Patient Encounter Part 3

Kidney Function Restoration Program

Alternative Cure for Kidney Disease

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The patient returns to your clinic in one week and states that her symptoms have not changed. She is asking about the results from her laboratory studies.

Labs: WBC 4.5 x 103 cells/m3 (4.5 x 109/L); RBC 2.3 x 106 cells/m3 (2.3 x 1012/L); Hgb 8.1 g/dL (81 g/L or 5 mmol/L); Hct 24% (0.24); mean corpuscular volume (MCV) 88 fL; mean corpuscular hemoglobin concentration (MCHC) 35 g/dL (350 g/L); iron 35 mcg/dL (6.26 p,mol/L); total iron binding capacity (TIBC) 450 mcg/dL (80.55 p,mol/L); ferritin 75 ng/mL (168 pmol/L); transferrin saturation (TSAT) 15% (0.15); stool guaiac negative x 3

What treatment would you recommend for this patient for treatment of anemia? How would you evaluate the effectiveness of treatment of anemia?

Pathophysiology

As kidney function declines in patients with CKD, decreased phosphorus excretion disrupts the balance of calcium and phosphorus homeostasis. Decreased vitamin D

activation in the kidney also decreases calcium absorption from the GI tract. The parathyroid glands release PTH in response to decreased serum calcium and increased serum phosphorus levels. The actions of PTH include the following:

• Increasing calcium resorption from bone

• Increasing calcium reabsorption from the proximal tubules in the kidney

• Decreasing phosphorus reabsorption in the proximal tubules in the kidney

• Stimulating activation of vitamin D by 1-a-hydroxylase to calcitriol (1,25-dihydroxyvitmin D3) to promote calcium absorption in the GI tract and increased calcium mobilization from bone

All of these actions are directed at increasing serum calcium levels and decreasing serum phosphorus levels, although the activity of calcitriol also increases phosphorus absorption in the GI tract and mobilization from the bone, which can worsen hyper-phosphatemia. Calcitriol also decreases PTH levels through a negative feedback loop. These measures are sufficient to correct serum calcium levels in the earlier stages of CKD.

As kidney function continues to decline and the GFR falls less than 40 mL/min/

1.73 m , phosphorus excretion continues to decrease and calcitriol production de-

creases, causing PTH levels to begin to rise significantly, leading to secondary hyperparathyroidism (sHPT). The excessive production of PTH leads to hyperplasia of the parathyroid glands, which decreases the sensitivity of the parathyroid glands to serum calcium levels and calcitriol feedback, further promoting sHPT.

The most dramatic consequence of sHPT is alterations in bone turnover and the development of BMMD. Other complications of CKD can also promote BMMD. Metabolic acidosis decreases bone formation and excessive aluminum levels cause aluminum uptake into bone in place of calcium, weakening the bone structure. The patho-genesis of sHPT and BMMD are depicted in Figure 26-5.

The increased serum phosphorus binds to calcium in the serum, which leads to deposition of hydroxyapatite crystals throughout the body. The calcium-phosphorus

(Ca-P) product reflects serum solubility. A Ca-P product greater than 75 mg /dL

(5.81 mmol /L ) promotes crystal deposition in the joints and eye, leading to arthritis and conjunctivitis, respectively. Soft tissue deposition primarily affects the coronary arteries of the heart, lungs, and vascular tissue and is associated with a Ca-P product

greater than 55 mg /dL (4.44 mmol /L ). The Ca-P product has been associated with a 40% increase in mortality54 and is a risk factor for calcification of vascular and

soft tissues.

Metabolic acidosis, a common complication of CKD, also contributes to BMMD by altering the solubility of hydroxyapatite, promoting bone dissolution. Additionally, metabolic acidosis inhibits the activity of osteoblasts to decrease bone formation, while stimulating osteoclasts to promote bone resorption. Finally, metabolic acidosis can worsen sHPT by reducing the sensitivity of the parathyroid gland to serum calcium levels.55

Treatment

General Approach

O Diagnosis and management of bone disease in CKD is based on corrected serum levels of calcium and phosphorus, the Ca-P (using corrected calcium levels), and intact PTH levels (iPTH)5 The target levels of each vary with the stage of CKD and are listed in Table 26-5. The primary target for treatment is control of serum phosphorus levels, as this is the initial parameter that disrupts homeostasis. However, serum phosphorus can be difficult to control, particularly in the latter stages of CKD. Management of sHPT often requires supplemental treatment in addition to phosphorus management.

Pathophysiology Hyperparathyroidism

FIGURE 26-5. Pathogenesis of secondary hyperparathyroidism and bone and mineral disorder in patients with CKD. *These adaptations are lost as kidney failure progresses. ([Ca] x [PO4], calcium-phosphorus product; PTH, parathyroid hormone. (From Hudson JQ. Chronic kidney disease: Management of complications.) In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill, 2008:767, with permission.)

FIGURE 26-5. Pathogenesis of secondary hyperparathyroidism and bone and mineral disorder in patients with CKD. *These adaptations are lost as kidney failure progresses. ([Ca] x [PO4], calcium-phosphorus product; PTH, parathyroid hormone. (From Hudson JQ. Chronic kidney disease: Management of complications.) In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill, 2008:767, with permission.)

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