Urogenital ImagingMultiple myeloma, renal involvement
a plasma cell dyscrasia characterized by
proliferation of plasma cells and abnormal serum and urine proteins. The disease results in excess production of immunoglobulins and is characterized by the presence of Bence Jones proteins in the urine.
Renal failure occurs in 3050% of such patients and has been attributed to precipitation of Bence Jones proteins in the tubules, which causes mechanical
obstruction and damages the
tubular cells. Other causes of
renal disease in multiple myeloma include hypercalcaemia, hyperuricosuria,
amyloidosis and urinary tract infection.
Hypercalcaemia can result from bone destruction that accompanies the myelomatous lesions in bone, resulting in nephrocalcinosis. Because there is excess uric acid production, uric acid calculi may also be found. Amyloidosis develops in approximately 10% of patients.
Radiologically, the kidneys are enlarged and there may be attenuation of the collecting system as a result of interstitial oedema. Intravascular contrast media causes in vitro precipitation of Bence Jones proteins and may worsen renal failure in these patients. However, many patients undergo contrast studies without difficulty if the kidneys are normal. Poor opacification on urography occurs commonly because of diminished renal function. On sonography, the kidneys are enlarged with decreased echogenicity, which reflects the abnormal fluid accumulation within the kidneys. It is suggested that risks associated with contrast administration can be minimized as long as dehydration is avoided, serum creatinine is not elevated and marked proteinuria is absent.
On unenhanced CT, both kidneys are of normal or increased size, with smooth outlines. In cases of nephrocalcinosis, medullary calcification is seen. After intravenous contrast, the tubular obstruction by precipitation of protein may cause dense, long-standing contrast enhancement within the renal parenchyma.
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