Kidney

2007-09-22T06:35:00.000-07:00

Kidney
From Wikipedia, the free encyclopedia

Human kidneys viewed from behind with spine removed
Latin ren
Gray's subject #253 1215
Artery renal artery
Vein renal vein
Nerve renal plexus
MeSH Kidney
Dorlands/Elsevier k_03/12470097

The kidneys are organs that filter wastes (such as urea) from the blood and excrete them, along with water, as urine. The medical field that studies the kidneys and diseases of the kidney is called nephrology [1]. The prefix nephro- meaning kidney is from the Ancient Greek word nephros (νεφρός); the adjective renal meaning related to the kidney is from Latin rēnēs, meaning kidneys.

In humans, the kidneys are located in the posterior part of the abdomen. There is one on each side of the spine; the right kidney sits just below the liver, the left below the diaphragm and adjacent to the spleen. Above each kidney is an adrenal gland (also called the suprarenal gland). The asymmetry within the abdominal cavity caused by the liver results in the right kidney being slightly lower than the left one while the left kidney is located slightly more medial.
The kidneys are retroperitoneal. They are approximately at the vertebral level T12 to L3. The upper parts of the kidneys are partially protected by the eleventh and twelfth ribs, and each whole kidney is surrounded by two layers of fat (the perirenal and pararenal fat) which help to cushion it. Congenital absence of one or both kidneys, known as unilateral or bilateral renal agenesis, can occur.

Organization
Above each human kidney is one of the two adrenal glands.

In a normal human adult, each kidney is about 10 cm long, 5.5 cm in width and about 3 cm thick, weighing 150 grams.[2] Together, kidneys weigh about 0.5% of a person's total body weight [citation needed]. The kidneys are "bean-shaped" organs, and have a concave side facing inwards (medially). On this medial aspect of each kidney is an opening, called the hilum, which admits the renal artery, the renal vein, nerves, and the ureter.

The outer portion of the kidney is called the renal cortex, which sits directly beneath the kidney's loose connective tissue/fibrous capsule. Deep to the cortex lies the renal medulla, which is divided into 10-20 renal pyramids in humans. Each pyramid together with the associated overlying cortex forms a renal lobe. The tip of each pyramid (called a papilla) empties into a calyx, and the calices empty into the renal pelvis. The pelvis transmits urine to the urinary bladder via the ureter.

Blood supply
Each kidney receives its blood supply from the renal artery, two of which branch from the abdominal aorta. Upon entering the hilum of the kidney, the renal artery divides into smaller interlobar arteries situated between the renal papillae. At the outer medulla, the interlobar arteries branch into arcuate arteries, which course along the border between the renal medulla and cortex, giving off still smaller branches, the cortical radial arteries (sometimes called interlobular arteries). Branching off these cortical arteries are the afferent arterioles supplying the glomerular capillaries, which drain into efferent arterioles. Efferent arterioles divide into peritubular capillaries that provide an extensive blood supply to the cortex. Blood from these capillaries collects in renal venules and leaves the kidney via the renal vein. Efferent arterioles of glomeruli closest to the medulla (those that belong to juxtamedullary nephrons) send branches into the medulla, forming the vasa recta. Blood supply is intimately linked to blood pressure.

Nephron
Parts of the kidney:
1. Renal pyramid
2. Efferent vessel
3. Renal artery
4. Renal vein
5. Renal hilum
6. Renal pelvis
7. Ureter
8. Minor calyx
9. Renal capsule
10. Inferior renal capsule
11. Superior renal capsule
12. Afferent vessel
13. Nephron
14. Minor calyx
15. Major calyx
16. Renal papilla
17. Renal column

Nephron
The basic functional unit of the kidney is the nephron, of which there are more than a million within the cortex and medulla of each normal adult human kidney. Nephrons regulate water and solute within the cortex and medulla of each normal adult human kidney. Nephrons regulate water and soluble matter (especially electrolytes) in the body by first filtering the blood under pressure, and then reabsorbing some necessary fluid and molecules back into the blood while secreting other, unneeded molecules. Reabsorption and secretion are accomplished with both cotransport and countertransport mechanisms established in the nephrons and associated collecting ducts.

Collecting duct system
Main article: Collecting duct system

The fluid flows from the nephron into the collecting duct system. This segment of the nephron is crucial to the process of water conservation by the organism. In the presence of antidiuretic hormone (ADH; also called vasopressin), these ducts become permeable to water and facilitate its reabsorption, thus concentrating the urine and reducing its volume. When the organism must eliminate excess water, such as after excess fluid drinking, the production of ADH is decreased and the collecting tubule becomes less permeable to water, rendering urine dilute and abundant. Failure of the organism to decrease ADH production appropriately, a condition known as syndrome of inappropriate ADH (SIADH), may lead to water retention and dangerous dilution of body fluids, which in turn may cause severe neurological damage. Failure to produce ADH (or inability of the collecting ducts to respond to it) may cause excessive urination, called diabetes insipidus (DI).
A second major function of the collecting duct system is the maintenance of acid-base homeostasis.
After being processed along the collecting tubules and ducts, the fluid, now called urine, is drained into the bladder via the ureter, to be finally excluded from the organism.

Functions
Main article: Renal physiology

Excretion of waste products
The kidneys excrete a variety of waste products produced by metabolism, including the nitrogenous wastes: urea (from protein catabolism) and uric acid (from nucleic acid metabolism) and water.

Homeostasis
The kidney is one of the major organs involved in whole-body homeostasis. Among its homeostatic functions are acid-base balance, regulation of electrolyte concentrations, control of blood volume, and regulation of blood pressure. The kidneys accomplish these homeostatic functions independently and through coordination with other organs, particularly those of the endocrine system. The kidney communicates with these organs through hormones secreted into the bloodstream.

Acid-base balance
The kidneys regulate the pH, by eliminating H ions concentration called augmentation mineral ion concentration, and water composition of the blood.

By exchanging hydronium ions and hydroxyl ions, the blood plasma is maintained by the kidney at a slightly alkaline pH of 7.4. Urine, on the other hand, is acidic at pH 5 or alkaline at pH 8.

The pH is maintained through four main protein transporters: NHE3 (a sodium-hydrogen exchanger), V-type H-ATPase (an isoform of the hydrogen ATPase), NBC1 (a sodium-bicarbonate cotransporter) and AE1 (an anion exchanger which exchanges chloride for bicarbonate). Due to the polar alignment of cells in the renal epithelia NHE3 and the H-ATPase are exposed to the lumen (which is essentially outside the body), on the apical side of the cells, and are responsible for excreting hydrogen ions (or protons). NBC1 and AE1 are on the basolateral side of the cells, and allow bicarbonate ions to move back into the extracellular fluid and thus are returned to the blood plasma. [citation needed]

Blood pressure
Main article: Renin-angiotensin system

Sodium ions are controlled in a homeostatic process involving aldosterone which increases sodium ion reabsorption in the distal convoluted tubules.

When blood pressure becomes low, a proteolytic enzyme called Renin is secreted by cells of the juxtaglomerular apparatus (part of the distal convoluted tubule) which are sensitive to pressure. Renin acts on a blood protein, angiotensinogen, converting it to angiotensin I (10 amino acids). Angiotensin I is then converted by the Angiotensin-converting enzyme (ACE) in the lung capillaries to Angiotensin II (8 amino acids), which stimulates the secretion of Aldosterone by the adrenal cortex, which then affects the renal tubules.

Aldosterone stimulates an increase in the reabsorption of sodium ions from the kidney tubules which causes an increase in the volume of water that is reabsorbed from the tubule. This increase in water reabsorption increases the volume of blood which ultimately raises the blood pressure.

Plasma volume
Any significant rise or drop in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. A rise in osmolality causes the gland to secrete antidiuretic hormone, resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.

Hormone secretion
The kidneys secrete a variety of hormones, including erythropoietin, urodilatin, renin and vitamin D.

Deamination
In the case of starvation, in the kidneys, an amino group is removed from protein and glucose is formed in the process of gluconeogenesis.

Embryology
Main article: Development of the urinary and reproductive organs
The mammalian kidney develops from intermediate mesoderm. Kidney development, also called nephrogenesis, proceeds through a series of three successive phases, each marked by the development of a more advanced pair of kidneys: the pronephros, mesonephros, and metanephros.[3] (The plural forms of these terms end in -oi.)

Pronephros
Main article: Pronephros
During approximately day 22 of human gestation, the paired pronephroi appear towards the cranial end of the intermediate mesoderm. In this region, epithelial cells arrange themselves in a series of tubules called nephrotomes and join laterally with the pronephric duct, which does not reach the outside of the embryo. Thus the pronephros is considered nonfunctional in mammals because it cannot excrete waste from the embryo.

Mesonephros
Main article: Mesonephros
Each pronephric duct grows towards the tail of the embryo, and in doing so induces intermediate mesoderm in the thoracolumbar area to become epithelial tubules called mesonephric tubules. Each mesonephric tubule receives a blood supply from a branch of the aorta, ending in a capillary tuft analogous to the glomerulus of the definitive nephron. The mesonephric tubule forms a capsule around the capillary tuft, allowing for filtration of blood. This filtrate flows through the mesonephric tubule and is drained into the continuation of the pronephric duct, now called the mesonephric duct or Wolffian duct. The nephrotomes of the pronephros degenerate while the mesonephric duct extends towards the most caudal end of the embryo, ultimately attaching to the cloaca. The mammalian mesonephros is similar to the kidneys of aquatic amphibians and fishes.

Metanephros
During the fifth week of gestation, the mesonephric duct develops an outpouching, the ureteric bud, near its attachment to the cloaca. This bud, also called the metanephrogenic diverticulum, grows posteriorly and towards the head of the embryo. The elongated stalk of the ureteric bud, the metanephric duct, later forms the ureter. As the cranial end of the bud extends into the intermediate mesoderm, it undergoes a series of branchings to form the collecting duct system of the kidney. It also forms the major and minor calyces and the renal pelvis.

The portion of undifferentiated intermediate mesoderm in contact with the tips of the branching ureteric bud is known as the metanephrogenic blastema. Signals released from the ureteric bud induce the differentiation of the metanephrogenic blastema into the renal tubules. As the renal tubules grow, they come into contact and join with connecting tubules of the collecting duct system, forming a continuous passage for flow from the renal tubule to the collecting duct. Simultaneously, precursors of vascular endothelial cells begin to take their position at the tips of the renal tubules. These cells differentiate into the cells of the definitive glomerulus.

Terms

Microscopic photograph of the renal cortex.

Microscopic photograph of the renal medulla.

renal capsule: The membranous covering of the kidney.
cortex: The outer layer over the internal medulla. It contains blood vessels, glomeruli (which are the kidneys' "filters") and urine tubes and is supported by a fibrous matrix.
hilus: The opening in the middle of the concave medial border for nerves and blood vessels to pass into the renal sinus.
renal column: The structures which support the cortex. They consist of lines of blood vessels and urinary tubes and a fibrous material.
renal sinus: The cavity which houses the renal pyramids.
calyces: The recesses in the internal medulla which hold the pyramids. They are used to subdivide the sections of the kidney. (singular - calyx)
papillae: The small conical projections along the wall of the renal sinus. They have openings through which urine passes into the calyces. (singular - papilla)
renal pyramids: The conical segments within the internal medulla. They contain the secreting apparatus and tubules and are also called malpighian pyramids.
renal artery: Two renal arteries come from the aorta, each connecting to a kidney. The artery divides into five branches, each of which leads to a ball of capillaries. The arteries supply (unfiltered) blood to the kidneys. The left kidney receives about 60% of the renal bloodflow.
renal vein: The filtered blood returns to circulation through the renal veins which join into the inferior vena cava.
renal pelvis: Basically just a funnel, the renal pelvis accepts the urine and channels it out of the hilus into the ureter.
ureter: A narrow tube 40 cm long and 4 mm in diameter. Passing from the renal pelvis out of the hilus and down to the bladder. The ureter carries urine from the kidneys to the bladder by means of peristalsis.
renal lobe: Each pyramid together with the associated overlying cortex forms a renal lobe

Diseases and disorders

Congenital
Congenital hydronephrosis
Congenital obstruction of urinary tract
Duplicated ureter
Horseshoe kidney
Polycystic kidney disease
Renal dysplasia
Unilateral small kidney
Multicystic dysplastic kidney

Acquired
Diabetic nephropathy
Glomerulonephritis
Hydronephrosis is the enlargement of one or both of the kidneys caused by obstruction of the flow of urine.
Interstitial nephritis
Kidney stones are a relatively common and particularly painful disorder.
Kidney tumors

Lupus nephritis
Minimal change disease
In nephrotic syndrome, the glomerulus has been damaged so that a large amount of protein in the blood enters the urine. Other frequent features of the nephrotic syndrome include swelling, low serum albumin, and high cholesterol.
Pyelonephritis is infection of the kidneys and is frequently caused by complication of a urinary tract infection.
Renal failure

The failing kidney
Generally, humans can live normally with just one kidney, as one has more functioning renal tissue than is needed to survive, possibly due to the nature of the prehistoric human diet. Only when the amount of functioning kidney tissue is greatly diminished will chronic renal failure develop. If the glomerular filtration rate (a measure of renal function) has fallen very low (end-stage renal failure), or if the renal dysfunction leads to severe symptoms, then renal replacement therapy is indicated, either dialysis or renal transplantation.

Medical terminology
Medical terms related to the kidneys involve the prefixes renal- and nephro-.
Surgical removal of the kidney is a nephrectomy, while a radical nephrectomy is removal of the kidney, its surrounding tissue, lymph nodes, and potentially the adrenal gland. A radical nephrectomy is performed for the removal of the cancers.

Animal kidneys as food
The kidneys of animals can be cooked and eaten by humans (along with other offal). If prepared properly, they can be nutritious and pleasant tasting (if somewhat bland). Veal kidneys and lamb kidneys are particularly prized for their tenderness and flavour. Kidneys can be grilled or sautéed, though they become tough and unpleasant if overcooked.

Chinese cuisine includes sauteed pork kidneys, which are first soaked in water and then cleaned with scissors to remove nephrons and excess urine.

Pork kidneys, along with pork tongue and beef tongue, are some of the most cholesterol intense sources. A serving of pork kidney or beef tongue can yield more than 200% of the allotted daily intake of cholesterol.

World Kidney Day
World Kidney Day is observed on the second Thursday of March every year. [4] It was held for the first time in 2006, to increase awareness of kidney disease and educate persons at risk regarding the importance of prevention and early detection. [5] It is a joint initiative by the International Society of Nephrology (ISF) and International Federation of Kidney Foundations (IFKF). The next World Kidney Day will be held on 13 March 2008. In 2007, it was held on 8th March.

References

Wikimedia Commons has media related to:
Kidney
^ Nephrology. Dictionary.com. Retrieved on 2007-08-04.
^ Martini F.. Fundamentals of Anatomy and Physiology 5th edition. Prentice Hall International Inc. 2001.
^ Bruce M. Carlson (2004). Human Embryology and Developmental Biology, 3rd edition, Saint Louis: Mosby. ISBN 0-323-03649-X.
^ http://www.ifkf.net/worldkidneyday.php
^ http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5608a1.htm

External links
American Kidney Fund
European Renal Genome project kidney function tutorial
Information on the Kidneys
Kidney Foundation of Canada kidney disease information
Kidney Foundation (Canada)
National Kidney Disease Education Program (NKDEP)
National Kidney Foundation
National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC)
BC Renal Agency - Official site for the province-wide network of renal care providers in British Columbia, Canada
World Kidney Day website
UNC Nephropathology

v • d • e Urinary system - Kidney

Renal fascia • Renal capsule • Renal cortex (Renal column) • Renal medulla (Renal sinus, Renal pyramids) • Renal lobe • Cortical lobule • Medullary ray • Nephron
Afferent circulation
Renal artery → Segmental arteries → Interlobar arteries → Arcuate arteries → Cortical radial arteries → Afferent arterioles → Renal corpuscle (Glomerulus, Bowman's capsule)
Renal tubule
Proximal tubule → Loop of Henle (Descending, Thin ascending, Thick ascending) → Distal convoluted tubule → Connecting tubule → Collecting ducts → Duct of Bellini → Renal papilla → Minor calyx → Major calyx → Renal pelvis → Ureter
Efferent circulation
Glomerulus → Efferent arterioles → Peritubular capillaries/Vasa recta → Arcuate vein → Interlobar veins → Renal vein
Juxtaglomerular apparatus
Macula densa • Juxtaglomerular cells • Extraglomerular mesangial cells
Filtration
Glomerular basement membrane • Podocyte • Filtration slits • Intraglomerular mesangial cells

v • d • e Anatomy: urinary system
Kidneys • Ureters • Urinary bladder (Uvula) • Urethral sphincters • Urethra
Retrieved from "http://en.wikipedia.org/wiki/Kidney"

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Kidney Stone

2007-09-22T04:35:00.000-07:00

Kidney stone
From Wikipedia, the free encyclopedia

Classification & external resources

Ultrasonic instrument and kidney stone

ICD-10
N 20.0
ICD-9
592.0
DiseasesDB
11346
MedlinePlus
000458
eMedicine
med/1600

Kidney stones, or Renal calculi, are solid concretions (crystal aggregations) of dissolved minerals in urine; calculi typically form inside the kidneys or ureters. The terms nephrolithiasis and urolithiasis refer to the presence of calculi in the kidneys and urinary tract, respectively. Renal calculi can vary in size from as small as grains of sand to as large as grapefruit. Kidney stones typically leave the body by passage in the urine stream, and many stones are formed and passed without causing symptoms. If stones grow to sufficient size before passage — on the order of at least 2-3 millimeters — they can cause obstruction of the ureter. The resulting spasm of muscle, trying to move the stone, can cause severe episodic pain, most commonly felt in the flank, lower abdomen and groin (a condition called renal colic). Renal colic can be associated with nausea and vomiting due to the embyrological association of the kidneys and the intestinal tract. Hematuria is commonly present due to damage to the wall of the urethra as well as dysuria (when passing stones). Recurrence rates are estimated at about 10% per year.

Star shaped bladder urolith

Staghorn calculus

Causes
Kidney stones can be due to underlying metabolic conditions, such as renal tubular acidosis, Dent's disease and medullary sponge kidney. Many centers will screen for such disorders in patients with recurrent kidney stones. However, most stones are idiopathic.
The most common type of kidney stone is composed of calcium oxalate crystals, and factors that promote the precipitation of crystals in the urine are associated with the development of these stones.

Conventional wisdom and common sense has long held that consumption of too much calcium can promote the development of kidney stones. However, current evidence suggests that the consumption of low-calcium diets is actually associated with a higher overall risk for the development of kidney stones. 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.
Other types of kidney stones are composed of struvite (magnesium, ammonium and phosphate); uric acid; calcium phosphate; and cystine.

The formation of struvite stones is associated with the presence of urea-splitting bacteria, most commonly Proteus mirabilis (but also Klebsiella, Serratia, Providencia species). These organisms are capable of splitting urea into ammonia, decreasing the acidity of the urine and resulting in favorable conditions for the formation of struvite stones.

The formation of uric acid stones is associated with conditions that cause high blood uric acid levels, such as gout, leukemias/lymphomas treated by chemotherapy (secondary gout from the death of leukemic cells), and acid/base metabolism disorders.

The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis.

The formation of cystine stones is uniquely associated with people suffering from cystinuria, who accumulate cystine in their urine.

Clinical presentation and diagnosis
Symptoms of kidney stones include:

Colicky Pain: "loin to groin". Described to be the worst pain ever felt.
Hematuria: due to damage to wall of ureter and/or urethra (blood in urin)
Dysuria: when passing stones (painful urination)
Oliguria: obstruction of bladder or urethra by stone, or extremely rarely, simultaneouus obstruction of both ureters by a stone. (low urin output, less 1mL/kg/h in infants, less than o.5 mL/kg/h in children, and less than 400 mL a day in adults.)
Nausea/vomiting: embryological link with intestine — stimulates vomiting center

Diagnosis is usually made on the basis of the location and severity of the pain, which is typically colic in nature (comes and goes in spasmodic waves). Radiological imaging is used to confirm the diagnosis and a number of other tests can be undertaken to help establish both the possible cause and consequences of the stone. Ultrasound imaging is also useful as it will give details about the presence of hydronephrosis (swelling of the kidney - suggesting the stone is blocking the outflow of urine). It can also be used to show the kidneys during pregnancy when standard x-rays are discouraged. About 10% of stones do not have enough calcium to be seen on standard x-rays (radiolucent stones) and may show up on ultrasound although they typically are seen on CT scans.

The relatively dense calcium renders these stones radio-opaque and they can be detected by a traditional X-ray of the abdomen that includes Kidneys, Ureters and Bladder—KUB. This may be followed by an IVP (Intravenous Pyelogram; IntraVenous Urogram (IVU) is the same test by another name) which requires about 50ml of a special dye to be injected into the bloodstream that is excreted by the kidneys and by its density helps outline any stone on a repeated X-ray. These can also be detected by a Retrograde pyelogram where similar "dye" is injected directly into the ureteral opening in the bladder by a surgeon, usually a urologist.

Computed tomography (CT or CAT scan), a specialized X-ray, is considered the gold-standard diagnostic test for the detection of kidney stones, and in this setting does not require the use of intravenous contrast, which carries some risk in certain people (eg, allergy, kidney damage). All stones are detectable by CT except very rare stones composed of certain drug residues in urine. The non-contrast "renal colic study" CT scan has become the standard test for the immediate diagnosis of flank pain typical of a kidney stone. If positive for stones, a single standard x-ray of the abdomen (KUB) is recommended. This additional x-ray provides the physicians with a clearer idea of the exact size and shape of the stone as well as its surgical orientation. Further, it makes it simple to follow the progress of the stone without the need for the much more expensive CT scan just by doing another single x-ray at some point in the future.

Investigations typically carried out include:

Microscopic study of urine, which may show proteins, red blood cells, pus cells, cellular casts and crystals.
Culture of a urine sample to exclude urine infection (either as a differential cause of the patient's pain, or secondary to the presence of a stone)
Blood tests: Full blood count for the presence of a raised white cell count (Neutrophilia) suggestive of infection, a check of renal function and if raised blood calcium blood levels (hypercalcaemia).
24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate.

Treatment

An 8-mm kidney stone.

90% of stones 4 mm or less in size usually will pass spontaneously, however the majority of stones greater than 6 mm will require some form of intervention. In most cases, a smaller stone that is not symptomatic is often given up to 30 days to move or pass before consideration is given to any surgical intervention as it has been found that waiting longer tends to lead to additional complications. Immediate surgery may be required in certain situations such as in people with only one working kidney, intractable pain or in the presence of an infected kidney blocked by a stone which can rapidly cause severe sepsis and toxic shock.

One modern medical technique uses a ureter stent (a small tube between the bladder and the inside of the kidney) to provide some relief of a blocked kidney. This is especially useful in saving a failing kidney due to swelling and infection from the stone. This tubing allows urine to drain from kidney and in some cases medicine to be injected directly. Ureter stents vary in shape and size, but most are designed to allow urine to drain and be retained for some length of time as infections reside and as stones are dissolved or sonar blasted. Most stents can be removed during a final office visit. This can range from little associated pain to extreme pain.
Management of pain from kidney stones varies from country to country and even from physician to physician, but may require intravenous medication (eg, narcotic or nonsteroidal anti-inflammatories) in acute situations. Similar classes of drugs may be effective orally in an outpatient setting for less severe discomfort. Intravenous ketorolac has been found to be quite effective in many cases of acute renal colic to control the pain without the need for narcotic medications. Ketorolac is a non-steroidal anti-inflammatory drug that is related to aspirin and ibuprofen. Most acute kidney stone pain will last less than 24 hours and not require hospitalization. Patients are encouraged to strain their urine so they can collect the stone when it eventually passes and send it for chemical composition analysis [citation needed].

In many cases non-invasive Extracorporeal Shock Wave Lithotripsy or (ESWL) may be used. Otherwise some form of invasive procedure is required; with approaches including ureteroscopic fragmentation (or simple basket extraction if feasible) using laser, ultrasonic or mechanical (pneumatic, shock-wave) forms of energy to fragment the stones. Percutaneous nephrolithotomy or open surgery may ultimately be necessary for large or complicated stones or stones which fail other less invasive attempts at treatment.

A single retrospective study in the USA, at the Mayo Clinic, has suggested that lithotripsy may increase subsequent incidence of diabetes and hypertension,[1] but it has not been felt warranted to change clinical practice at the clinic.[2] The study reflects early experience with the original lithotripsy machine which had a very large blast path, much larger than what is used on modern machines. Further study is believed necessary to determine how much risk this treatment actually has using modern machines and treatment regimens.

Calgranulin
Crystallization of calcium oxalate (CaOx) appears to be reduced by molecules in the urine that retard the formation, growth, aggregation, and renal cell adherence of calcium oxalate. By purifying urine using salt precipitation, preparative isoelectric focusing, and sizing chromatography, some researchers have found that the molecule calgranulin is able to inhibit calcium oxalate crystal growth.[3] Calgranulin is a protein formed in the kidney.
Given the large amounts of calcium oxalate in the urine, and considering its potency, calgranulin could become an important contribution to the normal urinary inhibition of crystal growth and aggregation. If so it will be an important tool in the renal defense against kidney stones.

Prevention
Preventive strategies include dietary modifications and sometimes also taking drugs with the goal of reducing excretory load on the kidneys:[4]

Drinking enough water to make 2 to 2.5 liters of urine per day.
Aquaretics
A diet low in protein, nitrogen and sodium intake.
Avoiding excess Vitamin C, especially Vitamin C supplements.
Restriction of oxalate-rich foods and maintenance of an adequate intake of dietary calcium. There is equivocal evidence that calcium supplements increase the risk of stone formation, though calcium citrate appears to carry the lowest, if any, risk.
Taking drugs such as thiazides, potassium citrate, magnesium citrate and allopurinol, depending on the cause of stone formation.
Depending on the stone formation disease, vitamin B-6 and orthophosphate supplements may be helpful, although these treatments are generally reserved for those with Hyperoxaluria. Cellulose supplements have also shown potential for reducing kidney stones caused by hypercalciuria (excessive urinary calcium) although today other means are generally used as cellulose therapy is associated with significant side effects.

Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which is important for kidney stone sufferers to avoid, there are no conclusive data demonstrating any cause and effect regarding kidney stones. However, some have theorized that frequent and binge drinkers create situations that set up dehydration, (alcohol consumption, hangovers, and poor sleep and stress habits). In this view, it is not the alcohol that creates a kidney stone but it is the alcohol drinker's associated behavior that sets it up.[5]

One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs usually thought of as diuretic. These drugs prevent stones through an effect independent of their diuretic properties: they reduce urinary calcium excretion. Nonetheless, their diuretic property does not preclude their efficacy as stone preventive. Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Though some have said that the effect probably fades after two years or so of therapy (tachyphylaxis), in fact it is only randomized controlled trials lasting 2 years or more that show the effect; there is really no good evidence from studies of calcium metabolism that the thiazide effect does not last indefinitely. Thiazides are the medical therapy of choice for most cases of hypercalciuria (excessive urinary calcium) but may not be suitable for all calcium stone formers; just those with high urinary calcium levels.

Allopurinol (Zyloprim) is another drug with proven benefits in some calcium kidney stone formers. Allopurinol interferes with the liver's production of uric acid. Hyperuricosuria, too much uric acid in the urine, is a risk factor for calcium stones. Allopurinol reduces calcium stone formation in such patients. The drug is also used in patients with gout or hyperuricemia, but hyperuricosuria is not the critical feature of uric acid stones. Uric acid stones are more often caused by low urine pH. Even relatively high uric acid excretion will not be associated with uric acid stone formation if the urine pH is alkaline. Therefore prevention of uric acid stones relies on alkalinization of the urine with citrate. Allopurinol is reserved for patients in whom alkalinization is difficult. For patients with increased uric acid levels and calcium stones, alloprinol is one of the few treatments that has been shown in double-blinded placebo controlled studies to actually reduce kidney stone recurrences. Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/dL is often the goal of the drug's use in patients with gout or hyperuricemia.

Potassium citrate is also used in kidney stone prevention. This is available as both a tablet and liquid preparation. The medication increases urinary pH (makes it more alkaline), as well as increases the urinary citrate level, which helps reduce calcium oxalate crystal aggregation. Optimal 24 hour urine levels of citrate are thought to be over 320 mg/liter of urine or over 600 mg per day. There are urinary dipsticks available that allow patients to monitor and measure urinary pH so patients can optimize their urinary citrate level.

Though caffeine does acutely increase urinary calcium excretion, several independent epidemiologic studies have shown that coffee intake overall is protective for stones.[6]
Measurements of food oxalate content have been difficult and issues remain about the proportion of oxalate that is bio-available, versus a proportion that is not absorbed by the intestine. Oxalate-rich foods are usually restricted to some degree, particularly in patients with high urinary oxalate levels, but no randomized controlled trial of oxalate restriction has been performed to test that hypothesis.

For those patients interested in optimizing their kidney stone prevention options, it's essential to have a 24 hour urine test performed. This should be done with the patient on his or her regular diet and activities. The results can then be analyzed for abnormalities and appropriate treatment given.

Though not a "cure", ease can sometimes be found during "mild" pain by walking (if possible), preferably in cold air. Some pain relief may also be derived by soaking in a hot tub of water.

Risk of high-protein diet
A high protein diet might be partially to blame. Protein from meat and other animal products is broken down into acids, including uric acid. The most available alkaline base to balance the acid from protein is calcium phosphate (hydroxyapatite) from the bones (buffering). The kidney filters the liberated calcium which may then form insoluble crystals (i.e., stones) in urine with available oxalate (partly from metabolic processes, partly from diet) or phosphate ions, depending on conditions. High protein intake is therefore associated with decreased bone density as well as stones. The acid load is associated with decreased urinary citrate excretion; citrate competes with oxalate for calcium and can thereby prevent stones. In addition to increased fluid intake, one of the simplest fixes is to moderate animal protein consumption. However, despite epidemiologic data showing that greater protein intake is associated with more stones, randomized controlled trials of protein restriction have not shown reduced stone prevalence. In this regard, it is not just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium. Some diseases (e.g., distal renal tubular acidosis) which cause a chronically acidic state also decrease urinary citrate levels; since citrates are normally present as potent inhibitors of stone formation, these patients are prone to frequent stone formation.

Famous sufferers

Trivia sections are discouraged under Wikipedia guidelines.The article could be improved by integrating relevant items into other sections and removing inappropriate items. (September 2007)

In 271 or 270 BC, the Greek Philosopher Epicurus died from a kidney stone blockage lasting a fortnight according to his successor Hermarchus and reported by his biographer Diogenes Laertius.
French Renaissance essayist Montaigne suffered from kidney stones. British statesman Samuel Pepys also suffered from kidney stones and was operated on, pre-anesthesia, to remove a large stone which he carried with him and used to try to persuade fellow sufferers to endure the painful surgery. His contemporary, John Wilkins, Bishop of Chester, could not face the prospect and died as a result.
Dutch blacksmith Jan de Doot is remembered for having his portrait painted with the large stone that he removed from himself in 1651.
Author Chuck Palahniuk wrote about his experience with a kidney stone in his nonfiction book Stranger Than Fiction: True Stories.
British General James Wolfe suffered from "the gravel" prior to the Battle of Quebec during the Seven Years War.
The eleventh President of the United States, James K. Polk, suffered from kidney stones which prevented him from receiving a formal education until the age of eighteen.
Author Isaac Asimov suffered from kidney stones, and wrote about how his pain was treated with morphine, saying that he feared becoming addicted to morphine if he ever needed it again.
Astronauts often get kidney stones because of an increase in the amount of calcium in their blood due to a loss of bone density in zero gravity.
In his book A Year At the Movies, Mystery Science Theatre 3000 writer/performer Kevin Murphy describes his ordeal with a kidney stone: "Being gut-stabbed with a dirty spoon in a prison cafeteria is less painful."
Former Speaker of the United States House of Representatives, Dennis Hastert, has had a number of kidney stones, necessitating kidney stone removal surgery.
Lyndon B. Johnson suffered from kidney stones at various times in his life. See Woods, LBJ: Architect Of American Ambition.
While DJ'ing at a student event, British DJ John Peel passed a kidney stone, and then proceeded to auction it off for charity at the same event.
On October 19, 2005, while working on the set of Boston Legal, actor William Shatner was taken to the emergency room for lower back pain. He eventually passed a kidney stone, but recovered and soon returned to work. Shatner sold his kidney stone in 2006 for $75,000 to GoldenPalace.com. The money will go to a housing charity. [1]
Minnesota Twins catcher Joe Mauer has also suffered from kidney stones. When asked about it he stated, "I don't wish that on anyone."
Reggaeton artist Tito El Bambino briefly suffered from kidney stones.
Karl Pilkington was diagnosed with kidney stones in late August 2006
John Hart, signer of the Declaration of Independence, died of kidney stones.
Tycho Brahe, astronomer.
Georges-Louis Leclerc, Comte de Buffon, French naturalist, had 57 stones at time of autopsy.
Peter Baulman (Australia) had a kidney stone removed from his right kidney in December 2003 at The Gold Coast Hospital, Southport, Queensland, Australia, weighing 356 g (12.5 oz) and measuring at its widest point, 11.86 cm (4.66 in). It holds the Guinness world record for largest and heaviest kidney stone removed from a human being.
Myles Standish, military officer of the Pilgrims at Plymouth Colony.
Washington Post columnist and Pulitzer Prize winner Art Buchwald suffered from a kidney stone late in his life.
Tim Snead, humanitarian and environmentalist
Buzz Kilman

See also
Nephrology
Urinary retention
Urology
Retrograde pyelogram
Cystinuria
Intravenous pyelogram

References and notes
Coe FL, Evan A, Worcester E (2005). "Kidney stone disease". J Clin Invest 115 (10): 2598-608. PMID 16200192.
^ Krambeck AE, Gettman MT, Rohlinger AL, Lohse CM, Patterson DE, Segura JW (2006). "Diabetes mellitus and hypertension associated with shock wave lithotripsy of renal and proximal ureteral stones at 19 years of followup". J Urol 175 (5): 1742-7. PMID 16600747.
^ Ed Edelson. "Kidney Stone Shock Wave Treatment Boosts Diabetes, Hypertension Risk - Study suggests link, but doctors say it's too early to abandon this therapy", HealthFinder, National Health Information Center.
^ http://ajprenal.physiology.org/cgi/content/abstract/275/2/F255 Calcim Oxalate crystallization experiment
^ Goldfarb DS, Coe FL (1999, November 15). "Prevention of recurrent nephrolithiasis". Am Fam Physician 60 (8): 2269-76. PMID 10593318.
^ Rodman, John, S (May, 1997). "No More Kidney Stones". Prevention.
^ Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ (1996, February 1). "Prospective Study of Beverage Use and the Risk of Kidney Stones". Am Jour Epidemiology 143 (3): 240-247. PMID 8561157.

External links
Patient Guide To Kidney Stone Diagnosis, Treatment and Prevention. Written by a nephrologist at the New York University School of Medicine.
International Kidney Stone Institute
Pictures of kidney stones, showing their crystalline shape
Renal calculi
International Cystinuria Foundation
Cystinuria Clearinghouse-"Kidney Stone Disease"
Pass Kidney Stones - Information on the causes, side effects, diagnosis, treatments, and prevention of kidney stones.
National Kidney and Urologic Diseases Information Clearinghouse
Patient Experiences with Kidney Stones
[hide]
v • d • e Urinary system - Pathology - Nephrology (N00-N39, 580-599)
Diseases of the glomerulus
Glomerulonephritis - Focal segmental glomerulosclerosis - Membranoproliferative glomerulonephritis - Membranous glomerulonephritis - Nephritic syndrome - Post-streptococcal glomerulonephritis - Nephrotic syndrome (Minimal change disease) - IgA nephropathy - Lupus nephritis - Diabetic nephropathy
Tubulointerstitial diseases of the kidney
Interstitial nephritis - Pyelonephritis - Hydronephrosis - Pyonephrosis - Balkan nephropathy - Reflux nephropathy
Renal failure
Acute renal failure - Chronic renal failure
Diseases of the renal tubule andother disorders of kidney and ureter
Renal osteodystrophy - Nephrogenic diabetes insipidus - Renal tubular acidosis - Nephroptosis - Ureterocele - Fanconi syndrome
Other diseases anddisorders of urinary system
Cystitis (Interstitial cystitis, Trigonitis) - Neurogenic bladder - Vesicointestinal fistula - Urethritis - Urethral stricture - Urinary tract infection - Kidney stone
Tumours of the kidney
Renal cell carcinoma - Wilms' tumor (children)
See also congenital conditions (Q60-Q64, 753)
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