Minimal Change Disease (MCD) and Human Chorionic Gonadotropin (hCG)-Mediated Thyrotoxicosis during Pregnancy

Introduction: Thyroid hormones influence cardiac output and RAAS activity with effects in GFR. Proteinuria has been associated with hypothyroidism but rarely with hyperthyroidism or Graves’ disease in non-pregnant adults. This is a case of AKI with severe proteinuria due to MCD in a woman presenting with hyperemesis gravidarum and gestational thyrotoxicosis. Case Description: A 19-year-old woman at 14 weeks of gestation presented with 4 weeks of hyperemesis accompanied by myalgias, fainting, and muscle weakness. Patient was normotensive, with dry skin and without peripheral edema. Labs showed AKI with creatinine (Cr) of 3.09mg/dL from a normal baseline, BUN of 123mg/dL, hypokalemia, hypophosphatemia, elevated CK of 663 U/L, transaminitis with direct bilirubinemia of 2.4 mg/dL and hypoalbuminemia of 3.0g/dL. TSH was undetectably at <0.005uIU/mL low with elevated free T4 at 4.07ng/dL and normal T3, antithyroid antibodies were negative. Diagnosis of HCG-mediated thyrotoxicosis was made. Urine studies showed total protein-to-Cr ratio of 10.3mg/mg and an albumin-to-Cr ratio of 5.7mg/mg. Kidney biopsy showed diffuse and severe acute tubular injury with myoglobin cast nephropathy. Electron microscopy showed global effacement of foot processes, vacuolization and microvillus transformation of podocytes and the absence of immune deposits. Patient received intravenous fluids, electrolyte replacement and symptomatic treatment of thyrotoxicosis with Propranolol. Emesis improved and she was able to tolerate an oral diet. At 17 weeks of gestation, creatinine had returned to baseline with mild proteinuria and no albuminuria. TSH and free T4 normalized. Discussion: MCD is rare in pregnancy, the etiology is unclear and management includes initiation of immunosuppression. High HCG levels during the first trimester of pregnancy can trigger thyrotoxicosis given structural homology with TSH and hyperemesis. In this case, we observed normalization of albuminuria and thyroid hormone levels as HCG levels dropped with pregnancy progression. We hypothesize that hyperfiltration from pregnancy and increased cardiac output due to increased thyroid activity could have played a role in proteinuria leading to podocyte effacement. Whether immune or inflammatory mechanisms are involved in the interaction between thyroid and kidney disease during pregnancy is unknown.