Page 140 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Abnormalities of Phosphate Balance
Phosphate is a constituent of a wide variety of mining the plasma phosphate level. Uptake of
compounds, for example, nucleotides (ATP, phosphate by the cells occurs when phosphate
cAMP, cGMP, etc.), nucleic acids, creatine phos- is incorporated into the body’s metabolism, for
phate, intermediary substrates of carbohy- example, the formation of glucose phosphate
drate metabolism (e.g., glucose phosphate), from free glucose. A dramatically increased
and phospholipids. Phosphate activates or in- uptake occurs after food intake by starving
activates many enzymes and is an essential people and alcoholics, after insulin adminis-
buffer in cells and in urine. It also plays a sig- tration in diabetic coma, and in severe alkalo-
Kidney, Salt and Water Balance function is normal, PTH reduces the plasma and cell damage (→ A4).
nificant role in the mineralization of bone.
sis (→ A3). This results in, at times marked, hy-
pophosphatemia. Conversely, phosphate is re-
PTH and calcitriol are essential for the regu-
leased from cells in acidosis, diabetic coma,
lation of phosphate balance. When kidney
phosphate level by inhibiting renal reabsorp-
Lastly, an excess of phosphate can occur as a
result of its mobilization from bone (e.g., by tu-
tion, but at the same time it promotes the mo-
mor, skeletal immobilization, hyperparathy-
bilization of phosphate in bone. Calcitriol
raises the plasma phosphate level by stimulat-
roidism), unless its renal elimination is stimu-
lated at the same time. In renal failure, skeletal
ing its enteric absorption and renal reabsorp-
Abnormal phosphate metabolism can be
thyroidism, contributes to the development of
caused by an uneven external balance or by
hyperphosphatemia (→ p.132).
The clinical effects of hypophosphatemia
changes in distribution within the body (intra-
5 tion. demineralization, stimulated by hyperpara-
cellular and extracellular spaces; bone). The depend on the duration and extent of the ab-
external balance is determined by the rela- normality. If the serum phosphate level is be-
tionship between enteric absorption and renal low 0.3 mmol/L, myopathy (muscular weak-
excretion. ness, myolysis), heart failure, hemolysis, and
Phosphate deficiency can be the result of re- nervous system dysfunction (convulsions,
duced enteric absorption, for example, the re- coma) will occur. The abnormalities are ex-
sult of inadequate supply in food (common in plained mainly by a reduced energy metabo-
alcoholics), due to malabsorption, vitamin D lism in the cells (ATP). The decrease of 2,3-bis-
deficiency, or chronic intake of phosphate- phosphoglycerate (2,3-BPG) in erythrocytes
binding aluminum hydroxide (→ A1). Renal leads to a decreased oxygen release to the tis-
loss of phosphate occurs in hyperparathyroid- sues. Skeletal demineralization occurs in pro-
ism, vitamin D deficiency, certain transport longed hypophosphatemia (osteomalacia;
defects in the proximal tubules (phosphate → p.132).
diabetes, Fanconi’s syndrome; → p. 96), and, Effects of hyperphosphatemia include pre-
to a lesser extent, in salt-losing nephritis, in cipitation of calcium phosphate with the de-
expansion of the extracellular space, during velopment of soft-tissue calcifications in tis-
diuretic treatment, and under the influence of sues of low metabolic turnover (e.g., mucous
glucocorticoids. bursae, joints, skin). Corresponding symptoms
Phosphate excess can be caused by a large are itching (pruritus), joint pain (arthritis), etc.
oral intake of phosphate as well as by vitamin The plasma Ca 2+ concentration falls and the re-
D intoxication (→ A2). The renal elimination of lease of PTH is stimulated. In renal failure a vi-
phosphate is impaired in reduced filtration cious circle develops (→ p.110ff.).
(renal failure) or if renal tubular reabsorption
is raised (hypoparathyroidism).
The phosphate concentration is markedly
higher in the cells than in the extracellular
space (see also potassium; → p.124). For this
130 reason shifts between intracellular and extra-
cellular space play an important role in deter-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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