Renal phosphate wasting

X-linked hypophosphatemic rickets is characterized by defective proximal renal tubular phosphate transport and impaired renal production of 1,25-dihydroxycolecalci-ferol. These abnormalities lead to renal phosphate wasting, hypophosphatemia with normocalcemia, low plasma 1,25-dihydroxycolecalciferol concentrations, and... 

Hypophosphatemia or phosphate depletion may be caused by (1) a shift of phosphate from extracellular to intracellular spaces, (2) renal phosphate wasting, (3) decreased intestinal absorption, and (4) loss from intracellular phos-phate. Box 49-5 lists the commonly encountered causes of hypophosphatemia and phosphate depletion. 

Renal phosphate wasting may also cause hypophosphatemia. Any cause of excessive PTH secretion (primary... 

Osteomalacia and rickets may also occur because of phosphate depletion. The most common cause of rickets in the United States is hypophosphatemic osteomalacia (also known as hypophosphatemic vitamin D-resistant rickets and vitamin D-resistant rickets).This disorder is an X-linked dominant inherited trait characterized by renal phosphate wasting. Tubular phosphate wasting can also occur sporadically in adults and as part of Fanconi syndrome. Certain rare mesenchymal tumors may also produce a phosphaturic factor (phosphatonin or FGF-23), resultmg in renal phosphate wasting and osteomalacia. 

Treatment of rickets and osteomalacia is dictated by the etiology of the disorder. Nutritional rickets and osteomalacia are healed by treatment with physiological doses of vitamin D, whereas higher doses may be required in malabsorption. Adequate dietary intakes of calcium and phosphorus are critical during therapy. Renal phosphate-wasting syndromes require frequent, pharmacological administration of oral phosphorus. 

Hemorrhagic cystitis always given with mesna and hydration nephrotoxicity renal tubular acidosis potassium, magnesium, and phosphate wasting, especially in high-dose regimens myelosuppression CNS effects somnolence, confusion, disorientation, cerebellar symptoms that are dose-related moderately emetogenic alopecia... 

The alkalinization of the urine caused by these drugs may contribute to an increase in urinary calcium and phosphate, which increases the formation of renal calculi. In addition, the bicarbonate wasting effect can cause hyperchloremic metabolic acidosis and excessive loss of potassium. In large doses, or in renally compromised patients, the drug may cause central nervous system (CNS) effects, such as sedation and paresthesias. 

About 40 years ago it was already established that long-term inhalation of cadmium oxide dust could cause a syndrome characterized by damage of the pulmonary and renal systems [66]. And it is a well known fact, that during the last decades in Japan a large population suffered from a chronic cadmium poisoning with severe bone damage ("Itai-Itai desease"), caused by the intake of highly cadmium contaminated rice. Waste disposal, especially by incineration, as well as phosphate fertilizers and acid rain are pronounced risks for cadmium exposure. 

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