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I’m going to have to throw myself on the mercy of the court this time. For the life of me I can’t figure out what the studies linked and excerpted below are saying. Other than MGUS or monoclonal gammopathy can cause kidney damage.
If you have been diagnosed with MGUS, SMM or MM and your creatinine or other kidney function tests are abnormal, please ask your oncologist to have an immunofluoresence study.
MGUS at a glance-
If you do not want to “watch and wait” to see if your MGUS progresses to Multiple Myeloma please watch the short video below:
Consider MGUS Therapies such as:
“Indeed, a growing number of pathologic renal conditions are being attributed to a clonal plasma cell disorder that is less “myeloma-like” and more “MGUS-like” in terms of its bulk and proliferative rate.11,12 Unfortunately, the current diagnostic schema fails to properly categorize the hematologic disorder in these patients. Because they do not meet conditions for smoldering multiple myeloma or MM, these patients are mistakenly diagnosed as MGUS...
Unfortunately, MGUS in this context is misrepresented because in these patients there is significance to the monoclonal gammopathy, and its significance is not “undetermined.” Despite their nonmalignant nature, these diseases are associated with a great deal of morbidity and even mortality.10,12,16
MGUS should not be used to describe hematologic disorders that result in kidney disease. It is because of this necessity that we propose the term “monoclonal gammopathy of renal significance” (MGRS) to discriminate the pathologic nature of these diseases from the truly benign MGUS…
Although the MGUS-like biology sometimes makes the hematologic disease less lethal, the effect on the kidney regrettably is not as benign…
“Plasma cell dyscrasias are frequently encountered malignancies often associated with kidney disease through the production of monoclonal immunoglobulin (Ig). Paraproteins can cause a remarkably diverse set of pathologic patterns in the kidney and recent progress has been made in explaining the molecular mechanisms of paraprotein-mediated kidney injury…”