Severe hypophosphatemia. Pathophysiologic implications, clinical presentations, and treatment.

Chapter 11 – Osteomalacia and Related Disorders

Drug-induced calculi represent 1–2% of all renal calculi. The drugs reported to produce calculi may be divided into two groups. The first one includes poorly soluble drugs with high urine excretion that favour crystallisation in the urine. Among them, drugs used for the treatment of patients with human immunodeficiency, namely atazanavir and other protease inhibitors, and sulphadiazine used for the treatment of cerebral toxoplasmosis, are the most frequent causes. Besides these drugs, about 20 other molecules may induce nephrolithiasis, such as ceftriaxone or ephedrine-containing preparations in subjects receiving high doses or long-term treatment. Calculi analysis by physical methods including infrared spectroscopy or X-ray diffraction is needed to demonstrate the presence of the drug or its metabolites within the calculi. Some drugs may also provoke heavy intra-tubular crystal precipitation causing acute renal failure. Here, the identification of crystalluria or crystals within the kidney tissue in the case of renal biopsy is of major diagnostic value. The second group includes drugs that provoke the formation of urinary calculi as a consequence of their metabolic effects on urinary pH and/or the excretion of calcium, phosphate, oxalate, citrate, uric acid or other purines. Among such metabolically induced calculi are those formed in patients taking uncontrolled calcium/vitamin D supplements, or being treated with carbonic anhydrase inhibitors such as acetazolamide or topiramate. Here, diagnosis relies on a careful clinical inquiry to differentiate between common calculi and metabolically induced calculi, of which the incidence is probably underestimated. Specific patient-dependent risk factors also exist in relation to urine pH, volume of diuresis and other factors, thus providing a basis for preventive or curative measures against stone formation.

Drug-Induced Kidney Stones and Crystalline Nephropathy: Pathophysiology, Prevention and Treatment

Literature data on the aluminium content of individual foods have been compiled, summarized and presented by food groups. The contribution of aluminium from food preparation and cooking utensils and from food additives is discussed. Literature data on the daily intake of aluminium are summarized, and the contribution of food groups to daily aluminium intake is estimated. The major sources of dietary aluminium include several with aluminium additives (grain products, processed cheese and salt) and several that are naturally high in aluminium (tea, herbs and spices). The aluminium that may migrate from aluminium utensils is probably not a major or consistent source of this element. Daily intakes of aluminium, as reported prior to 1980, were 18–36 mg per day. More recent data, which are probably more accurate, indicate intakes of 9 mg per day for teenage and adult females and 12–14 mg per day for teenage and adult males.

Aluminium content of foods and diets.

Effect of small doses of aluminum-containing antacids on calcium and phosphorus metabolism

A 36-year-old woman suffered from bone pain, muscle weakness, and renal stones after prolonged ingestion of antacids for esophageal reflux. Investigation disclosed hypophosphatemia, hypercalciuria, and osteomalacia by bone biopsy. All symptoms and abnormal laboratory findings reversed with a regimen of oral phosphate supplementation and cessation of antacid intake. ( Arch Intern Med 138:1007-1009, 1978)

Antacid-induced osteomalacia and nephrolithiasis.

The paper presents the case history of a 15-year-old boy with traumatic tetraplegia who developed hypercalcaemia within 6 weeks of injury. The condition was initially controlled by the infusion of intravenous fluids in large amounts and by the administration of calcitonin. After 3 weeks, calcitonin became ineffective. Eventually the hypercalcaemia responded to cortisone administered in low dosage. The endocrinologic implications of this observation are discussed.

/pdf/hypercalcaemia-in-adolescent-tetraplegic-patients-case-1f4otriegi.pdf

Hypercalcaemia in adolescent tetraplegic patients: case report and review

The effects of 7S nerve growth factor (NGF) and its isolated α, β, and γ subunits on bone resorption were assessed in a tissue culture system in which the degree of resorption was determined by measuring the release of45Ca from prelabeled fetal rat radii and ulnae. It was found that 7S-NGF, through the activity of its γ, subunit, inhibits parathyroid hormone (PTH)-stimulated but not-unstimulated bone resorption.

Inhibition of parathyroid hormone-induced fetal rat bone resorption in vitro by nerve growth factor.

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Antacid-induced osteomalacia and nephrolithiasis.

Hypercalcaemia in adolescent tetraplegic patients: case report and review

Inhibition of parathyroid hormone-induced fetal rat bone resorption in vitro by nerve growth factor.