Acute renal failure due to cast nephropathy in nonsecretory myeloma: A case report and review of the literature S. Karthik Kumar 1 , Preet M. Sohal 1 , Harbir S. Kohli 1 , Kamal Sud 1 , Krishan L. Gupta 1 , Kusum Joshi 2 , Vinay Sakhuja 1 , & Vivekanand Jha 1 1 Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India & 2 Department of Nephrology and Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Abstract. Multiple myeloma is characterized by marrow plamacytsois, M spike in serum or urine elec- trophoresis and skeletal lytic lesions. The M spike may be absent in rare instances. We describe a case of myeloma cast nephropathy with acute renal failure who did not exhibit an M spike. k-chain staining was documented on immunoperoxidase, suggesting paraprotein-related tubular damage. Key words: Myeloma nephropathy, Acute failure Introduction Multiple myeloma (MM) is characterized by the proliferation of a malignant clone of plasma cells that produce large amounts of immunoglobulins. This can be detected electrophoretically as a sharp monoclonal or M spike in serum or urine and is a hallmark of MM [1, 2]. In rare situations, this M spike is absent and can lead to problems in diag- nosis. Renal involvement is seen in about 10–20% of all MM cases and most commonly takes the form of acute renal failure (ARF) due to myeloma cast nephropathy [1]. There is little information in the literature about the nature of renal involvement in nonsecretory myeloma. We describe a case of nonsecretory MM who presented with ARF due to myeloma cast nephropathy. Case report A 45-year-old businessman was admitted to our Institute in October 2002 with a 5-day history of alteration in the level of consciousness. He was well till May 2002, when he developed a nagging pain in the lower part of back. There was no relief despite treatment at a local health facility, and the pain spread on to involve the upper back and rib cage. A few weeks later, his appetite started to decline and he lost weight. Occasional vomiting appeared in September 2002, and the alertness level started to decline about a week prior to admission. The urine output was adequate and his family denied a history of NSAID intake. On examination, he was pale, but had no jaundice, edema or lymphadenopathy. The pulse was 88 beats/min and blood pressure 122/74 mm of Hg. The cardiovascular, respiratory and abdomi- nal examinations were unremarkable. He was conscious, but exhibited flapping tremors. There was diffuse bony tenderness, and a tender soft tissue swelling was noted over the left iliac crest. Investigations revealed hemoglobin of 7 g/dl; the WBC was 8400/dl with a normal differential count and platelets were 2.2 · 10 5 /mm 3 . The serum cre- atinine was 17.3 mg/dl, calcium 11 mg/dl, uric acid 5.5 mg/dl, albumin 3.5 g/dl, globulins 2.9 g/dl and alkaline phosphatase 5 King-Armstrong units. The serum b-2 microglobulin was 28,925 lg/ml. Abdominal ultrasound revealed the kidneys to be 12.7 and 12.6 cms. Xrays of spine, pelvis and skull showed multiple lytic lesions. A computerized tomographic scan of the pelvis revealed an ex- pansile lytic lesion in the left iliac bone with extension into the surrounding tissues, and several International Urology and Nephrology (2005) 37:351–353 Ó Springer 2005 DOI 10.1007/s11255-004-2362-3