Multiple myeloma (MM) is a malignant plasma cell disorder characterized by clonal plasma cell proliferation in the bone marrow, leading to osteolytic lesions, anemia, renal impairment, and hypercalcemia. Renal involvement is common in MM, typically presenting as cast nephropathy or light chain nephropathy. However, nephrolithiasis, particularly staghorn calculi, is rarely reported in MM. The pathophysiology of nephrolithiasis in MM is complex, involving hypercalcemia-induced calcium excretion, light chain deposition, and altered renal tubular function. This case highlights a patient with MM presenting with nephrolithiasis and extensive osteolytic bone disease, emphasizing the role of imaging and early intervention in disease management.

A 53-year-old female with a history of hyperuricemia and pre-existing chronic kidney disease (CKD) presented with nausea, vomiting, weight loss, and worsening renal function. She had been diagnosed with CKD prior to the onset of MM-related symptoms. Laboratory tests revealed acute kidney injury (creatinine 1.99 to 3.8 mg/dL), anemia (Hb 7.4 g/dL), and hypercalcemia (13.3 mg/dL). Imaging studies identified a 1.3 cm right renal stone with staghorn morphology, extensive osteolytic skull lesions, and a paraspinal mass. The nephrolithiasis was obstructive, contributing to further renal function decline. Bone marrow biopsy confirmed MM, with 60% plasma cells expressing CD38, CD138, dim CD45, and partial CD56+. Immunofixation electrophoresis revealed a monoclonal IgA lambda band. Retrograde intrarenal surgery (RIRS) was chosen for stone removal due to the patient’s renal impairment and the minimally invasive nature of the procedure, which reduces perioperative risks compared to percutaneous nephrolithotomy (PCNL).

RIRS was successfully performed, and stone analysis revealed a composition of 66% calcium oxalate and 34% calcium phosphate. The presence of calcium phosphate stones suggested a strong correlation with the patient’s hypercalcemia, a hallmark of MM. Hypercalcemia-induced urinary calcium excretion, coupled with potential renal tubular damage from monoclonal light chains, likely contributed to stone formation. The patient was initiated on thalidomide, dexamethasone, and bortezomib for MM management, along with radiotherapy for the paraspinal mass. Following treatment, renal function stabilized, and hypercalcemia improved.

This case underscores the importance of comprehensive imaging and laboratory assessments in diagnosing MM, particularly in patients presenting with nephrolithiasis and hypercalcemia. While nephrolithiasis is uncommon in MM, its presence—especially in conjunction with osteolytic lesions—should prompt consideration of an underlying plasma cell dyscrasia. Early recognition of MM-related renal complications allows for timely intervention, improving overall patient outcomes.