Kidney Transplant Recipients With Rheumatic Diseases: Epidemiological Data From the Polish Transplant Registries 1998-2015.

Chronic kidney disease (CKD) is a common complication of rheumatic disorders. We analyzed the incidence of different rheumatic conditions as a primary diagnosis of end-stage renal disease (ESRD) in kidney transplant recipients in Poland. Data were received from the national waiting list for organ transplantation (Poltransplant) registries. Primary diagnosis leading to ESRD were analyzed in 15,984 patients who received kidney transplants between 1998 and 2015. There was no information about primary diagnosis in 4981 cases (31%) and in 1482 cases (9%) the diagnosis was described as unknown. Rheumatic diseases were specified in 566 (5.14%) kidney transplant recipients: lupus erythematosus, (systemic lupus erythematous nephritis) in 211 (1.92%), vasculitis in 176 (1.60%), amyloidosis AA in 82 (0.75%), hemolytic uremic syndrome in 59 (0.54%), secondary glomerulonephritis in 24 (0.22%), scleroderma in 9 (0.08%), rheumatoid arthritis in 4 (0.04%) and Sjögren syndrome in 1 (0.01%). Graft survival at 1 and 5 years were significantly better in the nonrheumatic versus rheumatic group (90 vs 87% and 76 vs 72% respectively, P = .04). Recipient survival at 5 years was significantly better in the nonrheumatic versus the rheumatic group (88 vs 84%, P = .02). Our study showed that systemic lupus erythematosus and systemic vasculitides are the major rheumatic causes of ESRD in the Polish population. Long-term graft and recipient survival were significantly better in the nonrheumatic versus the rheumatic group in the Poltransplant cohort.

Attenuated post-exercise heart rate recovery in patients with systemic lupus erythematosus: the role of disease severity and beta-blocker treatment.

Objective Sinus tachycardia is frequently reported in systemic lupus erythematosus (SLE), while there are limited data on post-exercise ability to slow heart rate (i.e. heart rate recovery, HRR) in this group of patients. Methods We studied consecutive 70 patients with SLE and 30 healthy controls. All examined individuals underwent detailed clinical examination, echocardiography, Holter monitoring with heart rate variability and treadmill stress test using Bruce's protocol. HRR values were calculated as the difference between maximum HR during exercise and HR at the first (HRR1) and third (HRR3) minute of rest. Individuals with coronary artery disease, diabetes mellitus and suspected pulmonary hypertension were excluded from further analysis ( n = 15). Results Fifty-five SLE patients were eligible for this study: aged 41.5 ± 12.4 years, 87.3% women, SLICC/ACR-DI score 3.58 ± 1.85. In the SLE group 36.4% patients received beta-blockers, usually for previously detected sinus tachycardia and/or arterial hypertension. Mean HRR1 (36.9 ± 12.6 vs 49.5 ± 18.6, p = 0.0004) and HRR3 (55.5 ± 14.3 vs 69.2 ± 16.4, p = 0.0001) were significantly lower in SLE than in healthy individuals. Significantly negative correlations between SLICC/ACR-DI score and HRR1 ( r = -0.299, p = 0.01), HRR3 ( r = -0.361, p = 0.001) and exercise capacity ( r = -0.422, p < 0.0001) were revealed. Additionally, beta-blocker treatment was also revealed to alter significantly HRR1, HRR3 and exercise capacity in SLE. Conclusion Patients with SLE are characterized by attenuated HRR after exercise. In our study impaired HRR was associated with disease severity and beta-blocker treatment and probably with disease duration. The use of HRR assessment in SLE can be used as an additional marker of cardiac autonomic nervous system dysfunction.

Differential association of juvenile and adult systemic lupus erythematosus with genetic variants of oestrogen receptors alpha and beta.

Oestrogens acting via nuclear receptors (encoded by ESR1 or ESR2) are important for pathogenesis of systemic lupus erythematosus (SLE). rs2234693 and rs4986938 are two single nucleotide polymorphisms (SNPs) whose C and A variants increase transcription of ESR1 and ESR2, respectively. The T allele of rs2234693 was associated with early onset SLE, whereas the role of rs4986938 in SLE was not reported. Our aim was to examine the role of rs2234693 and rs4986938 in conferring susceptibility to juvenile and adult SLE (jSLE and aSLE). Genotype distribution of both SNPs was analysed in 84 jSLE, 112 aSLE patients and 1001 controls. Allele C of rs2234693 was associated with jSLE (OR = 1.87, p = 0.006, p(corrected) = 0.02), whereas allele A of rs4986938 showed an association with aSLE (OR = 1.46, p = 0.008, p(corrected) = 0.03). In jSLE, rs2234693 C had lower frequency in patients with central nervous system involvement (OR = 0.39, p = 0.005, p(corrected) = 0.04) and showed a trend for increase among males, patients with renal involvement and those without DR2/3 (p < 0.05, p(corrected) > 0.05). Whereas our results are consistent with a role of ESR1 variation in jSLE, more studies are needed since the direction of association was the opposite of that reported previously. The association between rs4986938 (ESR2) and aSLE is a novel finding, consistent with our recent report associating this variant with Graves' disease.