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Diagnosis and acute management of suspected nephrolithiasis in adults

Gary C Curhan, MD, ScD
Mark D Aronson, MD
Glenn M Preminger, MD
Section Editors
Stanley Goldfarb, MD
Michael P O'Leary, MD, MPH
Deputy Editor
Albert Q Lam, MD


Renal and ureteral stones are a common problem in primary care practice [1]. Patients may present with the classic symptoms of renal colic and hematuria. Others may be asymptomatic or have atypical symptoms such as vague abdominal pain, acute abdominal or flank pain, nausea, urinary urgency or frequency, difficulty urinating, penile pain, or testicular pain.

Primary care clinicians need to be alert to the possibility of nephrolithiasis and its consequences to decide upon a diagnostic approach, therapy, and the need for referral to a urologist. These issues will be reviewed here. The epidemiology of nephrolithiasis and subsequent evaluation of such patients are discussed separately. (See "The first kidney stone and asymptomatic nephrolithiasis in adults" and "Evaluation of the adult patient with established nephrolithiasis and treatment if stone composition is unknown".)


Eighty percent of patients with nephrolithiasis form calcium stones, most of which are composed primarily of calcium oxalate or, less often, calcium phosphate [2,3]. The other main types include uric acid, struvite (magnesium ammonium phosphate), and cystine stones. The same patient may have more than one type of stone concurrently (eg, calcium oxalate and uric acid) [3].

There are different theories regarding calcium stone formation. One theory is that stone formation occurs when normally soluble material (eg, calcium, oxalate) supersaturates the urine and begins the process of crystal formation (eg, calcium oxalate crystal). It is presumed that crystal aggregates become large enough to be anchored (usually at the end of the collecting ducts), and then slowly increase in size over time. This anchoring is thought to occur at sites of epithelial cell injury, perhaps induced by the crystals themselves.

Another theory is that stone formation is initiated in the renal medullary interstitium [4-6]. Calcium phosphate crystals may form in the interstitium and eventually get extruded at the renal papilla, forming the classic Randall's plaque [5,6]. Calcium oxalate or calcium phosphate crystals may then deposit on top of this nidus, remaining attached to the papilla.


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Literature review current through: Sep 2016. | This topic last updated: Nov 11, 2015.
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