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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
LETTER TO THE EDITOR  
Year : 2014  |  Volume : 25  |  Issue : 6  |  Page : 1308-1311
A case of minimal change disease complicated by acute kidney injury in systemic lupus erythematosus


Nephrology Unit, Department of Medicine, Hospital Queen Elizabeth, Kota Kinabalu, Sabah, Malaysia

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Date of Web Publication10-Nov-2014
 

How to cite this article:
Wong KW. A case of minimal change disease complicated by acute kidney injury in systemic lupus erythematosus. Saudi J Kidney Dis Transpl 2014;25:1308-11

How to cite this URL:
Wong KW. A case of minimal change disease complicated by acute kidney injury in systemic lupus erythematosus. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2019 May 21];25:1308-11. Available from: http://www.sjkdt.org/text.asp?2014/25/6/1308/144295
To the Editor ,

The World Health Association (WHO) Clas­sification of lupus nephritis was first intro­duced in 1974, which was then modified in 1982. [1] By definition, any biopsy showing glomeruli that are normal by all techniques (light and electron microscopy and negative immunofluorescence) should be classified as Class Ia. The classification was further revised to the latest International Society of Nephrology/ Renal Pathology Society (ISN/RPS) classifi­cation in 2003. [1] In the latest classification, the biopsy of glomeruli with no immune deposits by immunofluorescence cannot be included into the diagnosis of lupus nephritis. However, there have been a few reports since 1989 of minimal change disease associated with sys­temic lupus erythematosus (SLE). We encoun­tered a case of SLE who presented with acute kidney injury requiring temporary hemodialysis, nephrotic syndrome and biopsy showing minimal change disease.

A 33-year-old lady was diagnosed SLE since 2000, when she presented with polyarthritis, malar rash, alopecia with vasculitic lesions and low complement levels. She had a cutaneous flare in 2003 and was treated with intravenous methylprednisolone and cyclophosphamide. Her ANA was positive, 1:1280 with speckled pattern, but anti-dsDNA was negative. She also had a history of bronchiectasis since 2000, the cause of which was unknown. Her lupus had been in the quiescent phase since 2005 and her oral steroid had been stopped. She was put on oral hydroxychloroquine as maintenance. She had no history of ingestion of non-steroidal anti-inflammatory drugs (NSAIDs). She presented in March 2011 with acute kidney injury and with features of nephrotic syn­drome. She was grossly edematous and her blood pressure was 91/52 mm Hg, with serum albumin 11 g/L, 24-h urine protein of 2.25 g/ day, serum creatinine of 517 umol/L, urea 49 mmol/L and normal C3C4. Urine protein was 4+ and urine red cells was 3+. In view of her progressively rising urea and creatinine, she was dialysed temporarily via a non-cuffed double-lumen catheter. She was given one dose of intravenous cyclophosphamide 750 mg because we suspected that it was active lupus nephritis Class III or IV. It was followed by high-dose oral prednisolone (1 mg/kg/day).

A percutaneous renal biopsy was performed. The renal histopathology showed two cores of renal cortex containing up to 16 glomeruli. One glomerulus showed global sclerosis and the others showed minor changes exhibiting mild mesangial expansion with mild mesangial hypercellularity. A tip lesion was noted at the focal area, but most glomeruli showed no remarkable changes. There were no active lesion and no obvious subepithelial spikes noted. The tubular epithelial cells showed marked cytoplasmic swelling and vacuolation with bleeds, and the vessels showed no ab­normality. The immunofluorescence repeated twice was negative. The biopsy basically showed features of acute tubular injury and the glomeruli showed minor changes with mild mesangial alteration. The impression of the renal biopsy was minimal change disease with acute tubular injury. Her clinical condition improved rapidly, with recovery of renal function. Alto­gether she required four dialysis sessions. Her serum creatinine was normal upon discharge from the hospital. She remained proteinuric on urine analysis on discharge, but went into re­mission by the 3 rd month of the high dose oral prednisolone which was then tapered down to a maintenance dose of 10 mg daily. Subse­quently, she had two more relapses (December 2010 and July 2012), both of which responded to high-dose oral steroid for two months. Since the diagnosis of her minimal change disease, she had no other features of active clinical lupus activity and her C3 and C4 were checked a few times since and were noted to be normal. She was not on any other additional immunosuppressives.

The histopathological diagnosis of minimal change disease was a surprise to us as we expected a diagnosis of more aggressive proliferative lesions. The normal complement le­vels were against the diagnosis of an active lupus renal flare. Clinically, she had no active cutaneous lesions suggestive of lupus flare. There was also no evidence of amyloidosis in the histology, even though this patient had a long-standing history of bronchiectasis diag­nosed since 2000. The fact that this patient res­ponded well to steroid, the history of relapses and the renal biopsy findings correlated well with the diagnosis of minimal change disease.

From the literature review, there have been about 30 cases reported of minimal change disease in SLE since 1989 [Table 1]. [2],[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18] Early on, many of the cases were reported from Japan and also from Korea. [1],[2],[3],[4],[5],[7],[9],[10],[13],[14],[15],[16] Later on, increasingly more cases are being noted from the Western countries. [6],[8],[11],[12],[17],[18]
Table 1: Thirty cases of SLE that showed an association with minimal change disease

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The nephrotic syndrome due to minimal change disease may present before the diag­nosis of SLE, along with it or long after the SLE diagnosis. Most of the cases were females (including ours) and only two were males. [3],[11] In some cases, as in ours, the nephrotic syndrome was associated with renal impair­ment, and most resolved as the disease respon­ded to steroid. Dube et al [11] described seven cases, with various ethnic groups of white, African-American and Hispanic. Three of the cases had a history of NSAIDs or celecoxib ingestion prior to the development of nephrotic syndrome. All of them responded to steroid and the NSAIDs were stopped. Four patients presented with renal impairment, which im­proved with response to steroid.

Class II lupus nephritis was believed to cause a mild to moderate degree of proteinuria and was unlikely to result in nephrotic syndrome. However, there were reports in which nephrotic syndrome was associated with Class II lupus nephritis. [18] Therefore, the authors con­cluded that the nephrotic syndrome was most likely due to the minimal change nephropathy.

Almost all cases reported were treated with steroid, and all were documented to be steroid sensitive. Hong et al [16] treated the patient with mycophenolate mofetil, presumably due to ste­roid toxicity, and the patient responded too. A few cases were noted to relapse, as happened to our patient as well, and they again res­ponded to re-introduction of high-dose steroid.

The causal relationship between SLE and minimal change disease is still unclear. A few authors have suggested that the two were linked, and that minimal change disease should be considered as a type of lupus nephritis. [19] Hertig et al in their analysis of 11 SLE patients who developed nephrotic syndrome suggested that there might be a relevant association between the two diseases, and that SLE itself could be a precipitating factor for the nephrotic syndrome. [12]

In conclusion, minimal change disease is rarely diagnosed in patients with SLE and, with the current classification, there is no re­cognition of this entity in SLE. Our case indi­cates the fact that this classification may be flawed, but further studies are still needed to confirm the relationship between the two diseases.


   Acknowledgment Top


The author would like to thank the Director General of Ministry of Health, Malaysia for the approval to publish this paper.

Conflict of Interest: None.

 
   References Top

1.
Weening JJ, D'Agati VD, Schwartz MM, et al. The Classification of Glomerulonephritis in Systemic Lupus Erythematosus Revisited. J Am Soc Nephrol 2004;15:241-50.  Back to cited text no. 1
    
2.
Matsumura N, Dohi K, Shiiki H, et al. Three cases presenting with systemic lupus erythematosus and minimal change nephrotic syn­drome. Nihon Jinzo Gakkai Shi 1989;31:991-9.  Back to cited text no. 2
    
3.
Okai T, Soejima A, Suzuki M, et al. A case report of lupus nephritis associated with mini­mal change nephrotic syndrome -comparison of various histological types of 67 cases with lupus nephritis. Nihon Jinzo Gakkai Shi 1992; 34:835-40.  Back to cited text no. 3
    
4.
Makino H, Haramoto T, Shikata K, Ogura T, Ota Z. Minimal-change nephrotic syndrome associated with systemic lupus erythematosus. Am J Nephrol 1995;15:439-41.  Back to cited text no. 4
    
5.
Horita Y, Nazneen A, Cheng M, et al. A case of systemic lupus erythematosus associated with minimal change nephrotic syndrome. Nihon Jinzo Gakkai Shi 1997;39:759-64.  Back to cited text no. 5
    
6.
Guery B, Martinez F, Beaufils H, Deray G. Minimal-change nephropathy associated with systemic lupus erythematosus. Nephrol Dial Transplant 1997;12:2030-1.  Back to cited text no. 6
    
7.
Nishihara G, Nakamoto M, Yasunaga C, et al. Systemic lupus erythematosus in a patient with remitting minimal change nephrotic syndrome. Clin Nephrol 1997;48:327-30.  Back to cited text no. 7
    
8.
Perakis C, Arvanitis A, Sotsiou F, Emmanouel DS. Nephrotic syndrome caused by minimal-change disease in a patient with focal proliferative SLE nephritis (WHO III) in remission. Nephrol Dial Transplant 1998;13:467-70.  Back to cited text no. 8
    
9.
Sugimoto T, Yamasaki Y, Kobayashi M, et al. A case of minimal change nephrotic syndrome manifesting acute renal failure in the course of systemic lupus erthematosus. Nihon Jinzo Gakkai Shi 2002;44:476-82.  Back to cited text no. 9
    
10.
Seo DB, Lee SW, Song JH, Lee KJ, Han JY, Kim MJ. Acute renal failure associated with a minimal change nephrotic syndrome in a sys­temic lupus erythematosus patient. Yonsei Med J 2002;43:114-8.  Back to cited text no. 10
    
11.
Dube GK, Markowitz GS, Radhakrishnan J, Appel GB, D'Agati VD. Minimal change disease in systemic lupus erythematosus. Clin Nephrol 2002;57:120-6.  Back to cited text no. 11
    
12.
Hertig A, Droz D, Lesavre P, Grunfeld JP, Rieu P. SLE and Idiopathic Nephrotic Syn­drome: Coincidence or Not? Am J Kidney Dis 2002;40:1179-84.  Back to cited text no. 12
    
13.
Horino T, Takao T, Morita T, Ito H, Hashimoto K. Minimal change nephrotic syndrome asso­ciated with systemic lupus erythematosus. Nephrol Dial Transplant 2006;21:230.  Back to cited text no. 13
    
14.
Wang YT, Chou HH, Chen FF, Chen MJ, Chiou YY. A case of minimal-change nephrotic syndrome in pediatric lupus erythematosus: Just a coincidence? Lupus 2006;15:244-7.  Back to cited text no. 14
    
15.
Deji N, Sugimoto T, Kanasaki M, et al. Emer­ging minimal-change nephrotic syndrome in a patient with chronic mesangial proliferative lupus nephritis. Intern Med 2007;46:991-5.  Back to cited text no. 15
    
16.
Hong YH, Yun DY, Jung YW, Oh MJ, Kim HJ, Lee CK. A case of minimal change disease treated successfully with mycophenolate mofetil in a patient with systemic lupus erythematosus. Korean J Intern Med 2011;26:470-3.  Back to cited text no. 16
    
17.
Moysés-Neto M, Costa RS, Rodrigues FF, et al. Minimal Change Disease: A variant of lupus nephritis. NDT(Plus) 2011;4:20-2.  Back to cited text no. 17
    
18.
Redondo-Pachón MD, Enríquez R, Sirvent AE, Andrada E, Millán I, Amorós F. Minimal-change nephropathy in systemic lupus erythematosus. Nefrologia 2012;32:412-3.  Back to cited text no. 18
    
19.
Stankeviciute N, Jao W, Bakir A, Lash JP. Mesangial lupus nephritis with associated nephrotic syndrome. J Am Soc Nephrol 1997; 8:1199-204.  Back to cited text no. 19
    

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Correspondence Address:
Dr. Koh-Wei Wong
Nephrology Unit, Department of Medicine, Hospital Queen Elizabeth, Kota Kinabalu, Sabah
Malaysia
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DOI: 10.4103/1319-2442.144295

PMID: 25394457

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