Search

The 3 leading causes of death in patients after solid organ transplantation (SOT) include cardiovascular diseases, malignancies, and infections. According to our current understanding, the latter play the key role in the pathogenesis of atherosclerosis. Similarly, infections (mainly viral) are implicated in the pathogenesis of at least 20% of known neoplasms. In other words, the implications of acute and chronic infectious diseases in modern medicine, not only transplantology, are significant and ever‑increasing. Immunosuppressive treatment impairs the immune function, which renders the patient more susceptible to infections. Furthermore, treatment of infections in immunocompromised patients poses a challenge and SOT. The current publication provides a brief summary of the key information provided in 20 lectures on viral infections in patients after SOT delivered during the 9th Practical Transplantology Course in Warsaw, Poland on September 15-16, 2017.

Atrial fibrillation (AF) frequently occurs in patients with chronic kidney disease (CKD), and the rate reaches even 30% in patients with end-stage renal disease (ESRD). Patients with AF and CKD have a significantly higher risk of thrombotic complications, particularly ischemic stroke, and at the same time, a higher bleeding risk (proportionally to the grade of renal failure). In addition, AF and CKD share a number of comorbidities and risk factors, which results in increased mortality rates. Moreover, disturbances in hemostasis are common complications of kidney disease. Their occurrence and severity correlate with worsening renal function, including ESRD. At present, the incidence of bleeding is declining, while thrombotic complications have become the predominant cause of mortality. Prophylactic antithrombotic treatment reduces the rate of stroke and other thrombotic complications. Vitamin K antagonists (VKAs) have long been used in anticoagulant therapy, and more recently, non-vitamin K oral anticoagulants (NOACs) have been introduced, which are direct thrombin inhibitors. NOACs are a valuable anticoagulant option in this group of patients as long as a summary of product characteristics is followed. They are at least as effective as warfarin, while being safer, especially when it comes to intracranial hemorrhage. Renal function should be evaluated before initiation of NOACs and reevaluated when clinically indicated. Importantly, disturbances in hemostasis in patients with CKD and ESRD may lead to unexpected complications, such as extensive bleeding. If anticoagulation is administered to patients on dialysis, effects of an individual dialysis modality as well as interactions with other drugs given (eg, heparin) should be considered.

Introduction The prognosis of takotsubo syndrome (TTS) was recognized as benign. However, patients with TTS and chronic kidney disease (CKD) more often experience severe complications in the acute phase of the disease, particularly sudden cardiac arrest. Objectives We aimed to assess the impact of CKD on early and long-term outcomes, including mortality, among 95 patients with TTS. Patients and methods All patients underwent coronary angiography. Clinical, biochemical, and other medical data were recorded. Estimated glomerular filtration rate was assessed using the CKD‑EPI formula. Results CKD was diagnosed in 32% of the patients. Contrast‑induced acute kidney injury (CI‑AKI) was not reported in any of the patients. Patients with CKD were older but had a lower prevalence of positive cardiovascular family history as well as higher creatine kinase activity and concentrations of inflammatory parameters. During hospitalization, sudden cardiac arrest was more common in CKD patients. In‑hospital, 1‑year, and long‑term mortality rates were the highest in CKD patients, reaching 33.3% in long‑term follow‑up. Predictors of death in a multivariate analysis were body mass index, ejection fraction, and serum creatinine concentrations. Conclusions CKD is a novel and still underestimated risk factor for TTS. It may trigger TTS but, more importantly, it adversely affects the outcomes. Thus, it is important to assess kidney function in all patients with TTS to evaluate the risk of morbidity and mortality in follow‑up, as well as to adjust drug doses and implement preventive measures to avoid CI‑AKI when coronary angiography or contrast‑enhanced computed tomography is performed.

INTRODUCTION Secondary hyperparathyroidism (SHPT) is a common hormonal disorder associated with chronic kidney disease (CKD). The treatment of SHPT should lead to a reduction in parathormone concentrations by calcimimetics or active vitamin D administration and stabilization of calciumand phosphate metabolism. In the event of failure of conservative treatment, complete or partial parathyroid resection should be considered. OBJECTIVES The aim of the study was to assess the beneficial effects of a combination treatment with paricalcitol and cinacalcet in comparison with paricalcitol alone. PATIENTS AND METHODS A total of 64 hemodialyzed patients (mean [SD] age, 58 [16] years) with inadequate control of serum parathyroid hormone levels were treated with intravenous paricalcitol, while 16 patients simultaneously received oral cinacalcet. Laboratory tests (intact parathormone [iPTH], calcium, phosphorus) were performed on a monthly basis. In the study, iPTH, calium, phosphorus, and alkaline phosphatase levels were assessed at baseline and after 24 weeks of treatment with paricalcitol alone or in combination with cinacalcet. RESULTS In both groups, a significant decrease in the iPTH level was observed. Although paricalcitol affects calcium levels, no hypercalcemia was observed. The combination treatment did not result in a significant lowering of iPTH levels in comparison with paricalcitol alone. CONCLUSIONS Treatment of SHPT with intravenous paricalcitol in patients on hemodialysis is effective and has a good safety profile. The combination of paricalcitol and cinacalcet does not improve the outcomes. Moreover, the combined treatment does not affect calcium and phosphorus concentrations. The cost‑effectiveness of therapy should also be considered.

INTRODUCTION Hypertension is associated with hemostatic abnormalities and endothelial dysfunction. thrombin activatable fibrinolysis inhibitor (TAFI) is a glycoprotein linking coagulation and fibrinolysis. Objectives. We evaluated TAFI concentrations in patients with essential hypertension in relation to blood pressure. Additionally, we studied TAFI activator, thrombin activity (thrombin-antithrombin complexes--TAT, prothrombin fragments F1 + 2), thrombomodulin (TM)--a marker of endothelial cell injury, degree of plasmin generation (plasmin-antiplasmin complexes [PAP]), other markers of endothelial cell injury--von Willebrand factor (vWF). PATIENTS AND METHODS Seventy-two patients with essential hypertension (27 untreated, 13 treated with enalapril (angiotensin-converting enzyme inhibitor [ACEI]), 32 with beta-blocker, betaxolol). In every hypertensive patients ambulatory blood pressure measurements and echocardiography were performed. RESULTS All hypertensive patients did not differ with respect to age, creatinine, fibrinogen, D-dimers. In ACEI-treated patients a significantly higher TAFI concentration was observed when compared to beta-blocker-treated patients. In beta-blocker-treated patients both diastolic and systolic blood pressure were lower than in ACEI treated patients as well as ejection fraction, while serum triglycerides were higher. Diastolic blood pressure correlated significantly with TAFI concentrations in untreated patients (r = 0.27, p < 0.05), and in beta-blocker-treated patients (r = 0.25, p = 0.05), TAFI activity was inversely associated with interventricular septal diameter (r = -0.75, p < 0.01) in patients treated with ACEI. CONCLUSIONS Elevated TAFI concentrations and enhanced thrombin generation in hypertensive patients may contribute to atherosclerosis progression in this population. Differences in the studied parameters may be due to a small sample size, monotherapy and potential effects of antihypertensive drugs on glicemia, ejection fraction and triglycerides.