Calcium stones

Calcific limestone is generally used by agronomists to denote a high calcium stone. This term can be misleading, however, because its use could suggest pure calcite, which calcitic limestone usually is not. 

Indiana high calcium stone 2 = Lehigh Valley, Pa., cement lock 3 = Pennsylvania cement lock 4 = Illinois Niagaian dolomitic stone ... 

Northwestern Ohio Niagaian dolomitic stone 6 = New York magnesian stone 7 = Virginia high calcium stone and 8 = Kansas Cretaceous high calcium stone (chalk). 

IP6 and phytates Kidney and gall bladder stone (calcium stones) management, hypercalcuria prevention (Ohkawa et al. 1984). Gastro-intestinal and colon health (Folino et al., 1995). 

Two renal responses are unique to the thiazide and thiazidehke diuretics. With these compounds, Na+ excretion is increased, while Ca++ excretion is decreased, primarily and directly because of increased distal Ca++ reabsorption, secondarily and indirectly because of a compensatory elevation of proximal solute absorption, making this class of diuretics useful in treating hypercal-ciuria. This effect, which may not be evident upon initial administration of the drug, is particularly benehcial in individuals who are prone to calcium stone formation. 

It is a potent antacid with rapid acid neutralizing capacity, but on long term use, it can cause hypercalcemia, hypercalciuria and formation of calcium stones in the kidney. 

Approximately two thirds of kidney stones contain Ca2+ phosphate or Ca2+ oxalate. Many patients with such stones exhibit a defect in proximal tubular Ca2+ reabsorption that causes hypercalciuria. This can be treated with thiazide diuretics, which enhance Ca2+ reabsorption in the distal convoluted tubule and thus reduce the urinary Ca2+ concentration. Salt intake must be reduced in this setting, since excess dietary NaCI will overwhelm the hypocalciuric effect of thiazides. Calcium stones may also be caused by increased intestinal absorption of Ca2+, or they may be idiopathic. In these situations, thiazides are also effective, but should be used as adjunctive therapy with other measures. 

Sodium cellulose phosphate (Calcisorb) binds calcium in the gut, reduces urinary calcium excretion and may benefit calcium stone-formers. 

Stone formation may occur in those with elevated levels of urinary calcium, Mormally adults excrctc less than 200 mg of calcium in the urine per day, even with relatively high intakes of calcium, A fraction of the population absorbs more calcium than normal and excretes more calcium in the urine, resulting in hyper-calciuria. Hypercalciuria is defined as urinary excretion of calcium of more than 300 mg/day. About half of patients with calcium stones have hypercalciuria and may be calcium hyper absorbers. Persons with hypercalciuria are advised to limit their calcium intake to one serving of milk or cheese per day. They are also advised to limit their protein intake to the RDA. Their protein intake should be limited to minimize the caiciuric effect of protein. They are also advised to fnerense their water intake to produce 2 liters of urine per day and to avoid oxalate-containing foods. Persons with hypercalciuria and with a familial history of stones should not lake calcium supplements to raise their intake above the RDA. 

Robertson WG. The effect of high animal protein uptake on the risk of calcium stone formation In the urinary tract. Clln.Scl. 1979 57(3) 285-8. 

Prevents recurrence of uric acid or calcium stone formation. 

Figure 45-16 Diagrammatic representation of the interplay of factors involved in kidney stone formation. High or low pH may act as a promoter or inhibitor of stone formation depending on the stone type in question (e.g., calcium stone formation is favored by inadequate acidification while urate is less soluble in acidic urine). Controversy exists as to whether formed stones become trapped as they pass through the nephron ( free particle theory ) or whether stone formation occurs at damaged sites on the tubule wall ( fixed particle theory ).

With calcium stone disease, magnesium is an inhibitor of stone growth. Magnesium forms complexes with oxalate that are more soluble than calcium oxalate. Increased urinary magnesium therefore inhibits stone formation. Administration of magnesium has been shown to reduce enteral calcium absorption and has been proposed as a treatment for idiopathic hypercalciuric stone formers. However, oral magnesium supplementation may have unpleasant side effects and a positive benefit in terms of reducing stone recurrence has not been demonstrated. ... 

Some investigators believe that urate may potentiate calcium stone formation, although this perception is not universally accepted. However, hyperuricosuria is common in calcium stone-forming patients, and treatment with allopurinol, thereby decreasing urate synthesis, reduces the rate of stone recurrence. Allopurinol treatment is therefore recommended for hyperuricosuric patients with calcium stone disease. The formation and management of pure urate stones are discussed in Chapter 24. 

De Swart PM JR, Busemann Sokole E, Wilmink JM. The interrelationship of calcium and magnesium absorption in idiopathic hypercalciuria and renal calcium stone disease. J Urol 1998 159 669-72. 

Robertson WG, Peacock M, Heyburn PJ, Marshall DH, Clark PB. Risk factors in calcium stone disease of the urinary tract. Br J Urol 1978 50 449-54. 

Tiselius HG. Possibilities for preventing recurrent calcium stone formation principles for the metabolic evaluation of patients with calcium stone disease. 

Trinchieri A, Nespoli R, Ostini F, Rovera F, Zanetti G, Pisani E. A study of dietary calcium and other nutrients in idiopathic renal calcium stone formers with low bone mineral content. J Urol 1998 159 654-7. 

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." ... 

Parks JH, Coe EL. Pathogenesis and treatment of calcium stones. Semin Nephrol 1996 16 398-411. 

Prevalence of hypocitraturia and hypopyrophosphaturia in recurrent calcium stone formers as isolated defects or associated with other metabolic abnormalities. Nephron 56 379-386... 

Moochhala SH, Sayer JA, Carr G et al (2008) Renal calcium stones insights from the control of bone mineralization. Exp Physiol 93 43—49... 

Fig. 1. A risk factor model of calcium stone formation GAGS, glycosaminoglycans (R2).

Another controversy surrounds the amount of glycoprotein (mucoprotein) excreted in the urine of adults with and without stones. Some reports showed that there is no difference in the excretion of uromucoids (B2, SI, S2), whereas others found that the excretion of uromucoid-rich material in calcium stone patients was greater than in their healthy counterparts (B3, K2, M5). This controversy may be attributed to different methods of urine storage, because it has been reported that the physical properties of the mucoproteins are altered by freezing (B3). Nevertheless, urine of black persons, who seldom develop stones, contains no uromu-coid (Kl, Ml). 

Sameul, C. T Uromucoid excretion in normal subjects, calcium stone formers and in patients with chronic renal failure. Urol. Res. 7, 5-12 (1979). 

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