Aim
Increased venous thrombosis and arterial embolism rates are observed in the general population during or after COVID‐19. Data regarding the kidney transplant population are scarce. In this study, ...we aim to investigate the thrombotic complications and risk factors associated with thrombotic complications in kidney transplant patients.
Methods
This retrospective observational study included adult kidney transplant recipients diagnosed with COVID‐19 between March 2020 and June 2022. The endpoint was the occurrence of thromboembolic events.
Results
Four hundred and sixty‐nine patients were followed for a median of 10.8 months after COVID‐19. Forty patients (8.5%) died. Thromboembolic complications developed in 51 (11.9%) of the surviving patients. Twenty‐four patients with thromboembolic events were receiving prophylactic anticoagulation before the event. The patients with mild, moderate, and severe COVID‐19 were 292, 129, and 48, respectively. Patients with moderate COVID‐19 had a significantly higher percentage of thromboembolic complications than patients with mild COVID‐19. Older age, prior heart disease, and moderate COVID‐19 were significantly associated with thromboembolic events. The incidence of thromboembolic events after COVID‐19 is 10.9 per 100 patient‐year.
Conclusion
Thromboembolic complications were observed at increased rates in kidney transplant recipients after COVID‐19. Therefore, prospective and cohort studies for post‐COVID‐19 complications regarding the treatment modalities are urgently needed.
Summary at a glance
This study reveals that thromboembolic complications occurred in kidney transplant recipients after COVID‐19. Older age, prior heart disease, and moderate COVID‐19 were significantly associated with thromboembolic events.
The dipeptide boronic acid analogue bortezomib as a potent and selective inhibitor of the proteasome is used for the treatment of plasma cell dyscrasias such as multiple myeloma (MM). Bortezomib may ...induce glomerular microangiopathy (GMA) with or without systemic thrombotic microangiopathy (TMA) in which vascular endothelial growth factor-nuclear factor (VEGF) -κ B pathway could be involved. MM itself can cause TMA but primarily at presentation. Case report: We present a case with GMA associated with clinical features supporting systemic TMA shortly after bortezomib. Case: A 54-year-old woman has been diagnosed as having POEMS syndrome. She had symmetric mild degree of peripheral neuropathy, scleroatrophic skin lesions, Raynaud's phenomenon, and retinopathy. IgG kappa type paraproteinemia with a monotypic increase of plasma cells and increased pulmonary artery pressure contributed to the diagnosis. Bortezomib based treatment was started. Methodology: At the 20th day she developed severe dyspnea. Bilateral pleural effusion and acute kidney failure with thrombocytopenia and microangiopathic hemolytic anemia were documented. Urgent steroid and plasmapheresis were started. ADAMTS13 level proved to be within normal and plasmapheresis did not contribute to improvement. She commenced on hemodialysis and kidney biopsy was decided. Light microscopy findings revealed glomerular capillary thrombus, basement membrane thickening and segmental Results: duplication. Hyperplastic arteriolar changes were present. No immune deposits were detected by immunofluorescence microscopy. Biopsy findings were diagnostic for thrombotic microangiopathy. The clinical picture deteriorated as sleepiness and confusion. Cranial imaging and cerebrospinal fluid analysis showed no abnormality. Eculizumab with off-label approval contributed to stabilization but no improvement. Conclusion: Conclusion: Proteasome inhibitors associated with TMA may be life-threatening along with organ dysfunction due to microangiopathy-related ischemia. Membrane attack complex (C5b-9) deposition was found on endothelial cells in culture exposed to plasma from patients during the acute phase of the disease which may point to complement blockade benefit.
Data to guide the evaluation of living-related donor candidates for kidney transplant recipients with Alport syndrome (AS) spectrum are limited. We aimed to examine a cohort of living-related donors ...to recipients with AS and compare their outcomes with a control group to improve understanding of the clinical course and outcomes of living donation in this context.
Living donors (LDs) of AS recipients and propensity score-matched control LDs without any family history of AS (control group) were followed for major cardiac events, death, post-donation estimated glomerular filtration rate (eGFR), and proteinuria.
There were 31 LDs (48.4% male), in whom relationship to AS recipient included mother (45.2%), father (32.3%), sibling (16.1%), grandparent (3.2%), and uncle (3.2%). Long-term outcomes over 10.0 (IQR, 3.0-15.0) years were evaluated in 25 and 25 LDs from study and control groups, respectively. During follow-up, 5 LDs (20.0%) in study group developed major cardiac event (acute coronary ischemia n = 4 and severe congestive heart failure n = 1) after 5.5 (IQR, 4.5-10.3) years, whereas only 2 (8.0%) LDs in control group developed major cardiac events (p = 0.221). New-onset hypertension was higher in study group (56.0%) compared to the control group (16.0%) (p = 0.003). Three donors in study and 2 donors in control group who developed new-onset hypertension died during follow-up (p = 0.297). Major cardiac event rate was significantly higher in donors who developed hypertension after donation (0 vs. 28.0%, p < 0.001). There were no differences between study groups regarding last eGFR and proteinuria levels (p = 0.558 and p = 0.120, respectively).
Although the risk of kidney disease can be minimized by careful donor evaluation, our findings suggest that hypertension risk after the donation is higher than expected in related donors of recipients with AS.
Background
Atypical hemolytic syndrome (aHUS) and C3 glomerulopathy (C3G) are complement-mediated rare diseases with excessive activation of the alternative pathway. Data to guide the evaluation of ...living-donor candidates for aHUS and C3G are very limited. The outcomes of living donors to recipients with aHUS and C3G (Complement disease-living donor group) were compared with a control group to improve our understanding of the clinical course and outcomes of living donation in this context.
Methods
Complement disease-living donor group
n
= 28; aHUS(53.6%), C3G(46.4%) and propensity score-matched control-living donor group (
n
= 28) were retrospectively identified from 4 centers (2003–2021) and followed for major cardiac events (MACE), de novo hypertension, thrombotic microangiopathy (TMA), cancer, death, estimated glomerular filtration rate (eGFR) and proteinuria after donation.
Results
None of the donors for recipients with complement-related kidney diseases experienced MACE or TMA whereas two donors in the control group developed MACE (7.1%) after 8 (IQR, 2.6–12.8) years (
p
= 0.15). New-onset hypertension was similar between complement disease and control donor groups (21.4% vs 25%, respectively,
p
= 0.75). There were no differences between study groups regarding last eGFR and proteinuria levels (
p
= 0.11 and
p
= 0.70, respectively). One related donor for a recipient with complement-related kidney disease developed gastric cancer and another related donor developed a brain tumor and died in the 4th year after donation (2, 7.1% vs none,
p
= 0.15). No recipient had donor-specific human leukocyte antigen antibodies at the time of transplantation. Median follow-up period of transplant recipients was 5 years (IQR, 3–7). Eleven (39.3%) recipients aHUS (n = 3) and C3G (n = 8) lost their allografts during the follow-up period. Causes of allograft loss were chronic antibody-mediated rejection in 6 recipients and recurrence of C3G in 5. Last serum creatinine and last eGFR of the remaining patients on follow up were 1.03 ± 038 mg/dL and 73.2 ± 19.9 m/min/1.73 m2 for aHUS patients and 1.30 ± 0.23 mg/dL and 56.4 ± 5.5 m/min/1.73 m2 for C3G patients.
Conclusion
The present study highlights the importance and complexity of living related-donor kidney transplant for patients with complement-related kidney disorders and motivates the need for further research to determine the optimal risk-assessment for living donor candidates to recipients with aHUS and C3G.
Graphical abstract
