Hypercalcemia nephrolithiasis

Diuretics have a wide range of clinical uses, including HTN, heart failure, edematous states, renal dysfunction, hypercalcemias, nephrolithiasis, glaucoma, and mountain sickness. Although they are classed as diuretics, recognize that both loops and thiazides cause significant vasodilation, an action that contributes to their clinical effectiveness, especially in HTN and heart failure. 

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-... 

Hypervitaminosis D apparently cannot arise from excessive exposure to sunlight but only occurs following inge.s-tion of large quantities of synthetic vitamin D for months The amount necessary has been estimated at 50,000 units or more in a person with normal parathyroid function. The mechanism may involve formation of excessive amounts of the vitamin D metabolite 25-OHD. Toxicity involves derangements of calcium metabolism, resulting in hypercalcemia and metastatic calcification of soft tissue. Most problems result from the hypercalcemia, which typically causes muscular weakness, anorexia, nausea, vomiting, and depression of the central nervous system (which can result in coma and death). In addition, deposition of calcium salts in the kidneys (nephrocalcinosis) and the tubules (nephrolithiasis)... 

Contraindications Hypercalcemia or evidence or vitamin D toxicity or use on the face Caution History of nephrolithiasis... 

Renal The most important renal manifestations of hypercalcemia are nephrolithiasis renal tubular dysfunction, particularly decreased concentrating ability and acute and chronic renal insufficiency. 

Adverse effects of oral calcium and vitamin D supplementation include hypercalcemia and hypercalciuria, especially in the hy-poparathyroid patient, in whom the renal calcium-sparing effect of parathyroid hormone is absent. Hypercalciuria may increase the risk of calcium stone formation and nephrolithiasis in susceptible patients. One maneuver to help prevent calcium stones is to maintain the calcinm at a low normal concentration. Monitoring 24-hour urine collections for total calcium concentrations (goal <300 mg/24 h) may also minimize the occurrence of hypercalciuria. The addition of thiazide dinretics for patients at risk for stone formation may result in a reduc-tionof both urinary calcium excretion and vitamin D requirements." ... 

Answer A. The effects described are typical of thiazide diuretics, which inhibit the Na+/Cr cotransporter in the distal convoluted tubule. This action facilitates reabsorption of Ca2+, which is the basis for the use of thiazides in nephrolithiasis, and which can result in hypercalcemia. The increased load of Na+ in the collecting tubules leads to increased excretion of both K+ and H+, so hypokalemia and alkalosis may occur. 

In healthy individuals - that is, with normal kidney function and with no history of nephrolithiasis - supplementation with up to 2-3 g calcium per day appears to be associated with only a minimal risk of hypercalcemia and kidney stone formation (Ringe... 

Renal effects of hypercalcemia include reduced glomerular filtration rate (GFR), polyuria, nephrocalcinosis, and renal stone disease. Hypercalcemia causes renal vasoconstriction which may contribute to decreased GFR. The hypercalcemia-induced polyuria results from 1) an impairment of active transport of NaCl in the loop of Henle, distal tubule and collecting duct and 2) an inhibition of vasopressin-facilitated absorption of water in the distal nephron. As a direct result of the polyuria, many side effects including polydipsia, thirst, nocturia and dehydration are common. Precipitation of calcium salts within the kidney leads to chronic inflammatory reactions (nephrocalcinosis), fibrosis, renal impairment, nephrolithiasis and urolithiasis. Further renal damage may occur indirectly from hypertension. 

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... 

Hypercalcemia/ 1. Increased serum calcium with no 1. Increased urine calcium 1. Nephrolithiasis-no stone... 

Calcium metabolism is disregulated in active sarcoidosis. The primary disorder in calcium metabolism stems from an increase 1-a hydroxylase activity in sarcoid alveolar macrophages that converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, the active form of the vitamin (177-179). This may manifest as hypercaluria, hypercalcemia, and nephrolithiasis with possible renal insufficiency (180). 

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. 

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