As hyperphosphatemia a serum phosphate concentration is referred> 4.5 mg / dl (> 1.46 mmol / l). The causes include kidney disease, hypoparathyroidism and a respiratory or metabolic alkalosis. The clinical symptoms are caused by the accompanying hypocalcemia and can range up to tetany. For diagnosis, the serum phosphate concentration is determined. The therapy consists of a limitation of phosphate uptake, and the administration of the phosphate-binding antacids such. As calcium carbonate.
(See also overview of disorders of phosphate concentration.)
As hyperphosphatemia a serum phosphate concentration is referred> 4.5 mg / dl (> 1.46 mmol / l). The causes include kidney disease, hypoparathyroidism and a respiratory or metabolic alkalosis. The clinical symptoms are caused by the accompanying hypocalcemia and can range up to tetany. For diagnosis, the serum phosphate concentration is determined. The therapy consists of a limitation of phosphate uptake, and the administration of the phosphate-binding antacids such. As calcium carbonate. (See also overview of disorders of the phosphate concentration.) Etiology The most common cause of hyperphosphatemia is a reduced urinary excretion of phosphate An advanced renal failure (GFR <30 ml / min) reduced to the extent the precipitation that a rise in serum phosphate levels occur can. Disorders of the renal excretion of phosphate without an existing renal failure also occur in a pseudohypoparathyroidism, a hypoparathyroidism and parathyroider suppression on (such. As of hyperkalemia caused by vitamin A or D or excretion granulomatosis). Now and again results in a hyperphosphatemia in a trans cellular shift of phosphate in the extracellular space, which is so extensive that the renal Exkretionsfähigkeit is exceeded. The transcellular shift happens mostly in the context of diabetic ketoacidosis (despite the reduction in total body phosphate), with trauma by pinching dangers, wherein the non-traumatic hemolysis and also in severe systemic infections or in a tumor lysis syndrome. Hyperphosphataemia also occurs with excessive oral phosphate administration and in some cases even with an exaggerated use of phosphate enemas. False high values ??for phosphate can occur in hyperproteinemia (multiple myeloma or macroglobulinemia), hyperlipidemia, hemolysis or hyperbilirubinemia. Pathophysiology hyperphosphatemia plays in the development of secondary hyperparathyroidism and renal osteodystrophy in patients with advanced chronic kidney disease and in patients on dialysis a role. Hyperphosphataemia can lead to Kalziumpräzipitation in soft tissues, when the serum calcium x phosphate product is mainly used in patients with chronic kidney disease permanently at> 55th Weichgewebekalzifikation the skin is a cause of the excessive itching in patients with end stage renal disease and chronic dialysis. A Gefäßkalzifikation also occurs in dialysis patients with chronic elevated calcium x phosphate product; the hardening of the arteries is a major risk factor for cardiovascular morbidity including stroke, myocardial infarction and intermittent claudication. Symptoms and signs Most patients with hyperphosphataemia are asymptomatic, although the symptoms of hypocalcemia may occur in the presence of concomitant hypocalcemia up to tetany. Weichgewebekalzifikationen often occur in patients with chronic kidney disease; they manifest themselves as easily palpable, hard subcutaneous nodules, often with overlying scratches. Means of imaging methods can often be detected vascular calcification along the major arteries. Diagnosis phosphate concentration> 4.5 mg / dl (> 1.46 mmol / l) hyperphosphatemia is diagnosed on the phosphate concentration. If the etiology is not obvious (eg. As rhabdomyolysis, tumor lysis syndrome, renal failure, abuse of phosphate laxatives), need further investigation to rule out hypoparathyroidism or Pseudohypoparathyroidism which (PTH) is due to a Endorganresistenz against parathyroid hormone, are performed. False high values ??for serum phosphate should be identified by means of the measurement of the concentrations of serum proteins, lipids and bilirubin. Treatment phosphate restriction phosphate binder Sometimes salt diuresis or hemodialysis, the most important in the treatment in patients with advanced chronic kidney disease is the reduction of phosphate uptake, mostly by the avoidance of foods with a high content of phosphate and by taking phosphate-binding drugs during meals will be achieved. Although very effective, aluminum-containing antacids should not be used as phosphate binders in patients with end-stage renal disease because of the possibility of aluminum-related dementia and osteomalacia is, calcium carbonate and calcium acetate are often used as a phosphate binder. But they require close monitoring because of the possibility of excessive calcium × vascular calcification in dialysis patients is taking calcium-containing binders. A phosphate-binding resin without calcium, sevelamer, is widely used in dialysis patients in doses 800-2400 mg p.o. 3 times a day with meals. Lanthanum is another phosphate binder without calcium, can also be used in dialysis patients. It is p.o. in doses of 500-1000 mg 3 times taken daily with meals. “Sucroferric” – oxyhydroxide combines the need for elemental iron that many dialysis patients with phosphate binding. It is p.o. in doses of 500 mg 3 times taken daily with meals. removed a lot of phosphate, but not enough to allow most that are available with end-stage renal disease patients to prevent hemodialysis significant hyperphosphatemia without the aforementioned nutritional interventions. Kochsalzdiurese can be used to improve phosphorus removal in acute hyperphosphatemia with intact renal function. Hemodialysis can reduce phosphate levels in cases of severe acute hyperphosphatemia. Summary The most common cause of hyperphosphatemia is advanced renal failure; Hypoparathyroidism and Pseudohypoparathyroidism are rarer causes. Most patients are asymptomatic; but those who are hypocalcemic can develop tetany. Treatment consists of restricted phosphate intake in the diet and, occasionally, with phosphate binders. Kochsalzdiurese or hemodialysis may be required.