2.3. Risk factors relating to chronic decline in graft function

With an increased risk of cardiovascular complications, homocysteine, infection, pathological coagulation and fibrinolysis are associated.

Anemia is a risk factor for the development of cardiovascular disease in patients with a transplanted kidney. The American Society of Transplantation (AST) defines anemia as a hemoglobin concentration lower than 120 g/l in men and lower than 110 g/l in women [29]. Anemia occurs in 20–60% of patients with a transplanted kidney, and its prevalence is the highest in the early post-transplant period (6–12 months after kidney transplantation). The main causes of its development in the early post-transplant period are: blood loss due to surgery, abrupt termination of erythropoietin administration, iron deficiency, bone marrow suppression caused by induction therapy, increased erythropoietin resistance due to infection (viral infection) and/or inflammatory status caused by systemic immune response on the presence of alloantigens, the use of drugs (mycophenolate mofetil). Reduced production of endogenous erythropoietin due to loss of allograft function, erythropoietin resistance due to secondary hyperparathyroidism and chronic microinflammatory disease are the main causes of anemia in late post-transplantation [30].

Post-transplantation anemia (a hemoglobin less than 110 g/l 3 months after renal transplantation) was associated with the development of congestive heart failure, a lower survival rate of allograft and patient, and a higher rate of acute rejection [31]. The relative risk for the cardiovascular incident was 1.32 with a decrease in hemoglobin by 0.5 g/dl, which is just slightly less than the relative risk of 1.37 related to an increase in systolic pressure of 15 mmHg. Anemia together with hypertension leads to left ventricular hypertrophy.

2.2. Risk factors related to the status of transplantation and its treatment

320 Organ Donation and Transplantation - Current Status and Future Challenges

vascular disease.

<60 ml/min/1.73 m2

especially when it is below 45 ml/min/1.73 m2

coagulation and fibrinolysis are associated.

of anemia in late post-transplantation [30].

patients with creatinine clearance <25, 25–50, and >50 ml/min [28].

2.3. Risk factors relating to chronic decline in graft function

In patients who at the moment of transplantation have no signs of atherosclerosis, reduced graft function and immunosuppressive therapy may cause hypertension, dyslipidemia, diabetes mellitus, and proteinuria, which can lead to myocardial infarction, stroke, or peripheral

Allograft function disorder is a risk factor for the development of cardiovascular disease [24]. A year after renal transplantation, chronic allograft disease at stage 3 (glomerular filtration

has 15% of patients [25]. With the decline in the allograft function, nontraditional risk factors appear. They occur when the glomerular filtration value falls below 60 ml/min/1.73 m2

. Reduced function of transplanted kidney in transplant recipient is an independent and important risk factor for the development of cardiovascular diseases due to adverse effects on hypertension, anemia, dyslipidemia, hyperhomocysteinemia [26]. The American National Kidney Foundation (NKF) reported that the value of glomerular filtration (GFR) measured or estimated is a better parameter of renal function than serum creatinine only [27]. The prevalence of left ventricular hypertension is inversely proportional to the level of glomerular filtration. In one study, the frequency of left ventricular hypertension was 45, 31 and 27% in

With an increased risk of cardiovascular complications, homocysteine, infection, pathological

Anemia is a risk factor for the development of cardiovascular disease in patients with a transplanted kidney. The American Society of Transplantation (AST) defines anemia as a hemoglobin concentration lower than 120 g/l in men and lower than 110 g/l in women [29]. Anemia occurs in 20–60% of patients with a transplanted kidney, and its prevalence is the highest in the early post-transplant period (6–12 months after kidney transplantation). The main causes of its development in the early post-transplant period are: blood loss due to surgery, abrupt termination of erythropoietin administration, iron deficiency, bone marrow suppression caused by induction therapy, increased erythropoietin resistance due to infection (viral infection) and/or inflammatory status caused by systemic immune response on the presence of alloantigens, the use of drugs (mycophenolate mofetil). Reduced production of endogenous erythropoietin due to loss of allograft function, erythropoietin resistance due to secondary hyperparathyroidism and chronic microinflammatory disease are the main causes

Post-transplantation anemia (a hemoglobin less than 110 g/l 3 months after renal transplantation) was associated with the development of congestive heart failure, a lower survival rate of allograft and patient, and a higher rate of acute rejection [31]. The relative risk for the cardiovascular incident was 1.32 with a decrease in hemoglobin by 0.5 g/dl, which is just slightly less

) has 60%, and in stage 4 (glomerular filtration value <30 ml/min/1.73 m<sup>2</sup>

)

, and

Treatment of patients with transplanted kidney and post-transplant anemia should be started with erythropoietin, when the hemoglobin concentration is less than 110 g/l and the target hemoglobin level should be 110–120 g/l.

Homocysteine concentration is an independent risk factor for cardiovascular disease after kidney transplantation [32]. In patients with a transplanted kidney, the concentration of homocysteine decreases compared to patients treated with dialysis but is higher than the concentration of homocysteine in healthy population, so hyperhomocysteinemia is common in patients after kidney transplantation [33]. For the treatment of hyperchomocysteinemia, we use folate and Vitamin B (12).

There is clear evidence that elevated levels of fibrinogen, factor VII, and von Willebrand factor in the general population are associated with an increased risk of acute insult or coronary disease [34]. These factors have also been elevated in patients following kidney transplantation, in more patients with cardiovascular disorders than in patients who do not have them.

Secondary hyperparathyroidism is a risk factor for the development of cardiovascular disease in patients with a transplanted kidney [35]. After transplantation of the kidney, hyperparathyroidism is maintained in 50% of patients, characterized by hypercalcaemia, hyperphosphatemia and increased parathormone concentration [36]. Secondary hyperparathyroidism in post-transplantation may also occur new, as a consequence of the decline in the function of the allograft and the lack of calcitriol. The disorder of metabolism of calcium and phosphate results in calcification of peripheral arteries, including coronary artery calcification. Cinacalcet may be useful in the treatment of persistent hyperparathyroidism after kidney transplant.

The effect of local inflammatory stimulus such as products of the oxidation process, the end products of glycosylation and chronic infectious processes alter the blood vessel in terms of the development of atherosclerosis. Microinflammation is a risk factor for the development of atherosclerotic cardiovascular diseases in patients with a transplanted kidney [24]. These patients have a low level of microinflammation as a consequence of a systemic immune response to the presence of all antigens but also because of chronic infections [25]. C-reactive protein >5 mg/l > 0.5 mg/dl) is associated with an increased risk of developing cardiovascular events in the population of patients with a transplanted kidney.

Proteinuria occurs in one-third of post-transplant patients and is a risk factor for the development of cardiovascular disease in patients with a transplanted kidney [37].
