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Kidney Week

Abstract: PO2173

Acute Acquired Fanconi Syndrome (FS) in Multiple Myeloma (MM) After Autologous Hematopoietic Stem Cell Transplantation (HCT): A Case Series

Session Information

  • Onco-Nephrology - 1
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Onco-Nephrology

  • 1500 Onco-Nephrology


  • Sy-Go, Janina Paula Tiulentino, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Leung, Nelson, Mayo Clinic Minnesota, Rochester, Minnesota, United States

Proximal tubular dysfunction can occur in patients with MM. The main clinical presentation is electrolyte abnormalities indicative of FS. The objective of the study was to describe and identify the rate and clinical predictors of developing acute acquired FS in adult patients with MM after autologous HCT.


We identified 2515 adult MM patients who underwent autologous HCT at Mayo Clinic from January 1, 2000 to December 31, 2018. 45 without research authorization were excluded. 13 patients were identified after searching for “Fanconi,” “Fanconis,” and “Fanconi’s” in the EMR. 6 patients did not have FS. 4 patients were diagnosed with FS prior to HCT. The remaining 3 patients (0.12% of cohort) were clinically diagnosed to have FS based on features indicative of FS - hypokalemia, hypophosphatemia, hypouricemia, proximal renal tubular acidosis, and normoglycemia glycosuria - within 14 days after HCT. Of note, these patients did not have features of FS prior to HCT.


The median age of the cohort was 65 years (range: 53-75). All were Caucasians. 2 were women and 1 was a man. Medical comorbidities included hypertension, dyslipidemia, CKD, hypothyroidism, and kidney stone. All had kappa-restricted light chain MM with a median M-spike of 1.2 g/dL (range: 0.4-2). All received dexamethasone while 2 received bortezomib and 1 each for cyclophosphamide and lenalidomide. They underwent HCT about 8.3 months after MM diagnosis and were clinically diagnosed with FS about 14.6 days after HCT. None underwent a kidney biopsy. All had hypokalemia, hypophosphatemia, and hypomagnesemia (<3.5, <2.5, and <1.7 respectively). 2/3 patients had AKI (≥1.5-fold increase in serum creatinine) and normoglycemia glycosuria. 1/3 had hypouricemia (low range of normal: 2.7-6.1) and proximal renal tubular acidosis (<22 and urine pH <5.3). Aminoaciduria was not checked. All received electrolyte replacement, whether PO or IV, and 2/3 received amiloride to help maintain normokalemia.


Although rare, severe electrolyte depletion after HCT in kappa MM patients could occur and should raise the suspicion for FS. Lenalidomide has been reported to induce FS. Concurrent GI symptoms could exacerbate these electrolyte losses, which concurrent AKI, conversely, could help correct. Timely electrolyte repletion and close monitoring are required.