Medical Management of Hypercalciuria




© Springer International Publishing Switzerland 2015
Manoj Monga, Kristina L. Penniston and David S. Goldfarb (eds.)Pocket Guide to Kidney Stone Prevention10.1007/978-3-319-11098-1_5


5. Medical Management of Hypercalciuria



Sushant R. Taksande1 and Anna L. Zisman 


(1)
Department of Medicine/Section of Nephrology, Pritzker School of Medicine, University of Chicago, 5841 S. Maryland Avenue, MC 5100, Suite S512, Chicago, IL 60637, USA

 



 

Anna L. Zisman



Keywords
HypercalciuriaNephrolithiasisOsteoporosisThiazideAlkali



Introduction


Nearly 80 % patients with nephrolithiasis have calcium-based stones. Hypercalciuria is the most common metabolic abnormality in calcium stone formers, with about 50 % of patients with stone disease demonstrating the trait. It may be defined as >250 mg/day of urine calcium in females and >300 mg/day in males. However, the risk of stones increases as urine calcium excretion increases even at values below these thresholds, suggesting that urine calcium should be considered a linear function, rather than a binary “normal” vs. “high.” Increasing urine calcium concentration alters the urinary supersaturation of calcium oxalate and calcium phosphate and is thus directly linked to increased risk of calcium stone disease [1].


Etiology


The most common etiology of hypercalciuria is genetic hypercalciuria, often termed idiopathic hypercalciuria. Approximately 50 % of first degree relatives of a patient with hypercalciuria without an apparent systemic cause will also demonstrate hypercalciuria, suggesting an autosomal dominant pattern of inheritance, though the trait appears to be polygenic. A careful history and a high index of suspicion may help guide further evaluation or will help eliminate secondary causes of increased urinary calcium excretion including:



  • Primary hyperparathyroidism—a normal serum calcium generally excludes this diagnosis, but a high index of suspicion is necessary for subtle cases.


  • Vitamin D excess—exogenous vitamin D, granulomatous disease (sarcoidosis, lymphoma, tuberculosis).


  • Hyperthyroidism—it is also important to make sure that in the setting of thyroid replacement therapy, the doses remain appropriate over time.


  • Renal Tubular Acidosis—the diagnosis is suggested by a low serum bicarbonate concentration.


  • Vitamin A toxicity


  • Medication use



    • Corticosteroids, acetazolamide, topiramate


  • Immobility


  • Paget’s disease


  • Genetic/congenital abnormalities [2]



    • Calcium sensing receptor (CaSR) mutations


    • Dent’s disease (chloride channel 5 mutations)


    • Bartter’s syndrome (mutations in multiple genes affecting ion transport in the ascending limb of the loop of Henle)


    • Liddle’s syndrome (ENaC mutations)


    • Hereditary hypophosphatemic rickets with hypercalciuria


    • Medullary sponge kidney


    • Beckwith—Weidmann syndrome


    • Familial hypomagnesemia (claudin 16, claudin 19 mutations)


    • Osteogenesis imperfecta type 1


Diagnosis


The diagnosis of hypercalciuria is established with at least one 24-h urine collection demonstrating excess calcium excretion [1] as defined by at least one of the following:



  • An absolute value of greater than 250 mg of calcium per day in females or >300 mg of calcium per day in males. Even values significantly below these “thresholds” however may be worth lowering in patients with recurrent stones.


  • Urinary calcium excretion of greater than 4 mg/kg of body weight.


  • Urinary calcium excretion of greater than 140 mg/g creatinine.

Definitions based on factoring calcium excretion for body weight or creatinine excretion may be useful in children and older people or others with reduced muscle mass.


Complications


In addition to risk of stone disease, hypercalciuria carries with it a risk of bone demineralization and osteoporosis [3].



  • Hypercalciuric patients often excrete more calcium than they absorb leading to a negative calcium balance and bone loss.


  • Bone mineral density is inversely correlated with degree of hypercalciuria in both male and female hypercalciuric stone formers (but not non-stone formers).


  • Stone formers have a higher incidence of both vertebral and long bone fracture compared to non-stone formers in multiple epidemiological studies.


  • Consider performing Dual Emission X-ray Absorptiometry (DEXA) in patients with hypercalciuria, particularly post-menopausal women and either gender with a family history of osteoporosis or bone fracture.


Treatment



General Considerations


Hypercalciuria portends a risk of kidney stone formation. General kidney stone prevention guidelines apply to patients with hypercalciuria including



  • High fluid intake to yield at least 2–2.5 L of urine volume.


  • Sodium restricted diet of less than 2,000–2,300 mg per day.


  • Moderation of animal protein intake to 0.8–1 g/kg per day.


  • Avoidance of calcium supplements and age-appropriate intake of dietary calcium (1,000 mg of elemental calcium between the ages of 19 and 50, 1,200 mg in patients older than 50 years).


Pharmacological Treatment of Hypercalciuria


Treatment of hypercalciuria to decrease supersaturation for calcium oxalate and calcium phosphate decreases the risk of recurrent nephrolithiasis. Given the linear nature of urine calcium excretion, applying these therapies only to patients meeting the threshold definitions of hypercalciuria discussed above may be too restrictive and will preclude giving effective therapy to all those who may benefit. As discussed below, thiazides have been shown to prevent stones even in patients who do not meet these threshold definitions of hypercalciuria.

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Nov 3, 2016 | Posted by in NEPHROLOGY | Comments Off on Medical Management of Hypercalciuria

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