) and plasma aldosterone concentration was 17 pg/ml (normal 36–240). Urinalysis demonstrated protein (4+) without hematuria. Daily urinary protein excretion was 11.1 g. Ultrasonography showed morphologically normal kidneys. Familial history was unremarkable. A kidney biopsy was performed (fig. 1, fig. 2); a total of 19 glomeruli were obtained from two pieces of specimen. Two glomeruli were globally sclerosed, the remaining 17 glomeruli were hypertrophic. Intraglomerular hypercellularity, adhesion or crescent formation were not observed. Mesangial matrix proliferation was not conspicuous and mesangial cell proliferation was absent. The thickness of the glomerular basement membrane (GBM) was almost normal and typical spike formation or bubble-like appearance was not obvious. Tubular atrophy, fibrosis and lymphocyte infiltration were mild in the interstitial space. Hyalinosis and moderate thickening of the vessel wall was noted in the intralobular arteries and arterioles. Inflammatory changes on the vascular walls were not apparent. Under immunofluorescence microscopy, IgG was found in a granular pattern along the GBM. Analysis of IgG subclass revealed strong deposition of IgG1 and IgG4 as well as mild deposition of IgG2. Staining for IgA, IgM, C3, C4, C1q and fibrinogen were negative. Under electron microscopy, foot process effacement and extensive subepithelial electron dense deposits with the projection of basement membrane between adjacent immune deposits were broadly observed. Endothelial tubuloreticular inclusions were not observed. Stage II MG was diagnosed. Malignancy survey including chest X-ray, CT scan, testing the stool for blood, upper gastrointestinal endoscopy, measurement of tumor markers (CEA, CA19-9, PSA) demonstrated no significant abnormality. The patient’s previous medical history of left subclavian artery stenosis strongly implied the presence of TA. After kidney biopsy, enhanced CT scan showed extensive thickening and enhancement of the vascular wall from the ascending portion to the abdominal aorta, resulting in narrowed and tortuous lumen. Involvement of the brachiocephalic trunk and bilateral vertebral arteries was detected, however, the bilateral renal arteries were unaffected. Considering the previous episode of subclavian artery stenosis, this patient met at least 3 of 6 American College of Rheumatology criteria (decreased brachial artery pulse, blood pressure difference >10 mm Hg and arteriogram abnormality) for the classification of TA [8]. TA was diagnosed and oral prednisolone (PSL) was initiated at a dose of 40 mg/day. Seven days after the PSL therapy, the CRP level had decreased to normal. Three month later, the urinary protein to creatinine ratio became <0.15 g/gCr. Enhanced CT scan 1 year later showed improvement of wall thickening in the entire aorta. PSL was gradually tapered to 5 mg daily and he remains free from relapse of both MG and TA (fig. 3)
- Primary MG IgG4 > IgG1, IgG3; IgA, IgM absent Mesangial Ig staining absent C1q negative or weak PLA2R positive and co-localizes with IgG Secondary MG IgG1, IgG3 > IgG4; IgA, IgM may be present Mesangial Ig staining may be present C1q positive PLA2R negative
- Though the true relationship between MG and TA was not revealed in present case, considering the fact that complete remission of nephrotic syndrome occurred following the improvement of C-reactive protein level in response to steroid therapy, TA might be the secondary cause of MG.
- References 1 Alibaz-Oner F, Aydin SZ, Direskeneli H: Advances in the diagnosis, assessment and outcome of Takayasu’s arteritis. Clin Rheumatol 2013;32:541–546. 2 Kuroda T, Ueno M, Sato H, Murakami S, Sakatsume M, Nishi S, Nakano M, Gejyo F: A case of Takayasu arteritis complicated with glomerulonephropathy mimicking membranoproliferative glomerulonephritis: a case report and review of the literature. Rheumatol Int 2006;27:103–107. 3 Cavatorta F, Campisi S, Trabassi E, Zollo A, Salvidio G: IgA nephropathy associated with Takayasu’s arteritis: report of a case and review of the literature. Am J Nephrol 1995;15:165–167. 4 Tiryaki O, Buyukhatipoglu H, Onat AM, Kervancioglu S, Cologlu S, Usalan C: Takayasu arteritis: association with focal segmental glomerulosclerosis. Clin Rheumatol 2007;26:609–611. 5 Hellmann DB, Hardy K, Lindenfeld S, Ring E: Takayasu’s arteritis associated with crescentic glomerulonephritis. Arthritis Rheum 1987;30:451–454. 6 Kitazawa K, Joh K, Akizawa T: A case of lupus nephritis coexisting with podocytic infolding associated with Takayasu’s arteritis. Clin Exp Nephrol 2008;12:462–466. 7 Nakashima A, Miyazaki R, Koni I, Tsugawa Y, Iwainaka Y, Kawano M, Tofuku Y, Takeda R: A case of aortitis syndrome (Takayasu’s arteritis) associated with glomerulonephropathy mimicking lupus membranous glomerulonephropathy (in Japanese). Nihon Jinzo Gakkai Shi 1988;30:233–238. 8 Arend WP, Michel BA, Bloch DA, Hunder GG, Calabrese LH, Edworthy SM, Fauci AS, Leavitt RY, Lie JT, Lightfoot RW Jr: The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990;33:1129–1134. 9 Kimura A, Kitamura H, Date Y, Numano F: Comprehensive analysis of HLA genes in Takayasu arteritis in Japan. Int J Cardiol 1996;54(suppl):S61–S69. 10 Weyand CM, Goronzy JJ: Medium- and large-vessel vasculitis. N Engl J Med 2003;349:160–169. 11 de Pablo P, García-Torres R, Uribe N, Ramón G, Nava A, Silveira LH, Amezcua-Guerra LM, Martínez-Lavín M, Pineda C: Kidney involvement in Takayasu arteritis. Clin Exp Rheumatol 2007;25(1 suppl 44):S10–S14. 12 Igarashi T, Nagaoka S, Matsunaga K, Katoh K, Ishigatsubo Y, Tani K, Okubo T, Lie JT: Aortitis syndrome (Takayasu’s arteritis) associated with systemic lupus erythematosus. J Rheumatol 1989;16:1579–1583. 13 Joh K, Taguchi T, Shigematsu H, Kobayashi Y, Sato H, Nishi S, Katafuchi R, Nomura S, Fujigaki Y, Utsunomiya Y, Sugiyama H, Saito T, Makino H: Proposal of podocytic infolding glomerulopathy as a new disease entity: a review of 25 cases from nationwide research in Japan. Clin Exp Nephrol 2008;12:421–431. 14 Beck LH Jr, Bonegio RG, Lambeau G, Beck DM, Powell DW, Cummins TD, Klein JB, Salant DJ: M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med 2009;361:11–21. 15 Haas M: IgG subclass deposits in glomeruli of lupus and nonlupus membranous nephropathies. Am J Kidney Dis 1994;23:358–364