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Published 4 November 2009
Cite this as: BMJ Case Reports 2009 [doi:10.1136/bcr.03.2009.1726]
Copyright © 2009 by the BMJ Publishing Group Ltd.

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Acute renal failure followed by low back ache

Mahesh Prasad1, Arjun Maitra2, Nimish Sethiya3, V K Bharadwaj4, Virendra Chowdhury1, Jyoti Valecha5, Rakesh Biswas3

1 People’s College of Medical Sciences, Medicine, Bhanpur Bypass Road, Bhopal, 462037, India
2 People’s College of Medical Sciences, Physiology, Bhanpur Bypass Road, Bhopal, 462037, India
3 People’s College of Medical Sciences, Medicine, People’s College of Medical Sciences, Bhopal, 462010, India
4 People’s College Of Medical Sciences, Pathology, Bhanpur Bypass Road, Bhopal, 462037, India
5 Jawaharlal Nehru Cancer Hospital and Research Centre, Radiology, Idgah Hills, Bhopal, Bhopal, 462001, India

Correspondence to:
Rakesh Biswas, rakesh7biswas{at}gmail.com

A 47-year-old man presented with a history of oliguria and uraemic symptoms such as anorexia, nausea and vomiting. His serum creatinine on admission was 8.5 mg/dl and his arterial blood gas revealed metabolic acidosis. He was enrolled for regular sessions of haemodialysis following which his symptoms improved remarkably and his serum creatinine returned to normal. A renal biopsy done at this time showed a moderate tubulo-interstitial nephritis with mild global glomerular sclerosis.

The patient returned 1 month later with severe back ache and a computed tomography (CT) scan of the lumbosacral spine was undertaken (fig 1).


 

A week later he developed sudden altered sensorium along with restless twitching of the limbs. Repeated serum creatinine showed a high value and arterial blood gas again showed metabolic acidosis.

A CT scan of the head was done as a work up for his altered sensorium (fig 2). Finally the diagnosis was established following a bone marrow examination (fig 3).


 


 

The CT of the spine taken for low back ache and of the cranium taken for altered sensorium revealed multiple punched out osteolytic lesions (evident on figs 1 and 2). This was immediately suggestive of myeloma-like plasma cell dyscrasia.

The bone marrow showed a severely depressed erythroid element, and the myeloid elements replaced with lymphoid cells showed reactive lymphocytes with moderate basophilic cytoplasm suggestive of a lymphoplasmacytic monoclonal proliferation.

These bone marrow findings are suggestive of Waldenstrom’s macroglobulinaemia (WM). A serum protein agarose gel electrophoresis revealed an M spike in the {gamma} globulin region.

WM is less common than multiple myeloma, and must be differentiated on predominantly clinical grounds from other entities presenting with monoclonal spikes of IgM. A diagnosis of WM can be made irrespective of IgM concentration if there is evidence of bone marrow infiltration by lymphoplasmacytoid lymphoma.1 Lytic bone disease is very uncommon in WM but well described in the literature.2 Although renal complications of plasma cell dyscrasias with IgM proliferations such as WM are rare, a wide spectrum of kidney lesions has been reported in patients, many of whom have presented with acute renal failure.3 The second hospital admission of our patient was with altered sensorium which was thought to be due to uraemic encephalopathy (along with twitching of the limbs that could again be a part of the uraemic encephalopathy).

Our patient received one cycle of chemotherapy with standard alkylating agents and steroids, following which he developed a severe bout of diarrhoea and fever. He was treated for the gastrointestinal sepsis but he could not recover and succumbed to the infection 4 weeks after.

To all professionals in People’s College and patient’s relatives involved in the care of this patient.

Competing interests: none.

Patient consent: Patient/guardian consent was obtained for publication

REFERENCES

  1. Dimopoulos, MA, Kyle, RA, Anagnostopoulos, A, et al. Diagnosis and management of Waldenstrom’s macroglobulinemia. J Clin Oncol 2005; 23: 1564–77.[Abstract/Free Full Text]
  2. Krausz, Y, & Slotnick, A. Macroglobulinemia of Waldenstrom associated with severe osteolytic lesions. Acta Haemat 1977; 58: 307–11.[CrossRef][Medline]
  3. Audard, V, Georges, B, Vanhille, P, et al. Renal lesions associated with IgM-secreting monoclonal proliferations: revisiting the disease spectrum. Clin J Am Soc Nephrol 2008; 3: 1339–49.[Abstract/Free Full Text]

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