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Chapter 2: PRIMARY HYPERPARATHYROIDISM: DIAGNOSIS.

Ann Endocrinol (Paris)

January 2025

University of Brest, CHU Brest, UMR1304 GETBO, 29200 Brest, France; Endocrinology and Diabetology Department, CHU Brest, 29200 Brest, France.

Primary hyperparathyroidism is now predominantly an asymptomatic pathology, as blood calcium assay has become systematic. Diagnosis therefore requires screening for target organ damage when this is not already indicative of primary hyperparathyroidism.Classical clinical manifestations include bone, kidney and muscle signs, and are characterized by reversibility after parathyroid surgery.

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Serum uric acid is an end-product of purine metabolism. Uric acid concentrations in excess of the physiological range may lead to diseases such as gout, cardiovascular disease, and kidney injury. The kidney includes a variety of cell types with specialized functions such as fluid and electrolyte homeostasis, detoxification, and endocrine functions.

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Renal tubular acidosis (RTA) is a group of disorders in which there is an alteration in acid-base homeostasis because of the impairment of nephrons to excrete hydrogen ions or reabsorb bicarbonate ions, resulting in chronic metabolic acidosis. RTA is an important cause of rickets, particularly 'resistant rickets'. Dental manifestations frequently reported in patients with RTA include enamel hypoplasia and amelogenesis imperfecta, affecting permanent dentition.

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The contribution of the gut to the ingestion, production, absorption, and excretion of the extra ammonia and urea-N associated with feeding ("exogenous" fraction) has received limited prior attention. Analysis of commercial pellet food revealed appreciable concentrations of ammonia and urea-N. Long term satiation-feeding increased whole trout ammonia and urea-N excretion rates by 2.

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Background: The progression of diabetic kidney disease (DKD) affects the patient's kidney glomeruli and tubules, whose normal functioning is essential for maintaining normal calcium (Ca) and phosphorus (P) metabolism in the body. The risk of developing osteoporosis (OP) in patients with DKD increases with the aggravation of the disease, including a higher risk of fractures, which not only affects the quality of life of patients but also increases the risk of death.

Aim: To analyze the risk factors for the development of OP in patients with DKD and their correlation with Ca-P metabolic indices, fibroblast growth factor 23 (FGF23), and Klotho.

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