PHOSPHATE Phosphorus is naturally present in nearly all foodstuffs. It is absorbed by the human body in the form of phosphates.

s. The main sources of food phosphates are 1. proteins, in particular eggs, meat and dairy products, 2. Wholegrain cereals. 3. Sea creatures absorb and concentrate marine phosphates naturally in their scales, bones and shells. Their remains, accumulated on the seabed for millions of years, have formed huge deposits in certain places, such as Morocco, South Africa and the USA. Phosphoric acid is isolated from this natural phosphate ore using many different purification processes. WHY DO OUR BODIES REQUIRE PHOSPHATES ? Phosphorus is the sixth most important component of our bodies, mainly in the form of phosphates. Phosphates are 1. key components of DNA, 2. components of cell structures 3. components of bones and teeth 4. responsible for energy transmission in cells (ATP, GTP) 5. are involved in many biological processes (esp. in CHO metabolism) 6. They are essential to the health of all living creatures. Phosphates are used to improve foodstuffs. They have a wide range of properties which enable the best aspects of foodstuffs to be preserved. Without phosphates, many farm products would be past their best before they reached consumers plates. Phosphates are used for a number of purposes in the food industry: 1. To preserve natural taste and color 2. To preserve the natural juices of meat and crustaceans 3. To prevent the development of certain bacteria 4. To ensure even rising of cakes and pastries during baking 5. To ensure the homogeneity of dairy products

6. To encourage the development of good bacteria in cheeses 7. To improve the free-flowing properties of powdered foodstuffs 8. To reactivate certain ingredients in pharmaceuticals 9. To prevent contamination of drinking water As our bodies regularly excrete phosphates through the kidneys, it is vital that we constantly replenish our supplies. To ensure good health, the minimum RDA is 700 mg for adults, 800 mg for pregnant women and 1,250 mg for teenagers. Phosphorus and calcium intake need to be balanced, as high doses of either may prevent assimilation of the other. This is why some women who are given calcium supplements for osteoporosis also need to take phosphate supplements. (*)Hydrogen 63%; oxygen 25% (including body water content), carbon 9.5%; nitrogen 1.4%; calcium 0.33%; phosphorus 0.22%

PHOSPHATE: A VITAL ANION Body stores of phosphorus range from 700 to 1,000 g Primarily coupled to oxygen as an anion phosphate (PO4). Approximately 85% of phosphate is an inorganic component of the crystalline hydroxyapatite contained in phosphate reservoirs in bone and teeth. The hydroxyapatites have a general structural formula of Ca10(PO4)6(OH)2 and provide the rigid architectural framework characteristic of osseous tissue. 14% percent of phosphate is an organic intracellular anion that is essential for 1. Aerobic and anaerobic energy metabolism within RBCs. Via RBC 2,3diphosphoglycerate, phosphate preferentially transfers oxygen from hemoglobin to cells exhibiting greatest hypoxia. 2. In the cell membrane, phosphate provides for scaffolding as a phospholipid 3. Serves as a major constituent of DNA and RNA nucleic acids and phosphor-protein macromolecules. 4. In addition, phosphate is essential for carbohydrate, lipid, and protein metabolism;

5. it functions as a cofactor in numerous enzyme systems 6. As an integral component in serum or intracellular acid-base metabolism. 7. Finally, as adenosine triphosphate, phosphate undergoes hydrolysis to form adenosine diphosphate, yielding essential energy for all metabolic activity. The remaining 1% of inorganic phosphorus is found in the extracellular compartment, which is measurable within the serum. 1. This phosphate contributes to electrical and acid-base homeostasis, with up to 90% in the free, unbound form; 2. the other 10% remains bound to protein. A normal serum level, reflecting this extracellular phosphate, is 3.0 to 4.5 mg/dL.

PHOSPHATE METABOLISM Intake of elemental phosphorus ranges from 800 to 1,500 mg. Two-thirds of dietary phosphorus is absorbed in the duodenum and jejunum through both active and passivediffusion. Absorption of phosphate is enhanced by 1,25-dihydroxycholecalciferol. However, absorption is most efficient at lower dietary intake levels and diminishes with increased ingestion. Non-absorbed phosphate is excreted in the feces. Phosphate metabolism is rigorously regulated by sodium-coupled phosphate transporters located in the nephron, bones, and intestines7 in the body's concerted effort to maintain homeostasis. Phosphate excretion through the kidneys roughly equals absorption in the GI tract. Phosphate is principally absorbed via active transport at the proximal tubule, and the distal convoluted tubule provides an additional 10% to 15% of absorption. Reabsorption in the intestines and the kidneys is greater with dietary deficiencies and higher 1,25-dihydroxycholecalciferol levels and is lower with increased phosphorus intake.

 Additional mechanisms also facilitate phosphorus homeostasis; 1. PTH o PTH inhibits phosphate reabsorption at the proximal and distal convoluted tubules, thereby promoting phosphaturia. In the intestines, PTH and 1,25-dihydroxycholecalciferol prompt phosphate absorption. o PTH also determines plasma phosphate levels in conjunction with volume status. o Volume expansion with an absence of PTH results in minimal phosphaturia; a volume expanded state with increased PTH elevates urinary phosphate levels. 2. BONE o Approximately 3 mg/kg/d of phosphate enter bone, with an equal amount leaving the osseous reservoir through bony resorption. o Important regulatory factors that determine bone formation and destruction, and thus phosphate levels, include i. PTH, ii. vitamin D, iii. sex hormones, iv. acid-base balance, v. the presence of generalized inflammation

5. ARE FOOD PHOSPHATES HAZARDOUS TO HEALTH ? There have been many studies into the effect of food phosphates on the human body. All have demonstrated that industrial food phosphates are not toxic. They are assimilated in the same manner as the phosphates which occur naturally in foodstuffs. The quantities of food phosphates added to foodstuffs are tiny. Depending on the application, the authorized maximum ranges from 0.07% to 4%. On average, the proportions used by industry are 0.35% in meat, 2.5% in processed cheeses, 0.4% in cakes and 0.05% in colas. The vast majority of phosphates occur naturally in high-protein foods such as meat, eggs, fish and cereals.

Total phosphate intake therefore depends less on what has been added industrially than on the type of foods eaten. Contrary to a widespread belief, phosphates are no more toxic than other regularly consumed products such as vinegar, bicarbonate of soda or table salt. Of course, high doses administered in laboratories can have a negative impact on health, such as temporary nausea in humans or kidney malfunction (observed in rats injected with extreme doses). The European Food Safety Authority (EFSA) concluded in 2005 that excessive phosphorus intake does not negatively affect humans unless they are suffering from severe kidney trouble. In the United States and Canada, the health authorities have set the maximum daily phosphorus intake at 3,0005,000 mg per day, depending on body mass. In 2003, the average national daily intake was 1,260 mg per day.

CAUSES OF HYPERPHOSPHATEMIA
The etiology of hyperphosphatemia is identified through at least one of three underlying pathogenic states. These include excessive phosphate intake or renal reabsorption, diminished phosphate excretion, and transcellular shifting. Hyperphosphatemia is most often the culmination of several maladies rather than resulting from a single contributory cause.
7

Renal failure The most common cause of hyperphosphatemia is renal failure. Renal dysfunction greater than 40% or a glomerular filtration rate of less than 30 mL/min significantly impairs the glomerular filtration capabilities of inorganic phosphate, increasing the serum accumulation of phosphate. Acute and chronic renal failure is reportedly responsible for 50% of hyperphosphatemia cases among elderly patients.
1,7

Increased phosphate absorption High intake of phosphorus, regardless of route (oral, parenteral, or rectal), or increased renal reabsorption are less common causes. Excessive use of phosphate-containing laxatives or enemas, short-term parenteral administration of large quantities of phosphate, and vitamin D intoxication will elevate phosphorus intake. Absorbable antacids (sodium bicarbonate and calcium carbonate) in large amounts and calcium supplementation (ie, milk-alkali syndrome) promote a mild hyperphosphatemia.
9

Granulomatous diseases, such as sarcoidosis or tuberculosis, cause excessive vitamin D production,

10

and vitamin D increases intestinal phosphate and calcium absorption. Elevated serum calcium concentration diminishes urinary excretion through two mechanisms: it inhibits PTH secretion and impairs renal function through direct renal vasoconstriction. Most often, concomitant renal insufficiency is the contributory underlying pathology, rather than an isolated increase in phosphate intake.
1,7

Hypoparathyroidism, in addition to increasing GI phosphate absorption, also enhances renal phosphate reabsorption. Acromegaly and thyrotoxicosis are also noted for facilitating renal reabsorption. Familial
2,8

tumor calcinosis, a rare disorder with autosomal recessive and dominant inheritance patterns, enhances hyperphosphatemia by increasing the renal tubule's capacity to reabsorb filtered phosphate.
11,12

Transcellular shifting The third main mechanism of hyperphosphatemia is transcellular shifting. Cellular destruction causes expeditious phosphate efflux from internal cellular compartments irrespective of the histologic source. These etiologies include rhabdomyolysis, malignant hyperpyrexia, cytotoxins, myonecrosis, crush injuries, healing fractures, tumor lysis syndrome, sepsis, the hemolytic anemias, and hemolyzed blood specimens. Laboratory findings that support cell lysis as the cause of hyperphosphatemia include concomitant elevations in LDH, potassium, magnesium, indirect bilirubin, myoglobin, or creatine phosphokinase levels. Other causes of transcellular shifting of phosphate to the extracellular space include insulin deficiency, certain medications (such as beta-blockers), and acidosis. The compensatory buffering mechanism that occurs during respiratory or metabolic acidosis prompts an exchange of intracellular phosphate for increasing external hydrogen ion concentrations.

Hyperphosphatemia is present in 94.7% of all patients with diabetic ketoacidosis (DKA) before therapy initiation; both insulin deficiency and metabolic acidosis are hallmarks of DKA.
13

Other clinical settings Plasma phosphate levels are increased in other clinical scenarios. Pseudohyperphosphatemia should be considered in patients with elevated phosphate levels but normal serum calcium levels and normal renal function. The differential diagnosis for spurious pseudohyperphosphatemia includes hyperlipidemia, hemolyzed samples, hyperbilirubinemia, and paraproteinemia, which is the most common. The presence of tissue plasminogen activator or alteplase,
14

used as catheter lock solutions to prevent clot formation during hemodialysis, may manifest as clinical pseudohyperphosphatemia. In this setting, erroneously elevated phosphate levels are the result of specimen contamination caused by an improper collection technique from the catheter. phosphate levels.
17 15,16

Plasma

samples taken from heparinized saline infusion indwelling catheters will similarly demonstrate increased

Phosphate levels may be elevated as a consequence of a malignancy-associated increase in bone mobilization. Etiologies include solid tumor osteolytic metastases, advanced lymphoma, multiple myeloma, and myelocytic leukemia. Volume status also affects phosphate levels. Contingent on the
3,8

presence of PTH, volume expansion reduces renal reabsorption of phosphate, thereby lowering plasma phosphate levels. Volume expansion devoid of PTH and volume contracted states increase renal reabsorption of phosphate at the distal tubule, facilitating hyperphosphatemia. Nonpathologic conditions Epidemiologic, dietary, seasonal, and temporal variability can cause fluctuations in plasma phosphate levels. Phosphate values exhibit diurnal variance; levels are lowest in the late morning and highest in the afternoon to late evening. Likewise, phosphate levels increase during the summer months because of a corresponding increase in sun exposure-induced vitamin D production. Age also affects phosphate levels. Concentrations steadily decrease with age; levels are
2,8

30% higher in children than in adults, 50% higher in infants. Higher demand for essential phosphatemediated growth processes in infants and children is the likely reason for the higher levels. A notable
4

exception is the concentration found in women entering postmenopause. Hypoestrogenemia, present during the fifth to sixth decades, contributes to a 3% increase in serum phosphate levels; whereas increased phosphate retention is the likely cause of an 8% to 9% increase observed during the sixth through eighth decades.
1

Various pharmacologic agents are known to induce hyperphosphatemia as an adverse reaction, including penicillin, corticosteroids, some diuretics, furosemide, and thiazides. Pseudohyperphosphatemia has
8

been documented in patients who received liposomal amphotericin B. Other liposomal formulations (cytarabine, doxorubicin, and amphotericin B) can also have this effect. phosphate reabsorption.
2,18,19

The bisphosphonates,

particularly etidronate, may elicit a mild hyperphosphatemia, in part as a direct stimulation of renal

MANIFESTATIONS AND COMPLICATIONS

Most patients with hyperphosphatemia are asymptomatic. If symptoms are present, they are usually reflective of underlying contributory pathologies. Clinically, manifestations common to hypocalcemia
1,4

evolve and represent sequelae of hyperphosphatemia; phosphorus complexes and precipitates ionized calcium, thereby lowering calcium levels. In addition, these calcium-phosphorus complexes cause a myriad of maladies. CNS and cardiovascular system changes are predominant in the clinical presentation of hyperphosphatemia. Delirium, coma, seizures, neuromuscular hyperexcitability (Chvostek's sign and Trousseau's phenomenon), hyperreflexia, muscle cramping (eg, carpopedal spasm) or tetany, and perioral or extremity paresthesias are possible CNS manifestations. Cardiovascular changes include hypotension and development of heart failure.
6,7

Hyperphosphatemia-induced hypocalcemia elicits elevations in PTH secretion, prompting secondary hyperparathyroidism. Subsequently, increased PTH furthers liberation of calcium from bony reservoirs, thereby diminishing calcium stores via increased bone turnover. Furthermore, high phosphate levels inhibit renal enzyme 1-alpha hydroxylase. This enzyme produces active vitamin D by addition of a hydroxyl group to circulating 25-hydroxycholecalciferol. The decrease in active vitamin D results in impaired GI absorption of calcium, reduced renal reabsorption of calcium and phosphate, and impaired bone mineralization. The collective metabolic ramifications of hyperphosphatemia, therefore, include a higher incidence of bone demineralization and bone fractures. Patients with end-stage renal disease (ESRD) and those on hemodialysis have higher cardiovascular morbidity and mortality because of a higher risk for metastatic vascular and soft-tissue calcification formation, a pervasive condition in chronic hyperphosphatemia. Studies led by Block and Ganesh demonstrate increased rates of cardiovascular mortality and sudden cardiac death in patients with hyperphosphatemia who are on dialysis.
20,21

Hyperphosphatemia results in deposits of calcium-phosphate

complexes throughout the body, a process mediated by sodium-phosphorus co-transporters. Human smooth muscle cells upregulate the transcription of osteocalcin, a promoter of vascular calcium deposition, when cultured in high-phosphate medium. In vascular smooth muscle cells, the ensuing
22

osteochondrogenic changes accelerate vascular calcification and arteriosclerosis. The resultant effects
23

are systolic hypertension, widened pulse pressure, and subsequent left ventricular hypertrophy. More specifically, three basic forms of vascular calcifications may occur: Capillary and small arteriole deposition results in distal extremity ischemic necrosis and hemorrhagic subcutaneous lesions. Medial layer arterial calcium deposition occurs with increased phosphate levels in the uremic state. Higher phosphate levels in conjunction with increased uremia characteristic of ESRD is linked to increased arterial medial layer calcification, a major factor in the development of arteriosclerosis. This process is mediated by platelet-derived growth factor, bone morphogenetic protein 2, fibroblast growth factor 23,

osteopontin, and osteonectin.

22,24

Calcium phosphate crystal deposition within the renal tubules of

nephrons may cause acute renal failure. Oral sodium phosphate solutions used for bowel cleansing prior to colonoscopy have been linked to nephrocalcinosis with ensuing acute renal failure characterized by calcium phosphate crystal deposition.
11,25-27

Increased phosphate load is an independent cause of mitral

and aortic stenosis. Further cardiac dysfunction secondary to hyperphosphatemia is characterized by aberrations in cardiac conduction, resulting in dysrhythmias. Those with familial tumor calcinosis may also demonstrate skin, soft tissue and periarticular calcifications, owing to increased plasma phosphatecalcium complexes. Familial tumor calcinosis disorder is characterized by masses of metastatic calcifications in soft tissues around the major joints, most often the shoulders, hips, and ankles.
11,12

Other notable systemic connective tissue sequelae of chronic hyperphosphatemia are found in the joints and subcutaneous and other soft-tissue areas. Systemic symptoms, as observed in vascular complications, result from increased phosphorus and calcium linkage and ensuing deposition. Cutaneous phosphate deposition may contribute to a papular rash that can progress to uremic pruritus and peripheral ischemic ulceration. Deposition in the joints and tendons causes painful, limited ranges of motion with an increased likelihood for tendon rupture. Manifestations in the eye include band-shaped keratopathy, cataracts, red eye, or conjunctivitis.
6,7

EVALUATION OF HYPERPHOSPHATEMIA
A plasma phosphate level higher than 4.5 mg/dL is diagnostic. A comprehensive metabolic profile should be obtained with special attention focused on renal competence and calcium levels. The clinician should suspect underlying hypoparathyroidism if the results indicate low PTH and calcium levels with normal renal function and a high phosphate level. An increased BUN and creatinine with intact to elevated PTH and low calcium levels suggest renal insufficiency or frank renal failure. High calcium and phosphate levels are found in patients with vitamin D intoxication or milk-alkali syndrome; the former will demonstrate relatively normal PTH levels with high 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and vitamin D levels, whereas the latter will demonstrate low PTH and vitamin D levels. Pseudohyperphosphatemia should be suspected if results show normal renal function and calcium levels; serum protein, bilirubin, and lipid assessments should then be obtained. A low anion gap may indicate
4

abnormal globulins or paraprotein etiology. Serum protein electrophoresis, immunoelectrophoresis, and serum deproteination are acceptable methods of differentiating protein-induced pseudohyperphosphatemia from genuine hyperphosphatemia. Confirmation of diagnosis via repeat phosphate determination is advised. ECG analysis may reveal QT interval prolongation.
1 6

Urinary phosphate assessment should be obtained for patients who exhibit normal renal function. Urinary phosphate levels higher than 1,500 mg/dL imply an endogenous (eg, cytotoxins, rhabdomyolysis, malignant hyperpyrexia) or exogenous (eg, laxative or enema use, phosphate toxicity) source of excess phosphate. Urinary phosphate levels of less than 1,500 mg/dL suggest increased renal reabsorption, as

seen with hyperparathyroidism, extracellular fluid volume contraction, or tumoral calcinosis, and in postmenopausal women. Tumoral calcinosis is characterized by serum calcium, alkaline phosphatase,
28

and PTH concentrations within the normal range and normal renal function; elevated serum 1,25dihydroxyvitamin D and calcitriol levels are typical.
11,12

Radiographic imaging is helpful in diagnosing clinical symptoms that often accompany chronic elevated serum levels. Plain film roentgenography may demonstrate metastatic calcifications (eg, bilateral, symmetric calcifications of the basal ganglia; periarticular calcifications around the large joints; soft-tissue calcifications at the pressure point areas). Bone densitometry may be indicated for patients with suspected demineralized bone as a result of primary or secondary hyperparathyroidism. If metabolic panel results indicate renal dysfunction, renal abnormalities can be assessed on a renal sonogram. Electron beam computed tomography (EBCT) and multidetector computed tomography (MDCT), although not routinely employed, are recognized as specialized imaging modalities that can identify increased coronary calcium deposition. EBCT and MDCT assessment of coronary calcium score is most appropriate for patients with chronic hyperphosphatemia who are on dialysis.
22

TREATMENT
Efficacious treatment of hyperphosphatemia, where applicable, consists of successful treatment of the underlying pathologies. Otherwise, treatment centers on lowering phosphate intake and increasing renal excretion. Acute severe hyperphosphatemia with symptomatic hypocalcemia can be life threatening. Phosphate excretion can be increased with saline infusions; however, this may exacerbate hypocalcemia by diluting serum calcium concentration. Hemodialysis is often indicated for patients with symptomatic hypocalcemia, particularly if renal function is impaired.
11

Hyperphosphatemia related to renal failure is predominantly treated by limiting phosphate ingestion and through dialysis. Hyperphosphatemia as a result of tumor lysis responds to the use of forced saline diuresis to enhance urinary losses. Reduced ingestion may be accomplished by curtailing phosphatecontaining foods, such as meat and dairy, as well as phosphate-containing supplements. Limiting phosphate ingestion to 600 mg/d is desirable, primarily for patients with mild renal insufficiency. As renal failure progresses, dietary restriction becomes less feasible and less effective. Phosphatebinding drugs and antacids as a second phosphate-lowering mechanism are then indicated. These drugs are taken concomitantly with meals and block GI absorption of phosphate in the intestines. Aluminum hydroxide and aluminum hydroxide sucrose gels were commonly used phosphate binders; however, calcium carbonate (calcium acetate) and calcium citrate binders have largely replaced aluminumcontaining binders for patients with ESRD because of the risk of aluminum-related osteomalacia, dementia, and anemia. Although calcium carbonate is a less effective phosphate binder than aluminum, calcium carbonate has a lower toxicity profile and the added benefit of calcium supplementation.

A phosphate-binding resin without calcium (sevelamer), is available in doses of 800 to 2,400 mg, three times a day with meals, for patients on dialysis. A second PO binder without calcium is lanthanum
4

carbonate, which can also be given to dialysis patients in doses of 500 to 1,000 mg three times a day with meals. In a comparative crossover study of calcium acetate and sevelamer conducted with patients on
4

hemodialysis, both drugs demonstrated similar efficacy in controlling hyperphosphatemia; however, calcium acetate was far more cost-effective. A trend toward higher serum calcium concentrations and lower PTH concentrations during treatment with calcium acetate was observed. In addition, vascular
22

calcification is possible in patients on dialysis who were taking calcium-containing phosphate binders; these agents should thus be avoided in patients who demonstrate coronary artery or systemic calcification.
6,7

CONCLUSION
The most common cause of hyperphosphatemia is compromised renal function. Other important causes include excessive phosphate intake, vitamin D intoxication, hypoparathyroidism, hyperthyroidism, malignancy, and transcellular-shifting. Evaluation of pseudohyperphosphatemia resulting from paraproteinemia, hyperlipidemia, and hemolysis should also be considered. Most patients with hyperphosphatemia are asymptomatic; however, coexisting hypocalcemia may cause neurologic manifestations. Chronic, severe hyperphosphatemia induces renal dysfunction, as well as extensive soft tissue, vascular, organ, and periarticular calcifications. The diagnostic assessment should include a CBC, complete metabolic panel, lipid and thyroid panels, a PTH assay, and vitamin D and urinary phosphate levels. Ancillary diagnostic studies, such as ECG, plain film radiography, and renal ultrasonography, may also be indicated. Evaluation of coronary arterial calcification by EBCT and MDCT may be useful but is reserved for patients with chronically elevated hyperphosphatemia who are on hemodialysis. Underlying causes of hyperphosphatemia should be identified and treated. Otherwise, reducing phosphate intake, blocking GI absorption, and enhancing phosphate excretion are the mainstays of treatment.JAAPA Daniel Podd is an assistant professor at the Saint John's University PA program in Queens, New York, and practices in primary care and pain management in Howard Beach, New York. He has indicated no relationships to disclose relating to the content of this article.

Kidney StonesAdult
Definition

Kidney stones are pieces of a stone or crystal-like material in the urine. These stones form inside the kidneys or other parts of the urinary tract. The kidneys remove waste (in the form of urine) from the body. They also balance the water and electrolyte content in the blood by filtering salt and water. There are several types of kidney stones:

The most common type has mostly calcium along with oxalate or phosphate. Others types contain uric acid, struvite, and/or cystine.

Kidney Stone

Copyright Nucleus Medical Media, Inc.

Causes
Some of the known causes include:

Chemotherapy (ie, uric acid stone) Too much oxalate in urine (hyperoxaluria) Too little magnesium in urine (hypomagnesemia) Too much calcium in the urine (hypercalciuria) Too much calcium in the blood (hypercalcemia) Too little citrate in the urine (hypocitraturia)

 Bacteria around which a stone can form Too much uric acid in the urine (hyperuricuria, gout) Bacteria that produce enzymes that increase the amount of ammonia and struvite in the urine Inherited abnormality in the way the body handles cystine Certain medications (such as indinavir ) Foreign bodies in the urinary tract, such as stents or catheters Retention of urine

Risk
Risk factors that can increase your chance of developing kidney stones include:

Race: White Sex: male Age: 20 to 50 years old Geographic location (residents of the Southeast United States have an increased risk) Family members who have had kidney stones or gout Previous kidney stones Taking excess doses of calcium supplements or vitamin C Pregnancy Fasting Other medical conditions, including:
Kidney disease Overactive parathyroid Chronic diarrhea Ulcerative colitis Crohn's disease

Leukemia Lymphoma Urinary tract infections Sarcoidosis

Immobility, paralysis, being bedridden Medications, including some AIDS medications, chemotherapydrugs, diuretics, and antacids Previous intestinal bypass surgery Reduced fluid intake or increased fluid loss in hot weather ( dehydration) Urinary tract obstruction or failure to empty the bladder Foreign material in the urinary tract (eg, catheter)

Symptoms
Occasionally, kidney stones do not cause symptoms. They leave the body in the urine. The condition, though, can cause severe pain. Symptoms include:

Sharp, stabbing pain in the mid-back that may occur every few minutes and last from 20
minutes to one hour

Pain in the lower abdomen and groin area, labia, or testicles Nausea, vomiting, or diarrhea Blood in the urine Frequent urge to urinate Burning pain during urination Fever Urinary tract infection