Primary hyperparathyroidism and the kidney: biochemical and clinical spectrum.

摘要: Primary hyperparathyroidism manifests biochemically as a disturbance in serum calcium homeostasis. The central organ setting level is the kidney. It not only has highest rate of active transport, but kidney also modulates homeostasis by virtue its endocrine role 1,25-hydroxyvitamin D secretion. Receptors for PTH are widely expressed throughout renal tubule and involved both transport function. Biochemical manifestations primary include increased tubular reabsorption calcium, decreased phosphate bicarbonate, hypercalciuria. A reduction glomerular filtration may occur some patients with hyperparathyroidism, which perturbs diagnostic relationships among biochemical variables induces further increases Parathyroidectomy rapidly restores abnormalities to normal apart from chronic reduced filtration. Clinical nephrolithiasis, common, nephrocalcinosis, uncommon. Nephrocalcinosis or without nephrolithiasis. Risk factors nephrolithiasis oversaturation urine oxalate. nephrocalcinosis clearly defined. greatly reduces incidence little effect on nephrocalcinosis.