Urolithiasis is the most common cause of nonobstetrical abdominal pain that requires hospitalization among pregnant patients. [1, 2] The relative incidence and rate of recurrent calculi in pregnant patients (1 per 1500 pregnant patients) is similar to that in nonpregnant patients.  Symptomatic stones are found in the ureter twice as often as in the renal pelvis and affect both ureters in equal frequency. Eighty to ninety percent are diagnosed after the first trimester. [4, 5]
Urolithiasis in pregnancy is often a diagnostic and therapeutic challenge for multiple reasons. First, potential adverse effects of anesthesia, radiation, and surgery often complicate traditional diagnostic and treatment modalities. Second, many signs and symptoms of urolithiasis can be found in a normal pregnancy or may be associated with broad differential diagnoses of other sources of abdominal pathology. Appendicitis, diverticulitis, or placental abruption was mistakenly diagnosed in 28% of patients in a 1992 study by Stothers and Lee.
Finally, most stones (64-84%) pass spontaneously with conservative treatment. [6, 7] However, if the calculus does not pass, it may initiate premature labor, produce intractable pain, cause urosepsis in the setting of urinary tract infection, or interfere with the progression of normal labor.
Of the various imaging modalities currently available, renal ultrasonography has become the first-line screening test for urolithiasis in pregnant patients, while limited intravenous pyelography (IVP) or CT scanning is reserved for more complex cases. Ideally, no ionizing radiation should be used in the first or second trimesters, if at all possible. MRI has limited utility in urinary stone disease, and nuclear renography is reserved for functional studies to direct treatment. These are of limited value during pregnancy.
Treatment of stones in pregnancy ranges from conservative management (eg, bed rest, hydration, analgesia) to more invasive measures (eg, stent placement, ureteroscopy with stone manipulation, percutaneous nephrostomy). With appropriate diagnosis and management, the outcome for both the mother and baby is excellent.
Prevention is the best cure for urolithiasis, and multiple investigators have suggested prophylactic measures to prevent the difficult course of treating urolithiasis in pregnancy. Denstedt and Razvi (1992) suggested prophylactic treatment of asymptomatic caliceal stones in women of childbearing age who are planning pregnancies.  Biyani and Joyce (2002) recommended metabolic evaluation in known stone formers, as well as prophylactic treatment of asymptomatic stones prior to pregnancy.  In support of their recommendation, they sited Glowacki et al (1992), whose study monitored 107 asymptomatic patients with renal calculi over 31.6 months. They found that 31.8% became symptomatic over that period. 
Although pregnancy-induced urinary stasis and hypercalcemia of pregnancy have been proposed as likely etiologic factors in urolithiasis, this has been disputed. Pregnancy-related events that tend to enhance stone formation include decreased ureteral peristalsis, physiological hydronephrosis, infection, and increased urinary calcium excretion. Augmented excretion of urolithiasis inhibitors, such as citrate, magnesium, and glycosaminoglycans, neutralize these phenomena in pregnant patients, who are no more likely to form urinary calculi than nonpregnant patients.  Coincident to the increased hypercalciuria in pregnancy is an increase in total circulating blood volume, making the relative supersaturation of calcium insignificant.
Anatomic and physiologic changes during pregnancy
Hydroureteronephrosis is the most significant renal alteration during pregnancy. Physiologic dilatation of the collecting system begins in the first trimester at 6-10 weeks' gestation and persists until 4-6 weeks following delivery.  Early theories suggest that hydronephrosis of pregnancy may be a hormonally induced phenomenon whereby ureteral smooth muscles relax in response to high levels of circulating progesterone. In early pregnancy, increased progesterone secretion dilates the ureters and reduces ureteral peristalsis, causing hydronephrosis. Alternatively, the predominant theory ascribes ureteric dilatation to compression of the ureter by the enlarging gravid uterus at the level of the pelvic brim, where the ureter crosses the iliac vessels.
Dilatation is greater on the right side than on the left because of pressure due to physiologic engorgement of the right ovarian vein and dextrorotation of the uterus.  Swanson and associates (1995) observed that hydroureteronephrosis was not routinely found below the pelvic brim and was altogether absent in patients who had undergone urinary diversion. 
Volume changes during pregnancy
Glomerular filtration rate (GFR) and renal plasma flow (RPF) increase by as much as 25-50% during pregnancy. Both of these changes are attributable to increases in cardiac output, decreases in renal vascular resistance, and increases in serum levels of progesterone, aldosterone, deoxycorticosterone, placental lactogen, and chorionic gonadotropin. GFR and RPF enhancements also contribute to the increase in glucose, amino acid, protein, and vitamin secretion. As a result of the GFR and RPF modulations, which peak at 9-11 weeks' gestation, renal volume increases during pregnancy by as much as 30% above the reference range. The sustained elevation of prolactin levels in the pregnant patient has a growth hormone–type effect by increasing the glomerular surface area, which also contributes to an increase in renal volume.
Along with increases in GFR and RPF, the filtered load of sodium, calcium, and urate increases. Although calcium and urate excretion increases, sodium excretion remains unchanged. The urinary excretion rate of calcium stone inhibitors, such as citrate and magnesium, also increases in the pregnant patient; likewise, increased glycosaminoglycans and acidic glycoproteins inhibit oxalate stone formation (eg, nephrocalcin). This explains why pregnancy is not associated with a net increase in the rate of stone formation relative to nonpregnant patients. The net effect of these physiologic changes is a stable relative supersaturation of important ions such as calcium oxalate, urate, and phosphate.
Uric acid stone formation
The formation of uric acid stones requires continued and excessive oversaturation of urine with uric acid or extreme aciduria. Dehydration, hyperuricosuria, and significantly acidic urine contribute to uric acid supersaturation and stone formation. However, during gestation, urine tends to be more alkaline, probably because of greater intrinsic purine use and increased urinary citrate excretion. Thus, renal units are generally protected against uric acid stone formation during pregnancy.
Calcium oxalate and calcium phosphate stone formation
Although pathologic calcium oxalate supersaturation has been identified in the urine of pregnant women, the incidence of crystalluria is no higher than in women who are not pregnant. In the pregnant patient, physiologic absorptive hypercalciuria is due to elevated levels of serum 1,25 dihydroxycholecalciferol (1,25 vitamin D). This hormone, which is secreted by the placenta, augments calcium absorption in the GI tract and suppresses parathormone production, increasing renal excretion of calcium. Additionally, dietary supplementation of calcium during gestation further augments calcium excretion. Some reports suggest that calcium excretion increases 200-300% compared with that in healthy patients who are not pregnant. However, increased concentration of the aforementioned urolithiasis inhibitors present in urine during gestation and increased urine fluid output counters the increased risk imposed by any hypercalciuria.
Struvite stones form only when the urinary tract is infected with urea-splitting organisms (eg, Proteus species). These infected stones are usually composed of pure magnesium ammonium phosphate but may be formed around a coexisting calcium, uric acid, or cystine stone. Struvite stones appear to develop more commonly in the presence of a congenital abnormality of the collecting system.
Stone formation during pregnancy does not appear to have any etiologic factors that are unique to pregnancy. Risk factors associated with urolithiasis in general include the following:
Age (third to fifth decades of life)
Decreased water intake
Increased environmental temperature and/or dry climate
Diet (eg, high in calcium, sodium, and red meat consumption)
Occupation (eg, exposure to hot climate)
Geographic location (eg, southwest United States ["Stone Belt"])
Social class (related to occupation and diet)
Excessive weight or obesity (apparently a risk factor in women but not in men)
The reported incidence of urinary calculi in pregnant women is around one case per 1500 pregnant women, which is similar to that in nonpregnant patients.  In a review of data from a tertiary women's hospital, Riley et al found that the number of patients with nephrolithiasis increased significantly from 1991-2000 to 2001-2011, from 78 to 226 a year (P = 0.004). However, the number of pregnant patients with nephrolithiasis did not change significantly over that period, rising from 36 to 47 (P = 0.1). 
Approximately 80-90% of pregnant patients with urinary calculi present with symptoms during the second or third trimester, because spontaneous stone passage is more difficult at this stage of pregnancy. 
Ureteral stones occur twice as often as kidney stones in pregnant patients.
Urolithiasis associated with ureteral obstruction and upper urinary tract infection mandates immediate treatment; this is a true urologic emergency that can potentially lead to urosepsis, perinephric abscess formation, or even death in pregnant women. Urolithiasis in a pregnant patient may initiate premature labor or interfere with the progression of normal labor, which poses a significant health risk to the fetus.
Race-, Sex-, and Age-related Demographics
Hispanic people and white people are most commonly predisposed to urinary calculi. Black people are less predisposed to kidney stone formation. The exact cause of this discrepancy is not known, but dietary influences may play a role. Calculi in black individuals are more likely to become infected than those in white individuals.
The reported incidence of urolithiasis is higher in men, with a male-to-female ratio of 3:1, although this ratio is decreasing, possibly because of dietary or obesity trends in the United States.
Urinary stones in women usually manifest during the third to fifth decades of life, with an average age of 24.6 years. Urolithiasis occurs in pregnant women at rates similar to age-matched nonpregnant women. 
Diagnosis and treatment of urolithiasis in pregnancy is complex. However, advances in technology and experience allow urologists to provide accurate evaluation and succeed with either temporizing or definitive treatments. These can be accomplished safely, with little risk to the mother or fetus. With prompt evaluation and expeditious treatment, the prognosis is excellent.
Approximately 64-84% of renal calculi pass spontaneously with conservative management, [6, 7] especially if they 4 mm or smaller. Stones that are 7 mm or larger are much less likely to pass without intervention and often require some type of treatment.
Symptomatic urolithiasis does not appreciably worsen pregnancy outcome. Occurring in about 10-20% of patients, urinary tract infection is the most common nonobstetric complication of urolithiasis in pregnancy. Premature labor associated with renal colic is rare but can occur. In the past, spontaneous abortion has been associated with a history of urolithiasis but it is extremely rare today.
An excellent patient education guide, The Kidney Stones Handbook is available directly from the publisher, Four Geez Press, at 1-800-2KIDNEYS. It is the only book on kidney stones specifically written for patients and their families by a urology kidney stone expert. A quarterly newsletter is also available and can be ordered from the same publisher.
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