*Purpose: We present a case of acute renal failure and hyperkalemia due to osmotic nephropathy from a non-sucrose based IVIG infusion therapy.

*Methods: A 67-year-old man with history of ESRD due to diabetes who was status post kidney transplant, his post transplant history was significant for BK nephropathy for which he had undergone lowered immunosuppression regimen and 2 cycles of cidofovir therapy over a period of 6 months. As his BK viremia with nephropathy continued to persist, he was initiated on 55gm of IVIG treatment with a plan for a total of 3 doses. The patient developed chills, rigors and myalgia during the 1st IVIG therapy, he was subsequently admitted for the 2nd dose in the hospital. In addition to pretreatment with Tylenol and Benadryl along with adequate hydration as before he received 20 mg IV methyl prednisone. IVIG was provided at a very slow rate over 12 hours (1ml/kg/hour). Although, symptomatically the patient tolerated this therapy well, the following day, patient’s creatinine elevated to 3.8 from baseline 2.5, potassium of 7.1 from 5.2, bicarbonate of 17 from 21. Overall the clinical picture appeared to be due to IVIG induced osmotic nephropathy. The 3rd dose of IVIG was discontinued. The patient underwent conservative therapy. His renal function started to improve gradually and returned to baseline 2.43 at 1 week follow-up.

*Results: IVIG is generally well tolerated; the most common side effects include fever, nausea, chills and hypotension. Occasional aseptic meningitis, hemolysis and anaphylaxis have been reported. Acute renal failure after IVIG therapy is a rare complication. The estimated incidence is less than 1%, risk factors include age >65 years, pre-existing renal failure, diabetes, hypovolemia or concomitant use of nephrotoxic age. Renal insufficiency is typically reversible, and management consists of discontinuation of IVIG and supportive measures. In less than one-third of the cases, dialysis is required.

*Conclusions: The pathomechanism of the nephrotoxicity has not been clearly defined. Incidence of AKI are reported mainly with sucrose containing IVIG. The hypothetical association for acute renal failure with sucrose containing IVIG is likely related due to the similar histopathology finding of acute tubular interstitial nephropathy caused by osmotic stress to the proximal tubules seen in patients who received IVIG treatment and in patients who have historically received high doses of IV sucrose. A different study compared incidence of renal failure with IVIG therapy with different concentrations of sucrose which showed no significant differences in changes in serum creatinine between the groups. Data for non sucrose based IVIG causing AKI is lacking. In summary, no definite conclusion can be drawn concerning the role of the stabilizing agent in the genesis of acute renal failure.

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