Renal Calculai
Renal CalculaiKidney Stone
A kidney stone, 8 millimeters (0.31in) in diameter
History
The existence of kidney stones was first recorded thousands of years ago, andlithotomy for the removal of stones is one of the earliest known surgical procedures.
In 1901, a stone discovered in the pelvisof an ancient Egyptianmummy was dated to 4,800BC.
Medical texts from ancient Mesopotamia, India, China, Persia, Greece, and Romeall 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, and this work served as the basis for this procedure until the 18th century.
Famous people who were kidney stone formers include Napoleon I, 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.
New techniques in lithotomy began to emerge starting in 1520, but the operation remained risky.
After Henry Jacob Bigelow popularized the technique of litholapaxyin 1878, 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.
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.
Introduction to the Urinary Tract
The urinary tract, or system, consists of the kidneys, ureters, bladder, and urethra.
The kidneys are two bean-shaped organs located below the ribs toward the middle of the back, one on each side of the spine.
The kidneys remove extra water and wastes from the blood, producing urine.
They also keep a stable balance of salts and other substances in the blood.
The kidneys produce hormones that help build strong bones and form red blood cells.
The urinary tract.
Narrow tubes called ureters carry urine from the kidneys to the bladder, an oval-shaped chamber in the lower abdomen.
Like a balloon, the bladder's elastic walls stretch and expand to store urine. They flatten together when urine is emptied through the urethra to outside the body.
Definition And Explanation
A kidney stone, also known as a renal calculus (from the Latinren, "kidney" and calculus, "pebble") is a solid concretion or crystal aggregation formed in the kidneys from dietary minerals in the urine.
The kidneys are the master chemists of your body, primarily responsible for filtering metabolites and minerals from the blood circulation. These secretions are then passed to the bladder and then out of the body as urine through the urethra.
The urine has all the ingredients that form the stone, but all these ideally pass through without our knowledge. When there is an imbalance in any of these substances, the crystals cluster together into stones. In medical terminology these deposits are known as Renal Calculi.
Kidney stones are clumps developed from solidified crystals in the kidney or urinary tract. The size of stone can be as small as a grain of sand to one as large as the size of a golf ball.
Kidney stones are the commonest complaint and one of the most painful of the urological disorders. Kidney stones may modify the victim's behaviour with great fear of intense pain and threaten with failure of the kidney.
People who have already had more than one kidney stone are prone to develop more stones. A family history of kidney stones is also a risk factor for the development of kidney stones.
Urinary stones are typically classified by their location in the kidney (nephrolithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis), or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds).
About 80% of those with kidney stones are men. Men most commonly experience their first episode between 30 and 40 years of age, while for women the age at first presentation is somewhat later.
One in every twenty people develops a kidney stone at some point in their life. Recurrence rates are very high around 50% over a 5-10 year period and 75% over 20 years.
Men are affected approximately 4 times more often than women. The prevalance of kidney stones begins to rise when men reach their 40s, and it continues to climb into their 70s.
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 (usually at least 3 millimeters (0.12in)) they can cause obstruction of the ureter.
Ureteral obstruction causes postrenal azotemia and hydronephrosis (distension and dilation of the renal pelvis and calyces), as well as spasm of the ureter. This leads to pain, most commonly felt in the flank (the area between the ribs and hip), lower abdomen, and groin (a condition called renal colic).
Renal colic can be associated with nausea, vomiting, fever, blood in the urine, pus in the urine, and painful urination. Renal colic typically comes in waves lasting 20 to 60 minutes, beginning in the flank or lower back and often radiating to the groin or genitals.
The diagnosis of kidney stones is made on the basis of information obtained from the history, physical examination, urinalysis, and radiographic studies. Ultrasound examination and blood tests may also aid in the diagnosis.
Classification
Kidney stones are typically classified by their ;
- location and
- chemical composition.
Classification Based on Chemical composition
Scanning electron micrograph of the surface of a kidney stone showing tetragonal crystals of Weddellite (calcium oxalate dihydrate) emerging from the amorphous central part of the stone (the horizontal length of the picture represents 0.5 mm of the figured original)
Multiple kidney stones composed of uric acid and a small amount of calcium oxalate
Calcium-containing stones
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 phosphatein the form of apatite or brushite.
Factors that promote the precipitation of oxalate crystals in the urine, such as primary hyperoxaluria, are associated with the development of calcium oxalate stones.
The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis.
Calcium Oxalate Kidney Stone
The calcium oxalate kidney stone variety is the most common making up 80%-90% of all kidney stone formations. The problem develops when calcium in the body is not disposed of efficiently and builds up in the urine. As the calcium passes through the kidneys it binds itself to other nutrients such as oxalate or phosphate.
Oxalate, or oxalic acid, gets its name from the biological process of incomplete oxidation of carbohydrates.
It occurs naturally in
- rhubarb (especially leaves),
- black pepper,
- buckwheat,
- kiwi fruit,
- star fruit,
- chocolate,
- nuts,
- cocoa,
- spinach,
- beets,
- chard,
- berries and
- beans.
Tea leaves also contain a high concentration of oxalate.
So if you are prone to the development of calcium oxalate kidney stones, stay away from the foods and beverages listed above.
Research has shown that low calcium diets have actually led to a higher risk of developing kidney stones. As ones intake of calcium decreases, the amount of oxalate in the bloodstream increases, thus increasing the amount of oxalate in the kidneys that eventually binds with the calcium forming stones.
Upshot...moderate intake of calcium is advised. Don't be afraid of calcium. Potassium Citrate and Magnesium Citrate have proven effective in reducing calcium oxalate stones as discussed at Duke University.
Struvite stones
Struvite was first described from medievalsewer systems in HamburgGermany in 1845 and named for geographer and geologist Heinrich Christian Gottfried von Struve (1772-1851).
Struvite is occasionally found in canned seafood, where its appearance is that of small glass slivers, objectionable to consumers for aesthetic reasons but of no health consequence.
Use of struvite as an agricultural fertilizer was in fact first described in 1857.
Struvite (magnesiumammonium phosphate) is a phosphate mineral with formula: NH4MgPO4·6H2O.
Struvite crystallizes in the orthorhombic system as white to yellowish or brownish-white pyramidal crystals or in platey mica-like forms.
It is a soft mineral with Mohs hardness of 1.5 to 2 and has a low specific gravity of 1.7.
It is sparingly soluble in neutral and alkaline conditions, but readily soluble in acid.
Struvite urinary stones and crystals form readily in the urine of animals and humans that are infected with ammonia-producing organisms.
They are potentiated by alkaline urine and high magnesium excretion (high magnesium/plant-based diets).
They also are potentiated by a specific urinary protein, in domestic cats.
About 10–15% of urinary calculi are composed of struvite.
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 metabolizeurea into ammonia and carbon dioxide.
This alkalinizes the urine, resulting in favorable conditions for the formation of struvite stones.
Infection stones can grow rapidly, forming large calyceal staghorn (antler-shaped) calculi.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.
Even in the absence of infection, accumulation of struvite crystals in the urinary bladder is a problem frequently seen in housecats, with symptoms including difficulty urinating (which may be mistaken for constipation) or blood in the urine (hematuria).
The protein cauxin, a protein excreted in large amounts in cat urine that acts to produce a feline pheromone, has recently been found to cause nucleation of struvite crystals in a model system containing the ions necessary to form struvite.
This may explain some of the excess struvite production in domestic cats. In the past, surgery has been required to remove struvite uroliths in cats; today, special acidifying low magnesium diets may be used to dissolve sterile struvite stones.
Upper urinary tract stones that involve the renal pelvis and extend into at least 2 calyces are classified as staghorn calculi. Although all types of urinary stones can potentially form staghorn calculi, approximately 75% are composed of a struvite-carbonate-apatite matrix.
They are also commonly seen in people with underlying metabolic disorders, such as idiopathichypercalciuria, hyperparathyroidism, and gout.
Uric acid stones
Uric acid was first isolated from kidney stones in 1776 by Scheele.
As far as laboratory synthesis is concerned, in 1882, Horbaczewski claimed to have prepared uric acid by melting urea hydrogen peroxide with glycine, trichlorolactic acid, and its amide.
Soon after, repetition by Eduard Hoffmann shows that this preparation with glycine gives no trace of uric acid, but trichlorolactimide produces some uric acid. Thus, Hoffmann was the first to synthesize uric acid.
About 5–10% of all stones are formed from uric acid.
Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C5H4N4O3. It forms ions and salts known as urates and acid urates such as ammonium acid urate.
Uric acid is a product of the metabolic breakdown of purine nucleotides.
High blood concentrations of uric acid can lead to a type of arthritis known as gout. The chemical is associated with other medical conditions including diabetes and the formation of ammonium acid urate kidney stones.
People with certain metabolic abnormalities, including obesity, may produce uric acid stones.
Uric acid is a diprotic acid with pKa1=5.4 and pKa2=10.3. Thus in strong alkali at high pH, it forms the dually charged full urate ion, but at biological pH or in the presence of carbonic acid or carbonate ions, it forms the singly charged hydrogen or acid urate ion as its pKa1 is lower than the pKa1 of carbonic acid.
As its second ionization is so weak, the full urate salts tend to hydrolyze back to hydrogen urate salts and free base at pH values around neutral.
It is aromatic because of the purine functional group.
As a bicyclic, heterocyclic purine derivative, uric acid does not protonate like carboxylic acids.
X-Ray diffraction studies on the hydrogen urate ion in crystals of ammomium hydrogen urate, formed in vivo as gouty deposits, reveal the keto-oxygen in the 2 position of a tautomer of the purine structure exists as a hydroxyl group and the two flanking nitrogen atoms at the 1 and 3 positions share the ionic charge in the six membered pi-resonance-stabilized ring.[2]
Thus, while most organic acids are deprotonated by the ionization of a polar hydrogen-to-oxygen bond, usually accompanied by some form of resonance stabilization (resulting in a carboxylate ion), uric acid is deprotonated at a nitrogen atom and uses a tautomericketo/hydroxy group as an electron-withdrawing group to increase the pK1 value.
The five membered ring also possesses a keto group (in the 8 position), flanked by two secondary amino groups (in the 7 and 9 positions), and deprotonation of one of these at high pH could explain the pK2 and behavior as a diprotic acid.
Similar tautomeric rearrangement and pi-resonance stabilization would then give the ion some degree of stability. (On the structure shown at the upper right, the NH at the upper right on the six membered ring is "1", counting clockwise around the six membered ring to "6" for the keto carbon at the top of the six membered ring.
The upper most NH on the five membered ring is "7", counting counter clockwise around this ring to the lower NH, which is "9".)
Uric acid stones (see image below) are the most common cause of radiolucent kidney stones in children.
Several products of purine metabolism are relatively insoluble and can precipitate when urinary pH is low.
These include 2- or 8-dihydroxyadenine, adenine, xanthine, and uric acid.
The crystals of uric acid may initiate calcium oxylate precipitation in metastable urine concentrates .
Uric acid stones.
The terms gouty nephropathy, urate nephropathy, and uric acid nephropathy are used to describe renal insufficiency due to uric acid precipitation within the renal tubules.
Uric acid urolithiasis or uric acid kidney stones refer to development of a stone or calculus composed of significant amounts of urate in the renal pelvis, ureter, or bladder.
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.
Certain medical conditions may further trigger uric acid kidney stone formation. Theseinclude:-
Diabetes too may lead to uric acid kidney stones. Research reveals that people with type 2 diabetes have highly acidic urine, which may lead to uric acid stones.
Insulin Resistance.
Genetic factors.
Chronic diarrhea.
Binge Drinking.
Some rare types of anemia.
Blood cancers.
Lead poisoning.
Not eating for long periods of time.
Genetic Factors.
Hypocitraturia, a low amount of citrate in the urine
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.
Cystine Kidney Stones
Cystinuria (siss-tin-NYUR-Ree-Uh), and the chemical cystine (SISS-teen) were discovered in 1812 by Dr. William Hyde Wollaston (1766-1828), originally of Norfolk, England.
Wollaston ( a partially blind man), working with his colleague, Dr. Humphrey Davy, discovered a chemical in a stone found in the bladder which Wollaston named "cystic oxide."
Another doctor, Berzelius, recognized that this discovery was not an oxide, and he changed the name to cystine.
In the old school of writing, it was spelled "cystin". The name cystine has nothing to do with its chemical composition, but rather, for the place of its discovery. It was so named because of its location in the bladder ( cyst= bladder) (Note: the bladder is named "cyst" in reference to cyst, a pouch or closure, as the bladder takes the appearance of a pouch). Therefore, it was mistakenly thought that cystine stones originated only in the bladder.
Cystine was the first amino acid to be discovered thru medical research.
Dr. Wollaston says upon his finding of the unusual stone: "A new species of urinary calculus had been taken [by Dr. Reeve] from his brother when he was five years old. These calculi have a yellowish semi-transparency; and they have also a peculiar glistening luster. I am inclined to consider it as an oxide; and it may be convenient to give it the name of cystic oxide."