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Year : 2013  |  Volume : 2  |  Issue : 3  |  Page : 168

Multiple myeloma presenting with focal segmental glomerulosclerosis

1 Department of Hematology/Medical Oncology, Urmia University of Medical Sciences, Urmia, Iran
2 Department of Nephrology, Urmia University of Medical Sciences, Urmia, Iran
3 Department of Pathology, Urmia University of Medical Sciences, Urmia, Iran
4 Urmia University of Medical Sciences, Urmia, Iran

Date of Web Publication27-Jun-2013

Correspondence Address:
Nasim Valizadeh
Department of Hematology/Medical Oncology, Urmia University of Medical Sciences, Urmia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2278-330X.114146

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How to cite this article:
Valizadeh N, Makhdomi K, Noroozinia F, Behzadi F. Multiple myeloma presenting with focal segmental glomerulosclerosis. South Asian J Cancer 2013;2:168

How to cite this URL:
Valizadeh N, Makhdomi K, Noroozinia F, Behzadi F. Multiple myeloma presenting with focal segmental glomerulosclerosis. South Asian J Cancer [serial online] 2013 [cited 2020 Jun 1];2:168. Available from:

Dear Editor,

Focal segmental glomerulosclerosis (FSGS) is a non-inflammatory glomerulopathy characterized by nephritic range proteinuria and can lead to end-stage renal disease (ESRD) without treatment. [1]

FSGS has idiopathic and secondary forms. There are few reports regarding FSGS in patients with plasma cell disorders, in whom treatment of plasma cell disorders could resolve FSGS and prevent from ESRD. [2],[3],[4],[5]

We present a case of multiple myeloma (MM) preceding with FSGS and leading to ESRD before diagnosis of MM.

A 63 year old male was admitted with ESRD. Past medical history was positive for renal stones and recurrent urinary tract infections (UTIs). Seven months ago he had been admitted and undergone a renal biopsy due to proteinuria, hematuria, and renal failure, and histopathological findings showed renal tissue with 20 glomeruli in periodic acid schiff (PAS) stain, total 3 sclerotic glomeruli, segmental mild mesangial hypercellularity with mild mesangial matrix in 10 glomeruli and normal looking appearance in 7 glomeruli. Tubulointerstitium showed patchy to diffuse mononuclear inflammatory cell infiltration with areas of tubular atrophy, tubular destruction, tubular cast and interstitial fibrosis with thickened wall vessels and pathological findings were compatible with FSGS [Figure 1]. On recent admission, laboratory findings included: A normocytic anemia, leukopenia, elevated ESR, hypercalcemia with low parathyroid hormone (PTH) level and monoclonal gammopathy. Laboratory findings are shown in [Table 1]. Bone marrow aspiration and biopsy showed plasma cell dyscrasia [Figure 2] and the diagnosis of MM was made. In this case of MM, causes of renal failure included: FSGS, hypercalcemia, renal stones, and recurrent UTI.

Known causes of renal failure in patients with MM include: Hypercalcemia, recurrent UTIs, renal stones, urate nephropathy, analgesic nephropathy, cast nephropathy, amyloidosis, and rarely infiltration of kidneys by neoplastic plasma cells. [6]
Figure 1: Foci of segmental sclerosis in a glomerulus in PAS staining (magnification ×400)

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Figure 2: Increased in number of mononucleated and binucleated plasma cells in bone marrow aspiration (magnification × 1000)

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Table 1: Laboratory findings at recent admission

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FSGS may be another leading cause of ESRD in patients with MM. We should think for FSGS in any case of MM with nephrotic or nerphritic range proteinuria.

Any patient with idiopathic FSGS should be assessed for evidence of monoclonal gammopathy in serum and urine protein electrophoresis, lytic bone lesions in bone survey, and serum calcium level for ruling out an underlying plasma cell disorder because early diagnosis and treatment of plasma cell dyscrasia can induce remission of FSGS and may prevent from ESRD. [7]

  Acknowledgment Top

We express our appreciation to Drs. Aida Gheibi, Abbas Saffarifard and Pantea Rohanidoost, residents of the Pathology Department in Urmia University of Medical Sciences who helped us in taking photos from pathology slides of this patient.

  References Top

1.Kitiyakara CE, Kopp JB. Twenty-one-year trend in ESRD due to focal segmental glomerulosclerosis in the United States. Am J Kidney Dis 2004;44:815-25.  Back to cited text no. 1
2.Dingli D, Larson DR, Plevak MF, Grande JP, Kyle RA. Focal and segmental glomerulosclerosis and plasma cell proliferative disorders. Am J Kidney Dis 2005;46:278-82.  Back to cited text no. 2
3.Torun D, Canpolat T, Özelsancak R. Focal segmental glomerulosclerosis in a patient associated with Kappa-Light chain disease. Turk Neph Dial Transpl 2011;20:96-8.  Back to cited text no. 3
4.Schwimmer JA, Valeri A, Appel GB. Collapsing glomerulopathy. Semin Nephrol 2003;23:209-18.  Back to cited text no. 4
5.Paueksakon PR, Horn RG, Shappell S, Fogo AB. Monoclonal gammopathy: Significance and possible causality in renal disease. Am J Kidney Dis 2003;42:87-95.  Back to cited text no. 5
6.Katzel JA, Hari P, Vesole DH: Multiple myeloma: Charging toward a bright future. CA Cancer J Clin 2007;57:301-18.  Back to cited text no. 6
7.Shah S, Cavenagh J, Sheaf M, Thuraisingham RC . Remission of collapsing focal segmental glomerulosclerosis following chemotherapy for myeloma. Am J Kidney Dis 2004;43:e10-2.  Back to cited text no. 7


  [Figure 1], [Figure 2]

  [Table 1]

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