Kidney stones - Mayo Clinic Kidney stones Kidney stones Kidney stones (renal lithiasis, nephrolithiasis) are small, hard mineral deposits that form inside your kidneys. The stones are made of mineral and acid salts. Kidney stones have many causes and can affect any part of your urinary tract — from your kidneys to your bladder. Often, stones form when the urine becomes concentrated, allowing minerals to crystallize and stick together. Passing kidney stones can be quite painful, but the stones usually cause no permanent damage. Depending on your situation, you may need nothing more than to take pain medication and drink lots of water to pass a kidney stone. In other instances — for example, if stones become lodged in the urinary tract or cause complications — surgery may be needed. Your doctor may recommend preventive treatment to reduce your risk of recurrent kidney stones if you're at increased risk of developing them again. References Goldman L, et al. Goldman's Cecil Medicine. 24th ed. Philadelphia, Pa.: Saunders Elsevier; 2012. Accessed Dec. 10, 2014. Kidney stones in adults. National Institute of Diabetes and Digestive and Kidney Diseases. Accessed Dec.

10, 2014. Diet for kidney stone prevention. National Institute of Diabetes and Digestive and Kidney Diseases. Accessed Dec. 10, 2014. Rakel D. Integrative Medicine. 3rd ed. Philadelphia, Pa.: Saunders Elsevier; 2012. Accessed Dec. 10, 2014. Curhan GC, et al. Diagnosis and acute management of suspected nephrolithiasis in adults. Accessed Dec. 10, 2014. Preminger GM, et al. The first kidney stone and asymptomatic nephrolithiasis in adults. Accessed Dec. 10, 2014. Humphreys MR (expert opinion). Mayo Clinic, Phoenix/Scottsdale, Ariz. Jan. 21, 2015. Anderson CF (expert opinion). Mayo Clinic, Rochester, Minn. Jan. 16, 2015. Wein AJ, et al. Campbell-Walsh Urology. 10th ed. Philadelphia, Pa.: Saunders Elsevier; 2012. Accessed Dec.

10, 2014. Signs and symptoms of parathyroid disease. The American Association of Endocrine Surgeons. Accessed Jan. 15, 2015. Cook AJ. Decision Support System. Mayo Clinic, Rochester, Minn. Oct. 8, 2014. Kidney stone treatment: Shock wave lithotripsy. National Kidney Foundation. Accessed Feb. 5, 2015. Products and Services Definition of Nephrolithiasis Our Kidney Stones Main Article provides a comprehensive look at the who, what, when and how of Kidney Stones Definition of Nephrolithiasis Causes of a Heart Attack Slideshow Nephrolithiasis: The process of forming a kidney stone, a stone in the kidney (or lower down in the urinary tract). Kidney stones are a common cause of blood in the urine and pain in the abdomen, flank, or groin. Kidney stones occur in 1 in 10 people at some time in their life. The development of the stones is typically related to increased excretion of stone-forming components such as calcium, oxalate, urate or cystine.

The pain with kidney stones is usually of sudden onset, very severe and colicky (intermittent), not improved by changes in position, radiating from the back, down the flank, and into the groin. Nausea and vomiting are common. Treatment includes relief of pain, hydration and, if there is concurrent urinary infection, antibiotics. The majority of stones pass spontaneously within 48 hours. If a symptomatic stone does not pass, a procedure by a urologist may be needed. "Nephrolithiasis" is derived from the Greek nephros- (kidney) lithos (stone) = kidney stone. The stones themselves are also called renal caluli. The word "calculus" (plural: calculi) is the Latin word for pebble. Last Editorial Review: 5/13/2016 Nephrolithiasis | definition of nephrolithiasis by Medical dictionary Nephrolithiasis | definition of nephrolithiasis by Medical dictionary 1. the formation of kidney stones . 2. a condition marked by the presence of kidney stones .

neph·ro·li·thi·a·sis (nef'rō-li-thī'ă-sis), (nef″ro-lĭ-thi´ah-sis) presence of renal calculi . nephrolithiasis a disorder characterized by the presence of calculi in the kidney. See also renal calculus . nephrolithiasis The formal medical term for kidney stone(s) (see there), or urinary tract calculi. nephrolithiasis neph·ro·li·thi·a·sis (nef'rō-li-thī'ă-sis) nephrolithiasis a condition marked by the presence of renal calculi. See also urolithiasis . Want to thank TFD for its existence? Tell a friend about us , add a link to this page, or visit the webmaster's page for free fun content . Link to this page: artificial kidney References in periodicals archive ? While this study suggested an increase incidence of nephrolithiasis in male marathon runners, it has little ability to explain the relationship due to the lack of objective and numerical data.

Kidney stones and the long distance athlete 2001) investigated the effects of an Ammi visnaga extract in an animal model of nephrolithiasis and found that the plant extract significantly reduced the incidence of calcium oxalate deposition in the rat kidneys. An aqueous extract of Ammi visnaga fruits and its constituents khellin and visnagin prevent cell damage caused by oxalate in renal epithelial cells The rate of nephrolithiasis associated with Cushing's syndrome was found to be lower than that of the reported studies (7. Nephrolithiasis Nephrolithiasis References Definition The formation of crystal aggregates in the urinary tract results in kidney stones, the clinical condition referred to as nephrolithiasis. Kidney stones might produce no symptoms or may be associated with one or several of the following: flank pain, gross or microscopic hematuria, obstruction of one or both kidneys, and urinary infections. The stones are usually formed by one of four substances: calcium, uric acid, magnesium ammonium phosphates (or struvite), or cystine. 1 Occasionally, calcium salts and uric acid are present in the same stone.

Some rare types of kidney stones include xanthine and triamterene stones, which are seen in patients taking xanthine oxidase inhibitors and triamterene-containing diuretics, respectively. Indinavir stones have been reported in HIV-positive patients treated with this retroviral therapy. 2 In this chapter, I discuss the prevalence, pathophysiology, clinical presentation, and treatment of each of the four major types of stones. Among American adults, the prevalence of nephrolithiasis is 1 in 1000, with men being almost twice as likely as women to have stones. Among the pediatric population, kidney stones are much less common, but the exact prevalence is unknown. Back to Top General Pathophysiology Kidney stones result from the growth of crystals into stones. 3 Crystals form in urine that is supersaturated with particular salts such as calcium oxalate, sodium urate, magnesium ammonium phosphate, or cystine. There is a maximum to the amount of a compound that can be kept in stable solution, which is defined by its solubility or equilibrium concentration product.

Supersaturation results when the amount of a compound in solution exceeds the solubility; at that point, there is a process that begins to remove this excess by crystal formation. This can be manipulated in two ways: by changing the amount or concentration of compound available for crystallization or by changing the solubility of the compound. An example of the former is reducing the quantity of calcium or cystine in the urine of a patient with hypercalciuric or cystinuric stone disease, or reducing the concentration of the calcium or cystine by high fluid intake (dilution of the urine). An example of the latter is increasing the solubility by increasing the urinary pH in patients with uric acid or cystine stone disease or by increasing the urinary excretion of naturally occurring inhibitors of crystal formation, such as citrate. Summary Calcium Stone Disease Prevalence Calcium stone disease is the most common form of nephrolithiasis and represents about 70% of all cases of stone-forming disease. It occurs most often in the third to fifth decades of life and more often in men than women.

Pathophysiology In 60% to 70% of patients, hypercalciuria is present (defined by 24-hour urinary calcium excretion of >300 mg in males, >250 mg in females, or >4 mg/kg in males or females). In less than 5%, the hypercalciuria may be associated with hyperparathyroidism or sarcoidosis, with or without hypercalcemia. More often, the hypercalciuria occurs with a normal serum calcium level and in the absence of any systemic diseases; this is called idiopathic hypercalciuria. 4 Most patients with idiopathic hypercalciuria exhibit excessive gastrointestinal absorption of calcium (absorptive hypercalciuria). In many such cases, the 1,25-hydroxyvitamin D level is slightly elevated and the serum phosphorus level is slightly low, but parathyroid hormone (PTH) levels are normal. The mechanisms for these derangements are not known. These patients also have inappropriately high levels of urinary calcium excretion, even when on a calcium-restricted diet, which is why a calcium-restricted diet is not advised for these patients.

A minority of hypercalciuric patients have a renal leak of calcium (renal hypercalciuria). These patients have fasting hypercalciuria and slightly elevated levels of PTH and 1,25-hydroxyvitamin D. In these patients, thiazide diuretics reduce urinary calcium excretion, correct the secondary hyperparathyroidism, and return vitamin D levels to normal. In both forms of hypercalciuria, the degree of hypercalciuria is worsened by high dietary sodium intake, high animal protein intake, and loop diuretics; it is reduced by distally acting thiazide diuretics and amiloride, as well as dietary restriction of sodium and protein. Several studies have shown that a higher dietary calcium intake has been associated with fewer calcium stone events in men and women. 5,6 A study of 120 Italian hypercalciuric calcium oxalate stone patients has demonstrated that a diet with normal calcium, low sodium, and low animal protein resulted in reduced incidence of calcium stones compared with those on a low-calcium diet.

7 In this study, both diets were associated with a reduction in urinary calcium level; however, urinary oxalate excretion rose in the low-calcium diet group and fell in the high-calcium diet group. The reduction in urinary oxalate excretion in persons on a normal calcium diet was attributed to the intestinal binding of dietary oxalate by dietary calcium, thus decreasing the amount of free oxalate available for absorption. Although both groups had reduced calcium oxalate saturation of their urine, the normal-calcium diet group had a more significant reduction. Compared with the patients on a low-calcium diet, the patients on the normal calcium, low-sodium, low-protein diet had a 50% reduction in stone risk at 5 years. In some calcium stone patients, the mechanism for the increased rate of calcium oxalate stones is the presence of hyperoxaluria. 8 The hyperoxaluria is usually secondary to high dietary oxalate intake caused by ingestion of foods or liquids containing large quantities of oxalate. Some of these foods and liquids include baked beans, collard greens, green beans, rhubarb, tea, cocoa, peanut butter, and vegetable soup.

In other cases, the hyperoxaluria occurs in the setting of gastrointestinal malabsorption, seen in patients with inflammatory bowel disease. When patients malabsorb fat, dietary calcium binds to the fat rather than to dietary oxalate, which is the norm. This results in a larger amount of unbound intestinal oxalate that passes into the colon, from which it is absorbed. In patients with ileostomies (colon excluded), this enhanced oxalate absorption does not occur. A rare cause of hyperoxaluria is the inherited condition known as primary hyperoxaluria. 9 In this condition, the hepatic enzyme that converts glyoxylate to glycine is deficient. As a result, there is increased production of oxalate from glyoxylate. Other risk factors for calcium stones include chronic low urine output, hyperuricosuria, and low urine citrate, which occurs most often in patients with inflammatory bowel disease, chronic metabolic acidosis, and renal tubular acidosis (RTA).

Renal stones occur in the distal form of RTA, are often composed of calcium phosphate, manifest as multiple stones on radiography (nephrocalcinosis), and occur in the presence of a persistently alkaline urine (pH >5.5) despite metabolic acidosis. Signs and Symptoms Patients often present with episodes of flank pain that radiates to the anterior abdomen or even to the genitalia. The pain is typically severe and comes in waves. Often, there is microscopic or gross hematuria. Calcium oxalate crystals may be seen with urine microscopy, but this finding is not diagnostic because calcium oxalate crystals may be seen in the urine of non–stone-forming patients. In some patients, the renal stones are completely asymptomatic or produce painless hematuria. Diagnosis Stone analysis is the best method for diagnosing calcium oxalate or calcium phosphate stones. Calcium-containing stones are radiopaque on routine radiography but show up as bright objects on computed helical tomography without contrast. Ultrasonography detects all types of renal stones if the stone is larger than 3 mm and the ultrasound procedure is technically satisfactory.

At present, helical computed tomography without contrast is the procedure of choice for the initial radiographic investigation. All types of stones located anywhere in the kidneys, ureters, or bladder are demonstrated with this technology. In a patient with azotemia, there is no risk from contrast administration. The anatomic status of the urinary tract will be clarified, and other possible nonstone causes for the patient's symptoms or signs may be identified. 10 Of the conditions associated with calcium stones, only pyelotubular ectasia—medullary sponge kidney—is better demonstrated by intravenous urography. Treatment and Outcome In recurrent hypercalciuric stone patients, treatment should consist of high fluid intake, dietary sodium restriction, and thiazide diuretics. Thiazide diuretics (not loop diuretics) reduce urinary calcium excretion by inducing extracellular volume depletion, which in turn causes increased renal sodium and calcium reabsorption, and by directly increasing distal calcium reabsorption. An additional benefit of thiazide diuretics is that their chronic use is associated with preservation of bone mineral density.

11 Dietary calcium restriction is not advised because of the potential for negative calcium balance and because a low-calcium diet increases the gastrointestinal absorption of oxalate and increased oxaluria. This increase in urinary oxalate can significantly raise the supersaturation of the urine for calcium oxalate, which in turn increases the stone formation rate. In hypercalcemic hypercalciuric stone-forming patients, the cause of the hypercalcemia should be sought and corrected. Correcting the metabolic acidosis in RTA and inflammatory bowel disease increases the urinary citrate excretion, an inhibitor of crystallization, and lessens the urinary calcium excretion. Summary Calcium stones are the type found in 70% of patients with stones. Risk factors include hypercalciuria, low urine output, hyperuricosuria, low urine citrate level, and hyperoxaluria (usually secondary to high dietary intake). Most patients (60%-70%) have hypercalciuria. A minority have associated hypercalcemia. Idiopathic hypercalciuria is associated with excessive gastrointestinal calcium absorption (mechanism unknown), even on low-calcium diets. Hypercalciuria is aggravated by high dietary sodium intake.

Therapy should include high fluid intake, dietary sodium restriction, and thiazide diuretics. Uric Acid Stone Disease Prevalence Uric acid stone disease is found in about 5% to 10% of stone patients. 12 It is more common in patients with chronic diarrheal disorders and in those with hyperuricosuria. Most uric acid stone patients do not have gout. About 30% to 40% of patients have hyperuricosuria. Uric acid stones may also be partially composed of calcium oxalate, and some patients have both uric acid and calcium oxalate stones. In a study by Sakhaee and colleagues, 13 about 30% of normouricosuric stone patients have diabetes and another 23% have abnormal glucose tolerance. Pathophysiology Uric acid stones occur especially in patients with a very low urine pH (<5.0) and in those with hyperuricosuria. In some patients, this very low urine pH is caused by a defect in renal ammonia secretion that results in less buffering of secreted hydrogen ions and lower urine pH.

Sakhaee and associates 13 have suggested that the very low urine pH is in some way related to the insulin resistance. Uric acid is rather insoluble (15 mg/dL) in urine at a pH of 5.0, but becomes significantly more soluble in urine at a pH of 7.0 (150 mg/dL). Any combination of low urine pH, concentrated urine (as seen in chronic diarrheal states), and increased urinary uric acid excretion (as seen in patients with gout, chronic probenecid therapy, or high purine intake) increases the risk for uric acid stone disease. Rare congenital disorders of purine metabolism, such as Lesch-Nyhan syndrome, are associated with uric acid stones, hyperuricosuria, and hyperuricemia. Urate stones are radiolucent and can be visualized by ultrasonography and noncontrast helical computed tomography. If the uric acid is mixed with calcium oxalate, the stone will be radiopaque. Signs and Symptoms Patients often present with episodes of flank pain that radiates to the anterior abdomen or even to the genitalia, as in calcium stone disease.

The pain is frequently severe and comes in waves. Often there is microscopic or gross hematuria. Diagnosis Uric acid stone disease should be suspected in any patient with typical symptoms of renal colic in whom plain radiographs do not show a calcified stone. Urate crystals may be present in the urine, but they occur in patients without stones as well. The urine pH is usually lower than 5.5. Stone analysis provides a definitive diagnosis. Treatment and Outcome Because the solubility of uric acid is greatly increased when the urine pH is raised, treatment should consist of alkalinization of urine to a pH higher than 6.5 with potassium citrate solution, 30 to 90 mEq/day in divided doses, and hydration. This treatment has been shown to reduce uric acid stones by 90%. Such treatment, given to a patient with small stones in the kidneys, can also result in dissolution of the stones. When hyperuricosuria is also present, allopurinol may be used to reduce the serum uric acid level and thus reduce the renal excretion of uric acid. Restriction of animal protein is also recommended for patients with hyperuricosuria.

Alkalinization of the urine with sodium bicarbonate or sodium citrate is not recommended because the sodium salts will increase calcium excretion, which increases the tendency to form calcium oxalate stones. Summary Uric acid stones represent 5% to 10% of stone cases. Risk factors include chronic diarrhea and hyperuricosuria. Some patients have both uric acid and calcium oxalate stones. Uric acid stones occur in patients with a very low urine pH (<5.0), which reduces uric acid solubility. Therapy should include alkalinization of the urine pH to higher than 6.5 with potassium citrate. Uricosuric patients can benefit from allopurinol. Struvite Stone Disease Prevalence Infection stones, also known as struvite or magnesium ammonium phosphate stones, occur in about 10% to 12% of patients, more often in women. They occur more often also in patients with spinal cord injury, neurogenic bladder, vesicoureteral reflux, chronic indwelling Foley catheters, and recurrent urinary infections, and in those with chronic obstruction of the upper urinary tract.

Pathophysiology Struvite stones occur only in the presence of urine persistently infected with urease-producing bacteria that split urea and cause persistently alkaline urine. 14 Urea-splitting bacteria include Proteus (most commonly), Pseudomonas, Klebsiella, Escherichia coli, and some Staphylococcus species. Struvite stones are often branched (staghorn-shaped) and large. Because the stones contain ammonium, they have a tendency to adhere to the uroepithelium, which tends to accelerate the growth of these stones in a very short time. Treatment requires eradication of infection with antibiotics and the removal of the bacteria-laden stones by some interventional technique. Signs and Symptoms These stones can cause the typical symptoms of renal colic, but often they are discovered during the course of investigating a patient with recurrent urinary infections or in a patient with asymptomatic bacteriuria. Because these stones can grow to significant size, they are often found in the renal pelvis and infundibula of the kidneys. Diagnosis The diagnosis of struvite stones is suspected by finding large or branched stones in the kidneys of a patient with persistently infected urine. Stone analysis confirms the diagnosis.

Treatment and Outcome Treatment must eradicate the urinary infection. Because the stones themselves are often infected with bacteria, the urinary infection cannot be eradicated without also removing the stones. Thus, surgical removal of the stones accompanied by appropriate antibiotic therapy is necessary. Acetohydroxamic acid is a urease inhibitor and has been used to prevent recurrence. Its effectiveness depends on its presence in the urine; hence, it has limited effectiveness in patients with azotemia. The use of this drug is further compromised because it has potentially serious side effects that include gastrointestinal upset, neurologic deficits, and thrombophlebitis. 15 Summary Magnesium ammonium phosphate stones represent 10% to 12% of stone cases. Risk factors include female sex, spinal cord injury, history of obstructive uropathy, and recurrent urinary tract infections. They occur only in the presence of persistently infected urine with urease-producing bacteria. They are often discovered during a workup for recurrent urinary tract infections. Treatment should include eradication of the infection and often requires removal of the stone by some interventional technique.

Cystine Stone Disease Prevalence Cystine stone disease occurs in less than 1% of all adult stone patients and in about 6% to 8% of children with nephrolithiasis. 16 Pathophysiology Cystine stone disease occurs in persons who have inherited an autosomal recessive gastrointestinal and renal tubular transport disorder of four amino acids: cystine, ornithine, arginine, and lysine. Of these, cystine is the most insoluble in normally acid urine and thus precipitates into stones. Signs and Symptoms The patient presents with symptoms of nephrolithiasis, often at a younger age than a person with calcium stone disease. The stones are radiopaque (ground-glass appearance) and amber. Family history is often helpful (i.e., siblings might have the disorder). Diagnosis Normal urine contains less than 20 to 30 mg/day (<100 mg/g creatinine) of cystine. Urinary cystine excretion of more than 250 mg/g creatinine in adults is clearly abnormal and is the usual amount found in patients with cystinuria.

The examination of a concentrated acidic urine specimen often reveals the presence of the cystine crystals, which are transparent and hexagonal. Cystine can be detected qualitatively by adding sodium nitroprusside to the urine and observing a purple-red color. Stone analysis is diagnostic. Treatment and Outcome Treatment is directed at reducing urinary cystine concentration in the urine or increasing urinary cystine solubility in the urine. The concentration of cystine in the urine is significantly helped by high fluid intake. There is a modest reduction of cystine excretion by reducing methionine in the diet by restricting red meat, fish, poultry, dairy products, and sodium. Alkalinization of the urine with potassium citrate to a pH of 6.5 to 7 is recommended. Sodium bicarbonate may be used for alkalinization, but the high sodium load increases cystine excretion. However, hydration and alkalinization alone are often ineffective at inhibiting recurrent stones. Cystine is made up of two cysteine molecules connected by a disulfide bond. Thiol derivatives are chelating agents.

They contain sulfhydryl groups that can bind with the cysteine molecules, reduce the formation of cystine, and render it more soluble. Therefore, these agents can also help dissolve cystine stones and prevent their formation. d -Penicillamine and α-mercaptopropionyl glycine are examples of such thiol-chelating agents. α-Mercaptopropionyl glycine is slightly more effective and produces fewer side effects. Captopril, which also has sulfhydryl groups, has been used in limited studies with success. 17 Summary Cystine stones occur in patients with an inherited disorder of tubular and intestinal transport of cystine, ornithines, arginine, and lysine. Cystine is poorly soluble at normal urine pH. Onset of clinical stone events is in the teens and early adulthood Therapy requires alkalinization of urine to a pH higher than 7.0, high fluid intake, and using cysteine-binding drugs such as penicillamine or captopril. Suggested Readings Asplin JR. Hyperoxaluric calcium nephrolithiasis. Endocrinol Metab Clin North Am.

2002; 31: 927-949. Borghi L, Schianchi T , Meschi T. et al: Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002; 346: 77-84. Coe FL, Evan A , Worcester E. Kidney stone disease. J Clin Invest. 2005; 115: 2598-2608. Curhan GC, Willett WC , Rimm EB , Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med. 1993; 328: 833-838. Curhan GC, Willett WC , Speizer FE. et al: Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med. 1997; 126: 497-504. Griffith DP. Struvite stones. Kidney Int.

1978; 13: 372-382. Katz DS, Scheer M , Lumerman JH. et al: Alternative or additional diagnoses on unenhanced helical computed tomography for suspected renal colic: Experience with 1000 consecutive examinations. Urology. 2000; 56: 53-57. Kok DJ. Clinical implications of physicochemistry of stone formation. Endocrinol Metab Clin North Am. 2002; 31: 855-867. Kopp JB, Miller KD , Mican JA. et al: Crystalluria and urinary tract abnormalities associated with indinavir. Ann Intern Med. 1997; 127: 119-125. Moe OW, Abate N , Sakhaee K. Pathophysiology of uric acid nephrolithiasis. Endocrinol Metab Clin North Am. 2002; 31: 895-914. Kidney stones: MedlinePlus Medical Encyclopedia Watch this video about: Kidney stones Kidney stones are common.

Some types run in families. They often occur in premature infants. There are different types of kidney stones. The cause of the problem depends on the type of stone. Stones can form when urine contains too much of certain substances that form crystals. These crystals can develop into stones over weeks or months. Calcium stones are most common. They are most likely to occur in men between ages 20 to 30. Calcium can combine with other substances to form the stone. Oxalate is the most common of these. Oxalate is present in certain foods such as spinach. It is also found in vitamin C supplements. Diseases of the small intestine increase your risk of these stones. Calcium stones can also form from combining with phosphate or carbonate. Other types of stones include: Cystine stones can form in people who have cystinuria . This disorder runs in families. It affects both men and women. Struvite stones are mostly found in women who have a urinary tract infection. These stones can grow very large and can block the kidney, ureter, or bladder. Uric acid stones are more common in men than in women. They can occur with gout or chemotherapy.

Other substances such as certain medicines also can form stones. The biggest risk factor for kidney stones is not drinking enough fluids. Kidney stones are more likely to occur if you make less than 1 liter of urine a day. Symptoms You may not have symptoms until the stones move down the tubes (ureters) through which urine empties into your bladder. When this happens, the stones can block the flow of urine out of the kidneys. The main symptom is severe pain that starts and stops suddenly: Pain may be felt in the belly area or side of the back. Pain may move to groin area ( groin pain ) or testicles ( testicle pain ). Other symptoms can include: Treatment depends on the type of stone and the severity of your symptoms. Kidney stones that are small most often pass through your system on their own. Your urine should be strained so the stone can be saved and tested. Drink at least 6 to 8 glasses of water per day to produce a large amount of urine. This will help the stone pass . Pain can be very bad. Over-the-counter pain medicines (for example, ibuprofen and naproxen), either alone or along with narcotics, can be very effective.

Some people with severe pain from kidney stones need to stay in the hospital. You may need to get fluids through a vein. For some types of stones, your provider may prescribe medicine to prevent stones from forming or help break down and remove the material that is causing the stone. These medicines can include: Tamsulosin to relax the ureter and help the stone pass Surgery is often needed if: The stone is too large to pass on its own The stone is growing The stone is blocking urine flow and causing an infection or kidney damage The pain cannot be controlled Today, most treatments are much less invasive than in the past. Lithotripsy is used to remove stones slightly smaller than a half an inch that are located in the kidney or ureter. It uses sound or shock waves to break up stones. Then, the stone fragments leave the body in the urine. It is also called extracorporeal shock-wave lithotripsy or ESWL. Procedures performed by passing a special instrument through a small surgical cut in your skin and into your kidney or ureters are used for large stones, or when the kidneys or surrounding areas are incorrectly formed. The stone is removed with a tube (endoscope).

Ureteroscopy may be used for stones in the lower urinary tract. Rarely, open surgery (nephrolithotomy) may be needed if other methods do not work or are not possible. Talk to your provider about what treatment options may work for you. You will need to take self-care steps. Which steps you take depend on the type of stone you have, but they may include: Drinking extra water and other liquids Eating more of some foods and cutting back on other foods Taking medicines to help prevent stones Taking medicines to help you pass a stone (anti-inflammatory drugs, alpha-blockers) Outlook (Prognosis) Kidney stones are painful but most of the time can be removed from the body without causing lasting damage. Kidney stones often come back. This occurs more often if the cause is not found and treated. You are at risk for: Urinary tract infection Urine that smells bad or looks cloudy A burning feeling when you urinate If you have been diagnosed with blockage from a stone, passage must be confirmed either by capture in a strainer during urination or by follow-up x-ray.

Prevention If you have a history of stones: Drink plenty of fluids (6 to 8 glasses of water per day) to produce enough urine. You may need to take medicine or make changes to your diet for some types of stones. Your provider may want to do blood and urine tests to help determine the proper prevention steps. Alternative Names Renal calculi; Nephrolithiasis; Stones - kidney; Calcium oxalate - stones; Cystine - stones; Struvite - stones; Uric acid - stones; Urinary lithiasis Images Lithotripsy procedure References Bushinsky DA. Nephrolithiasis. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 126. Fink HA, Wilt TJ, Eidman KE, et al. Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med. 2013;158(7):535-543. PMID: 23546565 .

Fink HA, Wilt TJ, Eidman KE, et al. Recurrent nephrolithiasis in adults: comparative effectiveness of preventive medical strategies [Internet]. Rockville, MD. Agency for Healthcare Research and Quality (US) 2012; Report No.: 12-EHC049-EF. PMID: 22896859 . Lipkin ME, Ferrandino MN, Preminger Glenn M. Evaluation and medical management of urinary lithiasis. In: Wein AJ, Kavoussi LR, Partin AW, Peters CA, eds. Campbell-Walsh Urology. 11th ed. Philadelphia, PA: Elsevier; 2016:chap 52. Qaseem A, Dallas P, Forciea MA, Starkey M, Denberg TD; Clinical Guidelines Committee of the American College of Physicians. Dietary and pharmacologic management to prevent recurrent nephrolithiasis in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2014;161(9):659-667. PMID: 25364887 .

Read More Nephrolithiasis: Practice Essentials, Background, Anatomy Practice Essentials Overview Practice Essentials Nephrolithiasis specifically refers to calculi in the kidneys, but renal calculi and ureteral calculi (ureterolithiasis) are often discussed in conjunction. The majority of renal calculi contain calcium. The pain generated by renal colic is primarily caused by dilation, stretching, and spasm because of the acute ureteral obstruction. Signs and symptoms The classic presentation for a patient with acute renal colic is the sudden onset of severe pain originating in the flank and radiating inferiorly and anteriorly; at least 50% of patients will also have nausea and vomiting. Patients with urinary calculi may report pain, infection, or hematuria. Patients with small, nonobstructing stones or those with staghorn calculi may be asymptomatic or experience moderate and easily controlled symptoms.

The location and characteristics of pain in nephrolithiasis include the following: Stones obstructing ureteropelvic junction: Mild to severe deep flank pain without radiation to the groin; irritative voiding symptoms (eg, frequency, dysuria); suprapubic pain, urinary frequency/urgency, dysuria, stranguria, bowel symptoms Stones within ureter: Abrupt, severe, colicky pain in the flank and ipsilateral lower abdomen; radiation to testicles or vulvar area; intense nausea with or without vomiting Upper ureteral stones: Radiate to flank or lumbar areas Midureteral calculi: Radiate anteriorly and caudally Distal ureteral stones: Radiate into groin or testicle (men) or labia majora (women) Stones passed into bladder: Mostly asymptomatic; rarely, positional urinary retention References [Guideline] Turk C, Knoll T, Petrik A, Sarica K, Skolarikos A, Straub M, et al. Guidelines on urolithiasis. European Association of Urology. Available at . 2015; Accessed: May 16, 2016.

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Stone disease in the Hmong of Minnesota: initial description of a high-risk population. J Endourol. 2004 Nov. 18 (9):853-7. [Medline] . Media Gallery Small renal calculus that would likely respond to extracorporeal shockwave lithotripsy. Complete staghorn calculus that fills the collecting system of the kidney (no intravenous contrast material in this patient). Although many staghorn calculi are struvite (related to infection with urease-splitting bacteria), the density of this stone suggests that it may be metabolic in origin and is likely composed of calcium oxalate. Percutaneous nephrostolithotomy or perhaps even open surgical nephrolithotomy is required to remove this stone. Distal ureteral stone observed through a small, rigid ureteroscope prior to ballistic lithotripsy and extraction. The small caliber and excellent optics of today's endoscopes greatly facilitate minimally invasive treatment of urinary stones. Two calculi in a dependent calyx of the kidney (lower pole) visualized through a flexible fiberoptic ureteroscope.

In another location, these calculi might have been treated with extracorporeal shockwave lithotripsy (ESWL), but, after being counseled regarding the lower success rate of ESWL for stones in a dependent location, the patient elected ureteroscopy. Note that the image provided by fiberoptics, although still acceptable, is inferior to that provided by the rod-lens optics of the rigid ureteroscope in the previous picture. Nephrolithiasis: acute renal colic. Anatomy of the ureter. Nephrolithiasis: acute renal colic. Distribution of nerves in the flank. Nephrolithiasis: acute renal colic. Nerve supply of the kidney. Nephrolithiasis: acute renal colic. Renal colic and flank pain. Nephrolithiasis: acute renal colic. Nerve supply of the kidney. Nephrolithiasis: acute renal colic. Distribution of renal and ureteral pain. Noncontrast helical CT scan of the abdomen demonstrating a stone at the right ureterovesical junction.

Intravenous pyelogram (IVP) demonstrating dilation of the right renal collecting system and right ureter consistent with right ureterovesical stone. of 12 Nephrolithiasis | Define Nephrolithiasis at Dictionary.com nephrolithiasis 1837, probably from German, from nephro- + lithos "stone" (see litho- ) + -iasis "pathological or morbid condition." Online Etymology Dictionary, © 2010 Douglas Harper Kidney stones Causes - Mayo Clinic Kidney stones Kidney stones often have no definite, single cause, although several factors may increase your risk. Kidney stones form when your urine contains more crystal-forming substances — such as calcium, oxalate and uric acid — than the fluid in your urine can dilute. At the same time, your urine may lack substances that prevent crystals from sticking together, creating an ideal environment for kidney stones to form. Types of kidney stones Knowing the type of kidney stone helps determine the cause and may give clues on how to reduce your risk of getting more kidney stones. Types of kidney stones include: Calcium stones. Most kidney stones are calcium stones, usually in the form of calcium oxalate.

Oxalate is a naturally occurring substance found in food. Some fruits and vegetables, as well as nuts and chocolate, have high oxalate levels. Your liver also produces oxalate. Dietary factors, high doses of vitamin D, intestinal bypass surgery and several metabolic disorders can increase the concentration of calcium or oxalate in urine. Calcium stones may also occur in the form of calcium phosphate. Struvite stones. Struvite stones form in response to an infection, such as a urinary tract infection. These stones can grow quickly and become quite large, sometimes with few symptoms or little warning. Uric acid stones. Uric acid stones can form in people who don't drink enough fluids or who lose too much fluid, those who eat a high-protein diet, and those who have gout. Certain genetic factors also may increase your risk of uric acid stones. Cystine stones. These stones form in people with a hereditary disorder that causes the kidneys to excrete too much of certain amino acids (cystinuria). Other stones. Other, rarer types of kidney stones also can occur.

Renal Calculi - National Library of Medicine - PubMed Health Increased water intake may help reduce the risk of recurrence of kidney stones but more studies are needed Kidney stones (also known as calculi) are masses of crystals and protein and are common causes of urinary tract obstruction in adults. For a long time, increased water intake has been the main preventive measure for the disease and its recurrence. In this review only one study was found that looked at the effect of increase water intake on recurrence and time to recurrence. Increased water intake decreased the chance of recurrence and increased the time to recurrence. Further studies are needed. Extracorporeal shock wave lithotripsy (ESWL) versus percutaneous nephrolithotomy (PCNL) or retrograde intrarenal surgery (RIRS) for kidney stones Stones in the urinary tract are a common medical problem. Half of patients with previous urinary stones have a recurrence within 10 years. Kidney stones can cause pain, blood in the urine, infection, decreased kidney function, and kidney failure. The treatment is to remove the stones from kidney. Extracorporeal shock wave lithotripsy (ESWL) disintegrates stones using shock waves and is a minimally invasive technique.

Other minimally invasive methods (percutaneous nephrolithotomy (PCNL)) and retrograde intrarenal surgery (RIRS)) are widely used for kidney stones management because ESWL had limited success rate. This review aimed to compare the effectiveness and complications between ESWL and stones removing using the nephroscopy through the skin at kidney level (PCNL) or ureteroscope through the bladder and ureter to the kidney (RIRS). Five small randomised studies (338 patients) were included. Four studies compared ESWL with PCNL and one study compared ESWL with RIRS. Patients with kidney stones who undergo PCNL have a higher success rate than ESWL whereas RIRS was not significantly different from ESWL. However, ESWL patients spent less time in hospital, duration of treatment was shorter and there were fewer complications. Pharmacological interventions for preventing complications in idiopathic hypercalciuria Idiopathic hypercalciuria is an inherited metabolic abnormality characterised by excessive amounts of calcium excreted into the urine in patients with normal serum levels of calcium. The main complications of this disease in adults are the formation of kidney stones and bone loss.

In children, hypercalciuria can cause recurrent haematuria (blood in the urine), frequency‐dysuria syndrome (frequent painful or difficult urination), urinary tract infection and abdominal and back pain. The aim of this review was to evaluate the benefits and harms of drug treatments for preventing the complications of idiopathic hypercalciuria. We identified four studies comparing thiazides (diuretics) with either standard treatment of clinical follow‐up and increased water intake or specific dietary recommendations and one study comparing thiazides plus a potassium salt. There was a decrease in the number of new stones in the group receiving thiazides as well as an increase in the time taken for new stone formation. The addition of potassium salts to thiazide treatment significantly reduced the amount of calcium excreted in the urine. No studies in children were identified and there were no studies investigating the use of drug treatment for those with hypercalciuria but were symptom free. Treating kidney stones Small kidney stones often pass on their own and don't need treatment as long as they don't cause any severe pain or complications. Larger kidney stones usually need to be removed.

Depending on how large the kidney stones are and where they're located, they can be destroyed, removed using endoscopy or operated on.Kidney stones with a diameter of less than 5 millimeters pass on their own 70% of the time, and stones that are between 5 and 10 millimeters are flushed out in about 50% of cases. The amount of time this takes varies greatly. Small kidney stones are often passed in your urine after one or two weeks.If a stone is expected to be flushed out with your urine without any treatment, it's usual to simply wait. Anti-inflammatory painkillers like diclofenac can provide relief if the kidney stone causes pain as it travels through the ureter.Larger stones will usually have to be broken up or surgically removed. This needs to be done in the following instances:The kidney stone isn't passed within four weeks.There are complications.It causes severe renal colic.The stone is larger than 10 mm in diameter.Uric acid stones can sometimes be dissolved using medication.

Increased water intake may help reduce the risk of recurrence of kidney stones but more studies are needed Kidney stones (also known as calculi) are masses of crystals and protein and are common causes of urinary tract obstruction in adults. For a long time, increased water intake has been the main preventive measure for the disease and its recurrence. In this review only one study was found that looked at the effect of increase water intake on recurrence and time to recurrence. Increased water intake decreased the chance of recurrence and increased the time to recurrence. Further studies are needed. Kidney stones: Overview Kidney stones are very common, especially in people between the ages of 20 and 40. These small, hard deposits form in the renal pelvis and can enter a ureter. Larger stones can be painful and often have to be surgically removed. There are several options for treatment and prevention.

Question: Nephrolithiasis is the medical name for which condition?
Answer: Kidney Stones