tacrolimus and Osteomalacia

After osteoporotic fracture or low bone mineral density measurements, it is necessary to look for secondary causes of osteoporosis, such as drugs. Corticosteroids are the most common cause of drug-induced metabolic bone disease. Other drugs responsible for bone disease include: aromatase inhibitors, GnRH agonists, anticonvulsants, heparin, and L thyroxin at TSH-suppressive doses. Confirmation is required of data about neuroleptics and antivitamin K.

Topics: Aged; Animals; Anticoagulants; Anticonvulsants; Antipsychotic Agents; Aromatase Inhibitors; Bone Density; Child; Cyclosporins; Densitometry; Disease Progression; Diuretics; Female; Follow-Up Studies; Fractures, Bone; Gonadotropin-Releasing Hormone; Humans; Hypoglycemic Agents; Iatrogenic Disease; Immunosuppressive Agents; Lithium Compounds; Male; Menopause; Methotrexate; Middle Aged; Osteomalacia; Osteoporosis; Osteoporosis, Postmenopausal; Placebos; Prospective Studies; Protease Inhibitors; Randomized Controlled Trials as Topic; Retrospective Studies; Risk Factors; Tacrolimus; Thyroid Hormones; Time Factors

Transient hypophosphatemia is frequently observed during the first months after renal transplantation and is usually asymptomatic. Phosphate diabetes is defined as inadequate tubular phosphorus reabsorption leading to persistent renal phosphorus wasting, which is an important but overlooked cause of osteodystrophy in the post-renal transplantation population. We report the case of a 58-year-old male who presented with severe multiple osteoarticular pains within 3 months after successful first kidney transplantation. Bone disease was attributed initially to mild hyperparathyroidism secondary to vitamin D deficiency. Despite the correction of the hyperparathyroidism, the withdrawal of corticosteroids, and the reduction of immunosuppressive treatment to tacrolimus-based monotherapy, the osteoarticular pains persisted. Skeletal investigations at month 9 post-transplantation demonstrated a significant bone mineral density loss associated with osteomalacia and osteoporosis on the bone biopsy. Laboratory data showed persistent hypophosphatemia, and phosphate diabetes was then diagnosed explaining the post-transplant bone disease. A tacrolimus-induced renal tubular disorder was suspected to contribute to the excessive renal phosphorus wasting. The replacement of tacrolimus by sirolimus, in addition to oral phosphorus and vitamin D supplementations, led to the disappearance of pains, the normalization of urinary and plasma phosphate level, and a significant improvement of bone mineralization.

Topics: Bone Density Conservation Agents; Humans; Hydroxycholecalciferols; Hypophosphatemia; Immunosuppressive Agents; Kidney Transplantation; Male; Middle Aged; Osteomalacia; Phosphorus; Sirolimus; Tacrolimus