**1.2 Accelerated atherosclerosis in CKD**

Despite all above mentioned uncertanities concerning the causal association between renal disease and accelerated atherosclerosis there is a considerable amount of knowledge in the field of pathophysiology and pathobiochemistry of this topic (Felström et al, 2003, Vaziri, 2006, Kwan et al, 2007, Saland &t Ginsberg, 2007, Tsimihodimos et al. 2008 and 2011, Basnakian at al, 2010; Karumanchi & Thadhani, 2010). An overview of different factors influencing the rate of atherosclerosis in CKD, CRI and ESRD is summarized in Table 2. These factors however do not act independently but in the frame of a complicated and not yet fully understood network (Fig 1.). They are present already in the early phases of kidney diseases and in many cases other pathological conditions associated with accelerated atherosclerosis (obesity, diabetes, hypertension, etc.) are present, too.

Dyslipidemia (increased triglycerides and LDL-cholesterol, decreased HDL-cholesterol) Atherogenic lipid fractions (oxidized and carbamylated LDL, small dense LDL, triglyceride rich particles) Abnormal values and forms of apolipoproteins (apoB, apoAI, Lp(a)) Uremic toxins Alterations of calcium and phosphorus metabolism Oxidative stress (increased formation of reactive oxygen species and advanced glycation endproducts, decreased acitivty of antioxidants) Immunodeficiency Inflammation Malnutrition, hypalbuminemia and proteinuria Anaemia Physical inactivity Ethnicity and genetic polymorphism Drug treatment Hemodialysis modalities Peritoneal dialysis

Table 2. Factors influencing atherosclerosis development in CKD, CRI and ESRD

### **1.3 The aim of this chapter**

In this chapter the authors try to answer some question conserning accelerated atherosclerosis and its assessment in CRI patients. In the subsequent parts they:

Chronic glomerulonephritis 30% 30% 9% 47% **Diabetic nephropathy** 16% 22% 43% 31% **Hypertension** 12% 14% 26% 10% **Chronic interstitial nephritis** 8% 10% 2% 2% **Polycystic degeneration** 6% 6% 2% 2% **Other/unkown** 28% 18% 13% 8%

Table 1. Etiology of end stage renal disease in different regions of word. (According to

Despite all above mentioned uncertanities concerning the causal association between renal disease and accelerated atherosclerosis there is a considerable amount of knowledge in the field of pathophysiology and pathobiochemistry of this topic (Felström et al, 2003, Vaziri, 2006, Kwan et al, 2007, Saland &t Ginsberg, 2007, Tsimihodimos et al. 2008 and 2011, Basnakian at al, 2010; Karumanchi & Thadhani, 2010). An overview of different factors influencing the rate of atherosclerosis in CKD, CRI and ESRD is summarized in Table 2. These factors however do not act independently but in the frame of a complicated and not yet fully understood network (Fig 1.). They are present already in the early phases of kidney diseases and in many cases other pathological conditions associated with accelerated

Dyslipidemia (increased triglycerides and LDL-cholesterol, decreased HDL-cholesterol) Atherogenic lipid fractions (oxidized and carbamylated LDL, small dense LDL,

Oxidative stress (increased formation of reactive oxygen species and advanced glycation

Table 2. Factors influencing atherosclerosis development in CKD, CRI and ESRD

atherosclerosis and its assessment in CRI patients. In the subsequent parts they:

In this chapter the authors try to answer some question conserning accelerated

**Britain Australia USA Japan** 

**Etiology of ESRD Great** 

atherosclerosis (obesity, diabetes, hypertension, etc.) are present, too.

Abnormal values and forms of apolipoproteins (apoB, apoAI, Lp(a))

Alterations of calcium and phosphorus metabolism

endproducts, decreased acitivty of antioxidants)

Malnutrition, hypalbuminemia and proteinuria

Ethnicity and genetic polymorphism

Viklický, 2006)

**1.2 Accelerated atherosclerosis in CKD** 

triglyceride rich particles)

Uremic toxins

Anaemia

Immunodeficiency Inflammation

Physical inactivity

Hemodialysis modalities Peritoneal dialysis

**1.3 The aim of this chapter** 

Drug treatment


Therapeutic attempts and possibilities to normalize the lipid abnormalities and decrease the high risk of cardiovascular events in CRI, ESRD and HD patients are not the topics of this chapter.

Fig. 1. Factors responsible for abnormal lipid metabolism and accelerated atherosclerosis in kidney disease form a complicated and intertwined network
