What is the cause of uric acid

what is the cause of uric acid

Uric Acid Test

Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C 5 H 4 N 4 O lovetiktokhere.com forms ions and salts known as urates and acid urates, such as ammonium acid lovetiktokhere.com acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. High blood concentrations of uric acid can lead to gout and are associated with other. If your body makes too much uric acid or doesn't release enough into your urine, it can make crystals that form in your joints. This condition is known as gout. Gout is a form of arthritis that causes painful inflammation in and around the joints. High uric acid levels can also cause other disorders, including kidney stones and kidney failure.

Urea vs Uric Acid. Though many get confused, urea and uric acid are two different compounds. We are very familiar with these compounds as these are found and used for various purposes in our daily lives. In human body, urea is a waste product. It is excreted along with other components in the urine. The other components are sodium chloride and other chemicals. Urea is excreted from the body through sweat also.

Uric acid also is excreted from the body, but it is the final product in the urine metabolism. So it is always excreted with urine. Uric acid is the excreta of birds and is usually solid. While human excreted urea is liquid in form. Both these compounds are organic in nature. A molecule of urea has two amine residues and these are joined by the functional group, carbonyl.

Uric acid is made from xanthine oxidase. It id toxic to the tissues. Urea is colorless, soluble in water, odorless, and neutral. It is not tthe and is widely used in the manufacture of the fertilizers. This is because it ackd a very good source for nitrogen and nitrogen promotes the effective growth of plants. The transportation cost of urea also is less as it is a solid fertilizer and how many years from abraham to jesus nitrogen content is high.

So the amount of nitrogen transported is more when urea is being transported. It is also used in the feedstock products. Urea has uses in the automotive industry and chemical industry as well. Uric acid also is a fertilizer owing to its nitrogen content. But the form of uric acid used is Guano. The uric acid has a crystalline form and this is used in the manufacture of some reflectors to repel fireflies.

The high level of blood urea causf humans can affect the kidney. If the uric acid content becomes high it can cause pains in your joints. More raised level of uric acid in the body leads to the formation of kidney stones. In human beings, the blood urea converts to uric acid. If this is in excess, the effect of this compound on the kidneys is high in diabetic patients.

Causf excess of urea deposit causr found in the body, it indicates the failure or less functioning of the kidneys. Sometimes it can be how to do wedding registry at bed bath and beyond to the renal failure as well.

Uric acid in bird causr matter is in the solid state and urea in humans is in the liquid form. Urea has widespread uses in different domains, but uric acid does not have that many uses. Urea is the more commonly used fertilizer than any forms of uric acid. Uric acid excess in the body leads to kidney stones, and excess levels of urea in the body shows the failure of the kidney. The prolonged deposit of uric acid is more harmful to the human body tissues than the deposit of urea.

Cite Manisha Kumar. October caid, Good explanation of the difference between urea and uric acid. But you say that urea is NH2 2CO. This is correct. I think avid is an error; there is no such thing as a N2H unit. What is ridden at a velodrome should be two units of NH2, one on either side causse the CO.

I have a problem that some times my uric acid rises to 7. Can somebody clarify on this issue. Os uric acid is 6. What actual comdition is?? I have hyperthyroidism useing methimizole 5mg tab is any co relation for this?? Name required. Email required. Please note: comment moderation is enabled and may delay your comment. There is no need to resubmit your comment. Notify me of followup comments via e-mail. Written by : Manisha Kumar. User vause all risk of use, damage, or injury.

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Being stones, uric acid stones cause the usual problems of pain, obstruction, bleeding and infection. But they have some special features. The most obvious is stone color – red to orange because the crystals take up a variety of pigments mostly derived from hemoglobin breakdown. Sep 30,  · Uric acid is a waste product in the body. Sometimes, uric acid can build up in the joints and tissues, causing a range of health problems. These include gout, a form of arthritis. Sep 17,  · If uric acid is deposited in the genital area, the uric crystals cause inflammation of the testicles, prostatitis. What Are Common Causes Of Uric Acid? Two phenomena that are increased intake of purines or reduction of uric acid excretion or both occurring in parallel in the blood leads to increased uric acid.

Uric acid stones, to me, means not just pure uric acid stones but any uric acid in stones. If this seems fey, let me explain. Uric acid is a peculiar kind of crystal. Low urine pH causes them and treatment that raise urine pH prevent them altogether. Whether they form combined with calcium stones or pure, treatment is the same. Why then scruple over percentages? If I find uric acid in any stone, I look at urine pH with a yellow eye.

Should it be low I treat it surely and on the moment so at least that crystal be banished forever. The Profligate Punished by Neglect, Edward Penny catches the common motif of diet excess, obesity, diabetes, and gout — the joint manifestations of uric acid crystals. Note the abdominal fat denoted by his overly tight vest.

All of these states can lower urine pH and lead to uric acid stones. This article has a pragmatic leaning and eschews excessive scientific details. I have written a more mechanistic article that explores how the low urine pH might arise and cause uric acid stones. Read this one first unless you are already reasonably expert. Given my prior reasoning, I call patients who have any uric acid in their stones uric acid stone formers but reserve the right to use compound names when needed.

If all stones are only uric acid, I call such patients pure uric acid stone formers. These niceties of naming have the practical value of calling to mind the perpetual need for dual or multiple treatments — for uric acid but also for whatever crystals might be present.

Commonly uric acid stones show poorly on routine flat plate x rays having only carbon, nitrogen, oxygen and no heavier atoms such as calcium. On CT scans they do not look different from calcium stones but radiographic density can be measured and tends to be lower.

As this article points out, machines differ in their results and evaluation may therefore be less than perfect. Dual energy scanners are more precise, but also prone to many potential artefacts. Multiple reports, by contrast, indicate that CT measurements of radiographic density can reliably distinguish uric acid stones from calcium stones.

A reasonable present view is that lower radiographic density is an excellent clue to uric acid in stones, but far from definitive as stone analysis is.

I hesitate to classify a patient on scanning evidence alone. Being stones, uric acid stones cause the usual problems of pain, obstruction, bleeding and infection. But they have some special features. The most obvious is stone color — red to orange because the crystals take up a variety of pigments mostly derived from hemoglobin breakdown.

Recently scientists have determined the structure of one of these — urorosein. Sometimes, coarse or fine orange or red gravel passes, made up of uric acid crystals. Because the crystals form not as a complex lattice like calcium with oxalate or with phosphate but simply as uric acid crystallizing with itself, the process can be swift to begin and require very little supersaturation. Said more technically the energy required to create the crystal is relatively low. This means the upper limit of metastability — the supersaturation needed to initiate crystal formation is not far from solubility, so values above 1 even if below 2, could suffice.

Practically it means that bursts of supersaturation during the day can bring on showers of gravel and growth of stones. Also, urine contains a lot of uric acid. Common daily losses of oxalate approximate perhaps 25 — 50 mg, compared to — 1, mg of uric acid. The sheer amounts available when coupled to the rapid and facile crystal formation and growth allow stones to enlarge rapidly and achieve very large sizes, enough to fill the renal pelvis and calyces — so called staghorn stones.

Very uncommonly, sudden lowering of urine pH coupled with low urine volume can cause crystallizations in the terminal collecting ducts with acute kidney failure. This was once not uncommon during treatment of malignancies, but modern attention to uric acid surges from tumor killing has made it rare indeed.

Today, one does not expect to see it apart from unusual situations. I made the figures for this section anew but from a lovely data file constructed some years ago by Joan Parks , who was my scientific colleague from until her retirement about 8 years ago. Her legacy of curated data files sustains a lot of my public writing, now, and she deserves a place in it. Uric acid crystals form like all crystals because of supersaturation.

In this instance, that supersaturation varies remarkably with urine pH. In the figure, supersaturation ranges from 0. The dashed line at 1 represents equilibrium, or saturation, the level where crystals neither form nor dissolve. The horizontal axis shows urine pH. The dashed lines at 5. The tiny points each are one 24 hour urine from patients and normal people. Like an ancient Persian scimitar, points curve downward from 8 to 0. Urine volume matters.

Low volumes red 0. But pH trumps volume. At pH 5. Below 5. In speaking about excretion of uric acid we need to insert a note about the molecular species involved. Uric acid is a weak acid, which means it can take up or donate a proton to water. When it has its proton, that proton neutralizes much of its charge , so water molecules cannot themselves form charge bonds with it to keep it in solution.

This means that the molecule becomes very poorly soluble and tends to crystallize. When it loses its proton into solution, it has a charged site for water to relate to and also requires a counterion, which in urine will be sodium, potassium, and ammonium ion.

But all three salts have much higher solubility than uric acid itself. When we measure and report urine uric acid excretion we show the sum of all salts and the acid in one number. Obviously this total should affect supersaturation, but the effect is relatively small because so much depends on pH that sets the percentage of uric acid per se — the fraction that has its proton and is therefore poorly soluble. One presumes that urine pH of uric acid stone formers must lie below that of other kinds of stone formers, and numerous reviews and case descriptions have proven this true.

The dot distribution just below shows individual 24 hour urine pH measurements for calcium oxalate blue , calcium phosphate green and uric acid red stone formers. Here I include among uric acid stone formers those with both pure and mixed stones. Calcium oxalate stone former pH ranges widely with an average at about 5. Calcium phosphate stone formers average a lot higher — around 6.

Uric acid stone formers lie in an acid range. Their average is about 5. So uric acid stone formers produce a very acid urine compared to other stone formers, and the pH is exactly in the range to produce supersaturation that can drive formation of uric acid stones and hold them steady or cause them to grow. To see this, just look back on the graphs showing supersaturation vs. I have said that any uric acid in stones means pH should be raised because at least that portion of the stone burden might dissolve or at leasts not grow.

The figure below shows urine pH associated not with the kind of patient — calcium oxalate, calcium phosphate or uric acid stone former, but by the fraction of a given stone made up of uric acid. Blue means no uric acid at all. With a scattered few points as exceptions, stones made of mainly uric acid go with urine pH values mostly below 5.

The graph makes a point we often speak of but rarely show. Oxalic acid has a very low pKa — is a strong weak acid. So it has charges available for binding to calcium that very hardly at all with urine pH all the way down to 4. So these stone crystals are indifferent to pH. I makes another point, too, one that a patient emphasized in a comment to this article and that I failed to mention in the original version.

Of all stones that contain any uric acid, at least in my collection of data, most are mainly composed of uric acid. See where the red — pure uric acid — stones make up the largest mass in the figure just above? This is not to say that patients are uncommon who make both calcium and uric acid stones — mixed stone formers. The graph shows the stones themselves. People who make both kinds of stones need treatment with alkali so they will stop making uric acid crystals.

They also may need treatment against their calcium stones. Stones that contain both uric acid and calcium — usually calcium oxalate — mean the patients may need treatment against both their uric acid stone formation — that would be alkali, and for their calcium stone forming.

So in the final analysis, whether the stones are mixed, or patients form both uric acid and calcium stones the answer is the same: Treat against both crystals. In a larger study urine pH seems as heritable as urine calcium excretion.

Of interest, such dietary traits as sugar, calcium, and protein consumption that could influence stone formation also had significant heritability. Historically, uric acid stones have been linked to gout. A recent but brief review repeats that fact. Likewise, another review. Given low urine pH drives uric acid crystallization, one has to ask whether some kinds of patients might be expected to produce acid urines. In answer, those most common are obese, older, diabetic , hypertensive , and prone to modest reduction of kidney function.

Obesity itself, without necessarily overt diabetes correlates with lower urine pH in a progressive manner — as obesity increases urine pH falls. Resistance to the actions of insulin — so called insulin resistance — is often invoked as a general paradigm to encompass the general class of abnormalities that lower urine pH. Metabolic syndrome, a mix of insulin resistance with lipid and vascular abnormalities is linked to kidney stones.

But not to uric acid stones per se.



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