Prevention of recurrence of calcium stones (which is usually composed mainly of calcium oxalate) is to decrease the concentration litogenih factors (calcium oxalate) and increasing concentrations of
inhibitors of stone formation, such as citrate.
Achieving these goals may require a change in diet and the use of appropriate medications. Medical therapy (and metabolic assessment) is usually carried out in the case of patients who have formed more than a stone. Even if the patient threw a stone, it is important to review the footage to determine whether there are other stones because of their passing is not equivalent to the formation. At least one stone patients are encouraged to increase their fluid intake and periodically controlled (usually renal ultrasonography), to determine whether there is a new rock.
Here we present the treatment of patients with recurrent calcium stone formation. Treatment of patients with re-formation of rocks of different origin, and unknown are displayed separately, as well as risk factors for recurrence of calcium.
STONES calcium oxalate - the re-emergence of calcium oxalate stones is a large number of dietary modification and drug therapy.
Dietary modification - From the child, change fluids, calcium, oxalate, animal protein, potassium, sucrose, fructose, sodium phytate and vitamin C may be useful. It is unclear what role vitamin D has in the formation of these types of stones.
Increased fluid intake - Increased intake of fluids during the day (although not necessarily the patient wakes up several times during the night to urinating), increase the rate of urine flow and decrease the concentration of substances dissolved in it. Both phenomena can affect the reduction of the occurrence of stone. In a prospective study, 199 patients with the first appearance of calcium stones randomly determined not to undergo the treatment and referral of increased fluid intake to form at least two urine a day. After five years, the incidence of new stones was significantly lower in the treated patients compared to the control group (12 vs. 27 percent).
Similar findings were obtained in another prospective study. Patients who developed a cornerstone had a larger volume of urine from patients with the disease reappeared (320 ml / day relative to no change).
Type of liquid - The risk of stone is considered to be influenced by the type of liquid. However, data to support this are limited and presented in more detail in a separate booklet.
Grapefruit juice may be linked to an increased risk of developing stones, although the potential mechanism has not yet been identified. Although data are limited, to avoid grapefruit and grapefruit juice may make sense in the case of patients with calcium oxalate stones.
Coffee, tea and alcohol in prospective observational studies linked to a reduced risk of developing stones
Cranberry juice, which is recommended as prophylaxis of developing urinary tract infections, increased urinary saturation of calcium oxalate when ingested in large amounts (one liter per day).Intake of moderate amounts is usually not harmful, but there is no evidence that this drink contributes to the prevention of stones.
Reducing intake of animal protein - negative changes in the excretion of calcium, uric acid and citrate in the urine may occur due to a diet high in protein, because amino acids containing sulfur acid load increases day by creating sulfuric acid. Animal proteins often lead to the appearance of the plant, because they have a higher sulfur content, and thus produce more acid. Therefore, the reduced intake of animal protein to bring positive changes in the urine. However, it has not been proven to reduce the appearance of stone. In observational studies, a diet rich in animal protein is a risk factor for kidney stones in men but not in women. The random testing reduced intake of animal protein, along with higher daily calcium intake and lower sodium was associated with a lower risk of recurrence of stone.
Higher intake of fruits and vegetables - Foods rich in potassium, especially fruits and vegetables, can have a positive impact. Increased intake of fruits and vegetables may reduce the risk of forming calcium oxalate stones, especially in patients who have consumed some fruits and vegetables. This positive impact is primarily the result of increased excretion of citrate.
Limited intake of oxalate - Some foods are high in oxalates and should be avoided (eg spinach and rhubarb). In addition, some nuts and legumes also have high concentrations of oxalate and their intake should be limited (eg, peanuts, cashews and almonds). However, there is little evidence that a diet low in oxalate reduces the risk of stone formation. In prospective observational studies, individuals who have never had a stone, a higher intake of oxalate is only slightly raised the risk of stone men and older women: there is no indication in younger women. Because of the documented health benefits of many foods traditionally regarded as rich in oxalate (but still have them 10 mg or less per serving), strict oxalate restriction is not supported.
Restricted sodium intake - calcium is passively reabsorbed in the proximal tubules sequence corresponding concentration gradient created reabsorpcijom sodium and water.
For this reason, a low sodium diet (80 to 100 meq / day) may improve the proximal reabsorption of sodium and calcium, which leads to reduction in excretion of calcium. In one study, for example, lowering sodium intake from 200 to 80 meq / day reduced the excretion of calcium and 100 mg / day (2.5 mmol / day). Although the independent contribution of a low sodium diet is unknown, it is part of the regime which has been shown to reduce the appearance of new stones.
Limited intake of sucrose and fructose - For sucrose was shown to increase the concentration of calcium in the urine regardless of calcium intake and is associated with an increased risk of developing new stones. Fructose also increases the risk.
Calcium intake - Although a higher concentration of calcium often found in people with kidney stones is not recommended restricted intake of this mineral. Reduction of free intestinal calcium can lead to increased absorption of dietary oxalate and increased excretion of these, the reduced binding of calcium oxalate in the lumen of the intestine. The net effect may be increased supersaturation of urine with respect to calcium oxalate and increased the possibility of forming stones.
Possibility of preventing the creation of new stones with normal calcium intake is partly demonstrated a five-year study that compared two children among men with idiopathic hiperkalcenurijom and relapsed stones of calcium oxalate. In this study, 120 men were randomly prescribed diet which consisted of the normal amount of calcium (1,200 mg / day [30 mmol / day]) and small amounts of animal protein (52 g / day) and salt (2900 mg / day [50 mmol / day] sodium chloride) or a diet with a small amount of calcium (400 mg / day [10 mmol / day]).
After five years, a significantly lower risk of stone recurrence was observed in men for whom the prescribed diet with normal calcium, a little animal protein and salt (unadjusted relative risk of 0.49, with a CI from 0.24 to 0.98). This selective advantage is likely a consequence of reduced excretion of oxalate in the urine, compared with the increase seen in the low-calcium diet; calcium in the urine actually declined in both groups. However, the independent effect of calcium is not clear because the amount of animal protein have entered ii salt in the group whose diet had little calcium were different.Nonetheless, based diets with small amounts of calcium has no benefits and is not recommended.
In addition to increased formation of stones, diets low in calcium may have an additional negative effect in patients with idiopathic hypercalciuria: the emergence of a negative calcium balance. This extra calcium loss may exacerbate already reduced bone density in some patients, a complication that may be due to increased absorption.
It should be noted that calcium supplements have no effect in preventing recurrence of stone and may even slightly increase the risk.
In the case of patients with a history of kidney stones that need calcium supplementation (eg, for the treatment of osteoporosis), suggesting the measurement of urinary excretion of calcium before and about a month after starting the use of additional calcium. If there is a clinically significant increase in urinary excretion of calcium, addition of thiazide diuretics may be useful in reducing urinary excretion of the mineral (and helps maintain bone density).
Other - Large doses of vitamin C appears to increase in some patients the excretion of oxalate in the urine, as well as the risk of stone, because high doses of this supplement should be avoided in patients with higher urinary oxalate excretion. Phytate appears to reduce the risk of developing stones in women. Although it is not only a consequence of diet, higher body mass index increases the risk of stone formation, particularly in women. For this reason, weight control can help prevent recurrence of stone.
Drug therapy - Drug therapy is indicated if the disease is caused by stones formed active (which indicates the formation of new stones or enlarge old. Goal of treatment is to prevent further precipitation of calcium oxalate; dissolve existing calcium stones is almost impossible (as compared with stones from uric acid or cystine stones). initial course varies according to the existing metabolic disorder:
Thiazide diuretics reduce urinary calcium
Allopurinol for hiperurikosuriju
Calcium citrate to hipocitraturiju
Patient adherence to prescribed medication or a child can become a significant issue for a long period of time. Studies that document the use of these interventions require at least three years before the results become significant. In an analysis of over 3000 patients followed in a well-organized Department of stumbling at the University of Chicago, reduction of urinary supersaturation was constant or improved over time in people who followed a yearly check. However, only 15 to 40 percent of patients complied with these requirements in three years. Adherence to long term therapies among those who did not, the control is not known.
Hypercalciuria - Patients with a high concentration of calcium in the urine, which is due to the hypercalcemia (idiopathic hypercalciuria) and continuous active disease that causes the stones should be treated with normal calcium diet, a little animal protein and salt, plus the need to use thiazide diuretics such as as hydrochlorothiazide or chlorthalidone (which has a longer shelf life).
Thiazide therapy may reduce excretion of calcium in the urine and 50 per cent. This is done primarily by inducing a slight volume decline, leading to compensatory increase in proximal reabsorption of sodium and thus to passive reabsorption of calcium. The net effect may be a reduction of 90 percentage incidence of stones to create a new (although there is a significant improvement from 50 to 65 percent of patients treated with placebo). This does not de [state if in addition to this therapy and no limit salt intake.
Diuretics are usually started at a dose of 25 mg / day chlorthalidone or hydrochlorothiazide (or its equivalent) to reduce the complications of diuretic therapy, but most patients need 50 to 100 mg / day to achieve adequate reduction of calcium in the urine. Chlorthalidone may be applied once a day, but hydrochlorothiazide in doses higher than 25 mg / day may have to be given twice a day because of the short half life. Should be avoided because hypokalemia low potassium levels reduce the excretion of citrate in the urine. Diet low in calcium should be avoided as it increases the risk of stones. The above mentioned drugs should not be used bey previous tests and they should always be prescribed by a doctor.
The tendency towards a positive balance of calcium with thiazide diuretics may have additional positive effects: increasing bone mineralization and reducing the incidence of hip fractures in elderly patients. This will be useful for patients who are mistakenly put on diets low in calcium and / or rich in sodium, which can lead to a negative balance of calcium and osteopenia in patients with high calcium in the urine.
Calcium in the urine and sodium excretion should be controlled after starting thiazide therapy. If the calcium in the urine remains higher than desired, it may be due to higher sodium intake and should try to reduce the excretion of sodium less than 100 meq (2300 mg) per day. Diuretic that does not lower the potassium, amiloride (5 to 10 mg / day) may also be added, as it may increase the reabsorption of calcium in the collective cortical tubules, thus more calcium excretion decreases.
If the calcium in the urine is reduced sufficiently, or if the patient does not tolerate tiayidne diuretics can try adding alkali - one of the options the administration of 60 to 80 meq of alkali per day in the form of potassium bicarbonate or potassium citrate (citrate is rapidly metabolized to bicarbonate) .Warning: potassium supplements should be given regularly with amiloride, because the combination can cause potassium retention and hyperkalemia. These preparations are also not be given in patients with impaired renal function or elevated serum potassium caused by other diseases. In any case, this type of therapy is always a doctor by statute. The administration of potassium citrate or calcium bicarbonate may have a positive impact by increasing the excretion of citrate in the urine, a potent inhibitor of calcium stone formation.
Another opinion is that the administration of neutral phosphate (orthophosphate) may reduce the excretion of calcium and increase the excretion of crystallization inhibitors (such as pyrophosphate).However, no clinical studies documenting the effectiveness of this strategy in the prevention of recurrence of stone.
Hyperuricosuria - Increased excretion of uric acid in the urine may contribute to formation of stones.
Some studies have shown that the application of the drug allopurinol may be useful in patients with elevated excretion of uric acid in the urine and stone formation in the urinary tract. Allopurinol therapy significantly reduced the likelihood of recurrence of calcium oxalate stones (0:12 versus 0:26 per patient per year with placebo). The results obtained in other studies have not confirmed this view at least when it comes to stones and calcium oxalate.
Hipocitraturija - Increased excretion of citrate in the urine is the goal for patients with hipocitraturijom as citrate prevents the formation of hard stone by building dissociative, but soluble complexes with calcium, which reduces the amount of calcium available for binding with oxalate or phosphate. Citrate excretion may increase plasma alkalinizing with daily application of 30 to 80 meq potassium citrate or potassium bicarbonate. In a controlled study of 57 patients, for example, the incidence of new stone was hipocitraturičnih lower in patients treated with potassium citrate (0.1 compared to 1.1 occurrences per patient per year in the placebo-treated group). This positive effect is associated with a doubling of citrate excretion.
Although orange juice and a good source of potassium citrate, it has some side effects: no lowers calcium excretion; moderately increased excretion of oxalate; increased caloric intake can lead to increased body weight. In contrast, the lemon juice is an effective source of citrate. In one report, for example, enter 120 ml of concentrated lemon juice a day (blended with water as lemonade, the total volume of 2 liters) resulted in increased levels of citrate in the urine in 11 of 12 patients (average increase of 142 to 346 mg / day, remained low), or who did not want to adhere to or did not tolerate conventional therapy substitution of citrate. Active treatment also reduced the excretion of calcium in the urine and did not change the excretion of oxalate. Should not be sweetened lemonade to avoid entry of additional calories.
Contrary to popular belief, cranberries sod while not increasing the levels of citrate in the urine. This was demonstrated in a study conducted on 24 people (12 had stones of calcium oxalate), in which the excretion of citrate was the same with water (control) or cranberry juice. A possible explanation for the lack of effect of the low content of potassium in the juice of cranberries.
Hyperoxaluria - high content of oxalate in the urine can be the result of ingestion of foods rich in oxalate, or factors that can be converted into them (eg vitamin C) and / or due to increased GI absorption of dietary oxalate (enteric Hyperoxaluria). Treatment of patients with enteric hyperoxaluria is to decrease the intestinal absorption of oxalate. The initial regimen consisting of large amounts of fluids, potassium citrate in the correction of metabolic acidosis, if present, and oral calcium carbonate or citrate (1 to 4 g / day) with meals for binding oxalate in the lumen of the intestine. Although the calcium absorbed much of the oxalate binds.
Diet low in fats and oxalates can also be useful when it comes to this disorder as the result of reduction of amount of free fatty acid and oxalate in the colon. However, reliable data on oxalate content in different types of food were obtained only recently and restriction diets can lead to malnutrition of patients suffering from malabsorption of nutrients and / or short gut syndrome.
No metabolic abnormalities - Some patients who are Calcium stones have recurred diagnosed metabolic abnormalities. However, careful analysis has shown that these patients often have more calcium, oxalate, and / or less citrate in the urine than normal, although no value does not reach the traditional value of the abnormal.
People who form stones also often have a smaller volume of urine, which is another factor that increases the likelihood of stone formation. In one report, for example, patients with the first stone who later developed another had a basic daily amount of urine for 250 to 350 ml lower than those who were not re-developed stone. In some patients, the only abnormality was the volume of urine that led to increased concentrations of calcium and oxalate.
Stresses the importance of the concentration of urinary factors, not just the total amount of ekskretovane. For example, even when calcium is traditionally accepted hiperkalcinurijskom range, the concentration of calcium in the urine will be greater when the volume of urine decreased. If the volume of urine can constantly maintain a higher level of calcium in the urine has to be reduced.
Short Review - From the food, change fluid intake, calcium, oxalate, potassium phytate, animal protein, sucrose, fructose, sodium and vitamin C may be useful. Therefore, we recommend the following:
Drinking enough fluids during the day to produce at least 2 liters of urine, including drinking water during the night (although it is not necessary that the patient wakes several times at night to urinating).This will increase the rate of urine flow and reduce the concentration of dissolved substances in the urine, which reduces the risk of stone formation.
To achieve this goal, it is best recommended amount needed extra fluid in relation to his or her 24-hour urine volume. For example, if the total volume of urine 1.5 liter, we recommend an additional 240 ml of fluid every day to achieve the target value of 2 liters.
Limited intake of animal protein. Although it is not proven that eating a little protein reduces the incidence of stone, food botaga animal protein is a risk factor for gallstone formation in men but not in women.
Limit the intake of salt (sodium) to 100 meq / day. Eating a low sodium can increase proximal reabsorption of sodium and calcium, which leads to reduced excretion of calcium and less tendency to form stones.
Higher dietary intake of potassium, as this reduces the risk in men and older women. Higher intake of potassium is not allowed in patients who have an impaired kidney function or elevated serum potassium levels due to other causes.
Limiting the intake of sucrose and fructose.
Limiting the intake of oxalate and vitamin C in patients with calcium oxalate stones. However, the restriction is not too useful, patients should continue to eat a variety of vegetables and fruits.
Drug therapy is indicated if the disease is still active (as shown by the formation of new stones or increasing old), or if you do not notice improvement despite adequate dietary changes for three to six months.
Initial drug therapy varies according to the existing metabolic disorder:
Thiazide diuretics to reduce the excretion of calcium in urine
Allopurinol for hiperurikozuriju
Potassium citrate for hipocitraturiju
MONITORING RESPONSE TO THERAPY - 24-hour urine is an essential component of the initial assessment and impact on recommendations for prevention. Response to dietary therapy or medication followed by a repeated 24-hour urine collection. It is essential that patients with calcium oxalate stones from urinary track all factors of importance because they often have more than one urinary abnormalities. Although the remains of stone could theoretically bind the ingredients of urine and thus reduce the measured concentration, potential bias due to the existing stone is much smaller than the variability as a result of diet.
The goal of treatment is reversal of disorders detected during the initial examination (eg, a small volume of urine, hiperkalcinurija, hipocitraturija and Hyperoxaluria). Routine work one or two 24-hour collection of urine six to eight weeks after the start of treatment in order to determine the impact of the intervention. If there is a desired change, the values are measured again after six months, then once a year. If urinary abnormalities persist, additional therapy.
Another component of monitoring is periodic ultrasound examination of the urinary tract. Ultrasound examination should be performed once a year and, if negative, every two to four years after that.
Calcium phosphate stones - Generally, patients with calcium phosphate stones have the same risk factors as those with calcium oxalate (except hyperoxaluria), because the therapy is repeated occurrence of similar rocks in all situations.
Achieving these goals may require a change in diet and the use of appropriate medications. Medical therapy (and metabolic assessment) is usually carried out in the case of patients who have formed more than a stone. Even if the patient threw a stone, it is important to review the footage to determine whether there are other stones because of their passing is not equivalent to the formation. At least one stone patients are encouraged to increase their fluid intake and periodically controlled (usually renal ultrasonography), to determine whether there is a new rock.
Here we present the treatment of patients with recurrent calcium stone formation. Treatment of patients with re-formation of rocks of different origin, and unknown are displayed separately, as well as risk factors for recurrence of calcium.
STONES calcium oxalate - the re-emergence of calcium oxalate stones is a large number of dietary modification and drug therapy.
Dietary modification - From the child, change fluids, calcium, oxalate, animal protein, potassium, sucrose, fructose, sodium phytate and vitamin C may be useful. It is unclear what role vitamin D has in the formation of these types of stones.
Increased fluid intake - Increased intake of fluids during the day (although not necessarily the patient wakes up several times during the night to urinating), increase the rate of urine flow and decrease the concentration of substances dissolved in it. Both phenomena can affect the reduction of the occurrence of stone. In a prospective study, 199 patients with the first appearance of calcium stones randomly determined not to undergo the treatment and referral of increased fluid intake to form at least two urine a day. After five years, the incidence of new stones was significantly lower in the treated patients compared to the control group (12 vs. 27 percent).
Similar findings were obtained in another prospective study. Patients who developed a cornerstone had a larger volume of urine from patients with the disease reappeared (320 ml / day relative to no change).
Type of liquid - The risk of stone is considered to be influenced by the type of liquid. However, data to support this are limited and presented in more detail in a separate booklet.
Grapefruit juice may be linked to an increased risk of developing stones, although the potential mechanism has not yet been identified. Although data are limited, to avoid grapefruit and grapefruit juice may make sense in the case of patients with calcium oxalate stones.
Coffee, tea and alcohol in prospective observational studies linked to a reduced risk of developing stones
Cranberry juice, which is recommended as prophylaxis of developing urinary tract infections, increased urinary saturation of calcium oxalate when ingested in large amounts (one liter per day).Intake of moderate amounts is usually not harmful, but there is no evidence that this drink contributes to the prevention of stones.
Reducing intake of animal protein - negative changes in the excretion of calcium, uric acid and citrate in the urine may occur due to a diet high in protein, because amino acids containing sulfur acid load increases day by creating sulfuric acid. Animal proteins often lead to the appearance of the plant, because they have a higher sulfur content, and thus produce more acid. Therefore, the reduced intake of animal protein to bring positive changes in the urine. However, it has not been proven to reduce the appearance of stone. In observational studies, a diet rich in animal protein is a risk factor for kidney stones in men but not in women. The random testing reduced intake of animal protein, along with higher daily calcium intake and lower sodium was associated with a lower risk of recurrence of stone.
Higher intake of fruits and vegetables - Foods rich in potassium, especially fruits and vegetables, can have a positive impact. Increased intake of fruits and vegetables may reduce the risk of forming calcium oxalate stones, especially in patients who have consumed some fruits and vegetables. This positive impact is primarily the result of increased excretion of citrate.
Limited intake of oxalate - Some foods are high in oxalates and should be avoided (eg spinach and rhubarb). In addition, some nuts and legumes also have high concentrations of oxalate and their intake should be limited (eg, peanuts, cashews and almonds). However, there is little evidence that a diet low in oxalate reduces the risk of stone formation. In prospective observational studies, individuals who have never had a stone, a higher intake of oxalate is only slightly raised the risk of stone men and older women: there is no indication in younger women. Because of the documented health benefits of many foods traditionally regarded as rich in oxalate (but still have them 10 mg or less per serving), strict oxalate restriction is not supported.
Restricted sodium intake - calcium is passively reabsorbed in the proximal tubules sequence corresponding concentration gradient created reabsorpcijom sodium and water.
For this reason, a low sodium diet (80 to 100 meq / day) may improve the proximal reabsorption of sodium and calcium, which leads to reduction in excretion of calcium. In one study, for example, lowering sodium intake from 200 to 80 meq / day reduced the excretion of calcium and 100 mg / day (2.5 mmol / day). Although the independent contribution of a low sodium diet is unknown, it is part of the regime which has been shown to reduce the appearance of new stones.
Limited intake of sucrose and fructose - For sucrose was shown to increase the concentration of calcium in the urine regardless of calcium intake and is associated with an increased risk of developing new stones. Fructose also increases the risk.
Calcium intake - Although a higher concentration of calcium often found in people with kidney stones is not recommended restricted intake of this mineral. Reduction of free intestinal calcium can lead to increased absorption of dietary oxalate and increased excretion of these, the reduced binding of calcium oxalate in the lumen of the intestine. The net effect may be increased supersaturation of urine with respect to calcium oxalate and increased the possibility of forming stones.
Possibility of preventing the creation of new stones with normal calcium intake is partly demonstrated a five-year study that compared two children among men with idiopathic hiperkalcenurijom and relapsed stones of calcium oxalate. In this study, 120 men were randomly prescribed diet which consisted of the normal amount of calcium (1,200 mg / day [30 mmol / day]) and small amounts of animal protein (52 g / day) and salt (2900 mg / day [50 mmol / day] sodium chloride) or a diet with a small amount of calcium (400 mg / day [10 mmol / day]).
After five years, a significantly lower risk of stone recurrence was observed in men for whom the prescribed diet with normal calcium, a little animal protein and salt (unadjusted relative risk of 0.49, with a CI from 0.24 to 0.98). This selective advantage is likely a consequence of reduced excretion of oxalate in the urine, compared with the increase seen in the low-calcium diet; calcium in the urine actually declined in both groups. However, the independent effect of calcium is not clear because the amount of animal protein have entered ii salt in the group whose diet had little calcium were different.Nonetheless, based diets with small amounts of calcium has no benefits and is not recommended.
In addition to increased formation of stones, diets low in calcium may have an additional negative effect in patients with idiopathic hypercalciuria: the emergence of a negative calcium balance. This extra calcium loss may exacerbate already reduced bone density in some patients, a complication that may be due to increased absorption.
It should be noted that calcium supplements have no effect in preventing recurrence of stone and may even slightly increase the risk.
In the case of patients with a history of kidney stones that need calcium supplementation (eg, for the treatment of osteoporosis), suggesting the measurement of urinary excretion of calcium before and about a month after starting the use of additional calcium. If there is a clinically significant increase in urinary excretion of calcium, addition of thiazide diuretics may be useful in reducing urinary excretion of the mineral (and helps maintain bone density).
Other - Large doses of vitamin C appears to increase in some patients the excretion of oxalate in the urine, as well as the risk of stone, because high doses of this supplement should be avoided in patients with higher urinary oxalate excretion. Phytate appears to reduce the risk of developing stones in women. Although it is not only a consequence of diet, higher body mass index increases the risk of stone formation, particularly in women. For this reason, weight control can help prevent recurrence of stone.
Drug therapy - Drug therapy is indicated if the disease is caused by stones formed active (which indicates the formation of new stones or enlarge old. Goal of treatment is to prevent further precipitation of calcium oxalate; dissolve existing calcium stones is almost impossible (as compared with stones from uric acid or cystine stones). initial course varies according to the existing metabolic disorder:
Thiazide diuretics reduce urinary calcium
Allopurinol for hiperurikosuriju
Calcium citrate to hipocitraturiju
Patient adherence to prescribed medication or a child can become a significant issue for a long period of time. Studies that document the use of these interventions require at least three years before the results become significant. In an analysis of over 3000 patients followed in a well-organized Department of stumbling at the University of Chicago, reduction of urinary supersaturation was constant or improved over time in people who followed a yearly check. However, only 15 to 40 percent of patients complied with these requirements in three years. Adherence to long term therapies among those who did not, the control is not known.
Hypercalciuria - Patients with a high concentration of calcium in the urine, which is due to the hypercalcemia (idiopathic hypercalciuria) and continuous active disease that causes the stones should be treated with normal calcium diet, a little animal protein and salt, plus the need to use thiazide diuretics such as as hydrochlorothiazide or chlorthalidone (which has a longer shelf life).
Thiazide therapy may reduce excretion of calcium in the urine and 50 per cent. This is done primarily by inducing a slight volume decline, leading to compensatory increase in proximal reabsorption of sodium and thus to passive reabsorption of calcium. The net effect may be a reduction of 90 percentage incidence of stones to create a new (although there is a significant improvement from 50 to 65 percent of patients treated with placebo). This does not de [state if in addition to this therapy and no limit salt intake.
Diuretics are usually started at a dose of 25 mg / day chlorthalidone or hydrochlorothiazide (or its equivalent) to reduce the complications of diuretic therapy, but most patients need 50 to 100 mg / day to achieve adequate reduction of calcium in the urine. Chlorthalidone may be applied once a day, but hydrochlorothiazide in doses higher than 25 mg / day may have to be given twice a day because of the short half life. Should be avoided because hypokalemia low potassium levels reduce the excretion of citrate in the urine. Diet low in calcium should be avoided as it increases the risk of stones. The above mentioned drugs should not be used bey previous tests and they should always be prescribed by a doctor.
The tendency towards a positive balance of calcium with thiazide diuretics may have additional positive effects: increasing bone mineralization and reducing the incidence of hip fractures in elderly patients. This will be useful for patients who are mistakenly put on diets low in calcium and / or rich in sodium, which can lead to a negative balance of calcium and osteopenia in patients with high calcium in the urine.
Calcium in the urine and sodium excretion should be controlled after starting thiazide therapy. If the calcium in the urine remains higher than desired, it may be due to higher sodium intake and should try to reduce the excretion of sodium less than 100 meq (2300 mg) per day. Diuretic that does not lower the potassium, amiloride (5 to 10 mg / day) may also be added, as it may increase the reabsorption of calcium in the collective cortical tubules, thus more calcium excretion decreases.
If the calcium in the urine is reduced sufficiently, or if the patient does not tolerate tiayidne diuretics can try adding alkali - one of the options the administration of 60 to 80 meq of alkali per day in the form of potassium bicarbonate or potassium citrate (citrate is rapidly metabolized to bicarbonate) .Warning: potassium supplements should be given regularly with amiloride, because the combination can cause potassium retention and hyperkalemia. These preparations are also not be given in patients with impaired renal function or elevated serum potassium caused by other diseases. In any case, this type of therapy is always a doctor by statute. The administration of potassium citrate or calcium bicarbonate may have a positive impact by increasing the excretion of citrate in the urine, a potent inhibitor of calcium stone formation.
Another opinion is that the administration of neutral phosphate (orthophosphate) may reduce the excretion of calcium and increase the excretion of crystallization inhibitors (such as pyrophosphate).However, no clinical studies documenting the effectiveness of this strategy in the prevention of recurrence of stone.
Hyperuricosuria - Increased excretion of uric acid in the urine may contribute to formation of stones.
Some studies have shown that the application of the drug allopurinol may be useful in patients with elevated excretion of uric acid in the urine and stone formation in the urinary tract. Allopurinol therapy significantly reduced the likelihood of recurrence of calcium oxalate stones (0:12 versus 0:26 per patient per year with placebo). The results obtained in other studies have not confirmed this view at least when it comes to stones and calcium oxalate.
Hipocitraturija - Increased excretion of citrate in the urine is the goal for patients with hipocitraturijom as citrate prevents the formation of hard stone by building dissociative, but soluble complexes with calcium, which reduces the amount of calcium available for binding with oxalate or phosphate. Citrate excretion may increase plasma alkalinizing with daily application of 30 to 80 meq potassium citrate or potassium bicarbonate. In a controlled study of 57 patients, for example, the incidence of new stone was hipocitraturičnih lower in patients treated with potassium citrate (0.1 compared to 1.1 occurrences per patient per year in the placebo-treated group). This positive effect is associated with a doubling of citrate excretion.
Although orange juice and a good source of potassium citrate, it has some side effects: no lowers calcium excretion; moderately increased excretion of oxalate; increased caloric intake can lead to increased body weight. In contrast, the lemon juice is an effective source of citrate. In one report, for example, enter 120 ml of concentrated lemon juice a day (blended with water as lemonade, the total volume of 2 liters) resulted in increased levels of citrate in the urine in 11 of 12 patients (average increase of 142 to 346 mg / day, remained low), or who did not want to adhere to or did not tolerate conventional therapy substitution of citrate. Active treatment also reduced the excretion of calcium in the urine and did not change the excretion of oxalate. Should not be sweetened lemonade to avoid entry of additional calories.
Contrary to popular belief, cranberries sod while not increasing the levels of citrate in the urine. This was demonstrated in a study conducted on 24 people (12 had stones of calcium oxalate), in which the excretion of citrate was the same with water (control) or cranberry juice. A possible explanation for the lack of effect of the low content of potassium in the juice of cranberries.
Hyperoxaluria - high content of oxalate in the urine can be the result of ingestion of foods rich in oxalate, or factors that can be converted into them (eg vitamin C) and / or due to increased GI absorption of dietary oxalate (enteric Hyperoxaluria). Treatment of patients with enteric hyperoxaluria is to decrease the intestinal absorption of oxalate. The initial regimen consisting of large amounts of fluids, potassium citrate in the correction of metabolic acidosis, if present, and oral calcium carbonate or citrate (1 to 4 g / day) with meals for binding oxalate in the lumen of the intestine. Although the calcium absorbed much of the oxalate binds.
Diet low in fats and oxalates can also be useful when it comes to this disorder as the result of reduction of amount of free fatty acid and oxalate in the colon. However, reliable data on oxalate content in different types of food were obtained only recently and restriction diets can lead to malnutrition of patients suffering from malabsorption of nutrients and / or short gut syndrome.
No metabolic abnormalities - Some patients who are Calcium stones have recurred diagnosed metabolic abnormalities. However, careful analysis has shown that these patients often have more calcium, oxalate, and / or less citrate in the urine than normal, although no value does not reach the traditional value of the abnormal.
People who form stones also often have a smaller volume of urine, which is another factor that increases the likelihood of stone formation. In one report, for example, patients with the first stone who later developed another had a basic daily amount of urine for 250 to 350 ml lower than those who were not re-developed stone. In some patients, the only abnormality was the volume of urine that led to increased concentrations of calcium and oxalate.
Stresses the importance of the concentration of urinary factors, not just the total amount of ekskretovane. For example, even when calcium is traditionally accepted hiperkalcinurijskom range, the concentration of calcium in the urine will be greater when the volume of urine decreased. If the volume of urine can constantly maintain a higher level of calcium in the urine has to be reduced.
Short Review - From the food, change fluid intake, calcium, oxalate, potassium phytate, animal protein, sucrose, fructose, sodium and vitamin C may be useful. Therefore, we recommend the following:
Drinking enough fluids during the day to produce at least 2 liters of urine, including drinking water during the night (although it is not necessary that the patient wakes several times at night to urinating).This will increase the rate of urine flow and reduce the concentration of dissolved substances in the urine, which reduces the risk of stone formation.
To achieve this goal, it is best recommended amount needed extra fluid in relation to his or her 24-hour urine volume. For example, if the total volume of urine 1.5 liter, we recommend an additional 240 ml of fluid every day to achieve the target value of 2 liters.
Limited intake of animal protein. Although it is not proven that eating a little protein reduces the incidence of stone, food botaga animal protein is a risk factor for gallstone formation in men but not in women.
Limit the intake of salt (sodium) to 100 meq / day. Eating a low sodium can increase proximal reabsorption of sodium and calcium, which leads to reduced excretion of calcium and less tendency to form stones.
Higher dietary intake of potassium, as this reduces the risk in men and older women. Higher intake of potassium is not allowed in patients who have an impaired kidney function or elevated serum potassium levels due to other causes.
Limiting the intake of sucrose and fructose.
Limiting the intake of oxalate and vitamin C in patients with calcium oxalate stones. However, the restriction is not too useful, patients should continue to eat a variety of vegetables and fruits.
Drug therapy is indicated if the disease is still active (as shown by the formation of new stones or increasing old), or if you do not notice improvement despite adequate dietary changes for three to six months.
Initial drug therapy varies according to the existing metabolic disorder:
Thiazide diuretics to reduce the excretion of calcium in urine
Allopurinol for hiperurikozuriju
Potassium citrate for hipocitraturiju
MONITORING RESPONSE TO THERAPY - 24-hour urine is an essential component of the initial assessment and impact on recommendations for prevention. Response to dietary therapy or medication followed by a repeated 24-hour urine collection. It is essential that patients with calcium oxalate stones from urinary track all factors of importance because they often have more than one urinary abnormalities. Although the remains of stone could theoretically bind the ingredients of urine and thus reduce the measured concentration, potential bias due to the existing stone is much smaller than the variability as a result of diet.
The goal of treatment is reversal of disorders detected during the initial examination (eg, a small volume of urine, hiperkalcinurija, hipocitraturija and Hyperoxaluria). Routine work one or two 24-hour collection of urine six to eight weeks after the start of treatment in order to determine the impact of the intervention. If there is a desired change, the values are measured again after six months, then once a year. If urinary abnormalities persist, additional therapy.
Another component of monitoring is periodic ultrasound examination of the urinary tract. Ultrasound examination should be performed once a year and, if negative, every two to four years after that.
Calcium phosphate stones - Generally, patients with calcium phosphate stones have the same risk factors as those with calcium oxalate (except hyperoxaluria), because the therapy is repeated occurrence of similar rocks in all situations.
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