Kidney transplantation from a systemic lupus erythematosus donor and 1-year follow-up: A case report.

Systemic lupus erythematosus (SLE) is usually regarded as a relative contraindication for deceased kidney donation. The pathological variations because of the changes in the immune environment after kidney transplantation (KT) are unclear, and the recovery of renal function is poorly understood. We present a case of KT from a deceased donor with SLE who was followed-up for one year. Although SLE-related hemangioma developed during the perioperative period, it was cured after interventional treatment. A pre-planned biopsy was performed one year after KT, and it was found that most of the pathological changes and immunofluorescent markers of lupus had resolved. Renal function was stable, and urinary protein and occult blood levels reduced one year after KT.

Passenger lymphocyte syndrome after ABO-mismatched kidney transplantation: A case report and literature review.

BACKGROUND: Passenger lymphocyte syndrome (PLS) is a rare post solid organ transplantation complication, usually occurring after ABO- or Rh-mismatched transplantation. In general, PLS can lead to severe hemolytic anemia, but it is usually a self-limited disease. Most PLS cases start with a decreased hemoglobin (Hb) level and require donor type RBC transfusion as the only treatment. CASE REPORT: In our case, the allograft was given by an O-type Rh-D(+) donor and received by an A-type Rh-D(+) recipient. The PLS was developed on the post-operative day (POD) 10 with an increased indirect bilirubin (IDBIL) level as the first clinical symptom, while the Hb level did not significantly decrease. The PLS was diagnosed on POD 17 by a direct antiglobulin test (DAT) and a blood group test. The patient quickly became stable on POD 18 after a total of eight units of O-type RBC transfusion. Kidney function was uneventful in the entire PLS period. CONCLUSION: In ABO-mismatched kidney transplantation, an increased level of IDBIL should be considered as the first symptom of PLS even without an Hb decrease. The kidney function may be not affected by the PLS symptoms.

Protective effect of estradiol copreservation against kidney ischemia-reperfusion injury.

Ischemia-reperfusion injury (IRI) is the major cause of delayed graft function (DGF) during the posttransplantation period. Estradiol (E2) prevents IRI-induced kidney dysfunction and tissue injury. However, many side effects limit E2's in vivo application. Recent evidence uncovers E2's expanded use in the field of transplantation. We aimed to study if and how E2 exerts protective activity during the period of kidney organ preservation. The autologous kidney transplant model in rats was first established. Rats were divided into 5 groups: normal group (N), sham group (sham), static cold storage (SCS) 4 hours group (control), SCS 4 hours + ethanol (1 µL/mL) group (solvent), and SCS 4 hours + ethanol (1 µL/mL) + E2 (1000 ng/mL) group (E2). ERα expression under hypothermia was measured by western blotting. Moreover, biochemical analyses of plasma levels of creatinine, BUN, estradiol, and testosterone were examined. Among all groups, kidney tissues were collected and processed for further western blot analysis about ERα, eNOS, Bcl-2, and Bax expression, histological analyses such as H&E staining to evaluate pathological severity. In addition, a TUNEL assay is performed to evaluate apoptosis. E2 copreservation upregulated ERα expression under hypothermia. Moreover, E2 copreservation reduced levels of creatinine and BUN in plasma but without affecting estradiol and testosterone. Further, E2 copreservation increased expression of eNOS and antiapoptotic Bcl-2 and decreases expression of proapoptotic Bax. E2 copreservation significantly inhibited IRI-induced apoptosis and evidently improved pathological severity in the kidney of rats. E2 copreservation exerts protective activity against IRI-induced pro-inflammatory and proapoptotic effects in kidneys during organ preservation time and improves transplanted kidney function.

Aldehyde dehydrogenase 2 regulates autophagy via the Akt-mTOR pathway to mitigate renal ischemia-reperfusion injury in hypothermic machine perfusion.

AIMS: Ischemia-reperfusion injury (IRI) is harmful to patients following kidney transplantation. Hypothermic machine perfusion (HMP) can be adopted to preserve grafts and reduce consequential injury. We hypothesized that aldehyde dehydrogenase 2 (ALDH2) partly mitigates kidney IRI via regulating excessive autophagy in HMP. MATERIALS AND METHODS: The rabbits were assigned to 5 groups: Normal, HMP, HMP + Alda-1, HMP + CYA and cold storage (CS). After the rabbit autologous kidney transplantation, renal pathology and function were evaluated by histological analysis, glomerular related proteins (desmin, nephrin), tubular injury factors (NGAL, Ki67), serum creatinine (Cr) and blood urea nitrogen (BUN). Oxidative stress molecular Malondialdehyde (MDA) and superoxide dismutase (SOD2) expression, as well as inflammatory cytokines (TNF-α, IL-6, IL-10) were assessed by immunohistochemistry. The expression of LC3, p62, ALDH2, p-Akt, mTOR, PTEN, p-PTEN, and 4-HNE were measured by immunohistochemistry, RT-PCR, Western blot analysis or ELISA. KEY FINDINGS: HMP was more effective than CS for kidney preservation, with p- ALDH2 expressed in greater quantities in HMP. The results of kidney pathology and function in HMP + Alda-1 were the best. The MDA & SOD2 and the Vyacheslav score were improved in HMP + CYA. ALDH2 reduced 4-HNE-induced oxidative stress, inflammatory infiltration, the expression of LC3, p62 and inhibited autophagy accompanied by activation of p-Akt and mTOR via p-PTEN/PTEN. SIGNIFICANCE: Akt-mTOR autophagy pathway is a novel target for ALDH2 to reduce renal IRI partly by inhibition of 4-HNE in HMP, then protecting the donated kidney received after cardiac death (DCD).