document_title: Kidney stone disease

question_text: medical term meaning condition of stones in the ureters

question_tokens: medical term meaning condition of stones in the ureters

text: Kidney stone disease

text: Signs and symptoms[edit]

text: The hallmark of a stone that obstructs the ureter or renal pelvis is excruciating, intermittent pain that radiates from the flank to the groin or to the inner thigh.[11] This pain, known as renal colic, is often described as one of the strongest pain sensations known.[12] Renal colic caused by kidney stones is commonly accompanied by urinary urgency, restlessness, hematuria, sweating, nausea, and vomiting. It typically comes in waves lasting 20 to 60 minutes caused by peristaltic contractions of the ureter as it attempts to expel the stone.[11]

text: The embryological link between the urinary tract, the genital system, and the gastrointestinal tract is the basis of the radiation of pain to the gonads, as well as the nausea and vomiting that are also common in urolithiasis.[13] Postrenal azotemia and hydronephrosis can be observed following the obstruction of urine flow through one or both ureters.[14]

text: 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.

text: Risk factors[edit]

text: Dehydration from low fluid intake is a major factor in stone formation.[11][15] Obesity is a leading risk factor as well.

text: High dietary intake of animal protein,[11] sodium, sugars including honey, refined sugars, fructose and high fructose corn syrup,[16] oxalate,[17] grapefruit juice, and apple juice may increase the risk of kidney stone formation.[15]

text: Kidney stones can result from an underlying metabolic condition, such as distal renal tubular acidosis,[18] Dent's disease,[19] hyperparathyroidism,[20] primary hyperoxaluria,[21] or medullary sponge kidney. 3–20% of people who form kidney stones have medullary sponge kidney.[22][23]

text: Kidney stones are more common in people with Crohn's disease;[24] Crohn's disease is associated with hyperoxaluria and malabsorption of magnesium.[25]

text: 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.[14]

text: Calcium oxalate[edit]

text: Calcium is one component of the most common type of human kidney stones, calcium oxalate. Some studies[which?] suggest that people who take calcium or vitamin D as a dietary supplement have a higher risk of developing kidney stones. In the United States, kidney stone formation was used as an indicator of excess calcium intake by the Reference Daily Intake committee for calcium in adults.[26]

text: In the early 1990s, a study conducted for the Women's Health Initiative in the US found that postmenopausal women who consumed 1000 mg of supplemental calcium and 400 international units of vitamin D per day for seven years had a 17% higher risk of developing kidney stones than subjects taking a placebo.[27] The Nurses' Health Study also showed an association between supplemental calcium intake and kidney stone formation.[17]

text: Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development.[17][27] This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation—about 15 times stronger than calcium.

text: A 2004 study found that diets low in calcium are associated with a higher overall risk for kidney stone formation.[28] 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.[29]

text: Other electrolytes[edit]

text: 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.[17]

text: 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.[30] 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.[citation needed]

text: Kidney stones are more likely to develop, and to grow larger, if a person has low dietary magnesium. Magnesium inhibits stone formation.[31]

text: Animal protein[edit]

text: 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.[32] 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.[17] Low urinary citrate, too, promotes stone formation.[32]

text: Vitamins[edit]

text: The evidence linking vitamin C supplements with an increased rate of kidney stones is inconclusive.[33] 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.[17]

text: Other[edit]

text: There are no conclusive data demonstrating a cause-and-effect relationship between alcoholic beverage consumption and kidney stones. However, some people have theorized that certain behaviors associated with frequent and binge drinking can lead to dehydration, which can, in turn, lead to the development of kidney stones.[34]

text: 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.[35]

text: In one study, people with lymphoproliferative/myeloproliferative disorders who were treated with chemotherapy developed symptomatic kidney stones 1.8% of the time.[36]

text: Pathophysiology[edit]

text: Hypocitraturia[edit]

text: Hypocitraturia or low urinary-citrate excretion (defined as less than 320 mg/day) can cause kidney stones in up to 2/3 of cases. The protective role of citrate is linked to several mechanisms; in fact, citrate reduces urinary supersaturation of calcium salts by forming soluble complexes with calcium ions and by inhibiting crystal growth and aggregation. The therapy with potassium citrate, or magnesium potassium citrate, is commonly prescribed in clinical practice in order to increase urinary citrate and to reduce stone formation rates.[37]

text: Supersaturation of urine[edit]

text: When the urine becomes supersaturated (when the urine solvent contains more solutes than it can hold in solution) with one or more calculogenic (crystal-forming) substances, a seed crystal may form through the process of nucleation.[22] Heterogeneous nucleation (where there is a solid surface present on which a crystal can grow) proceeds more rapidly than homogeneous nucleation (where a crystal must grow in a liquid medium with no such surface), because it requires less energy. Adhering to cells on the surface of a renal papilla, a seed crystal can grow and aggregate into an organized mass. Depending on the chemical composition of the crystal, the stone-forming process may proceed more rapidly when the urine pH is unusually high or low.[38]

text: Supersaturation of the urine with respect to a calculogenic compound is pH-dependent. For example, at a pH of 7.0, the solubility of uric acid in urine is 158 mg/100 ml. Reducing the pH to 5.0 decreases the solubility of uric acid to less than 8 mg/100 ml. The formation of uric-acid stones requires a combination of hyperuricosuria (high urine uric-acid levels) and low urine pH; hyperuricosuria alone is not associated with uric-acid stone formation if the urine pH is alkaline.[39] Supersaturation of the urine is a necessary, but not a sufficient, condition for the development of any urinary calculus.[22] Supersaturation is likely the underlying cause of uric acid and cystine stones, but calcium-based stones (especially calcium oxalate stones) may have a more complex cause.[40]

text: Inhibitors of stone formation[edit]

text: Normal urine contains chelating agents, such as citrate, that inhibit the nucleation, growth, and aggregation of calcium-containing crystals. Other endogenous inhibitors include calgranulin (an S-100 calcium-binding protein), Tamm–Horsfall protein, glycosaminoglycans, uropontin (a form of osteopontin), nephrocalcin (an acidic glycoprotein), prothrombin F1 peptide, and bikunin (uronic acid-rich protein). The biochemical mechanisms of action of these substances have not yet been thoroughly elucidated. However, when these substances fall below their normal proportions, stones can form from an aggregation of crystals.[41]

text: Sufficient dietary intake of magnesium and citrate inhibits the formation of calcium oxalate and calcium phosphate stones; in addition, magnesium and citrate operate synergistically to inhibit kidney stones. Magnesium's efficacy in subduing stone formation and growth is dose-dependent.[17][31][42]

text: Diagnosis[edit]

text: Diagnosis of kidney stones is made on the basis of information obtained from the history, physical examination, urinalysis, and radiographic studies.[43] Clinical diagnosis is usually made on the basis of the location and severity of the pain, which is typically colicky in nature (comes and goes in spasmodic waves). Pain in the back occurs when calculi produce an obstruction in the kidney.[44] Physical examination may reveal fever and tenderness at the costovertebral angle on the affected side.[43]

text: Imaging studies[edit]

text: In people with a history of stones, those who are less than 50 years of age and are presenting with the symptoms of stones without any concerning signs do not require helical CT scan imaging.[45] A CT scan is also not typically recommended in children.[46]

text: Otherwise a noncontrast helical CT scan with 5 millimeters (0.2 in) sections is the diagnostic modality of choice in the radiographic evaluation of suspected nephrolithiasis.[13][43][47][48][7] All stones are detectable on CT scans except very rare stones composed of certain drug residues in the urine,[49] such as from indinavir. Calcium-containing stones are relatively radiodense, and they can often be detected by a traditional radiograph of the abdomen that includes the kidneys, ureters, and bladder (KUB film).[49] Some 60% of all renal stones are radiopaque.[47][50] In general, calcium phosphate stones have the greatest density, followed by calcium oxalate and magnesium ammonium phosphate stones. Cystine calculi are only faintly radiodense, while uric acid stones are usually entirely radiolucent.[51]

text: Where a CT scan is unavailable, an intravenous pyelogram may be performed to help confirm the diagnosis of urolithiasis. This involves intravenous injection of a contrast agent followed by a KUB film. Uroliths present in the kidneys, ureters, or bladder may be better defined by the use of this contrast agent. Stones can also be detected by a retrograde pyelogram, where a similar contrast agent is injected directly into the distal ostium of the ureter (where the ureter terminates as it enters the bladder).[47]

text: Renal ultrasonography can sometimes be useful, because it gives details about the presence of hydronephrosis, suggesting that the stone is blocking the outflow of urine.[49] Radiolucent stones, which do not appear on KUB, may show up on ultrasound imaging studies. Other advantages of renal ultrasonography include its low cost and absence of radiation exposure. Ultrasound imaging is useful for detecting stones in situations where X-rays or CT scans are discouraged, such as in children or pregnant women.[52] Despite these advantages, renal ultrasonography in 2009 was not considered a substitute for noncontrast helical CT scan in the initial diagnostic evaluation of urolithiasis.[48] The main reason for this is that, compared with CT, renal ultrasonography more often fails to detect small stones (especially ureteral stones) and other serious disorders that could be causing the symptoms.[11] A 2014 study confirmed that ultrasonography rather than CT as an initial diagnostic test results in less radiation exposure and did not find any significant complications.[53]

text:
Bilateral kidney stones can be seen on this KUB radiograph. There are phleboliths in the pelvis, which can be misinterpreted as bladder stones.

Axial CT scan of abdomen without contrast, showing a 3-mm stone (marked by an arrow) in the left proximal ureter

Renal ultrasonograph of a stone located at the pyeloureteric junction with accompanying hydronephrosis.

Measurement of a 5.6 mm large kidney stone in soft tissue versus skeletal CT window.

text: Laboratory examination[edit]

text: Laboratory investigations typically carried out include:[43][48][49][54]

text:
microscopic examination of the urine, which may show red blood cells, bacteria, leukocytes, urinary casts, and crystals;
urine culture to identify any infecting organisms present in the urinary tract and sensitivity to determine the susceptibility of these organisms to specific antibiotics;
complete blood count, looking for neutrophilia (increased neutrophil granulocyte count) suggestive of bacterial infection, as seen in the setting of struvite stones;
renal function tests to look for abnormally high blood calcium blood levels (hypercalcemia);
24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate, and phosphate;
collection of stones (by urinating through a StoneScreen kidney stone collection cup or a simple tea strainer) is useful. Chemical analysis of collected stones can establish their composition, which in turn can help to guide future preventive and therapeutic management.

text: Composition[edit]

text:
Kidney stone type
Population
Circumstances
Color
Sensitivity
Details

Calcium oxalate
80%
when urine is acidic (decreased pH)[55]
Black/dark brown
Radio-opaque
Some of the oxalate in urine is produced by the body. Calcium and oxalate in the diet play a part but are not the only factors that affect the formation of calcium oxalate stones. Dietary oxalate is found in many vegetables, fruits, and nuts. Calcium from bone may also play a role in kidney stone formation.

Calcium phosphate
5–10%
when urine is alkaline (high pH)
Dirty white
Radio-opaque
Tends to grow in alkaline urine especially when proteus bacteria are present.

Uric acid
5–10%
when urine is persistently acidic
Yellow/reddish brown
Radiolucent
Diets rich in animal proteins and purines: substances found naturally in all food but especially in organ meats, fish, and shellfish.

Struvite
10–15%
infections in the kidney
Dirty white
Radio-opaque
Prevention of struvite stones depends on staying infection-free. Diet has not been shown to affect struvite stone formation.

Cystine
1–2%[56]
rare genetic disorder
Pink/yellow
Radio-opaque
Cystine, an amino acid (one of the building blocks of protein), leaks through the kidneys and into the urine to form crystals.

Xanthine[57]

Extremely rare
Brick red
Radiolucent

text: Calcium-containing stones[edit]

text: By far, the most common type of kidney stones worldwide contains calcium. For example, calcium-containing stones represent about 80% of all cases in the United States; these typically contain calcium oxalate either alone or in combination with calcium phosphate in the form of apatite or brushite.[22][41] Factors that promote the precipitation of oxalate crystals in the urine, such as primary hyperoxaluria, are associated with the development of calcium oxalate stones.[21] The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism[20] and renal tubular acidosis.[58]

text: Oxaluria is increased in patients with certain gastrointestinal disorders including inflammatory bowel disease such as Crohn's disease or in patients who have undergone resection of the small bowel or small-bowel bypass procedures. Oxaluria is also increased in patients who consume increased amounts of oxalate (found in vegetables and nuts). Primary hyperoxaluria is a rare autosomal recessive condition that usually presents in childhood.[59]

text: Calcium oxalate crystals in urine appear as 'envelopes' microscopically. They may also form 'dumbbells.'[59]

text: Struvite stones[edit]

text: About 10–15% of urinary calculi are composed of struvite (ammonium magnesium phosphate, NH4MgPO4·6H2O).[60] Struvite stones (also known as "infection stones," urease, or triple-phosphate stones) form most often in the presence of infection by urea-splitting bacteria. Using the enzyme urease, these organisms metabolize urea into ammonia and carbon dioxide. This alkalinizes the urine, resulting in favorable conditions for the formation of struvite stones. Proteus mirabilis, Proteus vulgaris, and Morganella morganii are the most common organisms isolated; less common organisms include Ureaplasma urealyticum and some species of Providencia, Klebsiella, Serratia, and Enterobacter. These infection stones are commonly observed in people who have factors that predispose them to urinary tract infections, such as those with spinal cord injury and other forms of neurogenic bladder, ileal conduit urinary diversion, vesicoureteral reflux, and obstructive uropathies. They are also commonly seen in people with underlying metabolic disorders, such as idiopathic hypercalciuria, hyperparathyroidism, and gout. Infection stones can grow rapidly, forming large calyceal staghorn (antler-shaped) calculi requiring invasive surgery such as percutaneous nephrolithotomy for definitive treatment.[60]

text: Struvite stones (triple-phosphate/magnesium ammonium phosphate) have a 'coffin lid' morphology by microscopy.[59]

text: Uric acid stones[edit]

text: About 5–10% of all stones are formed from uric acid.[18] People with certain metabolic abnormalities, including obesity,[17] may produce uric acid stones. They also may form in association with conditions that cause hyperuricosuria (an excessive amount of uric acid in the urine) with or without hyperuricemia (an excessive amount of uric acid in the serum). They may also form in association with disorders of acid/base metabolism where the urine is excessively acidic (low pH), resulting in precipitation of uric acid crystals. A diagnosis of uric acid urolithiasis is supported by the presence of a radiolucent stone in the face of persistent urine acidity, in conjunction with the finding of uric acid crystals in fresh urine samples.[61]

text: As noted above (section on calcium oxalate stones), people with inflammatory bowel disease (Crohn's disease, ulcerative colitis) tend to have hyperoxaluria and form oxalate stones. They also have a tendency to form urate stones. Urate stones are especially common after colon resection.

text: Uric acid stones appear as pleomorphic crystals, usually diamond-shaped. They may also look like squares or rods which are polarizable.[59]

text: Patients with hyperuricosuria can be treated with allopurinol, which will reduce urate formation. Urine alkalinization may also be helpful in this setting.

text: Other types[edit]

text: People with certain rare inborn errors of metabolism have a propensity to accumulate crystal-forming substances in their urine. For example, those with cystinuria, cystinosis, and Fanconi syndrome may form stones composed of cystine. Cystine stone formation can be treated with urine alkalinization and dietary protein restriction. People afflicted with xanthinuria often produce stones composed of xanthine. People afflicted with adenine phosphoribosyltransferase deficiency may produce 2,8-dihydroxyadenine stones,[62] alkaptonurics produce homogentisic acid stones, and iminoglycinurics produce stones of glycine, proline, and hydroxyproline.[63][64] Urolithiasis has also been noted to occur in the setting of therapeutic drug use, with crystals of drug forming within the renal tract in some people currently being treated with agents such as indinavir,[65] sulfadiazine,[66] and triamterene.[67]

text: Location[edit]

text: Urolithiasis refers to stones originating anywhere in the urinary system, including the kidneys and bladder.[13] Nephrolithiasis refers to the presence of such stones in the kidneys. Calyceal calculi are aggregations in either the minor or major calyx, parts of the kidney that pass urine into the ureter (the tube connecting the kidneys to the urinary bladder). The condition is called ureterolithiasis when a calculus is located in the ureter. Stones may also form or pass into the bladder, a condition referred to as bladder stones.[68]

text: Size[edit]

text: Stones less than 5 mm (0.2 in) in diameter pass spontaneously in up to 98% of cases, while those measuring 5 to 10 mm (0.2 to 0.4 in) in diameter pass spontaneously in less than 53% of cases.[69]

text: Stones that are large enough to fill out the renal calyces are called staghorn stones, and are composed of struvite in a vast majority of cases, which forms only in the presence of urease-forming bacteria. Other forms that can possibly grow to become staghorn stones are those composed of cystine, calcium oxalate monohydrate, and uric acid.[70]

text: Prevention[edit]

text: 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.[71][72]

text: Dietary measures[edit]

text: 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.[28][73][74] Current dietary recommendations to minimize the formation of kidney stones include:[75]

text:
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.[76]
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 men[77]).
Limiting consumption of cola soft drinks,[71] which contain phosphoric acid, to less than one liter of soft drink per week.[78]

text: 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.[72] A high fluid intake has been associated with a 40% reduction in recurrence risk.[48] The quality of the evidence for this, however, is not very good.[72]

text: 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.[79] Because of this, some nephrologists and urologists recommend chewing calcium tablets during meals containing oxalate foods.[80] 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.[74]

text: 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.[81] 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.[80] Some evidence indicates magnesium intake decreases the risk of symptomatic nephrolithiasis.[81]

text: Urine alkalinization[edit]

text: 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.[39] 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).[82] 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.[39]

text: 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.[39]

text: Diuretics[edit]

text: 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.[11] 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.[41]

text: Allopurinol[edit]

text: 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).[83] 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.[39]

text: Treatment[edit]

text: Stone size influences the rate of spontaneous stone passage. For example, up to 98% of small stones (less than 5 mm (0.2 in) in diameter) may pass spontaneously through urination within four weeks of the onset of symptoms,[7] but for larger stones (5 to 10 mm (0.2 to 0.4 in) in diameter), the rate of spontaneous passage decreases to less than 53%.[69] Initial stone location also influences the likelihood of spontaneous stone passage. Rates increase from 48% for stones located in the proximal ureter to 79% for stones located at the vesicoureteric junction, regardless of stone size.[69] Assuming no high-grade obstruction or associated infection is found in the urinary tract, and symptoms are relatively mild, various nonsurgical measures can be used to encourage the passage of a stone.[39] Repeat stone formers benefit from more intense management, including proper fluid intake and use of certain medications. In addition, careful surveillance is clearly required to maximize the clinical course for people who are stone formers.[84]

text: Pain management[edit]

text: Management of pain often requires intravenous administration of NSAIDs or opioids.[11] NSAIDs appear somewhat better than opioids or paracetamol in those with normal kidney function.[85] Medications by mouth are often effective for less severe discomfort.[52] The use of antispasmodics does not have further benefit.[9]

text: Medical expulsive therapy[edit]

text: The use of medications to speed the spontaneous passage of stones in the ureter is referred to as medical expulsive therapy.[86][87] Several agents, including alpha adrenergic blockers (such as tamsulosin) and calcium channel blockers (such as nifedipine), have been found to be effective.[86] Alpha blockers appear to lead to both higher and faster stone clearance rates.[88] Alpha blockers; however, only appear to be effective for stones over 4 mm but less than 10 mm in size.[89] A combination of tamsulosin and a corticosteroid may be better than tamsulosin alone.[86] These treatments also appear to be a useful in addition to lithotripsy.[7]

text: Lithotripsy[edit]

text: Extracorporeal shock wave lithotripsy (ESWL) is a noninvasive technique for the removal of kidney stones. Most ESWL is carried out when the stone is present near the renal pelvis. ESWL involves the use of a lithotriptor machine to deliver externally applied, focused, high-intensity pulses of ultrasonic energy to cause fragmentation of a stone over a period of around 30–60 minutes. Following its introduction in the United States in February 1984, ESWL was rapidly and widely accepted as a treatment alternative for renal and ureteral stones.[90] It is currently used in the treatment of uncomplicated stones located in the kidney and upper ureter, provided the aggregate stone burden (stone size and number) is less than 20 mm (0.8 in) and the anatomy of the involved kidney is normal.[91][92]

text: For a stone greater than 10 mm (0.4 in), ESWL may not help break the stone in one treatment; instead, two or three treatments may be needed. Some 80 to 85% of simple renal calculi can be effectively treated with ESWL.[7] A number of factors can influence its efficacy, including chemical composition of the stone, presence of anomalous renal anatomy and the specific location of the stone within the kidney, presence of hydronephrosis, body mass index, and distance of the stone from the surface of the skin.[90] Common adverse effects of ESWL include acute trauma, such as bruising at the site of shock administration, and damage to blood vessels of the kidney.[93][94] In fact, the vast majority of people who are treated with a typical dose of shock waves using currently accepted treatment settings are likely to experience some degree of acute kidney injury.[90]

text: ESWL-induced acute kidney injury is dose-dependent (increases with the total number of shock waves administered and with the power setting of the lithotriptor) and can be severe,[90] including internal bleeding and subcapsular hematomas. On rare occasions, such cases may require blood transfusion and even lead to acute renal failure. Hematoma rates may be related to the type of lithotriptor used; hematoma rates of less than 1% and up to 13% have been reported for different lithotriptor machines.[94] Recent studies show reduced acute tissue injury when the treatment protocol includes a brief pause following the initiation of treatment, and both improved stone breakage and a reduction in injury when ESWL is carried out at slow shock wave rate.[90]

text: In addition to the aforementioned potential for acute kidney injury, animal studies suggest these acute injuries may progress to scar formation, resulting in loss of functional renal volume.[93][94] Recent prospective studies also indicate elderly people are at increased risk of developing new-onset hypertension following ESWL. In addition, a retrospective case-control study published by researchers from the Mayo Clinic in 2006 has found an increased risk of developing diabetes mellitus and hypertension in people who had undergone ESWL, compared with age and gender-matched people who had undergone nonsurgical treatment. Whether or not acute trauma progresses to long-term effects probably depends on multiple factors that include the shock wave dose (i.e., the number of shock waves delivered, rate of delivery, power setting, acoustic characteristics of the particular lithotriptor, and frequency of retreatment), as well as certain intrinsic predisposing pathophysiologic risk factors.[90]

text: To address these concerns, the American Urological Association established the Shock Wave Lithotripsy Task Force to provide an expert opinion on the safety and risk-benefit ratio of ESWL. The task force published a white paper outlining their conclusions in 2009. They concluded the risk-benefit ratio remains favorable for many people.[90] The advantages of ESWL include its noninvasive nature, the fact that it is technically easy to treat most upper urinary tract calculi, and that, at least acutely, it is a well-tolerated, low-morbidity treatment for the vast majority of people. However, they recommended slowing the shock wave firing rate from 120 pulses per minute to 60 pulses per minute to reduce the risk of renal injury and increase the degree of stone fragmentation.[90]

text: Surgery[edit]

text: Most stones under 5 mm (0.2 in) pass spontaneously.[28][7] Prompt surgery may, nonetheless, be required in persons with only one working kidney, bilateral obstructing stones, a urinary tract infection and thus, it is presumed, an infected kidney, or intractable pain.[95] Beginning in the mid-1980s, less invasive treatments such as extracorporeal shock wave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy began to replace open surgery as the modalities of choice for the surgical management of urolithiasis.[7] More recently, flexible ureteroscopy has been adapted to facilitate retrograde nephrostomy creation for percutaneous nephrolithotomy. This approach is still under investigation, though early results are favorable.[96] Percutaneous nephrolithotomy or, rarely, anatrophic nephrolithotomy, is the treatment of choice for large or complicated stones (such as calyceal staghorn calculi) or stones that cannot be extracted using less invasive procedures.[43][7]

text: Ureteroscopic surgery[edit]

text: Ureteroscopy has become increasingly popular as flexible and rigid fiberoptic ureteroscopes have become smaller. One ureteroscopic technique involves the placement of a ureteral stent (a small tube extending from the bladder, up the ureter and into the kidney) to provide immediate relief of an obstructed kidney. Stent placement can be useful for saving a kidney at risk for postrenal acute renal failure due to the increased hydrostatic pressure, swelling and infection (pyelonephritis and pyonephrosis) caused by an obstructing stone. Ureteral stents vary in length from 24 to 30 cm (9.4 to 11.8 in) and most have a shape commonly referred to as a "double-J" or "double pigtail", because of the curl at both ends. They are designed to allow urine to flow past an obstruction in the ureter. They may be retained in the ureter for days to weeks as infections resolve and as stones are dissolved or fragmented by ESWL or by some other treatment. The stents dilate the ureters, which can facilitate instrumentation, and they also provide a clear landmark to aid in the visualization of the ureters and any associated stones on radiographic examinations. The presence of indwelling ureteral stents may cause minimal to moderate discomfort, frequency or urgency incontinence, and infection, which in general resolves on removal. Most ureteral stents can be removed cystoscopically during an office visit under topical anesthesia after resolution of urolithiasis.[97]

text: More definitive ureteroscopic techniques for stone extraction (rather than simply bypassing the obstruction) include basket extraction and ultrasound ureterolithotripsy. Laser lithotripsy is another technique, which involves the use of a holmium:yttrium aluminium garnet (Ho:YAG) laser to fragment stones in the bladder, ureters, and kidneys.[98]

text: Ureteroscopic techniques are generally more effective than ESWL for treating stones located in the lower ureter, with success rates of 93–100% using Ho:YAG laser lithotripsy.[69] Although ESWL has been traditionally preferred by many practitioners for treating stones located in the upper ureter, more recent experience suggests ureteroscopic techniques offer distinct advantages in the treatment of upper ureteral stones. Specifically, the overall success rate is higher, fewer repeat interventions and postoperative visits are needed, and treatment costs are lower after ureteroscopic treatment when compared with ESWL. These advantages are especially apparent with stones greater than 10 mm (0.4 in) in diameter. However, because ureteroscopy of the upper ureter is much more challenging than ESWL, many urologists still prefer to use ESWL as a first-line treatment for stones of less than 10 mm, and ureteroscopy for those greater than 10 mm in diameter.[69] Ureteroscopy is the preferred treatment in pregnant and morbidly obese people, as well as those with bleeding disorders.[7]

text: Epidemiology[edit]

text:
Country
Earliest prevalence (years)[99]
Latest prevalence (years)[99]

United States
2.6% (1964–1972)
5.2% (1988–1994)

Italy
1.2% (1983)
1.7% (1993–1994)

Scotland
3.8% (1977)
3.5% (1987)

Spain
0.1% (1977)
10.0% (1991)

Turkey
n/a
14.8% (1989)

text:
Country
New cases per 100,000 (year)[99]
Trend

United States
116 (2000)
decreasing

Germany
720 (2000)
increasing

Japan
114.3 (2005)
increasing

Spain
270 (1984)
decreasing

Sweden
200 (1969)
increasing

text: Kidney stones affect all geographical, cultural, and racial groups. The lifetime risk is about 10 to 15% in the developed world, but can be as high as 20 to 25% in the Middle East. The increased risk of dehydration in hot climates, coupled with a diet 50% lower in calcium and 250% higher in oxalates compared to Western diets, accounts for the higher net risk in the Middle East.[100] In the Middle East, uric acid stones are more common than calcium-containing stones.[22] The number of deaths due to kidney stones is estimated at 19,000 per year being fairly consistent between 1990 and 2010.[101]

text: In North America and Europe, the annual number of new cases per year of kidney stones is roughly 0.5%. In the United States, the frequency in the population of urolithiasis has increased from 3.2% to 5.2% from the mid-1970s to the mid-1990s.[18] In the United States, about 9% of the population has had a kidney stone.[2]

text: The total cost for treating urolithiasis was US$2 billion in 2003.[49] About 65–80% of those with kidney stones are men; most stones in women are due to either metabolic defects (such as cystinuria) or infection.[60][102] (p. 1057) Men most commonly experience their first episode between 30 and 40 years of age, whereas for women, the age at first presentation is somewhat later.[60] The age of onset shows a bimodal distribution in women, with episodes peaking at 35 and 55 years.[49] Recurrence rates are estimated at 50% over a 10-year and 75% over 20-year period,[18] with some people experiencing ten or more episodes over the course of a lifetime.[60]

text: A 2010 review concluded that rates of disease are increasing.[99]

text: History[edit]

text: The existence of kidney stones was first recorded thousands of years ago, and lithotomy for the removal of stones is one of the earliest known surgical procedures.[103] In 1901, a stone discovered in the pelvis of an ancient Egyptian mummy was dated to 4,800 BC. Medical texts from ancient Mesopotamia, India, China, Persia, Greece, and Rome all mentioned calculous disease. Part of the Hippocratic Oath suggests there were practicing surgeons in ancient Greece to whom physicians were to defer for lithotomies. The Roman medical treatise De Medicina by Aulus Cornelius Celsus contained a description of lithotomy,[104] and this work served as the basis for this procedure until the 18th century.[105]

text: Famous people who were kidney stone formers include Napoleon I, Epicurus, Napoleon III, Peter the Great, Louis XIV, George IV, Oliver Cromwell, Lyndon B. Johnson, Benjamin Franklin, Michel de Montaigne, Francis Bacon, Isaac Newton, Samuel Pepys, William Harvey, Herman Boerhaave, and Antonio Scarpa.[106]

text: New techniques in lithotomy began to emerge starting in 1520, but the operation remained risky. After Henry Jacob Bigelow popularized the technique of litholapaxy in 1878,[107] the mortality rate dropped from about 24% to 2.4%. However, other treatment techniques continued to produce a high level of mortality, especially among inexperienced urologists.[105][106] In 1980, Dornier MedTech introduced extracorporeal shock wave lithotripsy for breaking up stones via acoustical pulses, and this technique has since come into widespread use.[90]

text: Etymology[edit]

text: Renal calculus is from the Latin rēnēs meaning "kidneys," and calculus meaning "pebble". Lithiasis (stone formation) in the kidneys is called nephrolithiasis (/ˌnɛfroʊlɪˈθaɪəsɪs/), from nephro- meaning kidney + -lith meaning stone and -iasis meaning disorder.

text: Research directions[edit]

text: Crystallization of calcium oxalate appears to be inhibited by certain substances in the urine that retard the formation, growth, aggregation, and adherence of crystals to renal cells. By purifying urine using salt precipitation, isoelectric focusing, and size-exclusion chromatography, some researchers have found that calgranulin, a protein formed in the kidney, is a potent inhibitor of the in vivo formation of calcium oxalate crystals. Considering its extremely high levels of inhibition of growth and aggregation of calcium oxalate crystals, calgranulin might be an important intrinsic factor in the prevention of nephrolithiasis.[108]

text: Children[edit]

text: Although kidney stones do not often occur in children, the incidence is increasing.[109] These stones are in the kidney in two thirds of reported cases, and in the ureter in the remaining cases. Older children are at greater risk independent of sex.[110]

text: As with adults, most pediatric kidney stones are predominantly composed of calcium oxalate; struvite and calcium phosphate stones are less common. Calcium oxalate stones in children are associated with high amounts of calcium, oxalate, and magnesium in acidic urine.[111]

text: Other animals[edit]

text: Among ruminants, uroliths more commonly cause problems in males than in females; the sigmoid flexure of the ruminant male urinary tract is more likely to obstruct passage. Early-castrated males are at greater risk, because of lesser urethral diameter.[112]

text: Low Ca:P intake ratio is conducive to phosphatic (e.g. struvite) urolith formation.[112] Incidence among wether lambs can be minimized by maintaining a dietary Ca:P intake ratio of 2:1.[112][113]

text: Alkaline pH favors formation of carbonate and phosphate calculi. For domestic ruminants, dietary cation: anion balance is sometimes adjusted to assure a slightly acidic urine pH, for prevention of calculus formation[112]

text: Differing generalizations regarding effects of pH on formation of silicate uroliths may be found.[112][114] In this connection, it may be noted that under some circumstances, calcium carbonate accompanies silica in siliceous uroliths.[115]

text: Pelleted feeds may be conducive to formation of phosphate uroliths, because of increased urinary phosphorus excretion. This is attributable to lower saliva production where pelleted rations containing finely ground constituents are fed. With less blood phosphate partitioned into saliva, more tends to be excreted in urine.[116] (Most saliva phosphate is fecally excreted.[117])

text: Oxalate uroliths can occur in ruminants, although such problems from oxalate ingestion may be relatively uncommon. Ruminant urolithiasis associated with oxalate ingestion has been reported.[118] However, no renal tubular damage or visible deposition of calcium oxalate crystals in kidneys was found in yearling wether sheep fed diets containing soluble oxalate at 6.5 percent of dietary dry matter for about 100 days.[119]

text: Conditions limiting water intake can result in stone formation.[120]

text: Various surgical interventions, e.g. amputation of the urethral process at its base near the glans penis in male ruminants, perineal urethrostomy, or tube cystostomy may be considered for relief of obstructive urolithiasis.[120]


document_title: Honda Civic (sixth generation)

question_text: what engine is in a 2000 honda civic lx

question_tokens: what engine is in a 2000 honda civic lx

root

text: Honda Civic (sixth generation)

text: Trim packages and equipment (North America)[edit]

text: Coupe: Trims available in the coupe body style were the EJ6 (US DX, Canadian DX and DX-V), EJ7 (US HX), EJ8 (US EX, Canadian Si) and EM1 (only 1999 and 2000; US Si, Canadian SiR).

tag: p

text: Hatchback: Trims available in the hatchback body style were the EJ6 (US CX and DX, Canadian CX/CX-G/DX/SE), EJ9[3] (1.4L SOHC model), EK1 (1.5L SOHC VTEC-E model), EK2 (1.3L model), EK3 (1.5L SOHC VTEC-E model), EK4 (Japanese SiR, European SiR and/or VTi), EK6 (Japanese 1.6L SOHC model), EK7 (Japanese 1.6L SOHC model) and the EK9 (Japanese Type R).

text: Sedan: Trims available in the sedan body style were the EJ6 (US DX/LX/VP, Canadian EX/LX), EJ8 (US EX), EJ9 (1.4L SOHC model), EK1 (1.5L SOHC VTEC-E model), EK2 (1.3L model), EK3 (1.5L SOHC model), EK4 (Japanese SiR, European SiR and/or VTi), EK5 (Japanese 1.6L SOHC 4WD model), EK8 (Japanese 1.6L SOHC model) and EN1 (US GX).

text: CX: The base trim package, available as a hatchback only. Appointed very sparingly (no standard radio or power steering), it came equipped with 13-inch wheels, 4-wheel double wishbone suspension, dual airbags, split/folding rear seat, and seating for five people. In 1997, the CX added 14-inch wheels as standard equipment. In 2000, the CX added tilt steering as standard equipment.[4]

text: DX: Available as a hatchback, coupé, or sedan. It included all standard equipment from CX plus tilt steering and AM/FM radio. Power steering was standard on all sedans, and on the coupes when ordered with automatic transmission. For 1997, the DX added 14-inch wheels as standard equipment.[5]

text: LX: Available as a four-door only. It included all standard equipment from DX plus 14-inch wheels, power windows, power locks, power mirrors, power steering, front stabilizer bar, front center armrest with storage compartment, cargo area light, cruise control, and tachometer. For 1997, the LX added air conditioning as standard equipment.

text: EX: Available as a coupé or sedan. It included all standard equipment from LX plus a higher-horsepower SOHC VTEC engine, power sunroof, air conditioning, remote entry system, plus body-colored side mirrors and side molding. ABS was standard on sedan only and optional on the coupe if equipped with an automatic transmission. For 1999, the EX added a CD player as standard equipment.[6]

text: HX: Available as coupé only, this trim package was specially tooled for higher fuel efficiency. It was the only trim available with a CVT (continuously variable transmission), though customers could also choose a 5-speed manual transmission. It included all standard equipment from DX, plus a slightly higher horsepower VTEC-E engine, alloy wheels, power windows, power locks, power steering, and tachometer.[7][8]

text: GX: Introduced in 1997 and available as a sedan for fleet-purchase only, this trim package was specially designed to run on natural gas. See Honda Civic GX for detail and references.

text: VP: Introduced in 1998 and available as a sedan only, this trim was designed as a “Value Package” above the DX. It included all standard equipment from DX plus automatic transmission, power locks, CD player, air conditioning, keyless entry, and special paint.

text: Most trim packages had a standard AM/FM radio in the center dashboard with a backlit LCD display (except CX had no radio), but a slave cassette player or CD player was available through dealer-installed options and was installed in the forward portion of the console and was hidden from view when the cupholder was open. EX trims had the slave cassette player standard. Dealers also offered AM/FM cassette and AM/FM CD decks to replace the stock radio. All vehicles were equipped with four speakers (except for the EX which included two extra tweeters located on the front doors), radio wiring (prep), and an antenna regardless of whether or not they had a radio.

text: Si[edit]

text: After a brief hiatus, the Civic Si reappeared in 1999, available as a coupé only. With the adoption of the VTi badge in Europe and the SiR and Type R badges in Japan for the sports variants of Civics, the Si became primarily a US-specific badge, a branding trend that would continue in subsequent Civic generations. Accelerating from 0-60 in 7.1 seconds, the 1999 Civic Si trim package featured a 1.6-litre B16A2 engine that made 160 hp (119 kW) at 8,000 rpm and 111 ft-lbs of torque at 7,000 rpm. While similar to the powerplant in the Del Sol VTEC, the Civic Si saw some notable differences, which include a larger throttle body, improved intake manifold, strengthened connecting rods, low-friction/high-silicon pistons, a fully counterweighted crankshaft, and an exhaust system with larger-diameter piping. Due to its good fuel economy (27/31 city/hwy MPG), and a more popular coupe form, the trim package garnered a dedicated following in spite of its short production cycle.[9]

text: Changes from the standard Civic included stiffer, progressive-rate springs, stiffer front and rear anti-roll bars, and a tower brace, which contributed to a flatter-cornering ride. It was available with a five-speed manual transmission only, standard equipment also including disc brakes all around. Aesthetic exterior changes from the LX/EX trims were minimal, with the Si trim package featuring a lower-profile and wider 15-inch wheel/tire package, a subtle chin-spoiler, painted side sills, and Si badging. There are power locks, power windows, a CD player, cruise control, air conditioning, power sunroof, and tilt steering.[10] For the interior, the sixth generation Si also had tilt adjustment for the bottom cushion, a leather-wrapped steering wheel, remote keyless entry, and red-faced instrumentation with Si branding.

text: Paint colors[edit]

text: Colors available in the US were as follows:

text: 1996: Cyclone Blue Metallic (sedan), Cypress Green Pearl (coupe and sedan), Midori Green Pearl (hatch), Granada Black Pearl (hatch), Frost White (coupe and sedan), New Vogue Silver Metallic (hatch), Milano Red (coupe), Island Coral Pearl (coupe and sedan) and Roma Red (hatch).

text: 1997: Cyclone Blue Metallic (DX and LX sedan), Cypress Green Pearl (DX and EX coupe and sedan), Granada Black Pearl (LX and EX sedan, coupe and DX hatch) Frost White (DX and EX coupe and sedan), New Vogue Silver Metallic, Dark Amethyst Pearl (hatch), Milano Red (coupe), Inza Red Pearl (LX sedan) and Roma Red (hatch).

text: 1998: Cyclone Blue Metallic (sedan), Cypress Green Pearl (coupe and sedan), Taffeta White (coupe and sedan), New Vogue Silver Metallic, Flamenco Black Pearl, Dark Amethyst Pearl (hatch), Milano Red (coupe) and Roma Red (hatch).

text: 1999: Electron Blue Pearl (Si coupe), Iced Teal Pearl (sedan), Clover Green Pearl (coupe and sedan), Taffeta White (coupe and sedan), New Vogue Silver Metallic (hatch), Flamenco Black Pearl(hatch and coupe), Dark Amethyst Pearl (hatch), Milano Red (coupe) and Roma Red (hatch).

text: 2000: Electron Blue Pearl (Si coupe), Iced Teal Pearl (sedan), Clover Green Pearl (coupe and sedan), Taffeta White (coupe, hatch and sedan), New Vogue Silver Metallic, Flamenco Black Pearl, Milano Red (coupe), Roma Red (hatch), Vintage Plum Pearl (sedan) and Titanium Metallic (sedan).

text: Facelift[edit]

text: In 1998 for the 1999 model year, the Civic had some updates for both the interior and exterior. These redesigns could vary according to the country of origin for the car. For example, in some European countries there was no redesign to the climate control area or to the rear of the sedan models.

text: The updated cars received a facelift which included a new grille, new headlights, and a new front bumper, fenders and hood and redesigned taillights. The coupe and sedans models also received a slight redesign to the bottom of the rear bumper. On the pre-facelift sedans, the stop lights were on top of the reverse and turn lights; for the facelift version, the reverse and turn lights were on top of the stop lights. For the coupe and hatchback the layouts remained as before; however, the rear turn signal lenses became clear/white instead of amber to match the reverse lights (the turn light bulbs themselves now were amber).

text: Inside, the center console had a makeover. The sliding air system controls were replaced by rotary ones, which freed up space to accommodate an enlarged radio, which included the cassette player or Compact Disc player. Previously, the large size of the ventilation controls reduced the size of the radio, necessitating a slave cassette player or Compact Disc player at the bottom of the console.

text: Engines[edit]

text: United States Domestic Market (USDM)[edit]

text: The CX, DX, VP, and LX trim packages used the SOHC 16v D16Y7 engine. It produced 106 hp (79 kW) at 6,200 RPM, 103 lb⋅ft (140 N⋅m) of torque at 4,600 RPM, with a compression ratio of 9.6:1. Fuel injection was multi-point.[11]

text: The HX trim had the SOHC 16v D16Y5 lean-burn engine with VTEC-E. It produced 115 hp (86 kW) at 6,300 RPM, 104 lb⋅ft (141 N⋅m) of torque at 5,400 RPM, with a compression ratio of 9.4:1. Fuel injection was multi-point.[12][13]

text: The EX trim (Canadian Si trim) had the SOHC 16v D16Y8 engine with VTEC. It produced 127 hp (95 kW) at 6,600 RPM, 107 lb⋅ft (145 N⋅m) of torque at 5,500 RPM, with a compression ratio of 9.6:1. Fuel injection was multi-point.[14][15]

text: The Si trim (Canadian SiR trim) used the DOHC 16v B16A2 engine with VTEC. It produced 160 hp (119 kW) at 7,600 RPM, 111 lb⋅ft (150 N⋅m) of torque at 7,000 RPM, with a compression ratio of 10.2:1. Fuel injection was multi-point.[16][17]

text: The GX trim had the D16B5 engine designed to run on compressed natural gas. It had a compression ratio of 12.5:1.

text: Other Markets[edit]

text: In Japan, the least expensive trim package was the EL (and also a short-lived special EL-II trim), powered by a 1,343 cc D13B engine with 91 PS (67 kW) at 6,300 RPM. As for most of the sixth generation Civics, it was a SOHC 16v design.[18]

text: In the UK, Europe, South Africa and the Philippines, there were a number of sedans and Aerodecks between 1996 and 2000 produced with the B16A1, B16A2, B18B and even B18C motors.

text: In Japan, the Civic Ferio Si used the second generation B16A engine while the other trims used D15B, D16A or D13B engines.

text: In the Middle East market, the Civic came with a 105 hp (78 kW) D15Z4 engine for LXi and EXi trims.

text: in Australia, most trims came with the D16Y4 engine; the VTI sedan trim had the D16Y5, the VTI coupe the D16Y8 and the VTI-R Hatchback and Coupe had the B16A engine.

text: Transmissions[edit]

text: Most trim packages (DX, LX, EX, Si) were available with a standard 5-speed manual transmission with a hydraulic clutch, or an optional 4-speed automatic transmission. Various gear sets and final drives were used between trims and model years, resulting here are 4 different manual transmission combinations:

text: CX/DX hatchback, HX Coupe: Tall gearing with a 3.722 final drive

text: DX/LX coupe/sedan: Same transmission gearing as CX/DX hatchback and HX coupe but with a 4.058 final drive

text: EX hatchback/coupe/sedan: Shorter gearing than all the variants save for the Si with a 4.25 final drive

text: Si Coupe: Shortest gearing of all the 6th generation Honda Civics, 4.266 final drive, available in manual transmission only.

text: The HX trim was offered with the 5-speed manual or a CVT Continuously Variable Transmission which offered three driving ranges, D (standard transmission ratios for normal driving), S (secondary ratios for spirited driving with higher engine speeds), and L (lowest ratios to provide maximum engine braking and peak power). The conventional 4-speed automatic was not available on the HX trim. A JDM variant called the civic RTi was also produced and it featured either manual and automatic transmissions coupled to a Honda real-time all-wheel-drive layout.

text: For the DX/LX/EX Civics equipped with automatic transmissions, the only difference between the DX/LX vs. the EX is that the EX has slightly shorter gearing in 1st-3rd gear but otherwise shares same 0.638 4th gear ratio and 4.357 final drive ratio.[19]

text: Weights[edit]

text:
CX Hatch
DX Hatch
DX Coupe
HX Coupe
EX Coupe

Auto
Manual
Auto
Manual
Auto
Manual
Auto
Manual
Auto
Manual

1996
2297lbs
2222lbs
2317lbs
2242lbs
2339lbs
2262lbs
no data
2313lbs
2513lbs
2483lbs

1997
2338lbs
2304lbs
2253lbs
2319lbs
2271
2337
2399
2324
2460
2496

1998
2357
2295
2392
2339
2385
2342
2429
2361
2551
2504

1999
2423
2359
2434
2388
2405
2335
2445
2370
2560
2513

2000
2423
2359
2434
2388
2405
2359
2445
2370
2560
2513

tag: table

text:
DX Sedan
LX Sedan
EX Sedan
Si Coupe
Value Package Sedan

Auto
Manual
Auto
Manual
Auto
Manual
Manual
Auto

1996
2370
2319
2430
2387
2568
2518

1997
2319
2370
2387
2438
2568
2518

1998
2385
2339
2458
2412
2558
2511

1999
2388
2339
2456
2410
2562
2513
2612

2000
2388
2339
2456
2410
2562
2513
2612
2418

text: All weights listed in this table are in lbs.

text: Worldwide[edit]

text: The JDM Civic Sedan (known as the Civic Ferio Si) featured a 170 PS (125 kW) DOHC VTEC B16A engine, rear headrests, an Integra Type-R style shift knob, unique seating fabric and the same 15" alloy wheels that also appeared on the 1999-2000 US market Civic Si Coupé. Other JDM Ferio models included a model with the RealTime 4wheel drive and a rear wiper in the back window of the sedan, which was not seen in other markets.

text: Canada[edit]

text: Canadian trim packages were mostly similar to the United States, though with different designations. Canadian Civic sedans came in LX, EX and SE[20], which roughly correspond to the American DX and LX; there was no Honda-branded Canadian equivalent to the American EX sedan - the Canadian-market only Acura EL filled this spot. Canadian Civic coupes came in DX, Si, and SiR, the equivalent of the DX, EX, and Si in the United States. Only the EX sedan, Si coupe and SiR coupe had power locks and power windows, the Si and SiR coupes were the only Canadian Civic trims with a power moonroof. All sedans and coupes had a group option package available that added air conditioning and anti-lock brakes. The hatchbacks, available only in CX and DX trims, were sold as economy cars; as in the US, they had none of the amenities of other trims in the Civic lineup, not even as options. All sedans, coupes, and the hatchback DX had two front airbags; while the CX hatchback had the driver's side airbag only.

text: Canadian SiR and Si trims included ABS and heated mirrors, which better suited the Canadian climate of long winters, which were not included on the American Si trims. The Canadian SiR also was available in New Vogue Silver Metallic, which was not available for the American Si trim.

text: The Civic DX Special Edition (SE) hatchback was a special trim package released for the year 2000 only. The car was similar to the Canadian DX hatchback, but came with additional standard parts including mesh 14-inch wheels (similar in design to the more common third generation Integra mesh wheels), body-coloured side mirrors and side mouldings, a mid-wing and a Special badge on the rear of the hatch.

text: Australia[edit]

text: The Civic was introduced in 1996 initially with two 1.6-litre engines. The VTEC motor was found in the VTI, while the non-VTEC was standard across the range in the GLi and CXi models, with an optional 4-speed automatic in both the CXi and GLi or CVT in the VTi. The high output B16A2 engine was introduced later and available in the coupe and hatch, known as the VTi-R.

text: Asian SiRII[edit]

text: From 1996 to 2000, Honda produced Civic SiRII which came with a B16A engine, but it was only available in Asian market. This engine produced (160 hp (120 kW) at 7800 rpm with a displacement of 1595 cc.

text: Philippines[edit]

text: The sixth generation Civic was initially launched in 1996 with two trim packages: the LXi with a non-VTEC 1.5L SOHC D15Z4 engine, and the VTi with a 1.6L SOHC D16Y5 VTEC-E engine. Both came with regular front disk brakes and rear drum brakes. Transmission choices were a 5-speed manual or a 4-speed automatic, available in both trims. During the 1999 facelift, an SiR version was introduced. It had a B16a2 1.6L DOHC VTEC engine and was initially available in nighthawk black, tafetta white and passion orange variants. Formula red and sunburst yellow color variants followed aftwerwards with silver accents on the center console. Other notable differences were a mesh grill (similar with the EK9), three-spoked red stitched steering wheel, 15 inch Enkei rims (similar to the USDM Si & JDM Vi-RS), leather stitched shiftknob (similar with the JDM SiR), front upper strut bar, Kenwood CD player, bigger front and rear disc brakes, unique interior fabric colors and an optional front chin and spoiler. The only transmission choice was a 5-speed manual.

text: Japan[edit]

text: There was also the Civic Type R, sold only in the Japanese domestic market, and only available as a hatchback and 5-speed manual with LSD as the only available transmission. This model was equipped with the B16B (185 PS (136 kW) at 8,200 rpm) (AKA PCT), which is essentially a destroked, but powerful, version of the B18C engine from the Integra Type R. The chassis was given the designation EK9. The EK9 was very special as it was essentially based on the JDM EK4 SiR but taken out of the production line and given additional reinforcement to the chassis and body shell. Weight was also meticulously removed to create a light weight racecar feel. Other additions over the EK4 were bigger brakes, quicker steering ratio, specially tuned suspension, Recaro seats, Momo steering wheel, titanium shift knob, front lip spoiler, rear wing, smoked headlights and a hand built engine that embodied the racing spirit of Honda. This engine featured a hand polished cylinder head, lighter flywheel, redesigned cam profiles, high compression pistons and balanced crankshaft. The gearbox was fitted with a helical type limited slip differential.

text: Japanese Civic Ferio Vi-RS[edit]

text: Considered as the "extra sporty" version of the Honda Civic Ferio, the Honda Civic Ferio Vi-RS 1.5-litre, four-Door sedan was sold in the Japanese domestic market only. It has the 1.5-liter D15B three-stage VTEC, a five-speed manual or automatic transmission. The Civic Vi-RS had a three-way switch installed on the right side of steering wheel marked D, S1, or S2. These settings affected which cam was used, the ECU's air-fuel mapping, and gearbox behaviour (on automatics). S2 was the sportiest mode.

text: South Africa[edit]

text: In South Africa, the 3-door hatchback was sold under the "Civic" (pre-facelift) and "Civic Coupe" (facelift) nameplates. The 4-door sedan was marketed under the "Ballade" nameplate. In South Africa the 2-door Civic coupe (Si) was not available. Chassis codes also differed to other markets: SO3 (civic hatchback) and SO4 (Civic sedan/Ballade). The Type R was never released into the South African market. No SOHC VTEC motors were available either. South-African model options were Civic 150i (D15Z4) Civic 160i (D16Z4) Civic 160i VTEC (B16A6) Civic 180i (B18B). As Honda in SA were distributed by Mercedes-Benz SA at the time, many models used some Mercedes trim, such as their leather trim and alarm system on the Ballade and Civic Vtec models. An AMG version Ballade was also released featuring a performance exhaust system and AMG body pieces.

text: Europe - MA/MB/MC five-door Civic / two-door coupe Civic / Civic Aerodeck[edit]

text: Based on the Domani, this version was marketed in Europe as the MA/MB/MC Civic and Civic Aerodeck. It was built in five-door, two-door coupe and Aerodeck (Estate) models in various trim levels and engine sizes. The Aerodeck name was previously used on the Honda Accord Aerodeck, which was a two-door station wagon, popularly known in Europe as a shooting-brake. 1.4 L (D14A2/A5/A7), 1.5 L (D15Z8/Z6), 1.6 L (D16Y2/Y3, D16W2/W3, D16B2 etc.) and 1.8 litre (B18C4) petrol engines were available. These came with five-door body and fifty-five litre fuel tank, ABS, driver and passenger air bags, power steering and electric door mirrors, amongst other things. The later models came with air conditioning as standard. The 1.8 VTi model was the flagship model (explained in detail below) with the biggest petrol engine to be given to MA MB MC Civics. The Domani-based Civics were also available with the Rover L-Series diesel engine which was a 2-litre, eight-valve, direct-injection turbocharged unit (20T2N, 20T2R); an essential addition in the European market. Later diesel engines came with intercoolers. The chassis codes designated to this model and generation of Civics were chassis codes MA8, MA9, MB1, MB2, MB3, MB4, MB6, MB7, and MB8 for the liftback, while the Aerodeck chassis codes are MB9, MC1, MC2, MC3, and MC9. Compared to the original Domani, the Liftback and Aerodeck featured a new interior, similar to that of the more upmarket Rover 400. Honda had a long-serving partnership with the Rover group, who at the time didn't have enough funds for the tooling to produce an all new car, which allowed Rover to produce its own C-Segment competitor based around the design of the Domani shell and using a lot of its underpinnings to produce the Rover 400/45 and later MG ZS. Rover made mostly cosmetic changes (which included front fenders/wings, bonnet, headlights, bumpers, rear lights and tailgate were different on the Rover as well as more upmarket cabin materials and greater use of wood and decals) to have a brand new design in the showrooms, which was very cost effective but divided opinion amongst brand enthusiasts.

text: 1.8 /1.6 VTi[edit]

text: As with all Honda models of the age, VTi denoted the inclusion of Honda's VTEC technology. There was a rear VTi badge, and decals of "DOHC VTEC" on the rear doors, as well as front/rear bumper lips and side skirts (in VTI-S models). 1996 saw the introduction of the VTi model and then a limited edition VTI-S. The VTI came in two different flavours - the DOHC 1.6 VTi hatch and sedan (B16A2 engine) and the DOHC 1.8 VTi five-door (with the larger B18C4). The 1.6 VTi car was actually slightly faster in acceleration than the 1.8 due to the different gear ratios. The 1.6 was also a lighter engine in a lighter car, helping to reduce the 0-60 mph acceleration time by about 0.3 seconds. Front/rear disc brakes were standard on all VTi/VTi-S versions. The five-door versions (VTi/VTi-S) included a Torsen limited slip differential which meant they were quicker out of corners than the 1.6 (three-door) due to being able to accelerate out of corners more effectively.

text: The 1.8 VTi Civic came with a host of standard equipment, some of which was not available on the three-door (1.6) equivalents. Standard 1.8 spec includes:

text: Exterior: Front lip/spoiler, Rear boot spoiler with integral brake light, Headlight washers, electric sunroof, colour-coded mirrors, colour-coded door handles, colour-coded front rear bumpers, front fog lights, lightweight Speedline 5 spoke alloy wheels.

text: Interior: Unique half leather sports style seats (full leather optional), front/rear electric windows, Electrically operated/heated door mirrors, air conditioning, dashboard instrument light dimmer, front and rear head rests. Leather steering wheel with red stitching.

text: United Kingdom Limited Editions[edit]

text: The MB6 VTi-S five-door was made in a limited run of 500 of each body type, and only sold in the Honda colour 'Pirates Black', with body coloured bumpers. The VTI-S improved on the appearance of the standard Civic VTi five-door with a more pronounced front lip and also a rear lip on the bumpers, and different side skirts. The VTi-S specification also included chrome/aluminium gear-knob(silver/black plastic on later VTiS models), VTI-S floor-mats and tailgate badging. It also came fitted with lightweight 15" Speedline Chrono alloy wheels, with a split spoke design. The later VTi-S models came fitted with the lightweight Speedline "fan" alloy wheels. Other than this, the it is identical to the regular VTi. The instrument dials on later VTi-S models changed slightly, now with italic numbering.

text: The three-door EK4 VTi-S was produced in 1998 only and 200 were produced in this time, all on 'R' registration plates. Like the MB6 VTi-S, the EK4 VTi-S was based on the standard VTi hatch, with differences being the Starlight Black paint, front and rear bumper lips/skirts, rear mid-spoiler, 15" speedline chrono alloy wheels, the dashboard cluster used white numbering on the speedometer, fuel gauge etc., rather than orange/red as in the regular VTi, however it still retained the red needles. The boot badges spelling out 'Honda' 'Civic' '1.6VTi' and 'VTEC' were all replaced with a single VTi-S badge, and there was an alloy gear knob and VTi-S floor mats. Mechanically and in performance terms it is identical to a regular EK4 VTi. Due to a problem with the registration process many genuine VTi-S' were not on the log books as a VTi-S, but a VTi, and regular VTi Civic's were logged as VTi-S, this problem also affected the special edition EK4 Civic Jordan, of which some were also logged as a VTi-S.

text: To commemorate the Honda (Mugen) Jordan F1 team. A 500 car special limited edition Honda Civic VTi (EK4 3-door model) was created with their own signed Eddie Jordan Plaque with the specific number stamped on it in the centre console. This car was sold in 1999–2000. It had the same basic spec as the EK4 VTi, but the extras included: Sunlight Yellow paint work, yellow-and-black leather interior, Jordan decals on the sides and rear of the car as well as stitched into the seats and floor carpets.

text: Rover 200, 400, 25, 45 and MG ZR, ZS[edit]

text: Rover developed these vehicles from the Honda Domani (sold as a Civic in Europe) using their own engines. UK produced with styling and interior specifications were aimed primarily at the UK market.[citation needed]