What metabolic complication is commonly seen in chronic kidney disease due to phosphate retention and decreased calcium?

Study for the NCLEX Genitourinary Disorders Test. Prepare with flashcards and multiple choice questions, each with hints and explanations. Get ready for your exam!

Multiple Choice

What metabolic complication is commonly seen in chronic kidney disease due to phosphate retention and decreased calcium?

Explanation:
When kidney function declines, phosphate isn’t excreted effectively and tends to rise in the blood. High phosphate plus lower levels of active vitamin D reduce calcium absorption from the gut, so serum calcium falls. The parathyroid glands respond to this hypocalcemia (and hyperphosphatemia) by increasing parathyroid hormone secretion—secondary hyperparathyroidism. The elevated PTH drives bone turnover in an attempt to release calcium, which over time leads to renal osteodystrophy, the bone disease commonly seen with CKD. Vitamin D toxicity isn’t the issue here because the problem is insufficient activation of vitamin D, not excess. Primary hyperparathyroidism is a different disorder where the parathyroid glands themselves are the primary source of excess PTH. Renal osteitis fibrosa describes the bone changes from secondary hyperparathyroidism and involves high PTH levels.

When kidney function declines, phosphate isn’t excreted effectively and tends to rise in the blood. High phosphate plus lower levels of active vitamin D reduce calcium absorption from the gut, so serum calcium falls. The parathyroid glands respond to this hypocalcemia (and hyperphosphatemia) by increasing parathyroid hormone secretion—secondary hyperparathyroidism. The elevated PTH drives bone turnover in an attempt to release calcium, which over time leads to renal osteodystrophy, the bone disease commonly seen with CKD. Vitamin D toxicity isn’t the issue here because the problem is insufficient activation of vitamin D, not excess. Primary hyperparathyroidism is a different disorder where the parathyroid glands themselves are the primary source of excess PTH. Renal osteitis fibrosa describes the bone changes from secondary hyperparathyroidism and involves high PTH levels.

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