Hypophosphatemia in cats refers to severely low phosphate concentration in blood plasma which often results in various clinical signs. Gradual changes in total body phosphate can be accommodated without noticeable changes in serum phosphorus concentration, resembling the situation with potassium (the major intracellular cation). The source of dietary phosphorus markedly affects absorption and excretion of phosphorus in cats.56 The amount of phosphorus absorbed by the gastrointestinal tract, the amount excreted in the urine, and the extent of postprandial hyperphosphatemia were increased when monobasic and dibasic salts of phosphorus were fed but decreased when phosphorus originated from poultry, meat, and fish meal. Hemolytic anemia, thrombocytopenia, and impaired clot retraction occurred in starved dogs that were made hypophosphatemic by infusion of amino acids, ostensibly because of depletion of cellular ATP stores.178 Clinically, hemolysis has been reported in hypophosphatemic dogs and cats with diabetic ketoacidosis, hepatic lipidosis, and other disorders.2,80,173 Hemolysis was reported in four other hypophosphatemic diabetic cats, but cause and effect were obscured by the possibility of Heinz body anemia.23, Neuromuscular effects of hypophosphatemia include weakness and pain associated with rhabdomyolysis, as well as anorexia, vomiting, and nausea secondary to intestinal ileus.88,89 Decreased phosphate may impair central nervous system glucose use and ATP production, leading to metabolic encephalopathy, which has a wide range of manifestations in people (e.g., coma, seizure, confusion, irritability).99,177 Reversible impairment of cardiac contractility occurs in dogs with experimentally induced hypophosphatemia and in people with naturally occurring hypophosphatemia.65,66,180 Hypophosphatemia also causes proximal tubular bicarbonate wasting, reduction in titratable acidity, and impaired renal ammoniagenesis. Theoretically, adding phosphorus to fluids containing calcium may cause precipitation of calcium phosphate, but this appears to depend on relative concentrations of calcium and phosphorus. Energy for essential metabolic processes (e.g., muscle contraction, neuronal impulse conduction, epithelial transport) is stored in high-energy phosphate bonds of adenosine triphosphate (ATP). This page was last edited on 7 December 2012, at 04:17. Phosphorus in cats is very important. He is on a phosphate binder but it doesn't seem … Therefore, the dose necessary for repletion and the patient’s response to therapy cannot be predicted. The products available for oral and parenteral use are summarized in Tables 7-1 through 7-3. Excess phosphate in diet: Diets that are high in phosphate (and low in calcium) can increase serum phosphate and result in secondary nutritional hyperparathyroidism (e.g. Intestinal alkaline phosphatases may facilitate absorption by freeing inorganic phosphate for transport. Cats with decreased serum concentrations of cobalamin and folate have been found to be at increased risk for hypophosphatemia. Intestinal phosphate absorption occurs via two mechanisms. Neuromuscular effects of hypophosphatemia include weakness and pain associated with rhabdomyolysis, as well as anorexia, vomiting, and nausea secondary to intestinal ileus. 60-70% of ingested phosphate is hydrolyzed to an inorganic form that is absorbed actively and passively. Renal tubular disorders of phosphate transport have not been conclusively identified in dogs and cats, but hypophosphatemia, increased urinary FEPi, low serum 25-hydroxycholecalciferol concentration, osteopenia, and pathologic fractures were reported in a young cat believed to have abnormal renal tubular phosphate transport and defective hepatic 25-hydroxylation of vitamin D.74. Serum phosphorus concentrations typically are reported as elemental phosphorus and expressed as milligrams of elemental phosphorus per deciliter of serum. Hypophosphatemia & Weight Loss Symptom Checker: Possible causes include Vitamin D Deficiency. There is no evidence of a direct effect of parathyroid hormone (PTH) on intestinal phosphate absorption, and observed effects are probably mediated by the role of PTH in conversion of 25-hydroxycholecalciferol to calcitriol. N Engl J Med. The ECF compartment contains less than 1% of total body phosphorus stores. The effects of acid-base balance on proximal tubular transport of phosphate are complex.115 Acute metabolic acidosis does not affect renal tubular reabsorption of phosphate, but chronic metabolic acidosis results in decreased proximal tubular transport, an effect possibly mediated by glucocorticoids. Even though phosphorus circulates in organic and inorganic forms, clinical laboratories typically measure inorganic phosphate. Phosphatonins are circulating substances that increase renal loss of phosphorus. Not reported in veterinary medicine, cranial trauma is associated with renal losses of phosphorus and hypophosphatemia.132 Acquired diabetes insipidus has been suggested as a possible reason. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Currently, it seems safest to administer phosphate by constant-rate infusion at rates that have been used successfully in dogs and cats and to monitor the serum phosphorus concentration every 6 to 8 hours. The average phosphorus content of commercial pet foods is approximately 1% on a dry matter basis. However, as these patients frequently require nutritional supplementation (either enteral or parenteral), the need to avoid the refeeding syndrome was noted. However, serious acid-base disturbances do not arise in phosphate-deprived dogs.151 Phosphate deficiency produces bone demineralization via effects of PTH and calcitriol, and release of carbonate from bone may prevent serious metabolic acidosis. Innerhalb kürzester Zeit hatte ich vitale, zufriedenere Hunde mit glänzendem Fell und glücklichen Augen. Effects of hypophosphatemia. Intestinal phosphatonins (factors released from the intestines due to increased intraluminal phosphate concentration) have also been suggested to exist. The compound 2,3-diphosphoglycerate (2,3-DPG) decreases the affinity of hemoglobin for oxygen and facilitates the delivery of oxygen to tissues. Leukocytes in hypophosphatemic patients have impaired chemotaxis, phagocytosis, and bacterial killing.38 This altered function may promote sepsis in hypophosphatemic patients receiving total parenteral nutrition. In fact, hypophosphatemia in people with hepatic damage has been suggested to reflect healing and regeneration of the liver.144 Hypophosphatemia has been seen in dogs experimentally intoxicated with xylitol,176 but it is uncertain whether hypophosphatemia is due to hepatic damage or to other metabolic effects of xylitol. Asymptomatic animals with low serum phosphorus concentrations but without phosphorus depletion and those with serum phosphorus concentrations greater than 1.8 mg/dL and unlikely to decrease any lower (e.g., primary hyperparathyroidism) often do not require phosphate administration. Hypophosphatemia caused by dietary deficiency is unlikely in animals eating commercial diets with adequate protein content. Not reported in veterinary medicine, cranial trauma is associated with renal losses of phosphorus and hypophosphatemia. Therefore, it is not clear whether the changes in cobalamin and folate were epiphenomenon or cause-and-effect. * If 2.5 mg/dL is considered the lower limit of normal, serum phosphorus concentration was decreased in approximately one third of reported cases associated with parathyroid adenoma, but in six of six cases associated with parathyroid hyperplasia.44 Hypophosphatemia is seen inconsistently in cats with primary hyperparathyroidism.43,82 The fractional excretion of phosphorus (FEPi) was increased in a few affected dogs.172 The normal FEPi was found to be 7.5% ± 4.6% in 10 normal dogs but 10% to 23% in a dog with primary hyperparathyroidism.29. Prophylactic parenteral phosphate therapy (such as may be used for patients with diabetic ketoacidosis) may be reasonably estimated by giving one fourth to one half of the supplemented potassium as potassium phosphate and the rest as potassium chloride. Cats with decreased serum concentrations of cobalamin and folate have been found to be at increased risk for hypophosphatemia.135 Most of the hypophosphatemic cats had gastrointestinal tract disease or pancreatitis. At this pH, H3PO4 and PO43− are present in negligible amounts, and plasma inorganic phosphorus principally consists of H2PO41− and HPO42−. Hypophosphatemia is a disorder often characterized by muscle weakness (1). Interestingly, infusion of a higher concentration (e.g., 10% dextrose) for a shorter time seems to be less detrimental than infusing 4% glucose continuously.99 Malnourished patients receiving total parenteral nutrition are particularly susceptible to hypophosphatemia because of the accelerated rate of tissue repair as phosphate is incorporated into new cells and phosphate use during glycolysis.88,136 Hypophosphatemia as part of the “refeeding syndrome” (i.e., severe electrolyte changes in malnourished patients that are being fed parenterally or enterally) was more likely in patients that were more severely emaciated, had lower initial serum phosphate concentrations, and experienced more aggressive initial infusion of parenteral nutrition.107 Respiratory alkalosis likewise causes translocation because it stimulates glycolysis by activating phosphofructokinase.88 This effect has been demonstrated in experimental dogs but was marked only when hyperventilation was combined with glucose administration.19 Increased intracellular pH may be more important than increased extracellular pH for causing hypophosphatemia in respiratory alkalosis, which could explain why severe hypophosphatemia may occur in people with severe respiratory failure who are mechanically ventilated.99, Diabetic patients are especially at risk for hypophosphatemia. Vitamin D deficiency may cause hypophosphatemia because hypocalcemia increases PTH secretion, which increases renal phosphate excretion. It has been stated that 38% of hyperadrenocortical dogs have hypophosphatemia, but actual serum phosphorus concentrations were not reported. A severely ill diabetic patient, for example, is more likely to die from dehydration, hyperosmolality, metabolic acidosis, hypokalemia or hypophosphatemia than from hyperglycemia or lack of insulin therapy. Phosphate is also an important urinary buffer, and urinary phosphate constitutes the majority of titratable acidity (see Chapter 9). Hemolysis may affect laboratory results because phosphate is present in erythrocytes. Postsurgical hypophosphatemia is a well-established problem in people. Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. Orthophosphoric acid is governed by the following set of equilibria: The pKa for the reaction between H2PO41− and HPO42− is 6.8 at the ionic strength and temperature of extracellular fluid (ECF), and these are the two prevailing ionic species at the normal ECF pH of 7.4. Hypophosphatemia can be caused by decreased intestinal absorption, increased renal phosphorus loss, and transcellular shift of phosphorus from the blood into cells. Hypophosphatemia may be caused by translocation of phosphate from extracellular to intracellular fluid (maldistribution), increased loss (decreased renal reabsorption of phosphate), or decreased intake (decreased intestinal absorption of phosphate).99,136 Clinical conditions associated with hypophosphatemia are presented in Box 7-1. Similar results were obtained by Fuller (3) in dogs fed a phosphorus deficient diet. At a pH of 7.4, the HPO42−:H2PO41− ratio is 4.0, and the average valence of phosphate in serum reflects this ratio. Both transport mechanisms function in the duodenum, whereas diffusion is the primary mechanism in the jejunum and ileum. Hypophosphatemia may be caused by translocation of phosphate from extracellular to intracellular fluid (maldistribution), increased loss (decreased renal reabsorption of phosphate), or decreased intake (decreased intestinal absorption of phosphate). Hemolytic anemia (breaking down of red blood cells) secondary to severe hypophosphatemia 2. Normally, 80% to 90% of the filtered phosphate load is reabsorbed by the renal tubules, and renal dysfunction is the most common cause of hyperphosphatemia beside that found in young dogs. The effects of calcitriol on renal phosphate transport are difficult to separate from the effects of calcitriol on PTH secretion and on phosphate transport in other organs (e.g., intestine, bone). Internetinformationen bestärken sie, ihren Kindern auch ohne ärztliche Beratung unsinnige und strikte Diäten aufzuerlegen. 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