Etiology and Trigger Mechanisms
The pathology arises from two main causes. The first is the acute or chronic administration of excessive, toxic doses of vitamin D supplements. The second cause lies in genetics: some patients exhibit genetically determined hypersensitivity of cells to the vitamin. In such cases, even the intake of standard physiological doses leads to the clinical picture of poisoning.
The central link in the pathogenesis is hypercalcemia (excess calcium in the blood) and hypercalciuria (increased urinary calcium excretion). High concentrations of the mineral lead to its massive accumulation within the walls of blood vessels. As a result, irreversible calcinosis of internal organs develops, with the kidneys and heart suffering the most severe damage.
Renal Injury and Metabolic Shifts
In the early stages of the disease, vitamin D stimulates enhanced phosphorus reabsorption in the proximal renal tubules, leading to hyperphosphatemia. However, as calcinosis and toxic injury to the renal tissue progress, late manifestations develop—severe damage to the tubular apparatus.
The ability of the kidneys to reabsorb essential substances such as phosphorus, amino acids, glucose, and bicarbonate declines. This fundamentally alters the biochemical profile of the blood, resulting in hypophosphatemia, hypoglycemia, and metabolic acidosis. Ultimately, massive destruction of renal parenchyma inevitably leads to renal failure and uremia, which is one of the most frequent causes of death in this condition.
Cardiovascular System and Bone Tissue
An excess of Ca2+ ions in the blood, vascular wall cells, and cardiomyocytes causes persistent arterial hypertension and various arrhythmias. Due to calcification of the cardiac valves, development of aortic stenosis, and constant myocardial overload, severe heart failure develops.
Simultaneously, specific changes occur in the bone tissue. There is an enhanced accumulation of calcium in newly formed bone. The cortical layer of the bone thickens pathologically, and entirely novel ossification centers, not dictated by normal physiology, appear.
Immune System, Endocrine System, and CNS
Toxic doses of vitamin D and the accompanying hypercalcemia exert a direct damaging effect on the thymus gland, lymphoid structures, and parathyroid glands. Thymus involution occurs, leading to immunodeficiency states and a susceptibility to recurrent infections. Damage to endocrine glands results in pluriglandular insufficiency.
Oxidative stress inflicts additional damage: excessive activation of lipid peroxidation (LPO) generates free radicals that potentiate tissue destruction.
The patient's psychoneurological status is characterized by cyclicity. Periods of pronounced lethargy, depression, and somnolence suddenly give way to episodes of agitation and increased motor activity. In severe cases, loss of consciousness and coma develop.