Hyperparathyroidism Nephrolithiasis

Chronic hypercalcemia (i.e., hyperparathyroidism) is associated with metastatic calcification, nephrolithiasis, and chronic renal insufficiency. 

In 1930 and 1932, two separate reports were published, each describing the successful treatment of 2 patients with hypercalcemia secondary to hyperparathyroidism with inorganic phosphate [37-38]. Due to the potential for this treatment to lead to nephrolithiasis or extraskeletal calcifications, it was not widely employed. In 1966, Goldsmith and Ingbar reported... 

Features of lithium-induced hyperparathyroidism include a) a low urinary calcium excretion and the absence of nephrolithiasis b) normal urinary cyclic adenosine monophosphate excretion and c) normal plasma inorganic phosphate [32]. In lithium-induced hypercalcemia, a higher frequency of conduction defects has been noted [47]. Lithium also inhibits par-... 

Hyperparathyroidism disturbs calcium metabolism, and leads to hypercalcemia, bone atrophy, and nephrolithiasis. These three symptoms are usually present together, yet one of them may dominate the clinical picture. In recent decades, the incidence of renal disease seems to have increased, and that of bone disease decreased among patients with reported hyperparathyroidism. 

Two-thirds of the patients with hyperparathyroidism present nephrolithiasis. In the early stages, hypercalcemia leads to hypercalciuria and hyperphospha-turia with polyuria and occasionally polydypsia. Later, calcium phosphate stones form in the kidney, and nephrolithiasis with typical renal colics, hematuria, and a complicating pyelonephritis develop. The stones may reach sizes that make them visible on X-rays and make them responsible for hydronephrosis. Renal... 

If the semm calcium is greater than 11 mg/dL, the patient has nephrolithiasis, or the serum creatinine is elevated, dmg therapy is usually required. The drug of choice is prednisone at an initial daily dose of 20 to 40 mg/day (183). Corticosteroids cause a rapid decline in serum calcium within 5 days and in urinary calcium excretion in 7 to 10 days (183). Failure of the serum calcium to normalize within two weeks on this corticosteroid regimen should alert the clinician to an alternate or coexisting disorder such as hyperparathyroidism, lymphoma, carcinoma, and myeloma (183). Once the calcium disorder is brought under control, the corticosteroid dose can be lowered over four to six weeks (183). The serum calcium and urinary calcium excretion rate should be closely monitored. If the patient develops intolerable corticosteroid side effects or fails to respond, chloroquine (184), hydroxychloroquine (185), and ketoco-nizole (186) have been used successfully. 

Primary hyperparathyroidism, although the most frequent cause of hypercalcemic hypercalciuria in adults, is very rare in children (Fig. 20.6) (Damiani et al. 1998). NC and nephrolithiasis due to subcutaneous fat necrosis with hypercalcemia are described in neonates (Fig. 20.10) (Gu et al. 

---