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Abstract: PO1913

Beware of the "B": Type B Lactic Acidosis and Atypical Renal Interstitial Infiltrate

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology


  • Wilson, Sarah R., Geisinger Medical Center, Danville, Pennsylvania, United States
  • Anand, Prince Mohan, Geisinger Medical Center, Danville, Pennsylvania, United States
  • Kalra, Kartik, Geisinger Medical Center, Danville, Pennsylvania, United States

Lactic acid is an endogenous substrate for gluconeogenesis produced by muscle and other tissues. Lactate is the anion of lactic acid and is a source of base though Kreb's cycle. Lactic acid levels can increase due to impaired oxygen delivery (type A) or impaired oxygen utilization by cells (Type B). Here we describe a patient with an unusual presentation of lactic acidosis, and atypical renal interstitial infiltrate.

Case Description

A 32-year-old female with a history of chemotherapy and allogeneic bone marrow transplant in 2018 due to pre-B cell acute lymphoblastic leukemia (ALL) presented with concerns of sepsis due to suspected appendicitis and abnormal labs (pH 7.2, anion gap of 23, bicarbonate level of 10 mmol/L). Her lactate persistently ranged from 10-14 mmol/L despite antibiotics and bicarbonate containing fluids. Additionally, labs were consistent with acute kidney injury (Creatinine (Cr) 1.8 mg/dL from a baseline of 0.8 mg/dL). A kidney biopsy was performed given unexplained rise in Cr and enlarged kidneys (14 cm on renal ultrasound) which was suggestive of significant interstitial nephritis and tubulitis. Further immunohistochemical stains ordered due to suspicion of ALL reoccurrence, showed a mixture of CD3 and CD20-positive lymphocytes as well as CD68-positive cells. The atypical interstitial infiltrate was positive for CD10, CD45, CD79A, TDT, and PAX-5, consistent with B-cell leukemia. Flow cytometry and bone marrow biopsy confirmed the relapse of pre B-cell ALL. The patient was treated with steroids and blinatumomab, resulting in improvement in kidney function and resolution of lactic acidosis.


Although our patient had lactic acidosis and AKI in the setting of presumed sepsis, a common clinical presentation, she had a completely different diagnosis. Her persistent lactic acidosis and atypical interstitial infiltrate led to the diagnosis of relapsed ALL with kidney involvement. Malignancy causes Type B lactic acidosis due to increased tumor cells’ metabolism, overexpression of cellular glycolytic enzymes, mitochondrial dysfunction, thiamine, and riboflavin deficiency. Tumor cells have a high rate of glucose uptake and preferential production of lactate, even in the presence of oxygen, known as “Warburg effect.” Type B lactic acidosis from malignancy overall portends a poor prognosis. The goal of therapy is to target the underlying malignancy.