Introduction
Multiple myeloma (MM) is a malignant plasma cell neoplasm characterized by clonal proliferation of plasma cells in the bone marrow and the production of monoclonal immunoglobulins or free light chains. It is a biologically heterogeneous disease with a variable clinical course, and it is commonly associated with end‐organ damage, including hypercalcemia, renal impairment, anemia, and osteolytic bone lesions (CRAB criteria) [ 1 ].
Brucellosis is a prevalent zoonotic infection caused by Brucella species and remains an important public health problem in many regions worldwide, particularly in endemic areas. The disease can present with nonspecific systemic manifestations such as fever, night sweats, malaise, weight loss, and musculoskeletal pain, which may overlap with symptoms of hematological malignancies [ 2 ].
Renal impairment is a well‐recognized and relatively common manifestation of symptomatic MM and represents a myeloma‐defining event. In some cases, severe acute kidney injury requiring hemodialysis may occur at presentation, most frequently due to light‐chain cast nephropathy. The coexistence of infection may further exacerbate renal dysfunction and complicate the diagnostic process [ 1 , 3 ].
Although brucellosis and MM are distinct entities, their concurrent presentation may lead to diagnostic uncertainty, particularly in endemic regions where brucellosis is common and may mimic malignancy‐related symptoms. In this context, we present a case of a 58‐year‐old man with severe renal failure who was diagnosed with active brucellosis and underlying light‐chain predominant multiple myeloma. This case highlights the importance of considering dual pathology and performing comprehensive evaluation in patients presenting with overlapping systemic symptoms and severe renal dysfunction.
Case Presentation/Examination
A 58‐year‐old man with no significant past medical history or medication use was referred to the emergency department due to progressively worsening dyspnea, classified as functional class II. He also reported severe bone pain, significant weakness, loss of appetite, and episodes of nausea and vomiting. He further described intermittent fever associated with night sweats and an undulant (wave‐like) fever pattern over recent days.
Upon evaluation, his vital signs indicated a pulse rate of 103 beats per minute, blood pressure of 110/65 mmHg, temperature of 37.4°C, and oxygen saturation of 89% on room air. During physical examination, fine crackles were noted on pulmonary auscultation with reduced breath sounds at the lung bases. The patient exhibited pitting edema of the lower limbs and appeared pale. He was clinically volume overloaded with generalized edema. Tenderness was observed over the upper vertebrae.
Initial laboratory evaluation revealed severe renal dysfunction and anemia (Table 1 ). Serum creatinine at admission was 8.1 mg/dL. Complete blood count showed a white blood cell count of 4.8 × 10 9 /L. The patient reported gradually decreasing urine output starting approximately one week prior to admission. He became anuric two days before presentation, and anuria persisted despite adequate intravenous hydration. Serum potassium was 5.4 mEq/L (Table 1 ).
TABLE 1
Patient lab data to first assay.
| Test | Result | Reference value | Unit |
| WBC | 4.8 | 3.9–10 | 10 9 / L |
| RBC | 1.63 | 3.9–5.1 | 10 6 / μL |
| Hb | 4.1 | 11.8–15.5 | g/dl |
| PLT | 105 | 155–440 | 10 3 / μL |
| BUN | 110 | 7–18 | mg/dl |
| Cr | 8.1 | 0.6–1.3 | mg/dl |
| Alb | 4.2 | 3.5–5.5 | g/dl |
| AST | 18 | < 31 | U/L |
| ALT | 23 | < 31 | U/L |
| ALP | 831 | 64–306 | IU/L |
| ESR | 140 | Up to 15 | mm/h |
| CRP | 24 | Up to 6 | mg/L |
| LDH | 872 | 135–225 | U/L |
| Na | 141 | 135–145 | mEq/L |
| K | 5.4 | 3.5–5.1 | mEq/L |
| Mg | 3.1 | 1.7–2.2 | mEq/L |
| Ca | 10.9 | 8.6–10.3 | mg/dl |
| P | 9.2 | 2.6–4.5 | mg/dl |
| Uric A. | 19.4 | 2.8–6 | mg/dl |
| Urine 24 H/Pr | 1997 | < 200 | ml/day |
| Urine 24 H/vol | 1220 | 600–1800 | ml/day |
| Urine 24 H/cr | 827 | 800–2000 | mg/day |
In addition to uremic symptoms such as nausea, vomiting, and diaphoresis, the presence of volume overload with generalized edema and pulmonary findings consistent with fluid accumulation necessitated urgent hemodialysis for both metabolic control and volume management.
During the initial dialysis session, the patient received two units of cross‐matched packed red blood cells. Hemoglobin level on admission was approximately 4 g/dL, indicating severe anemia. Erythropoietin (Eprex) therapy was initiated at 4000 IU, and hemoglobin subsequently improved to approximately 7.8 g/dL.
After the initial session, the patient was placed on a routine hemodialysis schedule. Following three hemodialysis sessions, the patient's urine output gradually improved and renal replacement therapy was discontinued.
An infectious disease consultation was requested after positive serologic testing for brucellosis. Standard tube agglutination (Wright) test was positive at a titer of 1:640, and Coombs Wright test was positive at a titer of 1:1280. The patient denied consumption of unpasteurized dairy products or direct livestock exposure. Polymerase chain reaction (PCR) testing for Brucella species was not available at our center.
Investigations
A spiral CT scan of the chest and neck without contrast revealed multiple lytic lesions in the cervical vertebrae. Bilateral pleural effusion was noted. Further abdominopelvic CT imaging demonstrated multiple lytic lesions in the lumbar vertebrae and pelvic bones. A skull X‐ray also revealed multiple lytic lesions (Figure 1 ).
The liver, spleen, and pancreas appeared normal in size and density. Because the CT scan was performed without contrast, renal excretory (secretory) function could not be assessed. Structurally, both kidneys were of normal size with no evidence of hydronephrosis or obstructive uropathy.
Serum and urine electrophoresis were performed, revealing a free kappa/free lambda ratio of 4.54 (Table 2 ). Despite the absence of a prominent M‐spike on serum protein electrophoresis, the abnormal free light chain ratio together with Bence‐Jones proteinuria supported a diagnosis of light‐chain predominant multiple myeloma.
TABLE 2
Serum protein electrophoresis results.
| Factor | Fraction % | Ref % |
| Albumin | 59/2 | 55/8–66/1 |
| Alpha 1 | 5/6 | 2/9–4/9 |
| Alpha 2 | 14/3 | 7/1–11/8 |
| Beta 1 | 7 | 4/7–7/2 |
| Beta 2 | 5/3 | 3/2–6/5 |
| Gamma | 8/6 | 11/1–18/8 |
A bone marrow aspirate smear demonstrated numerous plasma cells (Figure 2 ). Despite a normal total leukocyte count (4.8 × 10 9 /L), the presence of circulating plasma cells suggested a high tumor burden and prompted further evaluation. Bone marrow biopsy demonstrated approximately 90% cellularity replaced by sheets of atypical plasma cells. Immunohistochemistry showed CD138 positivity in plasma cell sheets, CD20 positivity in scattered lymphocytes, CD3 positivity in some lymphocytes, and negative cytokeratin staining. Plasma cell dyscrasia compatible with multiple myeloma was confirmed.
Treatment
The patient was started on antimicrobial therapy with doxycycline 100 mg twice daily and rifampin 600 mg daily.
Chemotherapy was initiated using the CyBorD regimen. The patient received Cyclophosphamide 300 mg/m 2 orally on days 1, 8, 15, and 22; Bortezomib 1.5 mg/m 2 intravenously on days 1, 8, 15, and 22; and Dexamethasone 40 mg orally on days 1–4, 9–12, and 17–20 of each 28‐day cycle. This regimen was continued weekly for six months. After completion of induction therapy, the patient was transitioned to maintenance therapy with bortezomib and dexamethasone.
Outcome and Follow‐Up
After initiation of antimicrobial therapy, the patient's undulant fever gradually subsided and night sweats significantly decreased. His appetite improved and constitutional symptoms resolved. During follow‐up, Wright and Coombs Wright titers declined from 1:640 and 1:1280 to 1:160, respectively. In subsequent follow‐up visits, both serologic tests became negative, confirming an appropriate serologic response to treatment. Bone pain improved during therapy, likely reflecting a combined response to anti‐myeloma treatment and infection control.
Regarding renal function, the patient had experienced progressive oliguria beginning approximately one week prior to admission and became anuric two days before presentation. After three sessions of hemodialysis, urine output gradually increased, and dialysis was discontinued. Serum creatinine improved from 8.1 mg/dL at presentation to approximately 2 mg/dL during follow‐up. The patient was followed by the hematology team for one year, during which his general condition, functional status, and clinical appearance remained stable and satisfactory.
Discussion
Multiple myeloma (MM) is a malignant plasma cell disorder characterized by clonal proliferation of monoclonal plasma cells in the bone marrow, leading to the production of monoclonal immunoglobulins or free light chains and resulting in end‐organ damage. The clinical presentation is heterogeneous and may include anemia, bone pain, fatigue, hypercalcemia, and renal impairment, which collectively contribute to significant morbidity. The pathophysiology of MM involves disruption of normal hematopoiesis and increased osteoclast activity through cytokine‐mediated mechanisms, leading to bone resorption and skeletal‐related events such as lytic lesions and pathological fractures [ 4 ].
Brucellosis remains a significant public health concern in many developing countries due to its zoonotic transmission and endemic distribution. Because of its broad and nonspecific clinical manifestations, brucellosis can mimic malignancies and inflammatory disorders, leading to diagnostic delay or misdiagnosis. Several case reports have described diagnostic confusion between brucellosis and hematological malignancies, including MM, particularly in endemic regions. In our case, brucellosis was identified early; however, the subsequent investigations revealed an underlying plasma cell dyscrasia, emphasizing the importance of considering dual pathology in the appropriate clinical context [ 5 ].
Brucellosis commonly presents with systemic symptoms such as fever, sweating, malaise, myalgia, arthralgia, and weight loss. Osteoarticular involvement is one of the most frequent complications and may manifest as spondylitis, sacroiliitis, or peripheral arthritis [ 2 ]. The wide range of musculoskeletal symptoms may overlap with malignancy‐related bone pain, particularly in MM, and may obscure the diagnosis if not carefully evaluated. Although pulmonary manifestations such as pleural effusion and pneumonia are relatively uncommon, they have been reported. In our patient, pleural effusion was likely multifactorial, potentially reflecting both volume overload related to renal failure and systemic inflammation associated with infection.
Hematological abnormalities, including anemia, leukopenia, thrombocytopenia, and coagulopathy, are recognized complications of brucellosis [ 3 ] In contrast, MM is frequently associated with cytopenias due to marrow infiltration and is commonly complicated by renal impairment. Renal dysfunction is a myeloma‐defining event and constitutes one of the CRAB criteria, often occurring secondary to light‐chain cast nephropathy. In our patient, the combination of severe anemia, multiple lytic bone lesions, hypercalcemia, and renal failure prompted further evaluation for MM [ 2 ].
More than one‐third of patients with MM present with renal impairment at diagnosis, and a subset may require urgent hemodialysis. The primary mechanism is typically light‐chain–mediated tubular injury, particularly cast nephropathy, although other etiologies such as amyloidosis or light‐chain deposition disease may contribute. In our case, the presence of Bence‐Jones proteinuria and an abnormal serum free light chain ratio strongly supported light‐chain–mediated renal injury as the primary mechanism of renal failure. While brucellosis can rarely involve the kidneys through interstitial nephritis or immune‐complex mediated mechanisms, it was more likely a contributing factor that exacerbated renal dysfunction through dehydration, systemic inflammation, and metabolic stress rather than the main cause of kidney failure [ 6 , 7 ].
The relationship between MM and infection is clinically important, as patients with MM are immunocompromised due to both humoral immune dysfunction and treatment‐related immunosuppression [ 2 , 3 ] This immunocompromised state may predispose patients to infections, while infections themselves can worsen renal function, accelerate metabolic derangements, and further complicate diagnostic interpretation. Therefore, a multidisciplinary diagnostic approach is essential in patients presenting with overlapping infectious and malignant features [ 8 , 9 ].
In light‐chain predominant MM, serum protein electrophoresis may not demonstrate a prominent M‐spike, and the gamma fraction may remain within normal limits. Therefore, diagnosis in such cases relies heavily on serum free light chain assays and urine studies rather than electrophoretic findings alone. This explains the apparent discrepancy between the patient's electrophoresis pattern and the overall clinical picture [ 10 , 11 ].
An additional diagnostic challenge in this case was the interpretation of Brucella serologic testing. Although monoclonal gammopathies may occasionally interfere with agglutination‐based serologic assays, such false‐positive reactions are typically low‐titer and nonspecific. In endemic regions, titers ≥ 1:160 are generally considered diagnostic for active infection. In our patient, the markedly elevated Wright titer (1:640) and Coombs Wright titer (1:1280), followed by a progressive decline to 1:160 and eventual seronegativity after antimicrobial therapy, strongly supported true active brucellosis rather than serologic cross‐reactivity related to monoclonal protein interference. Furthermore, the patient demonstrated clinical improvement in undulant fever, night sweats, and appetite following doxycycline and rifampin therapy, which further supports the diagnosis of active brucellosis [ 12 , 13 ].
Renal impairment significantly affects prognosis and quality of life in patients with MM. Patients requiring dialysis represent a high‐risk subgroup and require careful supportive management in addition to prompt initiation of anti‐myeloma therapy [ 8 ]. In our patient, although urgent hemodialysis was required at presentation, urine output improved after three dialysis sessions and dialysis was discontinued, with serum creatinine stabilizing around 2 mg/dL during follow‐up. This suggests a component of reversible acute kidney injury superimposed on myeloma‐related renal involvement.
Overall, this case emphasizes the importance of considering concomitant infectious diseases such as brucellosis in endemic areas, even in patients with strong evidence of malignancy. Conversely, persistent bone pain, anemia, renal failure, and lytic lesions should prompt evaluation for MM even when an infectious diagnosis has been established. The overlapping manifestations of MM and brucellosis necessitate careful differential diagnosis and timely investigation. Early recognition of both conditions and coordinated multidisciplinary management may improve outcomes and prevent diagnostic delay.
Author Contributions
Maryam Ghaffari Rahbar: conceptualization, investigation, project administration, writing – original draft, writing – review and editing. Tahere Zarouk Ahimahalle: data curation, investigation, writing – review and editing. Marziyeh Ghalamkari: conceptualization, investigation, visualization, writing – review and editing. Maedeh Olya: data curation, resources, writing – original draft, writing – review and editing.
Funding
The authors have nothing to report.
Consent
Written informed consent for publication of this case report and any accompanying images was obtained from the patient. All patient information has been appropriately anonymized. A copy of the written informed consent is available for review by the Editor‐in‐Chief upon request.
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
Special thanks to the patient for their cooperation.
Data Availability Statement
All data produced or examined during this study are contained within this article. For any further inquiries, please contact the corresponding author.
References
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Associated Data
Data Availability Statement
All data produced or examined during this study are contained within this article. For any further inquiries, please contact the corresponding author.