Clinical impact using low-dose mycophenolate mofetil with tacrolimus on infectious, noninfectious complications and acute rejection, in renal transplant: A single hospital experience in Mexico.

Evidence supporting a starting dose of 2 g/day of mycophenolate mofetil (MMF) in combination with tacrolimus (TAC) for renal transplantation (RT) is still limited, but maintaining a dose of <2 g could result in worse clinical outcomes in terms of acute rejection (AR). This study aimed to determine the association between AR and infectious and noninfectious complications after RT with a dose of 1.5 g vs 2 g of MMF. A prospective cohort study was performed with a 12-month follow-up of recipients of RT from living donors with low (1.5 g/day) or standard (2 g/day) doses of MMF. The association between adverse effects and complications and doses of MMF was examined using Cox proportional hazard models, and survival free of AR, infectious diseases, and noninfectious complications was evaluated using the Kaplan-Meier test. At the end of the follow-up, the incidence of infectious diseases was 52% versus 50% (P = .71) and AR was 5% versus 5% (P = .86), respectively. The survival rate free of gastrointestinal (GI) complications requiring medical attention was higher in the low-dose group than in the standard-dose dose (88% vs 45%, respectively; P < .001). The use of 1.5 g/day of MMF confers a reduction in GI complications without an increase in infectious diseases or the risk of AR.

Humoral Acute Rejection in a Kidney Transplant Recipient with Idiopathic Thrombocytopenic Purpura.

A 47-year-old male was diagnosed with chronic kidney disease (CKD) in 2011; idiopathic thrombocytopenic purpura (ITP) was also diagnosed in 2011 refractory to medical treatment and finally treated with splenectomy (2017) without relapses since that date, 5 blood transfusions, and 4 platelet apheresis in 2017. Renal transplant from a living related donor (brother), ABO compatible, crossmatch were negative, sharing 1 haplotype. Donor-specific anti-HLA antibody was negative. Graft function was stable until the 5th day and graft biopsy on the 6th day; thrombotic microangiopathy (TMA), C4D negative and inflammatory infiltration of polymorphonuclear leukocytes inside peritubular capillary, and anti-MICA antibodies were positive. The treatment used were plasmapheresis, intravenous immunoglobulin, and rituximab. Serum creatinine began to decrease since the 14th day, and by day 33, post-RT graft function was restored.

Donor-specific antibodies development in renal living-donor receptors: Effect of a single cohort.

Minimization in immunosuppression could contribute to the appearance the donor-specific HLA antibodies (DSA) and graft failure. The objective was to compare the incidence of DSA in renal transplantation (RT) in recipients with immunosuppression with and without steroids. A prospective cohort from March 1st, 2013 to March 1st, 2014 and follow-up (1 year), ended in March 2015, was performed in living donor renal transplant (LDRT) recipients with immunosuppression and early steroid withdrawal (ESW) and compared with a control cohort (CC) of patients with steroid-sustained immunosuppression. All patients were negative cross-matched and for DSA pre-transplant. The regression model was used to associate the development of DSA antibodies and acute rejection (AR) in subjects with immunosuppressive regimens with and without steroids. Seventy-seven patients were included (30 ESW and 47 CC). The positivity of DSA class I (13% vs 2%; P < 0.05) and class II (17% vs 4%, P = 0.06) antibodies were higher in ESW versus CC. The ESW tended to predict DSA class II (RR 5.7; CI (0.93-34.5, P = 0.06). T-cell mediated rejection presented in 80% of patients with DSA class I (P = 0.07), and 86% with DSA II (P = 0.03), and was associated with DSA class II, (RR 7.23; CI (1.2-44), P = 0.03). ESW could favor the positivity of DSA. A most strictly monitoring the DSA is necessary for the early stages of the transplant to clarify the relationship between T-cell mediated rejection and DSA.

Urinary expression of long non-coding RNA TUG1 in non-diabetic patients with glomerulonephritides.

Metabolic alterations serve a significant role in the pathogenesis of kidney disease. Long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is a known regulator of podocyte health and mitochondrial biogenesis. Although TUG1 protects against podocyte loss in models of diabetic nephropathy, it is unknown if urinary TUG1 expression is associated with clinical and histopathological findings in non-diabetic patients diagnosed with glomerulonephritides. In the present study, the expression of TUG1, podocyte-specific markers (nephrin and podocin) and mitochondrial biogenesis-associated mRNAs (transcription factor A mitochondrial, cytochrome C oxidase subunit 5A and peroxisome proliferator-activated receptor γ coactivator 1α) were examined in urinary sediment of non-diabetic patients with biopsy-confirmed glomerulonephritides and healthy controls. Urinary expression of TUG1 was significantly lower in patients with glomerulonephritides, particularly those diagnosed with Focal Segmental Glomerulosclerosis (FSGS). Furthermore, TUG1 levels were associated with urinary expression of podocyte-specific markers and mRNAs associated with mitochondrial biogenesis. Loss of TUG1 expression in urinary sediment was strongly associated with FSGS, highlighting the potential of this lncRNA and its mitochondrial biogenesis-associated targets as non-invasive biomarkers of assessing podocytopathy.