Calcium phosphate kidney stones are less common than those formed with calcium oxalate. Calculi containing both phosphate (PO43−) and oxalate of calcium are common. However a greater proportion of the constituting chemical is usually oxalate.
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Kidney stones (renal calculi) of calcium phosphate (CaP) and those calculi containing greater amounts of phosphate are to be thoroughly investigated for the underlying medical cause.The most important calcium and PO43- involved renal stones are carbonate apatite, hydroxyapatite, and brushite. The struvite calculi are formed of magnesium, ammonium and phosphate. The basic cause is the supersaturation of calcium compounds in the urine. When the solubility threshold is exceeded under the given conditions in the kidney, nucleation begins. If the conditions are stable slow crystalline growth commences.
The existing supersaturation of calcium and phosphate in the urine is the driving force for the spontaneous precipitation and crystallization. One of the factors conducive to supersaturation of these salts is increase in urine pH. Carbonate apatite calculi may sometimes associate with urinary infection.
Causes of phosphate stone formation
Several medical conditions lead to calcium phosphate kidney stone formation. The primary hyperparathyroidism, secondary hyperparathyroidism, renal tubular acidosis, hyperphosphaturia, hypercalciuria and Fanconi syndrome are some of the causative factors. Certain medications, such as Topiramate (TPM), acetazolamide, zonisamide are associated with the development of metabolic acidosis, hypocitraturia, hypercalciuria and elevated urine pH.Hyperparathyroidism
The parathyroid glands produce parathyroid hormone (PTH). The parathyroid hormone regulates and maintains calcium and phosphate levels in the body.The primary hyperparathyroidism leads to hypercalcaemia (raised serum calcium levels). The serum PO43- levels tend to be low as a result of decreased renal tubular phosphate reabsorption and resultant loss in the urine. The hypercalcemia results in active removal of calcium into urine. The availability of Calcium and PO43- helps in seeding of renal calculi.
Hyperphosphaturia and Hypercalciuria
Phosphaturia is a condition wherein phosphate is excessively excreted by the kidney, making these ions easily available for calculi formation. There are two form of phosphaturia. The primary type is direct excess excretion of PO43− by the kidneys either due to generalized dysfunction of the proximal tubular cells in kidney (Fanconi syndrome) or due to the action of diuretics. The secondary phosphaturia is due to both primary and secondary types of hyperparathyroidism.Hypercalciuria is a condition wherein Calcium is excessively excreted by the kidney. Hypercalciuria is caused due excessive release from the bones, excessive calcium supplementation, elevated serum levels of calcium, excessive sodium intake or due to certain genetic disorders.
The conditions of hypercalciuria and hyperphosphaturia, individually or as a combined action, initiate calcium phosphate stone formation in the event of saturated levels of these ions in the urine. The stone formation is further helped by high pH of urine.
Renal tubular acidosis (RTA)
RTA is a medical condition is which there is acid accumulation in the body. The condition is due to inefficiency of kidney in resorbing and recovering bicarbonate ions from the filtrate in the proximal tubular cells or inefficiency in eliminating hydrogen ions into lumen of nephron at distal tubule. The distal renal tubular acidosis characterized by hyperchloremic acidosis, hypocitraturia, and high urine pH. The net effect is insufficient acidification of urine to a pH of less than 5.3 and accumulation of acid in the body and acidemia.Treatment and management
In the management of these renal calculi, reducing urine saturation and limiting of calcium excretion are important steps. With sufficient intake of water, urine can be diluted. Restricting sodium ingestion can reduce sodium excretion as well as calcium excretion. Citrate, though tends increase the urine pH, has the capacity to bind to ca2+ and eliminate it from the system. Thiazides also lower urine calcium excretion. The persisting calcium phosphate kidney stones are removed by extracorporeal shock wave lithotripsy (ESWL), Percutaneous stone removal or surgery.Advertisements
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References: 1.Vega D, Maalouf NM, Sakhaee K. Increased propensity for calcium phosphate kidney stones with topiramate use. Expert Opin Drug Saf. 2007 Sep;6(5):547-57. 2.David S. Goldfarb. A woman with recurrent calcium phosphate kidney stones. Clin J Am Soc Nephrol. 2012 Jul;7(7):1172-8. 3.Gault MH, Chafe LL, Morgan JM, Parfrey PS, Harnett JD, Walsh EA, Prabhakaran VM, Dow D, Colpitts A. Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. Medicine (Baltimore). 1991 Nov;70(6):345-59. 4.Fredric L. Coe, Andrew Evan, Elaine Worcester. Kidney stone disease. J Clin Invest. Oct 1, 2005; 115(10): 2598–2608. 5.Hesse A, Heimbach D. Causes of phosphate stone formation and the importance of metaphylaxis by urinary acidification: a review. World J Urol. 1999 Oct;17(5):308-15. |
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