KNOW ABOUT KIDNEY STONE

A kidney stone, also known as a renal calculus or nephrolith, is a solid piece of material which is formed in the kidneys from minerals in urine.Kidney stones typically leave the body in the urine stream, and a small stone may pass without causing symptoms. If stones grow to sufficient size (usually at least 3 millimeters (0.1 in)) they can cause blockage of the ureter. This leads to pain, most commonly beginning in the flank or lower back and often radiating to the groin. This pain is often known as renal colic and typically comes in waves lasting 20 to 60 minutes. Other associated symptoms include: nausea, vomiting, fever, blood in the urine, pus in the urine, and painful urination. Blockage of the ureter can cause decreased kidney function and dilation of the kidney.

Most stones form due to a combination of genetics and environmental factors.Risk factors include being overweight, certain foods, some medications, and not drinking enough fluids. The diagnosis is usually based on symptoms, urine testing, and medical imaging. Blood tests may also be useful.Urinary stones are typically classified by their location in the kidney (nephrolithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis), or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds).

In those who have previously had stones, prevention is recommended by drinking fluids such that more than two liters of urine is produced per day. If this is not effective enough, thiazide diuretic, citrate or allopurinol may be taken. It is recommended that soft drinks containing phosphoric acid (typically colas) be avoided. When a stone causes no symptoms, no treatment is needed. For stones which are causing symptoms, pain control is usually the first measure, using medications such as nonsteroidal anti-inflammatory drugs or opioids. More severe cases may require procedures. For example, some stones can be shattered into smaller fragments using extracorporeal shock wave lithotripsy. Others require cystoscopic procedures.

In 2013, 49 million cases of kidney stones occurred. This resulted in about 15,000 deaths globally.In the United States, about 9% of the population has had a kidney stone.Slightly more men are affected than women.

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.This pain, known as renal colic, is often described as one of the strongest pain sensations known.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.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.Postrenal azotemia and hydronephrosis can be observed following the obstruction of urine flow through one or both ureters. 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 close proximity of these two structures.

Risk factors

Dehydration from low fluid intake is a major factor in stone formation.

High dietary intake of animal protein,sodium, refined sugars, fructose and high fructose corn syrup,oxalate,grapefruit juice, and apple juice may increase the risk of kidney stone formation.

Kidney stones can result from an underlying metabolic condition, such as distal renal tubular acidosis, Dent's disease, hyperparathyroidism,primary hyperoxaluria,[lor medullary sponge kidney. 3–20% of people who form kidney stones have medullary sponge kidney.

Kidney stones are more common in people with Crohn's disease; Crohn's disease is associated with hyperoxaluria and malabsorption of magnesium.

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.

Calcite

Calcium is one component of the most common type of human kidney stones, calcium oxalate. Some studies[which?] suggest people who take calcium as a dietary supplement have a higher risk of developing kidney stones. In the United States, those findings were used[by whom?] as the basis for setting the Reference Daily Intake 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.The Nurses' Health Study also showed an association between supplemental calcium intake and kidney stone formation.

Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development.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. A 2004 study found that diets low in calcium are associated with a higher overall risk for kidney stone formation. For most individuals, other risk factors for kidney stones, such as high intakes of dietary oxalates and low fluid intake, play a greater role than calcium intake.

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.

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.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.

Kidney stones are more likely to develop, and to grow larger, if a person has low dietary magnesium. Magnesium inhibits stone formation.

Animal protein
Diets in Western nations typically contain a large proportion of animal protein. Consumption of 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. 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.[6] Low urinary citrate, too, promotes stone formation.

Vitamins
The evidence linking vitamin C supplements with an increased rate of kidney stones is inconclusive. The excess dietary intake of vitamin C might increase the risk of calcium oxalate stone formation, in practice this is rarely encountered. 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.

Other
There are no conclusive data demonstrating a cause-and-effect relationship between alcoholic beverage consumption and kidney stones. However, some 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.

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.

People with lymphoproliferative/myeloproliferative disorders who were treated with chemotherapy developed symptomatic kidney stones 1.8% of the time in one study.

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.

Dietary measures
Specific therapy should be tailored to the type of stones involved. Diet can have a profound influence 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.Current dietary recommendations to minimize the formation of kidney stones include:

Increasing total fluid intake to more than two liters per day of urine output.
Increasing citric acid intake; lemon/lime juice is the richest natural source.
Moderate calcium intake
Limiting sodium intake
Avoidance of large doses of supplemental vitamin C
Limiting animal protein intake to no more than two meals daily (an association between animal protein consumption and recurrence of kidney stones has been shown in ).
Limiting consumption of cola soft drinks, which contain phosphoric acid, to less than one liter of soft drink per week.
Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of nephrolithiasis, 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. A high fluid intake has been associated with a 40% reduction in recurrence risk.The quality of the evidence for this, however, is not very good.

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. Because of this, some nephrologists and urologists recommend chewing calcium tablets during meals containing oxalate foods. 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.

Aside from vigorous oral hydration and consumption of 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. However, no randomized, controlled trial of oxalate restriction has yet been performed to test the hypothesis that oxalate restriction reduces the incidence of stone formation.Some evidence indicates magnesium intake decreases the risk of symptomatic nephrolithiasis.

Urine alkalinization
The mainstay for medical management of uric acid stones is alkalinization (increasing the pH) of the urine. Uric acid stones are among the few types amenable to dissolution therapy, referred to as chemolysis. Chemolysis is usually achieved through the use of oral medications, although in some cases, intravenous agents or even instillation of certain irrigating agents directly onto the stone can be performed, using antegrade nephrostomy or retrograde ureteral catheters.Acetazolamide (Diamox) is a medication that alkalinizes the urine. In addition to acetazolamide or as an alternative, certain dietary supplements are available that produce a similar alkalinization of the urine. These include sodium bicarbonate, potassium citrate, magnesium citrate, and Bicitra (a combination of citric acid monohydrate and sodium citrate dihydrate). Aside from alkalinization of the urine, these supplements have the added advantage of increasing the urinary citrate level, which helps to reduce the aggregation of calcium oxalate stones.

Increasing the urine pH to around 6.5 provides optimal conditions for dissolution of uric acid stones. Increasing the urine pH to a value higher than 7.0 increases the risk of calcium phosphate stone formation. Testing the urine periodically with nitrazine paper can help to ensure the urine pH remains in this optimal range. Using this approach, stone dissolution rate can be expected to be around 10 mm (0.4 in) of stone radius per month.

Diuretics
One of the recognized medical therapies for prevention of stones is the thiazide and thiazide-like diuretics, such as chlorthalidone or indapamide. These drugs inhibit the formation of calcium-containing stones by reducing urinary calcium excretion. Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides work best for renal leak hypercalciuria (high urine calcium levels), a condition in which high urinary calcium levels are caused by a primary kidney defect. Thiazides are useful for treating absorptive hypercalciuria, a condition in which high urinary calcium is a result of excess absorption from the gastrointestinal tract.

Allopurinol
For people with hyperuricosuria and calcium stones, allopurinol is one of the few treatments that have been shown to reduce kidney stone recurrences. Allopurinol interferes with the production of uric acid in the liver. The drug is also used in people with gout or hyperuricemia (high serum uric acid levels). Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/100 ml) is often a therapeutic goal. Hyperuricemia is not necessary for the formation of uric acid stones; hyperuricosuria can occur in the presence of normal or even low serum uric acid. Some practitioners advocate adding allopurinol only in people in whom hyperuricosuria and hyperuricemia persist, despite the use of a urine-alkalinizing agent such as sodium bicarbonate or potassium citrate.