الفهرس 
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Abstract
Crystals in the urine is known as crystalluria. It is frequently found during routine examination of the urine. Sometimes crystals are found in healthy people and other times they are indicators of organ dysfunction the presence of urinary tract stone, or an infection in the urinary tract. They come in many different shapes and sizes.
Some forms of crystals appear in the urine of healthy individuals and most crystals, except for cystine are not considered cilinically significant. Freshy voided urine specimens are often devoid of crystals, but alkalization and refrigeration may promote crystals formation. While crystals are found in kidney stones, the presence of crystals in the urine doesn‘t necessarily relate to stone formation. Cystine crystals, however are found only in patients with cystinuria, agentic impairment of tubular reabsorption of basic amino acids lysine, arginine, ornithine, and cystine. There are many types of crystals like uric acid crystals, oxalate crystals and cystine crystals.
There was no significant difference in the incidence of each crystalluria type between males and females also there were no significant differences among age groups for both types of crystalluria. There were only two types of crystalluria are most predominant, those are uric acid and calcium oxalate and the incidence of uric acid crystalluria was significantly greater than oxalate in both genders and age groups.
There are many risk factors for crystals and stone formation like climate and geography. It is believed that individuals living in hot climates have an increased lifetime prevalence of stone disease secondary to dehydration. Also Urolithiasis incidence increases during summer and decreases during winter. It is generally attributed to the effect of seasonal variations in temperature on urinary volume.
Also BMI and weight are one of these risk factors, The prevalence and incident risk of stone disease were directly correlated with weight and body mass index in both sexes.
The risk of urolithiaisis is greater in individuals with a family history of stone disease. It is estimated to be more than 2.5 times greater in those individuals.
The most important risk factors is diet and water, low fluid intake and high dietary intake of animal protein, sodium, refined sugars, fructose and high fructose corn syrup, oxalate, grapefruit juice, apple juice, and cola drinks .
There are many causes for crystals and stone formation . the most important cause is metabolic causes like Hypercalciuria, Hyperoxaluria, Cystinuria, Hyperuricosuria and Hypocitraturia.
Also other causes include infection structural abnormalities of the urinary tract and use of drugs like loop diuretics, laxatives, ciprofloxacin, sulfa medications and indinavir.
For diagnosis you must take full history from patient. Examine him and then do investigations like metabolic evaluation and diagnostic imaging.
The metabolic evaluation for urolithiasis helps us to identify children those at increased risk for recurrent stone disease and also to diagnose specific treatable metabolic derangements.
Metabolic screening include Stone analysis, Blood test ( Bone Mineral Chemistry, that is serum calcium, phosphorus, alkaline phosphatase, albumin and parathyroid hormone- Renal tubular functions that is electrolytes such as sodium, potassium and chloride- Blood gas analysis) and Urine test ( Urine pH, Urine sediment for graveluria, pus cells, RBC, Urine culture and sensitivity test where indicated and 24-hour urine for calcium, phosphate, uric acid, sodium, citrate, oxalate and cystine (if cystinuria is suspected) .
Diagnostic Imaging of urolithiasis include Plain Radiography, Intravenous Urography, Ultrasound, Computed Tomography, Magnetic Resonance Imaging (MRI) and Retrograde Pyelography.
Dietary modifications may decrease stone formation in children dramatically. Increasing fluid intake reduces the risk of stone formation. The volume of fluid intake should be adjusted to maintain urine volume greater than750mL/d in infants, greater than1000mL/d in children younger than 5 years, greater than 1500 mL/d in children between 5 and 10 years, and more than 2000 mL/d in children older than 10 years. Almost all beverages, including coffee, tea, wine, beer, and fruit juices, are acceptable. Water is the best beverage for stone formers. It is non-caloric, non-caffeinated, and contains insignificant amounts of solutes. The mainstay for medical management of uric acid stones is alkalinization of urine (increasing the pH 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 on to 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 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 . Citrate potassium therapy is suggested in patients with chronic hypercalciuria. It is also useful in patients who have hypocitraturia and hypercalciuria concurrently. In this regard, the starting dose of citrate potassium is 1-2 meq/kg/day divided in two doses.