Kidney disease phosphate disorders

Osteitis fibrosa (hyperparathyroid bone disease) is the most common high-turnover bone disease. This disorder is caused by the high concentrations of serum PTH in secondary hyperparathyroidism. Secondary hyperparathyroidism is a consequence of the hypocalcemia associated with hyperphosphatemia and l,25(OH)2D deficiency. Hyperphosphatemia is a result of the kidneys inability to excrete phosphate. l,25(OH)2D deficiency results from the inability of the kidneys to synthesize l,25(OH)2 because of decreased renal mass and suppression of 25(OH)D-la-hydroxylase activity by high concentrations of phosphate. Deficiency of l,25(OH)2D leads to reduced intestinal absorption of calcium and reduced inhibition of PTH secretion by l,25(OH)2D. Skeletal resistance to PTH also contributes to the hypocalcemia and secondary hyperparathyroidism. 

The term chronic kidney disease-mineral and bone disorder (CKD-MBD) was introduced in a position statement by the Kidney Disease Foundation. According to the guidelines, CKD-MBD is a systemic disorder and patients with vascular or valvular calcification should be included in the group with the greatest cardiovascular risk. Therefore, the presence or absence of calcification is a key factor in strategy decisions for such patients. In particular, it is recommended that the use of calcium-based phosphate binders should be restricted in patients with hypercalcaemia, vascular calcification, low levels of parathyroid hormone or adynamic bone disease. 

Kidneys Dysfunction of the proximal tubule may occur as a late manifestation of Wilson s disease. Epithelial flattening, a loss of the brush-border membrane, mitochondrial anomalies and fatty cellular changes can be observed. These findings are, in turn, responsible for proteinuria with a predominance of hyperaminoaciduria (L. UzMAN et al., 1948). Enhanced calciuria and phosphat-uria may cause osteomalacia as well as hypoparathyroidism. (329, 344) Glucosuria and uricosuria, if present, are without clinical relevance. Due to decreased bicarbonate resorption, tubular acidosis may occur, with a tendency towards osteomalacia as well as the development of nephrocalcinosis and renal stones (in some 15% of cases). (344, 356, 392) The intensity of the copper deposits in the kidneys correlates closely with the cellular changes and functional disorders. The glomerular function is not compromised, with the result that substances normally excreted in the urine are not retained. 

In addition to an increase in serum urea and creatinine levels, uric acid and inorganic phosphate levels also increase in chronic renal failure. The increase in serum inorganic phosphate leads to deposition of calcium phosphate in bones, causing hypocalcemia. In the early stages of chronic renal failure, calcium levels are restored by the stimulation of parathyroid hormone. However, as the renal disease progresses, the ability of the kidney to hydroxylate vitamin D and thus convert it to the active form decreases, thereby affecting the uptake of calcium by the gut and thus perpetuating hypocalcemia. Serum alkaline phosphatase levels increase due to disordered bone metabolism. Loss of bicarbonate is seen in some patients with increased parathyroid hormone activity. 

While alcohol abuse may be associated with a variety of electrolyte and acid-base disorders, the role of the kidneys in this process has only recently been fully defined [164]. Renal functional abnormalities have now been related to chronic alcoholism in patients without liver disease and these defects have reverted to normal with abstinence from alcohol abuse. These abnor-mahties include decreases in the maximal reabsorptive abihty and threshold for glucose, a decrease in the threshold for phosphate excretion, and increases in the fractional excretion of P2-microglobulin, uric acid, calcium, magnesium, and amino acids. Defective tubular acidification and impaired renal concentrating ability... 

During the review of systems, the nurse should pay particular attention to the report of conditions such as Crohn disease, diabetes mellitus, and thyroid and kidney disorders owing to the possible impact of these conditions on phosphate absorption and movement into the cell. 

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