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Diagnosis and acute management of suspected nephrolithiasis in adults

Authors
Gary C Curhan, MD, ScD
Mark D Aronson, MD
Glenn M Preminger, MD
Section Editors
Stanley Goldfarb, MD
Michael P O'Leary, MD, MPH
Jorge A Soto, MD
Deputy Editors
Albert Q Lam, MD
Susanna I Lee, MD, PhD

INTRODUCTION

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".)

ETIOLOGY

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 a stone that contains more than one crystal type (eg, calcium oxalate and uric acid) [4].

There are different theories regarding calcium stone formation, and the different stone types may have different initiating events. Stone formation occurs when normally soluble material (eg, calcium, oxalate) supersaturates the urine and begins the process of crystal formation (eg, calcium oxalate crystal). For some calcium stones, particularly calcium oxalate, it appears that an important initiating event occurs in the renal medullary interstitium [5-7]. Calcium phosphate crystals may form in the interstitium and eventually erode through the renal papillary epithelium, forming the classic Randall's plaque [6,7]. Calcium oxalate or calcium phosphate crystals may then deposit on top of this nidus, remaining attached to the papilla. Calcium phosphate stones might also form initially in dilated ducts of Bellini and then grow out into the urinary space [8].

The pathogenesis of struvite, cystine, and uric acid stones is discussed separately. (See "Pathogenesis and clinical manifestations of struvite stones" and "Uric acid nephrolithiasis" and "Cystine stones".)

                           
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Literature review current through: Sep 2017. | This topic last updated: Jul 07, 2017.
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