Kidney stone

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

Nephrolithiasis is a common condition encountered in emergency rooms and also as an outpatient in the primary care setting. Its incidence and prevalence is increasing both in women and men, with women slightly incraing recently due to obesity and lifestyle changes. Nephrolithiasis may be classified into 4 subtypes/groups: calcium stones, struvite stones, uric acid stones and cystine stones. The common causes of nephrolithiasis include hypercalcemia, hyperparathyroidism, hypercalciuria, infection with urea splitting microorganisms like Proteus and Pseudomonas, gout, dehydration, inflammatory bowel disease. Less common causes of nephrolithiasis include drugs such as loop diuretics, Acetazolamide, ciprofloxacin, indinavir, guaifenesin triamterene and magnesium trisilicate. It is understood that nephrolithiasis is the result of combination of different mechanism responsible for different types of stones. Calcium stones are the most common type of kidney stones. Approximately 80% of all calcium stones are calcium oxalate stones. The pathophysiology of calcium stones is complex and involves dietary concerns, hypercalciuria, hypocitaturia, hyperoxaluria, hyperuricosuria and biomineralization. The underlying pathophysiological mechanisms responsible for uric acid stones are low urine volume, hyperuricosuria and high acidic urine. Cystinuria is a rare hereditary gene disorder which causes impaired renal reabsorption of cationic amino acids and cystine. It is caused by mutations in either of the two subunits (rBAT(SLC3A2) and b0,+AT(SLC7A9)) forming cystine stones. Struvite stones are usually seen in patients which have infection with urease +ve organisms. Urine pH is usually alkaline (>7.2). Nephrolithiasis can be passed on to following generations due to rare causes of hypercalciuria such as hereditary distal renal tubular acidosis, dent disease, Bartter syndrome types III and IV, autosomal dominant hypocalcemic hypercalciuria and familial hypomagnesemia. Nephrolithiasis associated with Hyperparathyroidism, Gout, Hypocitaturia, Sarcoidosis, chronic urinary tract infections and Obesity.On gross pathology, the characteristic findings of nephrolithiasis include location = 80% unilateral, usually in calyces, pelvis or bladder. The size=variable, 2-3 mm usually. All stones contain an organic matrix of mucoprotein. The shape of struvite stone is staghorn shaped. On microscopic histopathological analysis, the characteristic findings of nephrolithiasis include different shapes of stones/crystals are such as cystine= hexagonal, struvite= coffin lid shape, calcium oxalate= pyramid shape to dumbbell shape and uric acid= rectangular/rhomboidal. Oxalate crystals are highlighted by polarized light. Also, foreign body giant cells and macrophages are seen with the stones.It has increased from every 1 in 20 to 1 in 11 person in United States has kidney stones. If left untreated, <30% of patients with nephrolithiasis may progress to develop renal colicky pain due to increase in rate of growth.Most of the stones pass spontaneously. about 10-20% of symptom-causing stones fail to pass. Lower poles stones were significantly less likely to cause symptoms or pass spontaneously. They can progress to hydronephrosis especially when combined or superimposed by urinary tract infection. Common complications of nephrolithiasis include hydronephrosis, chronic renal failure, hypertension, cardiovascular disease, and increased risk of fracture. Prognosis is generally excellent. Approximately 80-85% resolve spontaneously. Recurrence rates for calcium stones after the initial event is 40–50% at the end of 5 years and 50–60% at the end of 10 years.The patients with nephrolithiasis may have a positive history of flank pain. Common symptoms of nephrolithiasis include flank pain progressing downward and anteriorly into the groin as the stone moves, hematuria, nausea and vomiting urinary frequency and urgency. Less common symptoms include burning micturition. Patients with nephrolithiasis usually appear in pain and trying to achieve a comfortable position. Common physical examination findings of nephrolithiasis include costovertebral angle tenderness, may accompany fever with increased heart rate and respiratory rate. They can have hypoactive bowel sounds due to ileus caused by severe pain. They can have hematuria in microscopic exmaination. Laboratory findings consistent with the diagnosis of nephrolithiasis include hypercalcemia, hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricemia and hyperuricosuria. Abdominal ultrasound may be helpful in the diagnosis of nephrolithiasis Findings on an ultrasound suggestive of/diagnostic of nephrolithiasis include: echogenic or hyperechogenic foci, acoustic shadowing, twinkle artefact on colour Doppler, colour comet-tail artefact , and increased resistive index which signifies acute obstruction. CT scan is the gold standard test for the diagnosis of nephrolithiasis. Abdominal and pelvic CT scan is helpful in the diagnosis of nephrolithiasis. Findings on CT scan diagnostic of nephrolithiasis include radiopacity showing the location, density and composition of stones calcium oxalate +/- calcium phosphate: 400-600 HU, struvite (triple phosphate): usually opaque but variable, pure calcium phosphate 400-600 HU, uric acid: 100-200 HU and cystine: opaque. The treatment of nephrolithiasis involves different measures e.g non pharmacological measures consisting of increased fluid intake, straining an dietary restrictions. Pharmacological measures include pain relief using NSAIDs and opioids., helping passage of stone spontaneously with drugs like tamsulosin and nifedipine. The treatment of underlying cause and being specific to type of stones is very important.It involves treating primary hyperparathyroidism and Renal tubular acidosis. For those having high urinary calcium, Hydrochlorothiazide or Chlorthalidone are used. For recurrent stones and high urine uric acid, Allopurinol is used. For recurrent stones and hypocitraturia, Potassium citrate is sued to alkalinize the urine. For uric acid stones, alkalinizing urine with potassium citrate/potassium bicarbonate is done and if needed Allopurinol is also used. For struvite stones, medical therapy is not of much help, although urease inhibitors such as acetohydroxamic acid can be given in urease +ve etiology. For cysteine stones, again alkalinizing urine helps along with Tiopronin. The Urological consult is needed when stone >10 mm in diameter, uncontrolled pain, Anuria, or there is Acute kidney injury. The mainstay of treatment for nephrolithiasis is medical therapy. Surgery is usually reserved for patients with either persistent and severe pain, renal failure, kidney infection and when stone fails to pass or move after 30 days. The surgeries which are being used currently include extracorporeal shockwave lithotripsy, ureteroscopy and percutaneous nephrolithotomy. Effective measures for the primary prevention of nephrolithiais include diet control and high fluid intake. Effective measures for the secondary prevention of nephrolithiasis include measures to prevent recurrence of the stones and prevent complications. It includes measures like correcting hydration and dietary habits. Drugs like allopurinol to prevent hyperuricemia, potassium citrate to alkalinize the urine and avoidance or judicious use of diuretics.

Urinary stones was first discovered by  E. Smith, an English archaeologist, in 1901 when he found bladder stone in Egyptian mummy aged 4500-7000 year. In the 4th century B.C., when Hipprocratic Oath was made,the line that refers to stones was mentioned:  “I will not use the knife, not even on sufferers from stone, but will withdraw in favor of such men as are engaged in this work….I will not cut for the stone, but will leave this to be done by practitioners of this work.”In the 8th century B.C, treatment strategy for stone removal was developed by an Indian surgeon, Sushruta as written in Sushruta Samhita. In 1976, the first percutaneous stone surgery was performed by Fernstrom and Johansson. The famous cases of nephrolithiasis includes: in 1549, Michelangelo was diagnosed and treated for uric acid stones;in 1724, Sir Isaac Newton noted that he passed two small pea-sized stones and in 1961, Roger Moore, aka James Bond, experienced three kidney stone episodes and treated with surgery.

Nephrolithiasis may be classified into 4 subtypes/groups: calcium stones, struvite stones, uric acid stones and cystine stones

It is understood that nephrolithiasis is the result of combination of different mechanism responsible for different types of stones. Calcium stones are the most common type of kidney stones. Approximately 80% of all calcium stones are calcium oxalate stones. The pathophysiology of calcium stones is complex and involves dietary concerns, hypercalciuria, hypocitaturia, hyperoxaluria, hyperuricosuria and biomineralization. The underlying pathophysiological mechanisms responsible for uric acid stones are low urine volume, hyperuricosuria and high acidic urine. Cystinuria is a rare hereditary gene disorder which causes impaired renal reabsorption of cationic amino acids and cystine. It is caused by mutations in either of the two subunits (rBAT(SLC3A2) and b0,+AT(SLC7A9)) forming cystine stones. Struvite stones are usually seen in patients which have infection with urease +ve organisms. Urine pH is usually alkaline (>7.2). Nephrolithiasis can be passed on to following generations due to rare causes of hypercalciuria such as hereditary distal renal tubular acidosis, dent disease, Bartter syndrome types III and IV, autosomal dominant hypocalcemic hypercalciuria and familial hypomagnesemia. Nephrolithiasis associated with Hyperparathyroidism, Gout, Hypocitaturia, Sarcoidosis, chronic urinary tract infections and Obesity.On gross pathology, the characteristic findings of nephrolithiasis include location = 80% unilateral, usually in calyces, pelvis or bladder. The size=variable, 2-3 mm usually. All stones contain an organic matrix of mucoprotein. The shape of struvite stone is staghorn shaped. On microscopic histopathological analysis, the characteristic findings of nephrolithiasis include different shapes of stones/crystals are such as cystine= hexagonal, struvite= coffin lid shape, calcium oxalate= pyramid shape to dumbbell shape and uric acid= rectangular/rhomboidal. Oxalate crystals are highlighted by polarized light. Also, foreign body giant cells and macrophages are seen with the stones.

The common causes of nephrolithiasis include hypercalcemia, hyperparathyroidism, hypercalciuria, infection with urea splitting microorganisms like Proteus and Pseudomonas, gout, dehydration, inflammatory bowel disease. Less common causes of nephrolithiasis include drugs such as loop diuretics, Acetazolamide, ciprofloxacin, indinavir, guaifenesin triamterene and magnesium trisilicate.

Nephrolithiasis should be differentiated from other conditions presenting with acute flank or upper abdominal pain, hematuria, nausea and vomiting.

In 2000, the incidence/prevalence of nephrolithiasis was estimated to be 116 cases per 100,000 individuals in the United States.The prevalence of nephrolithiasis is approximately 1116 per 100,000 individuals worldwide. It has increased from every 1 in 20 to 1 in 11 person in United States has kidney stones. According to American Journal of Kidney disease, 2016, 8% of women and 16% of men are developing nephrolithiasis by the age of 70 years. According to 2000 National Hospital Ambulatory Medical Care Survey of the United State,s there is an annual burden of more than 1,100,000 emergency department visits with a primary diagnosis of renal calculus or colic. Patients of all age groups may develop nephrolithiasis. The incidence of nephrolithiasis increases with age.  At initial diagnosis, the mean age was 44.8 years in men and 40.9 years in women. Nephrolithiasis usually affects individuals of the white/Caucasian ethnicity. Males are more commonly affected by nephrolithiaisis than females. The male to female ratio is approximately 2 to 1. The trend keeps on changing , a study in 2010 claims the incidence rate ratio of men to women with urinary tract stones has narrowed from 3.4 to 1.3. Females are having increasing incidence rates owing to increase lifestyle disease like obesity. The majority of nephrolithiasis cases are reported in southeast belt of the United States. The number of cases increase from north to south and from west to east. The states of North Carolina, South Carolina, Georgia, Alabama, Mississippi, and Tennessee are considered in the “stone belt.” The ambient temperature and sunlight levels as risk factors for stones and differences in exposure to temperature and sunlight and beverages are also responsible for geographic variability.

Common risk factors in the development of nephrolithiasis include dietary habits, low urinary pH, hypercalcemia, hypercalciuria, hyperoxaluria, hyperuricemia, hyperuricosuria, obesity, diabetes mellitus, environmental factors such as hot climate, drugs such as thiazide, furosemide, sulfadiazine, indinavir. Less common risk factors in the development of nephrolithiasis include hypocitraturia, beverage use, drugs like ciprofloxacin and triamterene.

There is insufficient evidence to recommend routine screening for nephrolithiaisis.

If left untreated, <30% of patients with nephrolithiasis may progress to develop renal colicky pain due to increase in rate of growth.Most of the stones pass spontaneously. about 10-20% of symptom-causing stones fail to pass. Lower poles stones were significantly less likely to cause symptoms or pass spontaneously. They can progress to hydronephrosis especially when combined or superimposed by urinary tract infection. Common complications of nephrolithiasis include hydronephrosis, chronic renal failure, hypertension, cardiovascular disease, and increased risk of fracture. Prognosis is generally excellent. Approximately 80-85% resolve spontaneously. Recurrence rates for calcium stones after the initial event is 40–50% at the end of 5 years and 50–60% at the end of 10 years.

CT scan is the gold standard test for the diagnosis of nephrolithiasis.

The patients with nephrolithiasis may have a positive history of flank pain. Common symptoms of nephrolithiasis include flank pain progressing downward and anteriorly into the groin as the stone moves, hematuria, nausea and vomiting urinary frequency and urgency. Less common symptoms include burning micturition.

Patients with nephrolithiasis usually appear in pain and trying to achieve a comfortable position. Common physical examination findings of nephrolithiasis include costovertebral angle tenderness, may accompany fever with increased heart rate and respiratory rate. They can have hypoactive bowel sounds due to ileus caused by severe pain. They can have hematuria in microscopic exmaination.

Laboratory findings consistent with the diagnosis of nephrolithiasis include hypercalcemia, hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricemia and hyperuricosuria.

There are no ECG findings associated with nephrolithiasis.

An x-ray may be helpfulin the diagnosis of nephrolithiasis. Findings on an x-ray suggestive of nephrolithiasis include radiopaque stones such as Calcium oxalate, calcium phosphate, struvite and radiolucent stones which includes uric acid stones and cystine stones.

Abdominal ultrasound may be helpful in the diagnosis of nephrolithiasis Findings on an ultrasound suggestive of/diagnostic of nephrolithiasis include: echogenic or hyperechogenic foci, acoustic shadowing, twinkle artefact on colour Doppler, colour comet-tail artefact , and increased resistive index which signifies acute obstruction.

Abdominal and pelvic CT scan is helpful in the diagnosis of nephrolithiasis. Findings on CT scan diagnostic of nephrolithiasis include radiopacity showing the location, density and composition of stones calcium oxalate +/- calcium phosphate: 400-600 HU, struvite (triple phosphate): usually opaque but variable, pure calcium phosphate 400-600 HU, uric acid: 100-200 HU and cystine: opaque.

There are no MRI findings associated with nephrolithiasis. However, a MRI may be helpful in the diagnosis of complications of nephrolithiasis, which include hydronephrosis.

There are no other imaging findings associated with nephrolithiasis.

There are no other diagnostic studies associated with nephrolithiasis.

The treatment of nephrolithiasis involves different measures e.g non pharmacological measures consisting of increased fluid intake, straining an dietary restrictions. Pharmacological measures include pain relief using NSAIDs and opioids., helping passage of stone spontaneously with drugs like tamsulosin and nifedipine. The treatment of underlying cause and being specific to type of stones is very important.It involves treating primary hyperparathyroidism and Renal tubular acidosis. For those having high urinary calcium, Hydrochlorothiazide or Chlorthalidone are used. For recurrent stones and high urine uric acid, Allopurinol is used. For recurrent stones and hypocitraturia, Potassium citrate is sued to alkalinize the urine. For uric acid stones, alkalinizing urine with potassium citrate/potassium bicarbonate is done and if needed Allopurinol is also used. For struvite stones, medical therapy is not of much help, although urease inhibitors such as acetohydroxamic acid can be given in urease +ve etiology. For cysteine stones, again alkalinizing urine helps along with Tiopronin. The Urological consult is needed when stone >10 mm in diameter, uncontrolled pain, Anuria, or there is Acute kidney injury.

The mainstay of treatment for nephrolithiasis is medical therapy. Surgery is usually reserved for patients with either persistent and severe pain, renal failure, kidney infection and when stone fails to pass or move after 30 days. The surgeries which are being used currently include extracorporeal shockwave lithotripsy, ureteroscopy and percutaneous nephrolithotomy.

Effective measures for the primary prevention of nephrolithiais include diet control and high fluid intake.

Effective measures for the secondary prevention of nephrolithiasis include measures to prevent recurrence of the stones and prevent complications. It includes measures like correcting hydration and dietary habits. Drugs like allopurinol to prevent hyperuricemia, potassium citrate to alkalinize the urine and avoidance or judicious use of diuretics.

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

Nephrolithiasis may be classified according to American Society of Nephrology based on stone composition into 4 subtypes/groups as calcium stones, struvite stones, uric acid stones and cystine stones.

• Nephrolithiasis may be classified according to American Society of Nephrology based on stone composition into 2 subtypes/groups:^[1][2]
• Calcium stones
  • Calcium oxalate stones
  • Calcium phosphate stones
• Struvite stones
• Uric acid stones
• Cystine stones

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

It is understood that nephrolithiasis is the result of combination of different mechanism responsible for different types of stones. Calcium stones are the most common type of kidney stones. Approximately 80% of all calcium stones are calcium oxalate stones. The pathophysiology of calcium stones is complex and involves dietary concerns, hypercalciuria, hypocitaturia, hyperoxaluria, hyperuricosuria and biomineralization. The underlying pathophysiological mechanisms responsible for uric acid stones are low urine volume, hyperuricosuria and high acidic urine. Cystinuria is a rare hereditary gene disorder which causes impaired renal reabsorption of cationic amino acids and cystine. It is caused by mutations in either of the two subunits (rBAT(SLC3A2) and b0,+AT(SLC7A9)) forming cystine stones. Struvite stones are usually seen in patients which have infection with urease +ve organisms. Urine pH is usually alkaline (>7.2). Nephrolithiasis can be passed on to following generations due to rare causes of hypercalciuria such as hereditary distal renal tubular acidosis, dent disease, Bartter syndrome types III and IV, autosomal dominant hypocalcemic hypercalciuria and familial hypomagnesemia. Nephrolithiasis associated with Hyperparathyroidism, Gout, Hypocitaturia, Sarcoidosis, chronic urinary tract infections and Obesity.On gross pathology, the characteristic findings of nephrolithiasis include location = 80% unilateral, usually in calyces, pelvis or bladder. The size=variable, 2-3 mm usually. All stones contain an organic matrix of mucoprotein. The shape of struvite stone is staghorn shaped. On microscopic histopathological analysis, the characteristic findings of nephrolithiasis include different shapes of stones/crystals are such as cystine= hexagonal, struvite= coffin lid shape, calcium oxalate= pyramid shape to dumbbell shape and uric acid= rectangular/rhomboidal. Oxalate crystals are highlighted by polarized light. Also, foreign body giant cells and macrophages are seen with the stones.

• It is understood that nephrolithiasis is the result of combination of different mechanism responsible for different types of stones:

• Calcium stones are the most common type of kidney stones.^[1]
• Approximately 80% of all calcium stones are calcium oxalate stones.^[2][3]
• The pathophysiology of calcium stones is complex and involves:^[4]
  • Dietary concerns^[5][6][7]
  • Hypercalciuria
  • Hypocitaturia
  • Hyperoxaluria
  • Hyperuricosuria
  • Biomineralization^[8]

• The underlying pathophysiological mechanisms responsible for uric acid stones are:
  • Low urine volume
  • Hyperuricosuria
  • High acidic urine.

• Cystinuria is a rare hereditary gene disorder which causes impaired renal rabsorption of cationic amino acids and cystine.
• The cationic amino acids commonly involved are called as COLA amino acids that stands for:
  • C= cystine
  • O=ornithine
  • L=lysine
  • A=arginine
• It is caused by mutations in either of the two subunits (rBAT(SLC3A2) and b0,+AT(SLC7A9)) forming the apical transporter for cationic amino acids system b0,+; thus excretion of the dibasic COLA amino acids is increased.^[9]

• These are usually seen in patients which have infection with urease +ve organisms.^[10][11]
• Urine pH is usually alkaline (>7.2)

The following table summarizes major mechanism of stone formation: ^{[12][13][14][15]}

• Nephrolithiasis can be passed on to following generations due to rare causes of hypercalciuria:
  • Hereditary distal renal tubular acidosis
  • Dent disease
  • Bartter syndrome types III and IV
  • Autosomal dominant hypocalcemic hypercalciuria
  • Familial hypomagnesemia

• Hyperparathyroidism
• Gout
• Hypocitaturia
• Sarcoidosis
• Chronic urinary tract infections
• Obesity

• On gross pathology, the characteristic findings of nephrolithiasis are:
  • Location = 80% unilateral, usually in calyces, pelvis or bladder
  • Size=variable, 2-3 mm usually
  • All stones contain an organic matrix of mucoprotein
  • Shape:
    • Struvite stone= staghorn calculus

• 
  Nephrolithiasis, Source: Wikimedia commons^[16]
• 
  Staghorn shape of struvite stones, Source: Wikimedia commons^[17]
• 
  Renal calculi, different shapes and sizes, Source: Wikimedia commons^[18]
• 
  Kidney stone with a maximum dimension of 5mm, Source: Wikimedia commons^[19]

• On microscopic histopathological analysis, the characteristic findings of nephrolithiasis are:
  • Shapes of different stones/crystals are different:
    • Cysteine= hexagonal
    • Struvite= coffin lid shape
    • Calcium oxalate= pyramid shape
    • Calcium oxalate= dumbbell shape
    • Uric acid= rectangular/rhomboidal
  • Oxalate crystals are highlighted by polarized light
  • Foreign body giant cells and macrophages are seen with the stones

• 
  Type of stones. Light microscopy of urine crystals. (A) Hexagonal cystine crystal (200X); (B) coffin-lid shaped struvite crystals (200X); (C) pyramid-shaped calcium oxalate dehydrate crystals (200X); (D) dumbbell-shaped calcium oxalate monohydrate crystal (400X); (E) rectangular uric acid crystals (400X); and (F) rhomboidal uric acid crystals (400X).^[20]
• 
  Deposits of oxalate with variable size and form; they occupy mainly distal tubules. The asterisks indicate proximal tubules, which usually do not contain these crystals, H&E seen with polarized light, X200^[21]
• 
  Medullary interstitial urate crystal deposits in chronic nephropathy by urates as seen after Masson’s trichome stain X400^[22]
• 
  Calcium oxalate dihydrate crystals under Scanning Electron Micrograph (SEM) taken at 30 KV. Source: Wikimedia commons^[23]
• 
  Density-dependent color scanning electron micrograph of kidney stone, Source: Wikimedia commons^[24]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

The common causes of nephrolithiasis include hypercalcemia, hyperparathyroidism, hypercalciuria, infection with urea splitting microorganisms like Proteus and Pseudomonas, gout, dehydration, inflammatory bowel disease. Less common causes of nephrolithiasis include drugs such as loop diuretics, Acetazolamide, ciprofloxacin, indinavir, guaifenesin triamterene and magnesium trisilicate.

The common causes of nephrolithiasis:

• Hypercalcemia
  • Hyperparathyroidism
• Hypercalciuria
• Infection with urea splitting microorganisms like Proteus and Pseudomonas
• Gout
• Dehydration
• Inflammatory bowel disease

Less common causes of nephrolithiasis include:

• Drugs:
  • Loop diuretics
  • Acetazolamide
  • Ciprofloxacin
  • Indinavir
  • Guaifenesin
  • Triamterene
  • Magnesium trisilicate
  • Cobicistat
  • Febuxostat
  • Sulfasalazine and other sulfa drugs
  • Topiramate
  • Zonisamide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2] Amandeep Singh M.D.[3]

Nephrolithiasis should be differentiated from other conditions presenting with acute flank or upper abdominal pain, hematuria, nausea and vomiting.

Nephrolithiasis should be differentiated from other conditions presenting with acute flank or upper abdominal pain, hematuria, nausea and vomiting. The differentials include the following:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]}

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

In 2000, the incidence/prevalence of nephrolithiasis was estimated to be 116 cases per 100,000 individuals in the United States.The prevalence of nephrolithiasis is approximately 1116 per 100,000 individuals worldwide. It has increased from every 1 in 20 to 1 in 11 person in United States has kidney stones. According to American Journal of Kidney disease, 2016, 8% of women and 16% of men are developing nephrolithiasis by the age of 70 years. According to 2000 National Hospital Ambulatory Medical Care Survey of the United State,s there is an annual burden of more than 1,100,000 emergency department visits with a primary diagnosis of renal calculus or colic. Patients of all age groups may develop nephrolithiasis. The incidence of nephrolithiasis increases with age.  At initial diagnosis, the mean age was 44.8 years in men and 40.9 years in women. Nephrolithiasis usually affects individuals of the white/Caucasian ethnicity. Males are more commonly affected by nephrolithiaisis than females. The male to female ratio is approximately 2 to 1. The trend keeps on changing , a study in 2010 claims the incidence rate ratio of men to women with urinary tract stones has narrowed from 3.4 to 1.3. Females are having increasing incidence rates owing to increase lifestyle disease like obesity. The majority of nephrolithiasis cases are reported in southeast belt of the United States. The number of cases increase from north to south and from west to east. The states of North Carolina, South Carolina, Georgia, Alabama, Mississippi, and Tennessee are considered in the “stone belt.” The ambient temperature and sunlight levels as risk factors for stones and differences in exposure to temperature and sunlight and beverages are also responsible for geographic variability.

Various studies have found epidemiological data based on time and population as mentioned:^[1][2][3][4]

• In 2000, the incidence/prevalence of nephrolithiasis was estimated to be 116 cases per 100,000 individuals in the United States.^[5]

• The prevalence of nephrolithiasis is approximately 1116 per 100,000 individuals worldwide.
• It has increased from every 1 in 20 to 1 in 11 person in United States has kidney stones.^[6]
• According to American Journal of Kidney disease, 2016, 8% of women and 16% of men are developing nephrolithiasis by the age of 70 years.
• According to 2000 National Hospital Ambulatory Medical Care Survey of the United State,s there is an annual burden of more than 1,100,000 emergency department visits with a primary diagnosis of renal calculus or colic.^[7]

• There is no independent association of prevalent kidney stone disease with all-cause and CV mortality.^[8]

• Patients of all age groups may develop nephrolithiasis.
• The incidence of nephrolithiasis increases with age.^[9]
•  At initial diagnosis, the mean age was 44.8 years in men and 40.9 years in women

• Nephrolithiasis usually affects individuals of the white/Caucasian ethnicity.

• Males are more commonly affected by nephrolithiaisis than females. The male to female ratio is approximately 2 to 1.^[10]
• The trend keeps on changing , a study in 2010 claims the incidence rate ratio of men to women with urinary tract stones has narrowed from 3.4 to 1.3.^[11]
• Females are having increasing incidence rates owing to increase lifestyle disease like obesity.

• The majority of nephrolithiasis cases are reported in southeast belt of the United States.
• The number of cases increase from north to south and from west to east
• The states of North Carolina, South Carolina, Georgia, Alabama, Mississippi, and Tennessee are considered in the “stone belt.”^[12]
• The ambient temperature and sunlight levels as risk factors for stones and differences in exposure to temperature and sunlight and beverages are also responsible for geographic variability.^[13]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

Common risk factors in the development of nephrolithiasis include dietary habits, low urinary pH, hypercalcemia, hypercalciuria, hyperoxaluria, hyperuricemia, hyperuricosuria, obesity, diabetes mellitus, environmental factors such as hot climate, drugs such as thiazide, furosemide, sulfadiazine, indinavir. Less common risk factors in the development of nephrolithiasis include hypocitraturia, beverage use, drugs like ciprofloxacin and triamterene.

• Common risk factors in the development of nephrolithiasis include:^[1]
  • Dietary habits
  • Low urinary pH
  • Hypercalcemia
  • Hypercalciuria
  • Hyperoxaluria
  • Hyperuricemia
  • Hyperuricosuria
  • Metabolic syndrome
  • Obesity
  • Diabetes mellitus
  • Environmental – such as hot climate
  • Drugs^[2]
    • Thiazide
    • Furosemide
    • Sulfadiazine
    • Indinavir

• Less common risk factors in the development of nephrolithiasis include:^[1]
  • Hypocitraturia
  • Beverage use
  • Drugs^[2]
    • Ciprofloxacin
    • Triamterene

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2]

If left untreated, <30% of patients with nephrolithiasis may progress to develop renal colicky pain due to increase in rate of growth.Most of the stones pass spontaneously. about 10-20% of symptom-causing stones fail to pass. Lower poles stones were significantly less likely to cause symptoms or pass spontaneously. They can progress to hydronephrosis especially when combined or superimposed by urinary tract infection. Common complications of nephrolithiasis include hydronephrosis, chronic renal failure, hypertension, cardiovascular disease, and increased risk of fracture. Prognosis is generally excellent. Approximately 80-85% resolve spontaneously. Recurrence rates for calcium stones after the initial event is 40–50% at the end of 5 years and 50–60% at the end of 10 years.

• If left untreated, <30% of patients with nephrolithiasis may progress to develop renal colicky pain due to increase in rate of growth.^[1]
• Most of the stones pass spontaneously. about 10-20% of symptom causing stones fail to pass.^[2]
• Lower poles stones were significantly less likely to cause symptoms or pass spontaneously.
• They can progress to hydronephrosis especially when combined or superimposed by urinary tract infection.

• Common complications of nephrolithiasis include:
  • Hydronephrosis
  • Chronic renal failure
  • Hypertension^[3]
  • Cardiovascular Disease^[4]
  • Increased risk of fracture^[5]

• Prognosis is generally excellent.
• Approximately 80-85% resolve spontaneously
• Recurrence rates for calcium stones after the initial event is 40–50% at the end of 5 years and 50–60% at the end of 10 years.^[6]

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