**5. References**

Al Nowaiser A.; Roberts GJ.; Trompeter RS.; Wilson M.; Lucas VS. (2003). Oral health in children with chronic renal failure. *Pediatr Nephrol*, 18, pp. 39-45.

**4.2 Possible association of periodontal disease with chronic renal failure** 

disease may have an effect on CRF through several possible mechanisms.

Periodontal disease may have an effect on CRF and also the treatment of CRF. Periodontal

a. Moderate to severe periodontal disease may increase the serum level of C-reactive protein (CRP). CRP is an acute phase protein and systemic marker of inflammation which is also a major risk predictor for cardiac disorder and all other mortality cause of CRF persons (Craig, 2008). Several studies have reported periodontal disease to be associated with elevated CRP as well as other serum components of the acute phase response including decreased high density lipoprotein cholesterol, low density lipoprotein cholesterol, blood glucose and decreased peripheral blood neutrophil function and count (Muntner et al., 2000). Since all these factors are also risk factors for CRF, it might be justifiable to assume that periodontal disease may be considered as a predisposing factor and/or marker of CRF. Moreover, periodontal disease in a person with CRF has a strong tendency to increase the possibility of the complication of

b. Several reports found that periodontitis may also contribute to the systemic inflammatory burden in ESRD. The level of IgG antibody particularly to *Porphyromonas gingivalis* correlated with elevated serum CRP (Muntner et al., 2000). Therefore, it is also important to consider an effective periodontal therapy in order to reduce the level of serum CRP which might eventually decrease the inflammatory

On the other hand, there are also some studies which failed to find the type of correlations mentioned above (Kitsou et al., 2000; Marakoglu et al., 2003; Duran et al., 2004; Bots et al., 2006). It is acknowledged that differences in research design, measurement methods instruments used, and other factors may have resulted in different findings. Therefore, it is still relevant and reasonable to execute further research using a more sophisticated and well-designed method to elucidate the relationship between CRF and periodontal

Al Nowaiser A.; Roberts GJ.; Trompeter RS.; Wilson M.; Lucas VS. (2003). Oral health in

children with chronic renal failure. *Pediatr Nephrol*, 18, pp. 39-45.

osteocalcin.

coronary atherosclerosis.

burden of ESRD or CRF.

disease.

**5. References** 

when resorption and formation are coupled and a specific marker of bone formation when formation and resorption are uncoupled (Bullon et al., 2005). Osteocalcin has also been found in the gingival crevicular fluid (GCF). Several studies found an increased level of serum osteocalcin in subjects with CRF. Moreover, the level of GCF osteocalcin was found to be significantly associated with periodontal disease, since there was an association with pocket depth, clinical attachment level and bleeding on probing (Bullon et al., 2005). Therefore, it might be reasonable to explain an effect of CRF on periodontal disease by its effect on bone metabolism (especially alveolar bone) which is specifically marked by the level of serum osteocalcin and/or GCF


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**6**

*USA* 

*Washington DC,* 

**Sarcoidosis and Kidney Disease** 

*Department of Medicine, Washington Hospital Center,* 

Tulsi Mehta, Anirban Ganguli and Mehrnaz Haji-Momenian

Sarcoidosis is an illness of granulomatous inflammation with multi-organ association. While most individuals exhibit pulmonary pathology, renal involvement is not without prevalence or significance. This chapter will review the current epidemiology of the disease and explore the two major pathways in the pathogenesis of renal sarcoidosis, mainly granulomatous deposition and deranged calcium management. With these concepts addressed, further inquiries into intrinsic renal disease will be provided along with explanations of renovascular complications, obstructive nephropathy, and transplant pathology. Each ailment will be accompanied by common presentation, more detailed pathophysiology, appropriate diagnostics, and current treatment recommendations. This chapter will seek to

Sarcoidosis can affect a wide range of racial and ethnic groups but it has high prevalence in northern European countries, Japan, and the United States1. Certain countries have skewed incidences, for example: black Americans are three times more likely than white Americans to develop the disease (Iannuzzi et al. 2007). However, across the racial and ethnic groups, females are more prone to the illness than males (Iannuzzi et al. 2007). The disease manifests itself typically in patients less than 50 years of age and mainly in the third of fourth decade of life (Iannuzzi et al. 2011). A patient with a first degree relative with the disease has a fivefold increase of developing sarcoidosis. Nevertheless, this risk still does not exceed 1% (Iannuzzi et al. 2011). Patient susceptibility also increases with certain associations of genetics and environmental factors. Discoveries into HLA gene products and the butyrophilin-like2 (BTNL2) gene are the latest areas of genetic interests (Iannuzzi et al. 2007). A variety of environmental triggers including wood-burning stoves, tree pollen, inorganic particles, insecticides, and mold have also been scrutinized in addition to mycobacteria and propionibacteria antigens (Iannuzzi et al. 2007, 2011). In fact, combinations of genetic and environmental activators have also been examined, for example: HLA-DQB1 and water damage or high humanity in the workplace (Iannuzzi et al. 2007). However, it seems that a ubiquitous number of agents may initiate a similar immunologic pathway that

purvey a comprehensive but concise exploration of renal sarcoidosis.

**2. Epidemiology & susceptibility** 

is pathognomonic for sarcoidosis.

**1. Introduction** 

Yoshihara, A.; Seida, Y.; Hanada, N; et al. (2004). A longitudinal study of the relationship between periodontal disease and bone mineral density in community-dwelling older adults. *J Clin Periodontol*, 31, pp. 680-684.
