Renal manifestations in multiple myeloma and in primary amyloidosis

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ONE of the important clinical features of plasmacytic dyscrasias is the frequency of renal complications.1 In patients who have multiple myeloma, acute or chronic renal failure may be produced by the precipitation of Bence Jones (light chain) proteins in the renal tubules. Moreover, patients with this disease are subject to a number of other renal abnormalities, including hypercalcemia, hyperuricemia, infection, and amyloid deposition in the glomeruli. Primary amyloidosis, another plasma cell dyscrasia, is frequently manifested as a nephrotic syndrome. Multiple myeloma and primary amyloidosis have been grouped together for the purpose of this report because of their close relation.2–4 Waldenstrom's macroglobulinemia may have renal complications resembling those of multiple myeloma5 but will not be included in this review.

Material and method of study

The records of 72 consecutive cases of multiple myeloma and 14 cases of primary amyloidosis seen at the Cleveland Clinic between August 30, 1965, and August 1, 1968, were reviewed. Particular attention was given to renal excretory function, degree and type of proteinuria, serum protein electrophoresis, serum calcium levels, as well as biopsy or autopsy findings. Proteinuria of any degree was recorded when it was more than 0.1 g per 24 hours. This low level of proteinuria was selected because of the finding of Bence Jones proteins in small amounts in the urine of some patients. The electrophoresis was done on paper at a pH of 8.6 with a barbital buffer. The urine specimens were first concentrated by pervaporation.

All cases that satisfied the usual criteria . . .



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