Case Report
A Case Report of Non-Secretorymyeloma with Renal Failure
Zhu Y1, Yan F2, He B2, Shen J3 and Xiao Z3*
1Department of Gastroenterology, The Third Affiliated Hospital of Soochow University, China
2Department of Hematology, The Third Affiliated Hospital of Soochow University, China
3Department of Pharmacology, School of Pharmacy, Southwest Medical University, China
*Corresponding author: Zhangang Xiao, Department of Pharmacology, School of Pharmacy, Southwest Medical University, China
Published: 02 Jul, 2016
Cite this article as: Zhu Y, Yan F, He B, Shen J, Xiao Z. A
Case Report of Non-Secretorymyeloma
with Renal Failure. Clin Oncol. 2016;
1: 1056.
Abstract
Non-secretory myeloma (NSM) is a rare form of multiple myeloma with the feature of absence of
monoclonal gammopathy in serum and urine by immunofixation electrophoresis. It accounts for
1-5% of all cases of multiple myeloma, and is supposed to be associated with longer survival. But
NSM usually presented with more advanced disease at initial stage than classic myeloma. Here we
present a case of NSM complicated with progressive renal failure and anemia.
Keywords: Non-secretory myeloma; Renal failure; Anemia; Osteolytic lesion
Introduction
Multiple myeloma, a cancer of plasma cells, accounts for about 1% of all tumors and 13% of hematological malignancy cases [1]. Of them, secretory type accounts for approximately 95-97% of all cases, where non-secretory type accounts for the other 1-5% [2]. Non-secretory myeloma (NSM) was first described by Serre in 1958 and is characterized by the absence of M protein band on serum or urine immunofixation electrophoresis [3]. The pathogenetic mechanisms underlying the incapability of neoplastic plasma cells to synthesize M proteins have been reported to differ from case to case. Moreover, with serum free light chain (FLC) assays, about three-fourths of nonsecretory cases were found to actually have elevated FLC levels and/or abnormal FLC ratios [4], and were considered as minimally secretory, hyposecretory, or oligosecretory cases [3]. NSM cases often fail to exhibit classical symptoms ofanaemia, neutropenia, thrombocytopenia, recurrent bacterial infection, and end organ damage [5], leading to the delaying of diagnosis. Here we reported a case of NSM with renal failure and anaemia.
Case Report
A 69-year-old man presented with a history of consistent chest pain lasting for at least 2 months.
Before coming to visit our hospital, the patient has already received routine blood and biochemical
tests as well as radiographic imaging studies one month ago in another hospital. Routine blood test
indicated slightly increased white blood cells of 10.8*109/L with leukocyte count of 0.9*109/L, no
anaemiaandthrombocytopenia were found. Serum lactate dehydrogenase (LDH) was significantly
increased (1319U/L). Haematuria and proteinuria were also seen in the patient, and blood test
revealed increased creatinine of 148.2μmol/L, which all indicated renal damage. Magnetic Resonance
Imaging (MRI) study showed diffuse degenerative changes in cervical spine, and bone lesions in
thoracic and cervical spine. Ultrasonographic findings were within normal limits and endoscopic
examination indicated esophagitis and erosive gastritis.
After admitted into our hospital, routine blood test was performed again, which indicated a
normal white blood cell count of 8.91*109/L, a normal leukocyte count of 1.60*109/L, and normocytic
nomochromic anaemia (9.70g/dl) which fell to 8.7g/dl four days later. His erythrocyte sedimentation
rate (ESR) was 21mm/h. Serum albumin (3.60g/dl) and total globulin (2.11g/dl) were within the
normal range, butthe levels of IgA, IgG, and IgM were significantly decreased. Additionally, FLC
assays showed that Kappa and Lambda were both in normal limits with their ratio significantly
decreased to 0.68. However, serum protein electrophoresis didn’t show any monoclonal protein
band and gamma globulin levels were normal. Urine bence-Jones protein was undetectable in this
patient. Bone SPECT-CT scan showed multiple increased intake, which suggested bone metastasis
or multiple myeloma. Yet no hypercalcemia was observed by biochemical blood test. Bone marrow
aspiration was performed from the posterior iliac spines of the patient, and the aspirates showed
numerous plasma cells of 65%. Binucleated, multinucleated forms and
occasional mitotic figures were also observed in these plasma cells. The
immunophenotyping results for bone marrow aspirates revealed cells
positive for CD38, CD138, Lambda, and HLA-DR. Cytogenetics were
performed with FISH showing the 1q21 amplification (38.7%), RB1
deletion (35.0%), D13S319 deletion (39.0%), p53 normal, and virtual
karyotype showing 2 deletion, 13 deletion, and 5q amplification.
The patient had already developed intorenal failure when
admitted into our hospital with serum creatinine increased to a high
level of 692.0μmol/L and serum blood urea nitrogen at a high level of
25.70mmol/L, and haematuria and proteinuria persistently existed.
Acute dialysis was then arranged. The patient was diagnosed as nonsecretorymyeloma
(NSM)in clinical stage IIIB according to Durie/
Salmon staging system and stage III according to the International
Staging System (ISS), and had a significantly high level of β2-
microglobin at 39.29mg/L (range 1.0-3.0mg/L), which indicated a
poor prognosis. However, the patient refused to accept further
chemotherapeutic regimen in our hospital.
Discussion
NSM was reported to have clinical features of elevated hemoglobin
levels, lower ESR values, higher neurological presentation incidence,
less aggressive osteolysis, low risk of renal myeloma, lower
hypercalcemia incidence, and elevated immunoglobulin levels [3].
Our patient here, however, presented anaemia, normal ESR values,
severe osteolytic lesions, renal failure, normal blood calcium, and
decreased IgA, IgG, IgM levels, whose complaint of bone pain was
extremely obvious. Therefore, the paradoxically clinical presentation
of the NSM case prompted us to discuss it here.
Anaemia is commonly presented in the majority of myeloma
patients, but anaemia in NSM cases was reported to be less frequent
than that in secretory myeloma cases. A case of megaloblastic anaemia
(MA) in NSM was described in 2013, which suggested the case of MA
was due to the increased cobalamin uptake and consumption and
paraprotein synthesis [6]. However, treatment with folic acid and
cobalamin significantly accelerated disease progression, and some
postulations were raised as cobalamin acted as a paracrine growth
factor to increase plasma cell growth and osteolytic activity [6]. Our
NSM case here presented normocytic normochromic anaemia with
hemaglobulin continuously decreasing. The bone marrow aspiration
confirmed the erythroid hypoplasia. And that, we thought, was due
to the occupation of neoplastic plasma cells into bone marrow and
caused the marrow hematopoietic cell replacement.
In multiple myeloma patients, renal damage commonly occurs
due to increased serum free light chain and/or hypercalcemia [7].
Our patient here presented a progressed renal damage to renal
failure, but no increased serum light chain and hypercalcemia were
detected. Someone reported a rare case of NSM associated with acute
renal failure due to massive renal infiltration by neoplastic plasma
cells, and increased renal size was observed in the reported case [8].
However, ultrosonographic examination for this patient did not show
swollen kidney. And no ongoing renal infection and hypotensive
episodes were presented in this case. Before admitting to our hospital,
the patient had a short history of using unknowing herbs, which may
have a risk leading to renal damage. Renal biopsy was not performed
in the patient, so we here can’t provide solid evidences to figure out
the association between NSM and renal failure and the actual cause of
renal failure in the patient.
In conclusion, paraprotein absence does not exclude the diagnosis
of multiple myeloma, especially in the case of NSM. Histologic,
serologic, and radiographic features should be carefully evaluated.
References
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