Focal Segmental Glomerulosclerosis (FSGS) recurrence after kidney transplantation (KTx) is relatively frequent and is associated with poor graft survival. The aim of this study was to investigate which management strategies were associated with better outcomes in our cohort of KTx recipients with primary FSGS. We retrospectively collected data on patients with primary FSGS who received a KTx between 1993 and 2019. A history of biopsy proven FSGS in native kidneys and new onset of significant proteinuria early post-KTx led to the diagnosis of recurrence, which was confirmed by graft biopsy. From 1993 to 2019 we performed 46 KTxs in patients with primary FSGS. We identified 26 episodes of recurrence in 25 patients, 67% of them occurring in males. They were younger at the time of KTx (33.8 vs. 41.1 years old, p = 0.067) and had progressed to end stage renal disease (ESRD) faster after FSGS diagnosis (61.4 vs. 111.2 months, p = 0.038), while they were less likely to have received prophylactic plasmapheresis (61.5% vs. 90%, p = 0.029). 76.7% of recurrences were found early, after a median of 0.5 months (IQR 0.1–1) with a median proteinuria was 8.5 (IQR 4.9–11.9) g/day. All patients with recurrence were treated with plasmapheresis, while 8 (30.7%) additionally received rituximab, 1 (3.8%) abatacept, and 4 (15.4%) ACTH. 7 (27%) patients experienced complete and 11 (42.3%) partial remission after a mean time of 3 (±1.79) and 4.4 (±2.25) months, respectively. Prognosis was worse for patients who experienced a recurrence. Eleven (42.3%) patients lost their graft from FSGS in a median time of 33 (IQR 17.5–43.3) months. In this series of patients, primary FSGS recurred frequently after KTx. Prophylacic plasmapheresis was shown efficacious in avoiding FSGS recurrence, while timely diagnosis and plasmapheresis-based regimens induced remission in more than half of the patients.

Background: Hypocomplementemic urticarial vasculitis syndrome is an infrequent condition characterized by ocular, renal, gastrointestinal and pulmonary involvement with low serum complement levels and autoantibodies. Renal manifestations vary from microscopic hematuria to nephrotic syndrome and acute kidney injury. Accordingly differing histologic patterns have been reported. Case presentation: We present the case of a 65 years old woman with a history of chronic uveitis who presented with arthralgias, urticarial rush, nephrotic syndrome, glomerular hematuria and low serum complement. Kidney biopsy revealed an immune-complex membranoproliferative glomerulonephritis. The patient received induction therapy with steroids, cyclophosphamide and hydroxychloroquine followed by rapid clinical improvement and remission of proteinuria. Maintenance treatment consisted of rituximab pulses. Conclusions: The majority of hypocomplementemic urticarial vasculitis syndrome cases is idiopathic, although an association to drugs, infections or other autoimmune disorders has been recorded. Given the rarity and heterogeneity of the disease, no standard treatment is established.

Erectile dysfunction (ED) is a common yet frequently underrecognized microvascular complication of diabetes, affecting up to three out of four individuals. Key contributing factors include advancing age, long-standing disease duration, and suboptimal glycemic control, as well as insulin resistance and androgen deficiency—the latter being particularly common in men with type 2 diabetes (T2D) and obesity. While numerous studies have investigated the effects of various antidiabetic therapies on diabetes-related ED, the results remain inconsistent, limiting definitive conclusions. In recent years, increasing attention has focused on a novel class of antidiabetic medications, namely glucagon-like peptide-1 receptor agonists (GLP-1 RAs). These agents have become central to the treatment of T2D due to their potent glucose-lowering properties and well-documented benefits on cardiovascular outcomes, and weight loss. Given these pleiotropic effects, GLP-1 RAs have been presumed to positively influence erectile function—a hypothesis supported by a growing body of experimental and clinical research. However, preliminary reports have also raised concerns about a possible association between GLP-1 RA use and ED. This narrative review aims to synthesize current evidence regarding the impact of GLP-1 RAs on erectile function, providing a platform for future research in this evolving field.

Allo- and autoimmune mechanisms are involved in kidney allograft rejection and loss. This study investigates the impact of anti-angiotensin II type-1 receptor antibodies (anti-AT1RAbs) detected alone or in association with HLA donor-specific antibodies (HLA-DSAs) on the outcome of kidney transplantation (KTx). Anti-AT1RAbs and HLA-DSAs were detected in 71 kidney transplant (KT) recipients who developed biopsy-proven acute or chronic active T-cell rejection (TCMR) (n = 51) or antibody-mediated rejection (ABMR) (n = 20), forming the rejection group (RG). The control group (CG) included 71 KTx recipients with comparable characteristics without rejection. All patients had been transplanted with negative T/B flow crossmatch (T/BFCXM). The median follow-up period was 3.7 years. Antibodies were determined pre- and periodically post-KTx by Luminex method for HLA-DSAs and enzyme-linked immunosorbent assay for anti-AT1RAbs. Before KTx, twenty-three (32.4%) patients in the RG, sixteen with TCMR and seven with ABMR, were found anti-AT1Rabs-positive (≥10 U/mL) versus eleven (15.5%) patients in the CG (p = 0.031). Simultaneous detection of preformed anti-AT1RAbs and HLA-DSAs was found in five patients of the RG versus two of the CG (p = 0.355). At the time of transplant biopsy, fifteen (21.1%) patients, four with ABMR and eleven with TCMR, were positive for anti-AT1RAbs. Anti-AT1RAbs and HLA-DSAs were detected simultaneously in 7/15 (46.7%) cases, three with ABMR and four with TCMR. During the follow-up, thirteen (18.3%) patients in the RG, eight with ABMR and five with TCMR, lost their graft compared to one patient (1.4%) in the CG (p = 0.001). Six out of thirteen (46.2%) RG patients who lost the graft were found positive for anti-AT1RAbs pretransplant. Patient survival with functioning graft did not differ significantly between anti-AT1Rabs-positive and negative KT recipients (log-rank p = 0.88). Simultaneous detection of anti-ATR1Abs and HLA-DSAs did not have a significant influence on patient survival with functioning graft (log-rank p = 0.96). Graft function at the end of the follow-up was better, but not significantly, in anti-AT1Rabs-negative patients, with serum creatinine 1.48 [1.20–1.98] mg/dL and eGFR (CKD-EPI) 48.5 [33.5–59.0] mL/min/1.73 m², compared to anti-AT1Rabs-positive ones who had serum creatinine 1.65 [1.24–2.02] mg/dL (p = 0.394) and eGFR (CKD-EPI) 47.0 [34.8–60.3] mL/min/1.73 m² (p = 0.966). Anti-AT1RAbs detection pretransplant characterizes KT recipients at increased risk of cellular or antibody-mediated rejection. Furthermore, anti-AT1RAbs, detected alone or simultaneously with HLA-DSAs, appear to be associated with impaired graft function, but their role in graft survival has not been documented in this study. Screening for these antibodies appears to complement pretransplant immunological risk assessment.

Background/Objectives: Malignancies constitute a major cause of death among kidney transplant recipients, and their incidence is increasing globally. We aimed to estimate the frequency of de novo malignancies and identify factors associated with their occurrence among kidney transplant recipients. Methods: Data were derived from the medical records of patients who received a kidney transplant between January 1979 and December 2023 in “Laiko” University Hospital in Athens, Greece. Κidney transplant recipients with a diagnosis of de novo malignancy were compared with recipients without malignancy and were matched for age, sex and year of transplantation. Demographic and clinical characteristics, data on immunosuppression and cancer type were recorded. Multivariate logistic regression was employed to identify possible risk factors for cancer occurrence. Results: Out of 2986 recipients, 268 (8.98%) developed malignancies within a median time of 8 (interquartile range—IQR: 4–16) years after transplantation. Of them, 59.3% were males, the median age at transplantation was 48 (IQR: 39–57) years and the median dialysis vintage was 31.5 (IQR: 9.5–70) months. In addition, 17.2% had a history of rejection. The majority (66.7%) received a combination of mycophenolate and a calcineurin inhibitor with or without steroids. The most frequent malignancies were lung cancer (13%) and post-transplant lymphoproliferative disease (13%), followed by Kaposi sarcoma (8.2%). At diagnosis, 37% had generalized end-stage disease and 19% had aggressive disease with poor prognosis. In multivariate analysis, a history of rejection (odds ratio—OR = 1.75, 95% CI = 1.04–2.94) and glomerulonephritis as primary kidney disease (OR = 2.23, 95% CI = 1.06–4.67) were both significantly associated with malignancy development, whereas immunosuppressive medication was not. Conclusions: Cancer occurrence among kidney transplant recipients was related to the cumulative burden of immunosuppression rather than a specific immunosuppressant.