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76-years-old male
He had been receiving treatment for hypertension at a local hospital since the age of 56, with a blood pressure of approximately 120/80 mmHg. He contracted COVID-19 in August of year X-1. At the time, his eGFR was 64.5 ml/min/1.73 m² and serum Cr 0.90 mg/dL. By November, his eGFR had worsened to 24.7 and Cr 2.12, respectively. He visited our hospital in January of year X. His BUN level had further deteriorated to 21.3 mg/dL, plasma Cr 2.53, and eGFR 20.35. His urine analysis showed urinary protein (±), occult blood (1+), urinary RBC 5-10/HPF. CT scan revealed no morphological abnormalities. COVID-19-associated nephropathy (COVAN) was also suspected, and a kidney biopsy was performed. No findings were found that could explain renal dysfunction. Subsequently, because the BUN was approximately 20 and the plasma Cr was in the 2.0-3.0 mg/dL range, we considered the possibility that plasma Cr might not accurately reflect renal function, and therefore measured cystatin C. Because the plasma Cr fluctuated despite the cystatin C being approximately 1 mg/L, pseudohypercreatinemia was suspected. Using our hospital's reagent (Pure Auto S CRE-N®), the plasma Cr was 4.16 and the serum Cr was 1.03. Simultaneously, a different company's reagent (enzymatic method) measured the plasma Cr and serum Cr at 1.03. Using the HPLC method, the plasma Cr was 1.23 and the serum Cr at 1.19. Only the plasma Cr, which we routinely measure, showed a discrepancy, leading to a diagnosis of pseudohypercreatinemia. We searched for paraproteins that could interfere with the enzymatic method to determine the cause of pseudohypercreatinemia. Protein fractionation revealed monoclonal high levels of gamma globulin (34.3%) and IgM (2757 mg/dL), and serum immunoelectrophoresis detected IgM-κ M protein.
Based on these findings, we diagnosed pseudohypercreatinemia as monoclonal hyper IgMemia.
Although enzymatic methods are the most commonly used for Cr measurement, the influence of abnormal proteins is not widely known. Similar reports of this case all involve hyper IgMemia with a molecular weight of 900,000. Possible causes include excessive B cell activation and induction of IgM after COVID-19 infection, but there are few reports and the causal relationship is unclear. It cannot be ruled out that this discovery was coincidental after COVID-19 infection. This is because the discrepancy between plasma and serum was discovered after COVID-19 infection. In any case, it is possible that fibrinogen, which is not present in serum, is chemically reacting with IgM. This report includes a literature review. We investigate the mechanism in detail in collaboration with the manufacturer.
