A patient with chronic renal disease would have an increased production of parathyroid hormone.
Renal osteodystrophy (ROD)is a pathologic bone condition in patients with underlying kidney disease. The most common endocrine abnormality is increased PTH secretion. Vitamin D, calcium and phosphate balance is carefully regulated by the kidneys, liver, parathyroid gland and bone. In patients with kidney disease, calcium is wasted, leading to low serum calcium concentrations. Serum phosphate is increased. In response to this, the parathyroid glands upregulate their production of PTH to affect bones, the GI tract and the kidney.
ROD can be classified as high and low-turnover. High-turnover is marked by an increase in PTH secretion and leads to parathyroid gland hyperplasia and elevated levels of PTH which persists after correction of the kidney disease. This manifests as bone disease and osteitis cystica. Low-turnover ROD is more common in the setting of dialysis and proper medical management leading to lower levels of PTH with characteristic bone lesions marked by low levels of bone formation.
Skeletal manifestations include metaphyseal enlargement, frontal bossing, bowing of long bones and genu varum. The histology is non-specific, as there are abundant multi-nucleated giant cells and abundant osteoclast activity in marrow stroma.
Tejwani et al. reviewed the pathophysiology of ROD. They reviewed the orthopedic implications of kidney disease and its effect on bone quality. They provided an overview of medical and surgical treatment of patients with kidney disease.
Illustration A shows the physiology of PTH. Decreased serum calcium leads to the release of PTH which stimulates the kidney, bone, and GI tract to increase serum calcium levels. High serum calcium levels in return act as negative feedback on the parathroid gland, lead to a decrease in PTH and subsequent decrease in the serum calcium levels.
Answer 1,2,3: PTH would be increased.
Answer 4 and 5: The thyroid gland is not involved with ROD, and therefore TSH would not be affected.
Einhorn TA. Metabolic bone disease. In: Einhorn TA, O'Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:415-426.
Tejwani NC, Schachter AK, Immerman I, Achan P. Renal osteodystrophy. J Am Acad Orthop Surg. 2006 May;14(5):303-11.
PMID:16675624 (Link to Abstract)