The tissue contained 49 glomeruli. chronic changes and a gradual decline in the renal allograft function. strong class=”kwd-title” Keywords: Lupus nephritis, Kidney transplant, Pregnancy Introduction Systemic lupus erythematosus (SLE) is an autoimmune disease that primarily affects women of reproductive Rabbit Polyclonal to NPY2R age. Lupus nephritis (LN) occurs in 22C54% of patients with SLE [1C3], and 14C17% of these patients progress to end-stage renal disease [3, 4]. Kidney transplantation is one of the treatment options for patients with LN-induced end-stage renal disease. Although LN is known to recur in 0C19% of renal allografts [7C18], protocol biopsies show a recurrence rate of 50% [19, 20]. However, kidney transplant recipients with LN have similar graft and patient survival to recipients with other etiologies [5, 7, 8, 14C18]. Its pathologic recurrence rate is high, but its impact on long-term prognosis is low. Kidney recipients with LN whose allografts are functionally stable (no proteinuria) may safely become pregnant 6?months to 2?years post-transplantation. Pregnant women with LN have a 5C46% risk of experiencing renal flares, depending on LN activity at conception [21C25]. During pregnancy, kidney transplant recipients with LN are at a risk of developing recurrent disease; however, this has not been reported. Herein, we present a kidney transplant recipient who developed proteinuria and deteriorating renal allograft function during pregnancy. This patient was diagnosed with recurrent LN on performing postpartum renal allograft biopsy. Case report The patient was a 37-year-old woman who was diagnosed with SLE at the age of 14?years. She presented with facial erythema, arthralgia, and Raynauds phenomenon. Blood tests indicated renal impairment and were positive for antinuclear and anti-double stranded DNA (dsDNA) antibodies. She was placed on steroids, cyclophosphamide, cyclosporine, and mizoribine. Her serum creatinine level then stabilized at 0.6C0.7?mg/dl, and proteinuria resolved. However, her renal dysfunction and proteinuria progressed at the age of 22?years. Renal biopsy at that time confirmed LN (International Society of Nephrology [ISN]/Renal Pathology Society [RPS] class IV?+?V). Despite receiving pulse steroids and cyclophosphamide therapy, she developed end-stage renal disease at the age of 26?years and was put on hemodialysis. Thereafter, SLE activity diminished and quiesced em . /em She underwent living donor kidney Dulaglutide transplantation at the age of 28?years, with the donor being her father. Basiliximab, methylprednisolone, tacrolimus, and mycophenolate mofetil (MMF) were administered as induction immunosuppressive therapy, followed by a maintenance regimen of methylprednisolone at a dose of 4?mg/day, tacrolimus at a dose of 2?mg/day, and MMF at a dose of 1000?mg/day. The trough level of tacrolimus was Dulaglutide 3C5?ng/ml. The serum creatinine level was Dulaglutide 1.0C1.2?mg/dl, without proteinuria after kidney transplantation. At the age of 31?years, given her desire to become pregnant, MMF was replaced by azathioprine (AZA) at a dose of 50?mg/day. This decision was reversed a year later as the serum creatinine level increased (1.2C1.4?mg/dl). A subsequent allograft biopsy did not contained glomeruli in light microscopy. No interstitial and vascular lesions caused by calcineurin inhibitor toxicity were observed. Immunofluorescence microscopy proved negative for immunoglobulins or complement components in the glomeruli. Electron microscopy revealed that there were no electron-dense deposits in the glomerular basement membrane to substantiate the recurrence of LN. Furthermore, she had no hypocomplementemia, and anti-dsDNA antibody testing was negative. The cause of deterioration of the renal allograft function was unclear, but since then, the renal allograft function was stable without proteinuria. MMF was again replaced with AZA at the age of 33?years. She became pregnant after intrauterine insemination, but had a miscarriage at 7?weeks of gestation. Tests for lupus anticoagulant, anticardiolipin antibodies, and anti-2glycoprotein-1 were negative, ruling out antiphospholipid syndrome. A second intrauterine insemination resulted in pregnancy at the age of 34?years and a viable birth at the Dulaglutide age of 35?years. Prior to this gestation, the serum creatinine level was 1.3C1.4?mg/dl and the Dulaglutide urine proteinCcreatinine ratio was 0.1C0.2?g/g creatinine. Urinary protein excretion increased at 14?weeks of gestation, plateauing at 2C3?g/g creatinine. The patient was hospitalized for abdominal pain and elevated blood pressure at 28?weeks of gestation. Her blood.
