Myeloma and the Kidney

and Christopher Isles²

(1)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK

(2)

Dumfries and Galloway Royal Infirmary, Dumfries, UK

Q1 What are plasma cells and what do they normally do?

Plasma cells are terminally differentiated B lymphocytes that produce large amounts of specific immunoglobulin. Immunoglobulins are the antibodies that make up part of our host defences. The immunoglobulins produced in health are polyclonal i.e. a mixture of IgG, IgA and IgM heavy chains with kappa and lambda light chains. Kappa and lambda light chains are not always attached to their heavy chains in which case they are known as free light chains (FLC).

Q2 What is myeloma?

Myeloma (sometimes known as multiple myeloma) is a malignant tumour of plasma cells producing immunoglobulins. Whereas normal immunoglobulin production is polyclonal (see above) the immunoglobulins produced in myeloma are monoclonal meaning that they derive from an abnormal clone of plasma cells (essentially a single plasma cell that becomes malignant and begins to multiply). This monoclonal protein is sometimes referred to as a paraprotein. Myeloma accounts for 1 % of all cancers and is the second most common haematological malignancy after non-Hodgkin’s lymphomas (Fig. 15.1).

Fig. 15.1

Plasma cells and immunoglobulins

Q3 Do all patients with myeloma produce monoclonal proteins?

Over 95 % do. Around 55 % of myelomas are known as IgG myeloma because the heavy chain class is IgG. Twenty percent are IgA myeloma for the same reason. IgG and IgA myelomas are usually associated with increased serum FLC which are either kappa or lambda but not both. When the serum FLC production rate exceeds the reabsorptive capacity of the renal tubules then the FLC are detectable in the urine as Bence Jones proteins. Around 10 % of patients with myeloma produce FLC only (aka Light Chain myeloma, previously known as Bence Jones myeloma). An IgM monoclonal protein usually means that the patient has a lymphoma (see later). IgD and IgE myelomas are extremely rare as are myelomas in patients who do not secrete immunoglobulins, so-called non-secretory myelomas.

Q4 How does myeloma present clinically?

Myeloma is a haematological disorder that frequently presents to general physicians and nephrologists. Myeloma may be asymptomatic and only detected because a doctor acted on a clinical clue e.g. anaemia with high ESR. Alternatively it can present with symptoms. Haematologists regularly use the acronym CRAB as an aide-memoire: hyperCalcaemia, Renal injury, Anaemia and Bony lesions. Acute kidney injury requiring dialysis is a renal emergency. Back pain due to myeloma causing spinal cord compression is a potentially devastating complication of myeloma.

Q5 What might lead you to suspect that myeloma was the cause of the renal failure?

There will usually be some clues. The important ones are as follows:

Anaemia with ESR >100.
Hypercalcaemia – this is unusual in other causes of renal failure which are more commonly associated with hypocalcaemia.
Serum total protein >100 g/l – if serum albumin is normal then this implies an excess of globulins and should prompt a request for serum electrophoresis.
Bone pain e.g. back pain.

Q6 How would you confirm a diagnosis of myeloma?

This requires at least two of the following three features to be present:

Monoclonal protein in serum and/or urine – usually IgG greater than 30 g/l or IgA greater than 20 g/l but there is no minimum level that excludes the diagnosis. Immune paresis i.e. suppression of the other immunoglobulin classes is commonly present.
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