Post-transplant erythrocytosis after kidney transplantation: A review.

Post-transplant erythrocytosis (PTE) is defined as persistently elevated hemoglobin > 17 g/dL or hematocrit levels > 51% following kidney transplantation, independent of duration. It is a relatively common complication within 8 months to 24 months post-transplantation, occurring in 8%-15% of kidney transplant recipients. Established PTE risk factors include male gender, normal hemoglobin/hematocrit pre-transplant (suggestive of robust native kidney erythropoietin production), renal artery stenosis, patients with a well-functioning graft, and dialysis before transplantation. Many factors play a role in the development of PTE, however, underlying endogenous erythropoietin secretion pre-and post-transplant is significant. Other contributory factors include the renin-angiotensin- aldosterone system, insulin-like growth factors, endogenous androgens, and local renal hypoxia. Most patients with PTE experience mild symptoms like malaise, headache, fatigue, and dizziness. While prior investigations showed an increased risk of thromboembolic events, more recent evidence tells a different story-that PTE perhaps has lessened risk of thromboembolic events or negative graft outcomes than previously thought. In the evaluation of PTE, it is important to exclude other causes of erythrocytosis including malignancy before treatment. Angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs) are the mainstays of treatment. Increased ACE-I/ARB use has likely contributed to the falling incidence of erythrocytosis. In this review article, we summarize the current literature in the field of post-transplant erythrocytosis after kidney transplantation.

Risk factors for progression from low level BK dnaemia to unfavorable outcomes after BK management via immunosuppressive reduction.

BACKGROUNDS: Effective management of BK viremia (BKPyV-DNAemia) in kidney transplant recipients (KTRs) involves regular monitoring and adjustment of immunosuppression. With this strategy, the majority of patients will clear BK or have ongoing, but non-significant, low-level BKPyV-DNAemia. However, despite adjustments, some will develop more severe sequelae of BK including BKPyV-DNAemia >5 log10 copies/mL and BK nephropathy, and others may develop de novo DSA (dnDSA) or acute rejection (AR). METHODS: This was a single-center study of KTRs transplanted at the University of Wisconsin-Madison between 01/01/2015 and 12/31/2017. In this study, we sought to elucidate characteristics associated with the progression of BKPyV-DNAemia to unfavorable outcomes after decreasing immunosuppressive medications for the management of BK viremia as described in consensus guidelines. RESULTS: A total of 224 KTRs fulfilled our selection criteria; 118 (53%) resolved or had persistent low DNAemia, 64 (28%) had severe BK/nephropathy, and 42 (19%) developed dnDSA or AR. In multivariable analysis, female gender (HR: 2.05; 95% CI: 1.08-3.90; P = .02); previous rejection (HR: 2.90; 95% CI: 1.04-8.12; P = .04), and early infection (HR: 0.81; 95% CI: 0.72-0.90; P < .001) were associated with the development of severe BK/nephropathy. Conversely, non-depleting induction at transplant (HR: 2.06; 95% CI: 1.03-4.11; P = .03), HLA mismatches >3 (HR: 2.27; HR: 1.01-5.06; P = .04), and delayed graft function (HR: 4.14; 95% CI: 1.12-15.28; P = .03) were associated with development of dnDSA and/or rejection. CONCLUSION: Our study suggests that almost half of KTRs with BKPyV-DNAemia managed by our immunosuppressant adjustment protocol progress unfavorably. Identification of these risk factors could assist the frontline clinician in creating an individualized immunosuppressive modification plan potentially mitigating negative outcomes.

Incidence, risk factors, and outcomes of post-transplant erythrocytosis after kidney transplantation.

The incidence, risk factors, and outcomes of kidney transplant recipients (KTRs) with post-transplant erythrocytosis (PTE) in the modern era of strong, protocolized immunosuppressive management are unknown. In this study, we aim to identify the incidence and risk factors of PTE and outcomes associated with PTE. This study examined adult KTRs transplanted at our hospital between 01/2001 and 12/2016. Controls were KTRs without PTE and selected in a 1:5 ratio using incident density sampling. Patient survival, graft survival, and vascular thromboembolism (VTE) incidence were outcomes of interest. Of 4,317 kidney transplants during the study period, 214 (5%) had PTE and were compared with controls. In the multivariate analysis, recipients with older age (HR: 0.97, 95% CI 0.96-0.99, p = .001) were less likely to develop PTE, while male gender (HR: 3.2; 95% CI: 1.92-5.3, p < .001) and non-preemptive transplant (HR: 3.86, 95% CI 1.56-9.56, p = .003) were associated with increased risk of PTE. After adjustment for confounding factors, PTE was not associated with patient mortality (HR: 0.99, 95% CI 0.69-1.42, p = .97), graft failure (HR: 1.11, 95% CI 0.68-1.80, p = .69), or VTE (HR: 1.07, 95% CI 0.59-1.96, p = .81). The incidence of PTE is still substantial in this era, but with proper management PTE does not impact patient or graft survival.