Pathogenesis (development of disease)
In chronic renal insufficiency (kidney weakness), various changes occur in the bone, which are called renal osteopathy. High-turnover osteopathy (high bone turnover and acute bone substance loss) can be distinguished from low-turnover osteopathy. In addition, mixed forms may also be present.
In high-turnover osteopathy, secondary hyperparathyroidism/parathyroid hyperfunction (parathyroid hormone level ↑, calcium level ↓) is present. Hypocalcemia (calcium deficiency) results from disturbances in vitamin D and phosphate metabolism:
- Decreased renal (“kidney-related”) calcitriol (vitamin D3) formation leads to a decrease in renal and intestinal (“gut-related”) calcium absorption. Furthermore, the inhibitory effect of calcitriol on parathyroid hormone secretion (parathyroid hormone excretion) is omitted.
- Phosphate retention leads to hyperphosphatemia (phosphate excess), which in turn inhibits the renal activation of vitamin D3.
- The decrease in serum calcium levels (ionized calcium) causes an increase in PTH. At the renal tubule, this leads to calcium reabsorption and inhibition of phosphate and bicarbonate reabsorption. At the bone, PTH stimulates osteoclasts (“bone-degrading cells”) and thus bone resorption (bone resorption).
Low-turnover osteopathy occurs predominantly in dialysis patients. There are predominantly aluminum overload (aluminum-induced osteopathy) and / or relative hypoparathyroidism / parathyroidism (adynamic bone disease).
Etiology (causes)
Disease-related causes.
Genitourinary system (kidneys, urinary tract-genital organs) (N00-N99).
- Chronic renal insufficiency (chronic renal failure).
Other causes
- Long-term dialysis (blood washing)
- Condition after kidney transplantation
