Two cases with the dramatic course of secondary hyperparathyroidism in patients with chronic kidney disease on long-term dialysis. Has anything possible been done in management of these patients? Complications associated with impaired bone mineralization among patients with chronic kidney disease on long-term dialysis are observed frequently with an array of pathologic processes being found. Kidney osteodystrophy may be associated with either increased or decreased (adynamic bone disease, osteomalacia, aluminum-induced osteopenia) bone metabolism, as well as mixed forms related to the B2 microglobulin amyloidosis. Differential diagnosis of various types of osteopathy is difficult and is usually based on the histologic assessment of the bone biopsy. The most typical bone complication in patients with impaired kidney function is osetodistophy with increased bone metabolism, caused by secondary hyperparathyroidism clinically manifesting as osteitis fibrosa. High serum levels of PTH induce osteoclast and osteoblast activity. Early changes, with characteristic increase in the woven osteoid suggesting early, increased osteoplastic bone resorption may be found in a significant percentage of patients with GFR>60ml/min/1,73m2 of the body surface. Lower values of the GFR are associated with both faster bone synthesis and more active resorption with progressive increase in the intraosseous fibrosis and decreased bone mineralization. As the abnormalities progress, which is especially marked in patients on long-term dialysis, a rage of clinical symptoms, such as: severe bone and joint pain, bone deformation, pathological fractures, especially in the spinal region, calcifications of the soft tissues and vessels, including heart valves and lungs. In children, the most common abnormality is growth impairment. In some patient’s skin calcifications, with subsequent necrosis, due to increased calcium deposition in small and medium arteries. The diagnosis is based on the typical clinical picture, biochemical parameters (calcium and phosphate ratio, parathormone levels, characteristic radiologic charges and sometimes, bone histology. Prevention and treatment of these complications includes effective dialysis, appropriate low-phosphate diet with limitation of the protein supply to the 0.8g/kg of the body mass, adequate calcium and active Vitamin D3 supply, introduction of the phosphate binding medications (sevelamer or lantan) as well as calcimimetic use (substances activating parathyroid gland calcium receptors inhibiting both its up-regulation and PTH secretion). In the severe cases, with insufficient effect of the treatment described above, parathyroidectomy is required after close ultrasound and scintigraphy-based assessment of these glands. However, even such treatment may be insufficient in some cases, as presented below.
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