**4. Mineral bone disease**

Many CKD patients are at an increased risk of developing CKD- Renal mineral bone disease (MBD). They develop bone lesions symptomatically showing up as pain, including back pain, tendon ruptures, pruritus, and an increased incidence of pathological fractures. Studies show that patients with renal mineral bone disorders are predisposed to calcification of the cardiovascular system and, consequently, increased morbidity and mortality.

This has led to a shift in the treatment of renal mineral bone diseases from just looking at a single biomarker, such as serum calcium levels, to further considering the disease's physiology, thus a look into serum phosphate and parathyroid hormone levels (PTH) [37].

Before the knowledge of fibroblast growth factor 23 (FGF23) and its influence on secondary hyperparathyroidism, phosphate retention was considered the main factor in the disorder occurring [38].

A series of physiological events are triggered by retained phosphate, including hyperphosphatemia, low vitamin D3, and reduced calcium levels, which stimulate parathyroid hormone secretion enhancing phosphate excretion and secondary hyperparathyroidism in end-stage renal disease [39].

There have been observations by authors that hyperphosphatemia and hypocalcemia were evidence of calcitriol deficiency, suggesting that it would be the main culprit to secondary hyperthyroidism noting the complexity of the disease because of the several elements in the pathophysiology [37].

Several studies have documented a strong relationship between serum Fibroblast growth factor 23 levels and creatinine clearance, noting that a decline in renal function had an increase in the FGF23 levels. Further, patients with End Stage renal disease would have up to a 1000-fold above the normal growth factor levels attributed to the reticence of phosphate and decline in renal clearance [40, 41].

The dire consequences associated with secondary hyperparathyroidism place an emphasis on the need to promptly manage CKD renal mineral bone diseases with a keen look and follow-up checks on markers such as serum calcium, phosphate, and parathyroid hormone and calcitriol levels. In light of this, the KDIGO guidelines recommend the onset of management dependent on serial trends of the markers [42].

Through proper nutrition education and counseling, there is a need to limit daily phosphate intake to less than 800 mg, and this is possible by educating the patients on how to read food labels to look out for high phosphate-containing foods and carbonated drinks as well as additives.

This should be done with close nutritional assessment and monitoring as most food sources that are protein in nature are rich in phosphorus. This, in turn, would help prevent protein-energy malnutrition in chronic kidney disease.

Individualized nutrition plans, as far as dietary sources of phosphates are concerned, should have the priority with consideration to intestinal absorption. Plant-based phosphate sources have lower intestinal absorption than those inorganic sources.

The use of phosphate binders has come a long way to help reduce intestinal absorption by allowing the formation of a non-absorbable complex with phosphorus in the food. Three classes of these binders are in use currently, that is, calcium-based binders, aluminum-based binders, and non-calcium-based binders. Caution should

be taken with aluminum-based binders as their long-term use has been related to osteomalacia and encephalopathy.

The choice between calcium-based and non-calcium-based binder should, on the other hand, be guided by serum calcium, calcitriol levels, and parathyroid hormones Lest hypercalcemia occurs.

Low cholesterol levels, low uric acid levels, and anti-inflammatory effects have been attributed to using Savelamer, a non-calcium phosphate binder making it have some prominence, particularly where the serum calcium levels are normal. Dialysis is another efficient way of eliminating phosphorus from the bloodstream, yet this is possible with consideration of the type of dialysis, length of dialysis, and type of dialysate.

The most common length of hemodialysis is 4 hours with thrice-a-week sessions that eliminate up to 2600 mg of phosphate levels. However, this may be slightly lower for low resources settings where dialysis is done twice a week. Peritoneal dialysis will succeed at up to 220mmg of phosphate elimination when done four times a day with two-liter exchanges.

#### **4.1 Emerging treatment options for CKD MBD**

A new class of phosphate binders, sucroferric oxyhydroxide (PA21) and ferric citrate (JTT-751), are iron-based, calcium-free phosphate binders recently advanced into clinical practice. These have also been used to fix anemia in CKD and attenuate vascular calcification.

Klotho supplementation has also been suggested as a prophylactic or therapeutic therapy for averting secondary hyperparathyroidism. Equally, the usage of anti-FGF23 monoclonal antibodies (FGF23-Ab) to counteract the negative effects of high levels of FGF23 in animal models has been assessed. While counteraction of FGF23 has been characterized by improvement in secondary hyperparathyroidism, increased levels of serum phosphate, aortic calcification, and higher risk of mortality have been reported. Therefore, the therapeutic applicability of FGF23-Ab in humans is yet to be proven.

### **5. Conclusion**

Renal replacement therapy has a great impact on the nutrition status and the overall well-being of renal patients. This chapter discussed medical nutrition therapy focusing on different modalities of renal replacement therapy. It delved into nutrition assessment. Its benefits, and nutrient requirements for each renal replacement therapy. It, finally, discussed the nutrition management of protein energy wasting and mineral bone disease, conditions which are very common among people with end-stage renal diseases.

### **Acknowledgements**

We acknowledge the contribution of Dr. Francis Aila from the Department of Health, Homa Bay County, Kenya.

### **Conflict of interest**

The authors declare no conflict of interest.

*Medical Nutrition Therapy in Renal Replacement Therapy DOI: http://dx.doi.org/10.5772/intechopen.111998*
