Dermatomyositis Sine Myositis with Membranoproliferative Glomerulonephritis

Owlia, Mohammad Bagher; Hemayati, Roya; Taghipour Zahir, Shokouh; Moeini Nodeh, Mohammad

doi:10.1155/2012/751683

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Dermatomyositis Sine Myositis with Membranoproliferative Glomerulonephritis

case-report

Author(s): Mohammad Bagher Owlia ¹ ^, ^* , Roya Hemayati ² , Shokouh Taghipour Zahir ³ , Mohammad Moeini Nodeh ⁴

Publication date (Electronic): 13 August 2012

Journal: Case Reports in Rheumatology

Publisher: Hindawi Publishing Corporation

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Abstract

Dermatomyositis (DM) is an autoimmune disease that is characterized by involvement of proximal musculature and skin. We report a 52-year-old woman with a 6-year history of dermatomyositis sine myositis, who developed lower extremity edema and proteinuria. Pathological examination of renal biopsy showed membranoproliferative glomerulonephritis. She received steroid, cyclophosphamide, and mycophenolate mofetil. Over the 9 to 10 months after the beginning of treatment, the proteinuria was improved.

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Most cited references 13

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Renal involvement in patients with polymyositis and dermatomyositis.

C. Chen, Charles P. Lai, S Hsueh … (2005)

Renal involvement in patients with polymyositis (PM)/dermatomyositis (DM) is previously thought to be uncommon, but two main types of renal lesion have been described. First, acute tubular necrosis with renal failure related to myoglobulinemia and myoglobulinuria is a well-recognised feature of acute rhabdomyolysis. Second, chronic glomerulonephritis has been infrequently reported in a small group of patients with PM/DM. This study aims at investigating the incidence, severity and prognosis of renal disease in PM/DM patients, admitted to a single centre in a 10-year interval. The hospital records of 65 Taiwanese patients with PM/DM, examined between 1992 and 2002, were studied retrospectively. Of the 65 patients, 14 were found to have suffered varying degree of renal involvement, and the incidence rate was 21.5%. All the 14 patients had varying degree of haematuria and proteinuria. Acute tubular necrosis with renal failure developed in four patients with PM and in five patients with DM. Renal biopsy in two DM patients with overt proteinuria revealed IgA nephropathy in one and membranous nephropathy in the other. We, therefore, concluded that renal involvement in PM/DM patients is not as uncommon as previously thought.

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Patterns of complement activation in idiopathic membranoproliferative glomerulonephritis, types I, II, and III.

William Varade, Judith Forristal, Clark D. West (1990)

Complement profiles on 22 hypocomplementemic patients with membranoproliferative glomerulonephritis (MPGN) type I, on 11 with MPGN II, and on 16 with MPGN III, gave evidence that the nephritic factor of the amplification loop (NFa) is responsible for the hypocomplementemia in MPGN II and the nephritic factor of the terminal pathway (NFt) for the hypocomplementemia in MPGN III. In contrast, in MPGN I, there was evidence for three complement-activating modalities, NFa, NFt, and immune complexes. As a result, four different patterns of complement activation were seen. NFa, found in MPGN II, produces a complement profile characterized mainly by C3 depression. In addition, four of seven (57%) severely hypocomplementemic MPGN II patients (C3 less than 30 mg/dL) had slightly depressed levels of factor B, and one of seven (14%) of properdin, but in all the C5 concentration was normal. In contrast, all eight severely hypocomplementemic patients with MPGN II had depressed C5 and properdin levels, and six of eight (75%) depressed levels of C6, C7, and/or C9. Of eight MPGN III patients with moderate hypocomplementemia, 50% had depressed C5 and properdin levels and the remainder, depressed C3 only. This spectrum of profiles is most likely produced by varying concentrations of NFt. In MPGN I, nine of 23 (39%) had a profile indicating only classical pathway activation; seven of 23 (39%), a pattern compatible with NFt alone; four of 23 (9%), evidence for both classical pathway activation and NFt; and three of 23 (13%), a pattern compatible with NFa. The unique multifactorial origin of the hypocomplementemia in MPGN I, often giving evidence of classical pathway activation, together with previously reported differences in glomerular morphology and clinical features at onset, makes it distinct from MPGN III. Depressed C8 levels were found to some extent in all hypocomplementemic states. The levels were uncommonly depressed in patients with NFa, most markedly depressed with NFt, and moderately reduced with classical pathway activation. The cause is not known. Diagnostically, profiles showing classical pathway activation and low levels of C6, C7, and/or C9 are specific for MPGN I. Those showing only classical activation are likewise diagnostic of MPGN I if systemic lupus erythematosus (SLE) and chronic bacteremia are ruled out.

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Unexpected IgA nephropathy during the treatment of a young woman with idiopathic dermatomyositis: case report and review of the literature.

Tzung-Hai Yen, Jeng-Yi Huang, Chen-Yin Chen (2015)

This article reports the unexpected discovery of IgA nephropathy in a 26-year-old Chinese woman 1.5 years after the onset of idiopathic dermatomyositis. The patient was taking immunosuppressive agents, prednisolone 25 mg and azathioprine 75 mg daily. Glomerulonephritis associated with idiopathic polymyositis/dermatomyositis is rare. A review of the medical literature indicates that the most common pattern seen in idiopathic polymyositis is mesangial proliferative glomerulonephritis. However, both membranous and mesangial proliferative glomerulonephritis are often seen in idiopathic dermatomyositis. It is still not clear, however, whether the humorally- mediated immune process in dermatomyositis and the cell-mediated immune process in polymyositis can explain the different patterns of occurrence of glomerular lesions in these two closely related disease entities.

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Author and article information

Journal

Journal ID (nlm-ta): Case Rep Rheumatol

Journal ID (iso-abbrev): Case Rep Rheumatol

Journal ID (publisher-id): CRIM.RHEUMATOLOGY

Title: Case Reports in Rheumatology

Publisher: Hindawi Publishing Corporation

ISSN (Print): 2090-6889

ISSN (Electronic): 2090-6897

Publication date (Print): 2012

Publication date (Electronic): 13 August 2012

Volume: 2012

Electronic Location Identifier: 751683

Affiliations

¹Department of Rheumatology, Shahid Sadoughi University of Medical Sciences, Yazd 89168-86938, Iran

²Department of Nephrology, Shahid Sadoughi University of Medical Sciences, Yazd 89168-86938, Iran

³Department of Pathology, Shahid Sadoughi University of Medical Sciences, Yazd 89168-86938, Iran

⁴Department of Internal Medicine, Shahid Sadoughi University of Medical Sciences, Yazd 89168-86938, Iran

Author notes

*Mohammad Bagher Owlia: bagherowlia@ 123456gmail.com

Academic Editors: H. Alexanderson, G. O. Littlejohn, J. C. Nossent, M. Salazar-Paramo, and A. Zoli

Article

DOI: 10.1155/2012/751683

PMC ID: 3424642

PubMed ID: 22937456

SO-VID: 5797b4c9-86ef-4c84-8e83-b7125f3232f6

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.