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Thread: myeloma kidney

  1. #1
    Join Date
    Apr 2007

    Unhappy myeloma kidney

    AAPC: Back to School
    Would myeloma kidney be coded as multiple myeloma? Some coders code malignancy kidney for this. Thanks.

  2. #2


    I feel that you need to have some more info to assign to the more closer proximity.
    On any account , you can not stay away from coding “multiple myeloma” because it is the underlying disease process. this is a plasma cell malignancy and it has a separate nomenclature.
    Your patient’s reason for encounter and the associated or ongoing renal problems are to be addressed which are presenting in your case. The following passage will give you which are the ones to pick up for assigning the code for (eg) like Multiple myeloma, with renal insufficiency (acute or chronic), or cast nephropathy or amyloidosis or simply Multiple myeloma with Nephropathy or only showing abnormal lab findings (all of them have seaprate diagnosis code , I believe).
    About a quarter of patients with multiple myeloma have renal insufficiency at diagnosis . There are a number of clinicopathologic responses to multiple myeloma that occur within the kidney and most often result in a condition termed myeloma kidney, which is specifically caused by a combination of myeloma cast nephropathy and inflammatory cascades triggered by the presence of light chains within the nephron tubules.
    [In addition to myeloma kidney, renal function in multiple myeloma may become compromised by hypercalcemia, acquired Fanconi syndrome, light chain deposition disease, and light-chain associated amyloidosis]
    { Pathophysiology:
    Light chain proteins are normally freely filtered by the glomerulus and are later endocytosed within the proximal tubule and returned to the bloodstream. In multiple myeloma, this mechanism of removal becomes overwhelmed and the light chains instead form aggregates with Tamm-Horsfall protein in the distal tubule. The hypervariable region of the light chain is primarily responsible for this interaction. Eventually the aggregate protein casts obstruct urinary flow and reduce the glomerular filtration rate. Furthermore, light chain endocytosis itself triggers numerous pro-inflammatory signaling cascades, such as the NF-kappaB pathway and with long-standing inflammatory changes comes excessive interstitial fibrosis and impaired tubular function
    In summary, the excess light chains produced in multiple myeloma are the key pathophysiologic factor responsible for renal damage. Light chains crowd the nephron tubules, initiate inflammation, and disrupt brush-border and glomerular function. Hypercalcemia frequently exacerbates. In sum, the kidneys of patients with multiple myeloma are essentially helpless bystanders. Only with aggressive tumor treatment, hydration, radiocontrast material restriction, and—if necessary as a final option—renal transplant, can this damage be minimized. }
    I hope this would help you .

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