Show Summary Details
Page of

Disorders of renal calcium handling, urinary stones, and nephrocalcinosis 

Disorders of renal calcium handling, urinary stones, and nephrocalcinosis

Disorders of renal calcium handling, urinary stones, and nephrocalcinosis

Elaine M. Worcester

, Andrew P. Evan

, and Fredric L. Coe


May 30, 2013: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.


Pathology and pathogenesis—enhanced discussion of mechanisms of formation of apatite plugs that form the nidus for many stones.

Primary hyperoxaluria Type III—brief details of this newly described condition.

Updated on 25 May 2011. The previous version of this content can be found here.
Page of

PRINTED FROM OXFORD MEDICINE ONLINE ( © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy).

date: 26 March 2017

Renal stones are common, with a prevalence of about 5% in the United States of America. Acute stone passage almost always produces the severe pain of renal colic, but stones are often asymptomatic and discovered incidentally on imaging.

Investigation and general management

The initial evaluation of patients with renal colic optimally includes noncontrast CT, which can accurately visualize the size and location of stones in the urinary tract. Initial management of stones less than 5 mm in diameter in patients without anatomical abnormalities of the urinary tract is to provide adequate analgesia, followed by watchful waiting to allow time for stone passage. The presence of urinary tract infection, inability to take oral fluids, or obstruction of a single functioning kidney requires hospitalization and active management. Once the acute episode of stone passage or removal is over, thought should be given to diagnosis of the underlying causes of stones, and steps taken towards prevention. Stone analysis is the cornerstone of diagnosis.

Particular types of urinary stone and nephrocalcinosis

Most stones (66–76%) are formed of calcium oxalate: other types include calcium phosphate (12–17%), uric acid (7–11%), struvite (magnesium ammonium phosphate, 2–3%), and cystine (1–2%). They form because urine becomes supersaturated with respect to the stone mineral, and treatment to lower supersaturation can prevent recurrence.

Calcium oxalate stones—systemic diseases such as primary hyperparathyroidism, renal tubular acidosis, and hyperoxaluria should be ruled out, but most cases are idiopathic, when onset is often in early adulthood, with recurrence in 40% at 5 years. Stones typically form on suburothelial calcium phosphate deposits, called Randall’s plaques, most commonly in the context of idiopathic hypercalciuria, which is a polygenic familial trait. Diets high in salt, protein, and sucrose may increase urinary calcium further. Treatments shown in randomized trials to decrease recurrence include increased fluid intake, a diet that is low in sodium and protein but with normal calcium intake, thiazide diuretics, and potassium citrate.

Calcium phosphate stones—form when hypercalciuria is combined with alkaline urinary pH, which is idiopathic in many cases. Treatment to lower urinary calcium excretion (thiazides, reduced protein and sodium intakes) can reduce the risk of recurrence.

Uric acid stones—most often the result of persistently low urinary pH, which decreases uric acid solubility. Poorly visualized on standard plain radiographs. Treatment with alkali can improve uric acid solubility and decrease stone recurrence.

Struvite stones—found in patients colonized with bacteria that possess the enzyme urease (e.g. proteus), which results in extremely alkaline urine with high levels of ammonia, leading to formation of stones made of magnesium ammonium phosphate. Individuals with chronic urinary tract instrumentation or neurogenic bladder are at particular risk. Effective treatment requires antibiotics and removal of all stone material.

Cystine stones—result from rare autosomal recessive abnormalities of cystine transport in the kidney, leading to high urinary cystine concentrations. Poorly visualized on standard plain radiographs. High fluid intake and alkali can increase cystine solubility, but may require treatment with drugs that chelate cysteine and form soluble hetero-dimers, such as d-penicillamine or tiopronin.

Nephrocalcinosis—this is defined as precipitation of calcium salts in renal tubules or interstitium. All calcium stones are accompanied by a small amount of such precipitation, but larger amounts are typically seen in diseases including distal renal tubular acidosis, primary hyperoxaluria, and a range of other monogenic conditions. Deposition of large amounts of mineral in medullary (and occasionally cortical) tissue may lead to renal failure.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can''t find the answer there, please contact us.