Kidney stone disease
Kidney stone disease, also known as nephrolithiasis or urolithiasis, is when a solid piece of material (kidney stone) develops in the urinary tract.[2] Kidney stones typically form in the kidney and leave the body in the urine stream.[2] A small stone may pass without causing symptoms.[2] If a stone grows to more than 5 millimeters (0.2 in), it can cause blockage of the ureter, resulting in severe pain in the lower back or abdomen.[2][7] A stone may also result in blood in the urine, vomiting, or painful urination.[2] About half of people who have had a kidney stone will have another within ten years.[8]
Most stones form due to a combination of genetics and environmental factors.[2] Risk factors include high urine calcium levels; obesity; certain foods; some medications; calcium supplements; hyperparathyroidism; gout and not drinking enough fluids.[2][8] Stones form in the kidney when minerals in urine are at high concentration.[2] The diagnosis is usually based on symptoms, urine testing, and medical imaging.[2] Blood tests may also be useful.[2] Stones are typically classified by their location: nephrolithiasis (in the kidney), ureterolithiasis (in the ureter), cystolithiasis (in the bladder), or by what they are made of (calcium oxalate, uric acid, struvite, cystine).[2]
In those who have had stones, prevention is by drinking fluids such that more than two liters of urine are produced per day.[4] If this is not effective enough, thiazide diuretic, citrate, or allopurinol may be taken.[4] It is recommended that soft drinks containing phosphoric acid (typically colas) be avoided.[4] When a stone causes no symptoms, no treatment is needed.[2] Otherwise pain control is usually the first measure, using medications such as nonsteroidal anti-inflammatory drugs or opioids.[7][9] Larger stones may be helped to pass with the medication tamsulosin[10] or may require procedures such as extracorporeal shock wave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy.[2]
Between 1% and 15% of people globally are affected by kidney stones at some point in their lives.[8] In 2015, 22.1 million cases occurred,[5] resulting in about 16,100 deaths.[6] They have become more common in the Western world since the 1970s.[8] Generally, more men are affected than women.[2] Kidney stones have affected humans throughout history with descriptions of surgery to remove them dating from as early as 600 BC
Most stones form due to a combination of genetics and environmental factors.[2] Risk factors include high urine calcium levels; obesity; certain foods; some medications; calcium supplements; hyperparathyroidism; gout and not drinking enough fluids.[2][8] Stones form in the kidney when minerals in urine are at high concentration.[2] The diagnosis is usually based on symptoms, urine testing, and medical imaging.[2] Blood tests may also be useful.[2] Stones are typically classified by their location: nephrolithiasis (in the kidney), ureterolithiasis (in the ureter), cystolithiasis (in the bladder), or by what they are made of (calcium oxalate, uric acid, struvite, cystine).[2]
In those who have had stones, prevention is by drinking fluids such that more than two liters of urine are produced per day.[4] If this is not effective enough, thiazide diuretic, citrate, or allopurinol may be taken.[4] It is recommended that soft drinks containing phosphoric acid (typically colas) be avoided.[4] When a stone causes no symptoms, no treatment is needed.[2] Otherwise pain control is usually the first measure, using medications such as nonsteroidal anti-inflammatory drugs or opioids.[7][9] Larger stones may be helped to pass with the medication tamsulosin[10] or may require procedures such as extracorporeal shock wave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy.[2]
Between 1% and 15% of people globally are affected by kidney stones at some point in their lives.[8] In 2015, 22.1 million cases occurred,[5] resulting in about 16,100 deaths.[6] They have become more common in the Western world since the 1970s.[8] Generally, more men are affected than women.[2] Kidney stones have affected humans throughout history with descriptions of surgery to remove them dating from as early as 600 BC
Signs and symptoms
The hallmark of a stone that obstructs the ureter or renal pelvis is excruciating, intermittent pain that radiates from the flank to the groin or to the inner thigh.[11] This pain, known as renal colic, is often described as one of the strongest pain sensations known.[12] Renal colic caused by kidney stones is commonly accompanied by urinary urgency, restlessness, hematuria, sweating, nausea, and vomiting. It typically comes in waves lasting 20 to 60 minutes caused by peristaltic contractions of the ureter as it attempts to expel the stone.[11]
The embryological link between the urinary tract, the genital system, and the gastrointestinal tract is the basis of the radiation of pain to the gonads, as well as the nausea and vomiting that are also common in urolithiasis.[13] Postrenal azotemia and hydronephrosis can be observed following the obstruction of urine flow through one or both ureters.[14]
Pain in the lower-left quadrant can sometimes be confused with diverticulitis because the sigmoid colon overlaps the ureter, and the exact location of the pain may be difficult to isolate due to the proximity of these two structures.
The hallmark of a stone that obstructs the ureter or renal pelvis is excruciating, intermittent pain that radiates from the flank to the groin or to the inner thigh.[11] This pain, known as renal colic, is often described as one of the strongest pain sensations known.[12] Renal colic caused by kidney stones is commonly accompanied by urinary urgency, restlessness, hematuria, sweating, nausea, and vomiting. It typically comes in waves lasting 20 to 60 minutes caused by peristaltic contractions of the ureter as it attempts to expel the stone.[11]
The embryological link between the urinary tract, the genital system, and the gastrointestinal tract is the basis of the radiation of pain to the gonads, as well as the nausea and vomiting that are also common in urolithiasis.[13] Postrenal azotemia and hydronephrosis can be observed following the obstruction of urine flow through one or both ureters.[14]
Pain in the lower-left quadrant can sometimes be confused with diverticulitis because the sigmoid colon overlaps the ureter, and the exact location of the pain may be difficult to isolate due to the proximity of these two structures.
Risk factors
Dehydration from low fluid intake is a major factor in stone formation.[11][15] Individuals living in warm climates are at higher risk due to increased fluid loss.[16] Obesity, immobility, and sedentary lifestyles are other leading risk factors.[16]
High dietary intake of animal protein,[11] sodium, sugars including honey, refined sugars, fructose and high fructose corn syrup,[17] and excessive consumption of tea or fruit juices may increase the risk of kidney stone formation due to increased uric acid excretion and elevated urinary oxalate levels.[16][15]
Kidney stones can result from an underlying metabolic condition, such as distal renal tubular acidosis,[18] Dent's disease,[19] hyperparathyroidism,[20] primary hyperoxaluria,[21] or medullary sponge kidney. 3–20% of people who form kidney stones have medullary sponge kidney.[22][23]
Kidney stones are more common in people with Crohn's disease;[24] Crohn's disease is associated with hyperoxaluria and malabsorption of magnesium.[25]
A person with recurrent kidney stones may be screened for such disorders. This is typically done with a 24-hour urine collection. The urine is analyzed for features that promote stone formation.
Dehydration from low fluid intake is a major factor in stone formation.[11][15] Individuals living in warm climates are at higher risk due to increased fluid loss.[16] Obesity, immobility, and sedentary lifestyles are other leading risk factors.[16]
High dietary intake of animal protein,[11] sodium, sugars including honey, refined sugars, fructose and high fructose corn syrup,[17] and excessive consumption of tea or fruit juices may increase the risk of kidney stone formation due to increased uric acid excretion and elevated urinary oxalate levels.[16][15]
Kidney stones can result from an underlying metabolic condition, such as distal renal tubular acidosis,[18] Dent's disease,[19] hyperparathyroidism,[20] primary hyperoxaluria,[21] or medullary sponge kidney. 3–20% of people who form kidney stones have medullary sponge kidney.[22][23]
Kidney stones are more common in people with Crohn's disease;[24] Crohn's disease is associated with hyperoxaluria and malabsorption of magnesium.[25]
A person with recurrent kidney stones may be screened for such disorders. This is typically done with a 24-hour urine collection. The urine is analyzed for features that promote stone formation.
Calcium oxalate
Spiculations, resembling the head of a morning star, can be seen for calcium oxalate monohydrate stones. Protrusions on uric acid stones are generally smaller.
Calcium is one component of the most common type of human kidney stones, calcium oxalate. Some studies[which?] suggest that people who take calcium or vitamin D as a dietary supplement have a higher risk of developing kidney stones. In the United States, kidney stone formation was used as an indicator of excess calcium intake by the Reference Daily Intake committee for calcium in adults.
In the early 1990s, a study conducted for the Women's Health Initiative in the US found that postmenopausal women who consumed 1000 mg of supplemental calcium and 400 international units of vitamin D per day for seven years had a 17% higher risk of developing kidney stones than subjects taking a placebo.[27] The Nurses' Health Study also showed an association between supplemental calcium intake and kidney stone formation.[28]
Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development.[28][27] This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation—about 15 times stronger than calcium.
Other electrolytes
Calcium is not the only electrolyte that influences the formation of kidney stones. For example, by increasing urinary calcium excretion, high dietary sodium may increase the risk of stone formation.[28]
Drinking fluoridated tap water may increase the risk of kidney stone formation by a similar mechanism, though further epidemiologic studies are warranted to determine whether fluoride in drinking water is associated with an increased incidence of kidney stones.[31] High dietary intake of potassium appears to reduce the risk of stone formation because potassium promotes the urinary excretion of citrate, an inhibitor of calcium crystal formation.[32]
Kidney stones are more likely to develop, and to grow larger, if a person has low dietary magnesium. Magnesium inhibits stone formation.[33]
Animal protein
Diets in Western nations typically contain a large proportion of animal protein. Eating animal protein creates an acid load that increases urinary excretion of calcium and uric acid and reduced citrate. Urinary excretion of excess sulfurous amino acids (e.g., cysteine and methionine), uric acid, and other acidic metabolites from animal protein acidifies the urine, which promotes the formation of kidney stones.[34] Low urinary-citrate excretion is also commonly found in those with a high dietary intake of animal protein, whereas vegetarians tend to have higher levels of citrate excretion.[28] Low urinary citrate, too, promotes stone formation.[34]
Vitamins
The evidence linking vitamin C supplements with an increased rate of kidney stones is inconclusive.[35][36] The excess dietary intake of vitamin C might increase the risk of calcium-oxalate stone formation.[37] The link between vitamin D intake and kidney stones is also tenuous. Excessive vitamin D supplementation may increase the risk of stone formation by increasing the intestinal absorption of calcium; correction of a deficiency does not.[28]
Other
There are no conclusive data demonstrating a cause-and-effect relationship between alcoholic beverage consumption and kidney stones. However, some people have theorized that certain behaviors associated with frequent and binge drinking can lead to dehydration, which can, in turn, lead to the development of kidney stones.[38]
The American Urological Association has projected that global warming will lead to an increased incidence of kidney stones in the United States by expanding the "kidney stone belt" of the southern United States
Spiculations, resembling the head of a morning star, can be seen for calcium oxalate monohydrate stones. Protrusions on uric acid stones are generally smaller.
Calcium is one component of the most common type of human kidney stones, calcium oxalate. Some studies[which?] suggest that people who take calcium or vitamin D as a dietary supplement have a higher risk of developing kidney stones. In the United States, kidney stone formation was used as an indicator of excess calcium intake by the Reference Daily Intake committee for calcium in adults.
In the early 1990s, a study conducted for the Women's Health Initiative in the US found that postmenopausal women who consumed 1000 mg of supplemental calcium and 400 international units of vitamin D per day for seven years had a 17% higher risk of developing kidney stones than subjects taking a placebo.[27] The Nurses' Health Study also showed an association between supplemental calcium intake and kidney stone formation.[28]
Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development.[28][27] This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation—about 15 times stronger than calcium.
Other electrolytes
Calcium is not the only electrolyte that influences the formation of kidney stones. For example, by increasing urinary calcium excretion, high dietary sodium may increase the risk of stone formation.[28]
Drinking fluoridated tap water may increase the risk of kidney stone formation by a similar mechanism, though further epidemiologic studies are warranted to determine whether fluoride in drinking water is associated with an increased incidence of kidney stones.[31] High dietary intake of potassium appears to reduce the risk of stone formation because potassium promotes the urinary excretion of citrate, an inhibitor of calcium crystal formation.[32]
Kidney stones are more likely to develop, and to grow larger, if a person has low dietary magnesium. Magnesium inhibits stone formation.[33]
Animal protein
Diets in Western nations typically contain a large proportion of animal protein. Eating animal protein creates an acid load that increases urinary excretion of calcium and uric acid and reduced citrate. Urinary excretion of excess sulfurous amino acids (e.g., cysteine and methionine), uric acid, and other acidic metabolites from animal protein acidifies the urine, which promotes the formation of kidney stones.[34] Low urinary-citrate excretion is also commonly found in those with a high dietary intake of animal protein, whereas vegetarians tend to have higher levels of citrate excretion.[28] Low urinary citrate, too, promotes stone formation.[34]
Vitamins
The evidence linking vitamin C supplements with an increased rate of kidney stones is inconclusive.[35][36] The excess dietary intake of vitamin C might increase the risk of calcium-oxalate stone formation.[37] The link between vitamin D intake and kidney stones is also tenuous. Excessive vitamin D supplementation may increase the risk of stone formation by increasing the intestinal absorption of calcium; correction of a deficiency does not.[28]
Other
There are no conclusive data demonstrating a cause-and-effect relationship between alcoholic beverage consumption and kidney stones. However, some people have theorized that certain behaviors associated with frequent and binge drinking can lead to dehydration, which can, in turn, lead to the development of kidney stones.[38]
The American Urological Association has projected that global warming will lead to an increased incidence of kidney stones in the United States by expanding the "kidney stone belt" of the southern United States
Prevention
Preventative measures depend on the type of stones. In those with calcium stones, drinking lots of fluids, thiazide diuretics and citrate are effective as is allopurinol in those with high uric acid levels in the blood or urine.[75][76]
Dietary measures
Specific therapy should be tailored to the type of stones involved. Diet can have an effect on the development of kidney stones. Preventive strategies include some combination of dietary modifications and medications with the goal of reducing the excretory load of calculogenic compounds on the kidneys.[29][77][78] Dietary recommendations to minimize the formation of kidney stones include:
Increasing total fluid intake to more than two liters per day of urine output.[79]
Limiting cola, including sugar-sweetened soft drinks,[75][79][80] to less than one liter per week.[81]
Limiting animal protein intake to no more than two meals daily (an association between animal protein and recurrence of kidney stones has been shown in men[82]).
Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of kidney stones, so increasing urine volume is a key principle for the prevention of kidney stones. Fluid intake should be sufficient to maintain a urine output of at least 2 litres (68 US fl oz) per day.[76] A high fluid intake has been associated with a 40% reduction in recurrence risk.[52] The quality of the evidence for this, however, is not very good.[76]
Calcium binds with available oxalate in the gastrointestinal tract, thereby preventing its absorption into the bloodstream, and reducing oxalate absorption decreases kidney stone risk in susceptible people.[83] Because of this, some doctors recommend chewing calcium tablets during meals containing oxalate foods.[84] Calcium citrate supplements can be taken with meals if dietary calcium cannot be increased by other means. The preferred calcium supplement for people at risk of stone formation is calcium citrate because it helps to increase urinary citrate excretion.[78]
Aside from vigorous oral hydration and eating more dietary calcium, other prevention strategies include avoidance of large doses of supplemental vitamin C and restriction of oxalate-rich foods such as leaf vegetables, rhubarb, soy products and chocolate.[85] However, no randomized, controlled trial of oxalate restriction has been performed to test the hypothesis that oxalate restriction reduces stone formation.[84] Some evidence indicates magnesium intake decreases the risk of symptomatic kidney stone
Preventative measures depend on the type of stones. In those with calcium stones, drinking lots of fluids, thiazide diuretics and citrate are effective as is allopurinol in those with high uric acid levels in the blood or urine.[75][76]
Dietary measures
Specific therapy should be tailored to the type of stones involved. Diet can have an effect on the development of kidney stones. Preventive strategies include some combination of dietary modifications and medications with the goal of reducing the excretory load of calculogenic compounds on the kidneys.[29][77][78] Dietary recommendations to minimize the formation of kidney stones include:
Increasing total fluid intake to more than two liters per day of urine output.[79]
Limiting cola, including sugar-sweetened soft drinks,[75][79][80] to less than one liter per week.[81]
Limiting animal protein intake to no more than two meals daily (an association between animal protein and recurrence of kidney stones has been shown in men[82]).
Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of kidney stones, so increasing urine volume is a key principle for the prevention of kidney stones. Fluid intake should be sufficient to maintain a urine output of at least 2 litres (68 US fl oz) per day.[76] A high fluid intake has been associated with a 40% reduction in recurrence risk.[52] The quality of the evidence for this, however, is not very good.[76]
Calcium binds with available oxalate in the gastrointestinal tract, thereby preventing its absorption into the bloodstream, and reducing oxalate absorption decreases kidney stone risk in susceptible people.[83] Because of this, some doctors recommend chewing calcium tablets during meals containing oxalate foods.[84] Calcium citrate supplements can be taken with meals if dietary calcium cannot be increased by other means. The preferred calcium supplement for people at risk of stone formation is calcium citrate because it helps to increase urinary citrate excretion.[78]
Aside from vigorous oral hydration and eating more dietary calcium, other prevention strategies include avoidance of large doses of supplemental vitamin C and restriction of oxalate-rich foods such as leaf vegetables, rhubarb, soy products and chocolate.[85] However, no randomized, controlled trial of oxalate restriction has been performed to test the hypothesis that oxalate restriction reduces stone formation.[84] Some evidence indicates magnesium intake decreases the risk of symptomatic kidney stone
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