Showing posts with label stones. Show all posts
Showing posts with label stones. Show all posts

Uric acid kidney stones

   ›      ›   Uric acid kidney stones.

What are uric acid kidney stones

Uric acid kidney stones are renal calculi formed by the crystallization of uric acid in the urine.
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Uric acid renal calculi are associated with disorders like hyperuricosuria with or without hyperuricemia. In healthy individuals diet rich in purines (explained below) can lead to increased amount of uric acid excretion (hyperuricosuria). A combination of factors like hyperuricosuria, low urinary volume and persistently low urinary pH lead to uric acid kidney stones. Certain food habits, metabolic abnormalities or hereditary factors may also play a part in the formation of these types of nephrolith. One positive fact about uric acid kidney stones is that they can be dissolved successfully.

Purines are heterocyclic aromatic organic compounds and some of them (adenine, guanine) are the building-blocks of deoxyribonucleicacid - DNA, and ribonucleicacid - RNA in the living cells. Other important purines are, hypoxanthine, xanthine, theobromine, caffeine, uric acid and isoguanine.
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Purines are biosynthesized and are found in high concentration in meat products (meat extracts, beef kidney, liver, brain and kidney), certain fish (anchovies, sardines, herring, mackerel), sweetbreads, asparagus, cauliflower, spinach, mushrooms, green peas and lentils. These purines are broken down into uric acid for excretion and when in excess cause hyperuricemia (excess uric acid in blood serum) and hyperuricosuria and uric acid kidney stones.

what causes uric acid kidney stones?

As said earlier, the pathogenesis of these uric acid kidney stones involves hyperuricosuria, low urinary volume, and persistently low urinary pH. Severe hyperuricosuria occurs in patients with certain medical conditions like chronic diarrhea, myeloproliferative disorders, metabolic disorders, Lesch-Nyhan syndrome and insulin resistance.

Acidic urine

The persistent low pH urine is a greater factor than hyperuricosuria in causing the uric acid kidney stones. It is to be noted that an individual with normal uric acid excretion but a persistent low pH urine can develop the nephrolith, whereas those with a higher urine pH but excessive urate excretion may not develop the calculi. Those with hyperuricosuria but normal urine pH may develop mixed calculi composed of calcium oxalate and urate.

Acidic urine is caused by factors like renal tubular disorders, chronic diarrhea or severe dehydration. In patients with chronic acidic urine production, it is found that defects in renal tubular ammonia production and secretion is a cofactor. A gene related to uric acid kidney stones has been identified but the pathophysiology has not been totally elucidated.

Resorption and secretion

Normally, uric acid exists as urate ions in the blood serum. In the human body nearly 300 to 400 mg of urate is accounted for by endogenous biosynthesis. The excess of it comes from the ingested purines. Normally almost entire urate is filtered out by the glomerulus. However only about ten percent is excreted and the balance is reabsorbed. Altogether only 70% of the excreted urate is handled by the kidneys and the rest is eliminated by the skin, hair and gut.

Tin C Ngo et al reported that nearly 99% of the filtered load of urate is reabsorbed in the S1 segment of the proximal tubule by the urate transporter URAT1. URAT1 is encoded by the gene SLC22A12. They further reported that "urate secretion occurs in the S2 segment via the organic acid transporters (OAT1 and OAT3) as well as a selective urate transporter, URAT. Post-secretory reabsorption of urate occurs in the S3 segment and is also mediated by URAT1."

Decreased urinary output

Uric acid nephrolithiasis is higher in people living in tropics as well as in those working in hot conditions. Obviously these situations cause concentration of urine. The solutes in the concentrated urine tend to precipitate. In high concentrations urate precipitates as uric acid and monosodium urate. In those predisposed to uric acid calculi formation, these hot conditions induce uric acid kidney stones.

Chronic diarrhea

Chronic diarrhea contributes to gastrointestinal bicarbonate loss from the body and leads to acidic urine and uric acid kidney stones. Diseases like inflammatory bowel disease, Crohn's disease, ulcerative colitis, familial adenomatous polyposis, colorectal cancer and total colonic Hirschsprung's disease may require removal of colon and ileostomy or colon resection. In such conditions hypovolemia may occur leading to supersaturation of solutes in the urine and acidity of urine as well as chronic gastrointestinal loss of bicarbonate.

Hyperuricosuria and dietary purines

In normal individuals hyperuricosuria is caused when purine and animal protein rich diet is taken. As said earlier, patients with hyperuricosuria but normal urine pH can develop kidney calculi containing urate and calcium oxalate compounds. It may be compounded by a mild protein-induced metabolic acidosis causing decrease in urine pH. Hyperuricosuria is also caused by renal diseases such as Fanconi syndrome, Hartnup disease, Wilson’s disease, and familial hypouricemic hyperuricosuria.

Diabetes, insulin resistance and obesity

There is an increase in the number of diabetes patients with uric acid kidney stones. The metabolic syndrome and type 2 diabetes cause insulin resistance. Insulin resistance lowers urine pH by impairing kidney ammoniagenesis. Daudon M et al observed that "it is suggested that patients with UA stones, especially if overweight, should be screened for the presence of type 2 diabetes or components of the metabolic syndrome."

Genetic predisposition

Genetic predisposition to uric acid nephrolithiasis is well established. The ZNF365 gene on chromosome 10q21–q22 is found associated with uric acid kidney stones. The functional characteristics are yet to be totally elucidated. However this trait requires influence of certain environmental factors for its expression.

Congenital hyperuricemia

Lesch–Nyhan syndrome (juvenile gout) is a rare X-linked recessive inherited disorder. It causes a deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase leading to hyperuricemia and hyperuricosuria. The purines from cell break down are not salvaged causing mental retardation, gout, uric acid kidney calculi. Glycogen storage disease type I (von Gierke's disease) is an autosomal recessive glycogen storage disease. It causes hyperuricemia, hypoglycemia and hyperlactacidemia. Patients affected by these disorders have the tendency form uric acid kidney stones.

Gout

Most of the patients suffering from gout also suffer from hyperuricemia. The buildup of uric acid in the blood causes its deposits in the joints causing severe pain. These patients may also develop excessive excretion of urate leading to uric acid nephrolithiasis. Gout can occur due a number of reasons, including diet, genetic predisposition, or underexcretion of urate.

Idiopathic uric acid nephrolithiasis

Some uric acid nephrolithiasis patients do not have identifiable congenital or acquired cause. Their condition is described as idiopathic uric acid nephrolithiasis. They have normal uric acid excretion and also normal urine pH. They also do not have any genetic predisposition or congenital hyperuricemia.

Malignancy

Myeloproliferative disorders and malignancy cause rapid cell turnover and also tumor necrosis during therapy. The tumor lysis and cell death can cause massive increase in purines leading to hyperuricemia and hyperuricosuria. Other conditions like sickle cell anemia and psoriasis also increase cell turnover leading to hyperuricemia, hyperuricosuria and uric acid kidney stone formation.

Uric acid kidney stones symptoms and diagnosis

The signs and symptoms of these calculi are similar to other nephrolith. Some of the common symptoms are back, flank and abdominal pain, nausea, renal colic, urinary tract infections, hematuria and groin pain. Persisting low urinary pH, less than 5.5 along with the above symptoms may indicate nephrolithiasis. Non-contrast-enhanced computed tomography or renal ultrasonography may help in uric acid calculus detection. Analysis of the expelled uric acid calculus can further guide in treatment modalities.

Uric acid kidney stones treatment

The treatment must focus on hydration, increasing urinary pH and reducing purine intake if hyperuricosuria is suspected. In cases where there is severe obstruction, severe infection and unremitting pain surgical options may be considered.

Hydration and dissolve uric acid kidney stones

The treatment is focussed on hydration to void more than 2,000 ml of urine daily. Simultaneously treatment with oral alkalies like potassium citrate or sodium bicarbonate to achieve urine pH between 6.2 to 7.0 is necessary. The treatment with potassium citrate can help in dissolving the existing uric acid calculi as well as prevent their recurrence. Urinary pH levels must be closely monitored to maintain high urine pH. However urine pH above 7.0 is conducive for calcium phosphate precipitation.

Uric acid kidney stones diet

Those patients who are suffering from hyperuricosuria as well as uric acid kidney stone formers must avoid foods rich in purines like red meat and meat products, certain types of fish, poultry, shellfish, sugar-sweetened foods, high fructose corn syrup, beer and legumes. The diet also should not be high in animal protein as it may produce a transient metabolic acidosis leading to acidic urine. Taking citrus fruits helps in increasing urine pH.

Allopurinol

Medicines like allopurinol block the uric acid excretion and kidney urolithiasis by inhibiting xanthine oxidase enzyme which catalyzes reactions producing urate. However as allopurinol may cause adverse reactions, its administration must be closely observed.

Surgical options

Surgical options are available for removing uric acid kidney stones that are not dissolving. Extracorporeal shockwave lithotripsy, retrograde endoscopic lithotripsy and extraction, ureteroscopy, percutaneous nephrostolithotomy, percutaneous nephrolithotomy, combination therapy and open surgery are the surgical options available for removing the uric acid kidney stones.
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References:
1.Ferrari P, Bonny O. Diagnosis and prevention of uric acid stones. Ther Umsch. 2004 Sep;61(9):571-4.
2.Tin C Ngo, Dean G Assimos. Uric Acid Nephrolithiasis: Recent Progress and Future Directions. Rev Urol. 2007 Winter; 9(1): 17–27.
3.Shekarriz B, Stoller ML. Uric acid nephrolithiasis: current concepts and controversies. J Urol. 2002 Oct;168(4 Pt 1):1307-14.
4.Cicerello E, Merlo F, Maccatrozzo L. Urinary alkalization for the treatment of uric acid nephrolithiasis. Arch Ital Urol Androl. 2010 Sep;82(3):145-8.
5.Bobulescu IA, Maalouf NM, Capolongo G, Adams-Huet B, Rosenthal TR, Moe OW, Sakhaee K. Renal ammonium excretion after an acute acidic load: blunted response in uric acid stone formers but not in patients with type 2 diabetes. Am J Physiol Renal Physiol. 2013 Nov 15;305(10):F1498-503.
6.Reichard C, Gill BC, Sarkissian C, De S1, Monga M. 100% uric Acid stone formers: what makes them different?. Urology. 2015 Feb;85(2):296-8.
7.Daudon M, Traxer O, Conort P, Lacour B, Jungers P. Type 2 diabetes increases the risk for uric acid stones. J Am Soc Nephrol. 2006 Jul;17(7):2026-33.
8.Sakhaee K, Maalouf NM. Metabolic syndrome and uric acid nephrolithiasis. Semin Nephrol. 2008 Mar;28(2):174-80.
9.Maalouf NM. Metabolic syndrome and the genesis of uric acid stones. J Ren Nutr. 2011 Jan;21(1):128-31.
10.Naim M. Maalouf. Metabolic Syndrome and the Genesis of Uric Acid Stones. J Ren Nutr. 2011 Jan; 21(1): 128–131.
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Cystine kidney stones from amino acid cystine

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What are cystine kidney stones?

Cystine kidney stones are renal calculi formed from the excessive cystine (an amino acid) present in the urine.
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In normal individuals only a relatively small amount of cystine is excreted in the urine. Cystine stones rarely form when the urine excretion of this amino acid is less than 150 mg per day. The amount of excretion of cystine and the dibasic amino acids, including ornithine, arginine and lysine, is regulated by the renal cystine transport.

Urine production is a complex process. More than 1200 ml of blood passes through the kidneys per minute. Each kidney has about one million nephrons. Each nephron is the primary functional unit of kidney and has a filtering system known as glomerulus. The renal tubule is the reabsorption, secretion and collecting system, through which the filtered liquid passes. Except for very large macromolecules and blood cells, the blood plasma is filtered into the tubule. 80% of the filtrate is reabsorbed at the proximal tubule by active and passive absorption. Several separate luminal transmembrane channels function to reabsorb and transport back minerals, vitamins, amino acids etc into the bloodstream.

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The cystine transporter (a high-affinity luminal transmembrane channel) promotes the reabsorption of the filtered cystine and dibasic amino acids from the luminal plasma fluid of the renal proximal convoluted tubules in the kidney. Any impairment to the renal cystine transport, as in cystinuria, results in decreased proximal tubular reabsorption of filtered cystine. The net result is increased urinary cystine excretion leading to its crystallization and stone formation.

Cystine kidney stones causes

Cystine stones are caused by cystinuria. Cystinuria is an inherited autosomal recessive disease. It causes defective renal tubular reabsorption of cystine and the three dibasic amino acids arginine, lysine and ornithine. It also affects the intestinal transport of these amino acids. Cystinuria patient has a lifelong risk of cystine stone formation because, unlike dibasic amino acids, cystine has low solubility in urine. Further in acidic urine, cystine is less soluble and precipitates faster, forming the calculus. Infections and obstructions in the urine flow can also give rise to formation these calculi.

Mutations within the SLC3A1 and the SLC7A9 genes are known to be associated with cystinuria. Cystinuria being an inherited recessive disease, the patient has to get the mutant genes from both the parents to become a cystinuric. Erik.Fjellstedt et al had reported that apart from the SLC3A1 and the SLC7A9 genes,
an additional gene or genes participate in the urinary cystine reabsorption in the cystinuric patients who currently are without a full genetic explanation for their disease.

Types of cystinuria

Earlier phenotypically distinctive groups of cystinuria, referred to as types I, II, and III were described. However in this classification it is cumbersome to differentiate type II cystinuria from type III. The type II homozygotes lack intestinal cystine absorption. With the identification of multiple mutations in the SLC3A1 and the SLC7A9 genes associated with the disorder, a genotypic classification of cystinuria has been introduced. Certain distinctive inheritance patterns are becoming clear.

The type I form of cystinuria is found to be completely recessive. Heterozygote individuals with type I mutations do not show any clinical manifestations. However the non-type I form (types II and III) of cystinuria is incompletely recessive. Heterozygote individuals with non-type I mutations have varying levels of urinary cystine excretion and even form cystine stones.

Cystine kidney stones symptoms

The individuals with these calculi, experience all the typical symptoms associated with renal calculi. Blood in the urine (hematuria), nausea, pain in the flanks, renal colic, obstruction to urine flow, urinary tract infections, pyelonephritis, renal insufficiency and end-stage kidney disease are some of the symptoms.

Cystine kidney stones diagnosis

The key finding in diagnosis is the presence of large amount of cystine in the urine. As cystine is a sulfur containing amino acid, the urine may have the characteristic odor of rotten eggs. Urinalysis may show typical hexagonal crystals. Sodium cyanide–nitroprusside test is done for qualitative determination of concentrations followed by ion-exchange chromatographic quantitative analysis for confirmation. There are also increased urinary levels of three other amino acids, lysine, arginine, and ornithine. These kidney stones may not be visible on most x-rays, CT's, and ultrasounds.

Cystine stones prevention

As cystine stone formation is a lifelong problem, the main focus must be on the prevention rather than the treatment.
  • Hydration, urinary alkalinization, urine dilution and increasing urine output are of prime importance.
  • The patient may be encouraged to take much more than one liter of water per twenty kilograms of body weight in a day. Additional water is necessary to compensate losses due to heat and sweating.
  • For avoiding nocturnal formation and aggregation of crystals, the patient is advised to take 300 ml of water overnight, as well as to void urine at least twice during the night.
  • Urine alkalinisation is to be maintained to dissolve existing calculi as well as to increase the solubility of cystine. Oral alkalinisation treatment with potassium bicarbonate is done to maintain the urine pH between 7.5 and 8.0. However oral alkalinisation treatment must be closely monitored, especially in patients with hypertension, impaired kidney function, diabetes and in those on diuretics.
  • The dietary restriction of the metabolic precursor of cystine, the amino acid methionine, may restrict the cystine excretion. Restriction of methionine-containing foods (milk, meat, eggs, etc.) results in a decrease in total urinary cystine excretion. However the total protein requirement of the body cannot be compromised. Hence dietary restriction may not work well for many patients, especially children.
  • Increase in sodium intake has a direct effect on the increase in cystine excretion. Hence sodium intake has to be restricted.

Cystine kidney stones treatment

Medication is available for decreasing the total urinary excretion of cystine. Penicillamine and alpha-mercaptoproprionylglycine (tiopronin or Thiola) are the usual medicines prescribed for decreasing the excretion of the amino acids. These are chelating agents that combines with cystine to form a soluble disulfide complex. However they carry the high risk of allergy, arthralgia, leukopenia, gastrointestinal intolerance, nephritic syndrome and toxicity. Hence these medications may be considered as a supplemental effort to hydration and urinary alkalinization. Though acetazolamide helps in rapid stone dissolution, it has adverse effects.

Surgical options are available for removing kidney stones that are negatively responding to the above non-surgical treatments. Extracorporeal shockwave lithotripsy, retrograde endoscopic lithotripsy and extraction, ureteroscopy, percutaneous nephrostolithotomy, percutaneous nephrolithotomy, combination therapy and open surgery are the surgical options available for removing cystine kidney stones.
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Related topics in nutritional deficiency diseases:
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References:
1.http://kidney.niddk.nih.gov/kudiseases/pubs/stonesadults/
2.http://www.kidney.org/atoz/content/diet.cfm
3.http://kidney.niddk.nih.gov/kudiseases/pubs/kidneystonediet/index.htm
4.Fjellstedt E, Harnevik L, Jeppsson JO, Tiselius HG, Söderkvist P, Denneberg T. Urinary excretion of total cystine and the dibasic amino acids arginine, lysine and ornithine in relation to genetic findings in patients with cystinuria treated with sulfhydryl compounds. Urol Res. 2003 Dec;31(6):417-25. Epub 2003 Oct 25.
5.Worcester EM, Coe FL, Evan AP, Parks JH. Reduced renal function and benefits of treatment in cystinuria vs other forms of nephrolithiasis. BJU Int. 2006 Jun;97(6):1285-90.
6.Trinchieri A, Montanari E, Zanetti G, Lizzano R. The impact of new technology in the treatment of cystine stones. Urol Res. 2007 Jun;35(3):129-32. Epub 2007 Apr 18.
7.Kamran Ahmed, Prokar Dasgupta, Mohammad Shamim Khan. Cystine calculi: challenging group of stones. Postgrad Med J. 2006 Dec; 82(974): 799–801.
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Uric acid kidney stones.
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Types of kidney stones

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Kidney stone, also known as kidney calculus or renal calculus, is a solid mass made of crystal-forming substances in the urinary system. Though all types of kidney stones originate in the kidneys, they may be found in the ureters, bladder and urethra.
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Many renal calculi of small sizes are formed and passed without causing symptoms. If the calculus is 3 mm or more, it may cause blockage of the ureter and associated renal colic pain.

Types of kidney stones

There are several different types of kidney stones. Urolithiasis refers to all types of calculi originating anywhere in the urinary system. In relation to the type of their location, renal calculi are categorized as nephrolithiasis (kidney), ureterolithiasis (ureter) and cystolithiasis (bladder). Another type of classification pertains to the type of crystal forming minerals and organic compounds constituting these calculi.

Renal calculi containing calcium

Most of the kidney stones are made of calcium compounds, especially calcium oxalate. Other calcium compounds are calcium phosphate in the form of calcium hydroxyphosphate (apatite), calcium phosphate carbonate (carbonate apatite) and brushite (CaHPO4·2H2O).

The calcium oxalate uroliths exist in combined monohydrate and dihydrate forms.
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The calcium oxalate dihydrate (CaC2O4·2H2O) type of crystals are octahedral in shape. The calcium oxalate monohydrate (CaC2O4·H2O) type of crystals vary in shape, and can be shaped like dumbbells, spindles and ovals.

The calcium oxalate calculi formation is much dependent upon the type of diet taken. Low calcium diet can lead to increased oxalate absorption from the intestine and its increased excretion in the urine. The concentration of urine and availability of oxalate in the urine increase the risk of oxalate urolith formation. High intakes of dietary oxalates, high dietary sodium, low fluid intake, low potassium intake, low citrate intake and low magnesium intake are other risk factors for developing calcium oxalate kidney stones.

Calcium phosphate renal calculi have an underlying medical cause. These types of calculi are usually associated with systemic disorders like primary hyperparathyroidism, secondary hyperparathyroidism, renal tubular acidosis, hyperphosphaturia and hypercalciuria. The availability of calcium and PO43- in the urine helps in seeding of these types of uroliths. Urine dilution with sufficient intake of water and reducing sodium intake to reduce sodium and calcium excretion can help in reducing the risk factors and recurrence.

Struvite type of renal calculi are mostly composed of struvite (magnesium ammonium phosphate). Struvite calculi also contain deposits of calcium carbonate-apatite. Infection in the upper urinary tract causes these types of uroliths. Struvite kidney stones can form only when the urine is alkaline and saturated levels of magnesium ammonium phosphate are present in urine. The urease-producing types of bacteria cause conversion of urea in the urine into carbon dioxide and ammonia by the catalytic action of the enzyme urease. Ammonia increases the pH of urine and also reacts with the magnesium and phosphate ions in the urine to form these types kidney struvite.

These types of calculi are associated with an excessive amount of uric acid in the urine (hyperuricosuria) with or without an excessive amount of uric acid in the serum (hyperuricemia). The major factors for the formation of uric acid uroliths are, chronic dehydration, low urine output, concentrated urine output, rich animal protein diet, excessively acidic urine, certain metabolic abnormalities, obesity and affliction by gout. Certain hereditary factors may also play a part in the formation of these types of kidney nephrolith. Uric acid and oxalate stones are common in patients with inflammatory bowel disease (Crohn's disease or ulcerative colitis) and in patients who had undergone colon resection.

Individuals suffering from cystinuria, cystinosis and Fanconi syndrome develop these uroliths. Cystinuria is a hereditary disorder running in families. It causes the kidneys to excrete the amino acid cystine in the urine. Cystine calculus formation can be treated by alkalinizing urine and restricting dietary animal protein, especially red meat.

Struvite have the potential to grow into staghorn uroliths. Staghorn nephrolith are branched and occupy a large portion of the renal pelvis and one or more of calices. Cystine or uric acid calculi, either in pure form or mixed with other components may also grow into staghorn. These type of kidney stones, if not treated early and properly, have the great risk of causing, permanent kidney damage, renal failure and life threatening sepsis.

Persons affected by xanthinuria often produce nephrolith composed of xanthine. In very rare cases, medications like indinavir, acyclovir, sulfadiazine and triamterene may get deposited as kidney stones.
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Related topics in nutritional deficiency diseases:
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References:
1.http://kidney.niddk.nih.gov/kudiseases/pubs/stonesadults/
2.http://www.kidney.org/atoz/content/diet.cfm
3.http://kidney.niddk.nih.gov/kudiseases/pubs/kidneystonediet/index.htm
4.Kristensen C, Parks JH, Lindheimer M, Coe FL. Reduced glomerular filtration rate and hypercalciuria in primary struvite nephrolithiasis. Kidney Int 1987; 32:749.
5.Viprakasit DP, Sawyer MD, Herrell SD, Miller NL. Changing composition of staghorn calculi. J Urol 2011; 186:2285.
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Current topic in nutritional deficiency diseases: Types of kidney stones.
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Staghorn kidney stones

   ›      ›   Staghorn kidney stones.

What is staghorn kidney stone?

Staghorn kidney stones are "staghorn-like" (branched antlers of deer) renal calculi. Staghorn stones are branched and occupy a large portion of the renal pelvis and one or more of calices.
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The staghorn calculus is termed "partial staghorn calculus" when it occupies part of the renal collecting system. If the calculus occupies the entire collecting system, it is termed as a "complete staghorn calculus".

Formation of staghorn kidney stones

Some of the main types of renal calculi are oxalate, phosphate, struvite, calcium carbonate apatite and cystine stones. The calcium oxalate stones are formed due to excessive oxalate and calcium, in acidic urine. The growth of oxalate calculi is slow and very rarely they grow into staghorn calculi. The phosphate calculi are formed due to certain medical conditions and disorders. The phosphate calculi also normally do not grow into staghorn stones.

The struvite calculi, which are composed of magnesium ammonium phosphate and/or in combination with calcium carbonate apatite, are formed due to infection in the upper urinary tract by urease forming organisms.
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The struvite calculi can grow fast into staghorn kidney stones filling the renal pelvis and the calices. Unlike other calculi, the struvite forms have the bacteria both on the surface as well as the inside of the calculi.

Renal calculi composed of cystine or uric acid, either in pure form or mixed with other components may also grow into staghorn filling the renal pelvis as well as the calices. Mucoproteins and biofilm exopolysaccharides produced by microbes may provide matrix for the formation of these renal calculi. Even after active treatment, there is always the possibility of recurrence due to persisting infection or staghorn calculi debris.

Renal failure

Active treatment is advised for the newly diagnosed patient. As the staghorn kidney stones may not cause renal colic, often show symptoms of dull pain only, the patient tend to neglect treatment. The staghorn kidney stones, if not treated early and properly, have the great risk of causing renal failure and/or life threatening sepsis.

Complete removal of the staghorn calculus along with its fragments and debris, eradication of the causative organisms and removal of obstructions, can only protect from the progressive renal damage. Nonsurgical conservative treatment and supportive measures such as use of antibiotics and urease inhibitors may give temporary relief, but active treatment is necessary for protection from permanent renal damage.

Treatment modalities

The American Urological Association (AUA) had in their guidelines report on the management of staghorn kidney stones recommended certain treatment modalities. Recommended treatment modalities are, percutaneous nephrolithotomy (PNL) monotherapy, shock-wave lithotripsy (SWL) monotherapy, combination therapy, open surgery or nephrectomy.

Percutaneous nephrolithotomy is the most prefered treatment option. Open surgery is considered in patients with extremely large staghorn calculi. Patients with extreme morbid obesity, skeletal abnormalities or unfavorable collecting-system are candidates for open surgery. In patients with chronic infection and severe renal damage, nephrectomy is the best option to prevent further patient morbidity and loss of life. Focus must be on complete removal of the staghorn calculus and treatment of infection.
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Related topics in nutritional deficiency diseases:
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References:
1.http://kidney.niddk.nih.gov/kudiseases/pubs/stonesadults/
2.http://www.kidney.org/atoz/content/diet.cfm
3.http://kidney.niddk.nih.gov/kudiseases/pubs/kidneystonediet/index.htm
4.Kristensen C, Parks JH, Lindheimer M, Coe FL. Reduced glomerular filtration rate and hypercalciuria in primary struvite nephrolithiasis. Kidney Int 1987; 32:749.
5.Viprakasit DP, Sawyer MD, Herrell SD, Miller NL. Changing composition of staghorn calculi. J Urol 2011; 186:2285.
Interesting topics in nutritional deficiency diseases:
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Current topic in nutritional deficiency diseases: Staghorn kidney stones.
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Struvite kidney stones

   ›      ›   Struvite kidney stones.
What are struvite kidney stones?
Struvite kidney stones are mostly composed of struvite (magnesium ammonium phosphate). Struvite calculi also contain deposits of calcium carbonate-apatite.
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Struvite kidney stones can form only when saturated levels of magnesium ammonium phosphate are present in urine. Magnesium ammonium phosphate solubility decreases with the increase in the urine pH. In alkaline urine, struvite crystals form readily and get deposited. Struvite stones account for 10-15% of renal calculi in USA and they can grow rapidly to form staghorn calculi.

Cause of struvite kidney stones

Magnesium ammonium phosphate calculus form when the ammonium, magnesium and phosphate ions are present at saturation levels and also the urine pH is high. In the first instance, ammonium phosphate (NH4+) has to be formed in the urine for these struvite stones to develop. In ureotelic organisms, including humans, the proteinaceous nitrogenous waste from the body is disposed off as urea in the urine. When there is upper urinary tract infection by certain urease-producing bacteria, urea is converted into ammonia.

Some of the urease-producing bacteria are, Proteus mirabilis, Staphylococcus species, Klebsiella species, Providencia species, Pseudomonas species, Corynebacterium species and Ureaplasma urealyticum. Struvite calculi are more common in women as they are more prone urinary infections.

Urease is a enzyme that catalyzes the hydrolysis of urea into carbon dioxide and ammonia. The reaction is as follows:
(NH2)2CO [urea] + H2O —> CO2 + 2NH3 [ammonia]
The ammonia readily combines with water to form ammonium hydroxide.
NH3 + H2O —> NH4+ + OH- —> NH4OH.
Ammonium hydroxide is a weak alkali and it increases the pH of urine. It reacts with the magnesium and phosphate ions in the urine to form struvite.
6 H2O + Mg2+ + NH4+ + PO43- —> MgNH4PO46H2O
When the pH of the urine is greater than the nucleation pH, there is rapid formation and growth of crystals.

Symptoms of struvite calculi presence

As there is concurrent infection along with struvite calculi development, fever and chills may be present. Other common symptoms are, nausea, loss of appetite, dull, burning, persistent pain, appearance of blood in the urine, cloudy urine and foul smelling urine. The calculi may grow rapidly to form staghorn calculi. The staghorn calculi may grow many branches and fill the renal pelvis. The branches may extend into the renal calyces.

In some cases struvite calculi may remain asymptomatic. An untreated struvite staghorn stone can damage the soft renal tissues, leading to end-stage pyelonephritis. The end-stage pyelonephritis may result in life-threatening sepsis and renal failure. As struvite stones are usually radiopaque, they can be detected by radiography or sonography.

Treatment and management of struvite calculus

Struvite calculus is always associated with the danger of rapidly developing into staghorn calculus.
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Struvite calculus must be removed completely, in the early course of the disease in order to prevent complications and renal deterioration. Conservative treatment of patients without removal of struvite stones had resulted in death of nearly 30% of the patients due to pyelonephritis, sepsis or renal failure.

With the calculus clearance, the patient must be treated with antibiotics to cure the renal infection. Persisting infection can cause recurrence of the struvite kidney stones. The recurrence rate is nearly 10%. Ineffective infection clearance, residual fragments or scar tissues had caused recurrence of struvite kidney stones in 80% of the patients.

In struvite calculi patients with significant medical comorbidities or acute infections wherein surgical procedures are contraindicated, nonsurgical measures are advised. Bacterial urease inhibitors such as, oral acetohydroxamic acid (AHA) are given. As AHA administration is associated with several adverse effects, the patients health status must be closely monitored.

Minimally invasive procedures like extracorporeal shockwave lithotripsy (SWL), flexible ureteroscopy and percutaneous nephrolithotomy (PNL) are resorted to remove the persisting struvite kidney stones. A percutaneous nephrostomy (PCN) tube may be required to allow adequate renal discharge.
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References:
1.http://kidney.niddk.nih.gov/kudiseases/pubs/stonesadults/
2.http://www.kidney.org/atoz/content/diet.cfm
3.http://kidney.niddk.nih.gov/kudiseases/pubs/kidneystonediet/index.htm
4.Kristensen C, Parks JH, Lindheimer M, Coe FL. Reduced glomerular filtration rate and hypercalciuria in primary struvite nephrolithiasis. Kidney Int 1987; 32:749.
5.Gnessin E, Mandeville JA, Handa SE, Lingeman JE. Changing composition of renal calculi in patients with musculoskeletal anomalies. J Endourol 2011; 25:1519.
6.Viprakasit DP, Sawyer MD, Herrell SD, Miller NL. Changing composition of staghorn calculi. J Urol 2011; 186:2285.
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Calcium phosphate kidney stones

   ›      ›   Calcium phosphate kidney stones.
Calcium phosphate kidney stones are less common than those formed with calcium oxalate. Calculi containing both phosphate (PO43−) and oxalate of calcium are common. However a greater proportion of the constituting chemical is usually oxalate.
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Kidney stones (renal calculi) of calcium phosphate (CaP) and those calculi containing greater amounts of phosphate are to be thoroughly investigated for the underlying medical cause.

The most important calcium and PO43- involved renal stones are carbonate apatite, hydroxyapatite, and brushite. The struvite calculi are formed of magnesium, ammonium and phosphate. The basic cause is the supersaturation of calcium compounds in the urine. When the solubility threshold is exceeded under the given conditions in the kidney, nucleation begins. If the conditions are stable slow crystalline growth commences.

The existing supersaturation of calcium and phosphate in the urine is the driving force for the spontaneous precipitation and crystallization. One of the factors conducive to supersaturation of these salts is increase in urine pH. Carbonate apatite calculi may sometimes associate with urinary infection.

Causes of phosphate stone formation

Several medical conditions lead to calcium phosphate kidney stone formation. The primary hyperparathyroidism, secondary hyperparathyroidism, renal tubular acidosis, hyperphosphaturia, hypercalciuria and Fanconi syndrome are some of the causative factors. Certain medications, such as Topiramate (TPM), acetazolamide, zonisamide are associated with the development of metabolic acidosis, hypocitraturia, hypercalciuria and elevated urine pH.

Hyperparathyroidism

The parathyroid glands produce parathyroid hormone (PTH). The parathyroid hormone regulates and maintains calcium and phosphate levels in the body.
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Primary hyperparathyroidism and the over secretion of PTH results from a hyperfunction of the parathyroid glands. This hyperactivity can be due to parathyroid adenoma, parathyroid hyperplasia, parathyroid carcinoma or genetic disorders.

The primary hyperparathyroidism leads to hypercalcaemia (raised serum calcium levels). The serum PO43- levels tend to be low as a result of decreased renal tubular phosphate reabsorption and resultant loss in the urine. The hypercalcemia results in active removal of calcium into urine. The availability of Calcium and PO43- helps in seeding of renal calculi.

Hyperphosphaturia and Hypercalciuria

Phosphaturia is a condition wherein phosphate is excessively excreted by the kidney, making these ions easily available for calculi formation. There are two form of phosphaturia. The primary type is direct excess excretion of PO43− by the kidneys either due to generalized dysfunction of the proximal tubular cells in kidney (Fanconi syndrome) or due to the action of diuretics. The secondary phosphaturia is due to both primary and secondary types of hyperparathyroidism.

Hypercalciuria is a condition wherein Calcium is excessively excreted by the kidney. Hypercalciuria is caused due excessive release from the bones, excessive calcium supplementation, elevated serum levels of calcium, excessive sodium intake or due to certain genetic disorders.

The conditions of hypercalciuria and hyperphosphaturia, individually or as a combined action, initiate calcium phosphate stone formation in the event of saturated levels of these ions in the urine. The stone formation is further helped by high pH of urine.

Renal tubular acidosis (RTA)

RTA is a medical condition is which there is acid accumulation in the body. The condition is due to inefficiency of kidney in resorbing and recovering bicarbonate ions from the filtrate in the proximal tubular cells or inefficiency in eliminating hydrogen ions into lumen of nephron at distal tubule. The distal renal tubular acidosis characterized by hyperchloremic acidosis, hypocitraturia, and high urine pH. The net effect is insufficient acidification of urine to a pH of less than 5.3 and accumulation of acid in the body and acidemia.

Treatment and management

In the management of these renal calculi, reducing urine saturation and limiting of calcium excretion are important steps. With sufficient intake of water, urine can be diluted. Restricting sodium ingestion can reduce sodium excretion as well as calcium excretion. Citrate, though tends increase the urine pH, has the capacity to bind to ca2+ and eliminate it from the system. Thiazides also lower urine calcium excretion. The persisting calcium phosphate kidney stones are removed by extracorporeal shock wave lithotripsy (ESWL), Percutaneous stone removal or surgery.
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References:
1.Vega D, Maalouf NM, Sakhaee K. Increased propensity for calcium phosphate kidney stones with topiramate use. Expert Opin Drug Saf. 2007 Sep;6(5):547-57.
2.David S. Goldfarb. A woman with recurrent calcium phosphate kidney stones. Clin J Am Soc Nephrol. 2012 Jul;7(7):1172-8.
3.Gault MH, Chafe LL, Morgan JM, Parfrey PS, Harnett JD, Walsh EA, Prabhakaran VM, Dow D, Colpitts A. Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. Medicine (Baltimore). 1991 Nov;70(6):345-59.
4.Fredric L. Coe, Andrew Evan, Elaine Worcester. Kidney stone disease. J Clin Invest. Oct 1, 2005; 115(10): 2598–2608.
5.Hesse A, Heimbach D. Causes of phosphate stone formation and the importance of metaphylaxis by urinary acidification: a review. World J Urol. 1999 Oct;17(5):308-15.
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Vitamin C and kidney - Oxalate stones

› › Vitamin C and kidney - Oxalate stones

Kidney regulates the plasma levels of vitamin C. The feared formation of oxalate stones due to high vitamin C is unfound. In fact vitamin C helps in the dissolution of other types of kidney stones.

Renal resorption threshold and excretion of vitamin C by kidney

The optimum renal resorption threshold levels of vitamin C in healthy men and women are 1.5 mg/dl and 1.3 mg/dl respectively. The body pool levels of 1500-3000 mg are considered tissue saturation levels of ascorbic acid. Once the plasma levels of vitamin C exceeds this level it is not further resorbed by the kidney and gets excreted in urine.

Further the water soluble properties of vitamin C leads to urinary excretion as ascorbic acid in case of elevated levels. In higher plasma levels the half-life of vitamin C is about 30 minutes. When the concentrations are less than the renal resorption threshold the vitamin C is resorbed actively and the half-life is greatly extended in depleted conditions.

Ascorbic acid has an average half-life of about 15-20 days. The half-life is inversely decreases or increases with its intake. The metabolic products of vitamin C, like 2-ketoascorbitol, 2-O-methyl ascorbate, dehydroascorbate and oxalic acid are excreted by the kidney.

Does vitamin C cause Oxalate stones in kidney?

There are various types of kidney stones made up of urate, calcium phosphate, struvite, cystine. Oxalate and urate are the main deposits in renal stones. A section of the medical community believes that ascorbic acid in high doses can cause kidney stones. As one of the by-product of vitamin C metabolism is oxalic acid, it is being concluded that, these ions on combining with calcium, form calcium salt and get deposited in kidney and form stones.

There are conflicting reports of studies conducted on these deposits formation. One study conducted on 45,250 men for 6 years and another on 85,557 women for 14 years, had given the conclusion that daily consumption of more than one gram of ascorbic acid did not result in oxalate deposit formation in the subjects. Another recent study on 45,619 men for 14 years had given a conflicting report that there is 41% higher risk in people consuming more than one gram of vitamin C in developing oxalate stones.

However this study had also concluded that persons consuming less than 250 mg/ day of ascorbic acid were also under high risk. The acidic vitamin C in urine may bind to calcium and reduce its availability for getting bound to oxalate. The possibility of deficiency of vitamin B6 and magnesium rather than the excess of ascorbic acid for the formation of calculi must be probed.

Though we may not fear for the risk of oxalate stones on high dose ascorbic acid consumption, it is prudent to evaluate the status of the individual prone to oxalate deposits and its recurrence, before embarking on high-dose vitamin C consumption. A person prone to calculi may also avoid excessive use of oxalate rich spinach, chocolate and rhubarb.

Vitamin C in the role of removing other types of kidney stones

Vitamin C has a diuretic action when consumed in high doses and this helps in flushing out the possible deposits, including calcium oxalate. Many calcium oxalate and other deposits usually form around a nucleus of infection. Ascorbic acid due to its pH lowering action, appears to retard, kill and flush out the causative agents like bacteria and nanobacteria.

Calcium phosphate stones, unlike calcium oxalate stones are alkaline in nature and get dissolved by the ascorbic acid in the urine. Struvite kidney stones ( formed by magnesium ammonium phosphate) also differ in nature and are easily soluble in urine due to high ascorbic acid.

Vitamin C depletion due to maintenance hemodialysis in kidney impaired patients

In maintenance hemodialysis, the water soluble ascorbic acid is depleted. The food intake of ascorbic acid must be monitored, so as avoid development of deficiency. If necessary supplements in regulated doses must be given.

Doses in excess of 100-200 mg must be avoided in chronic renal disease as oxalates can accumulate in the body causing oxalosis. This can even cause acute renal failure. Oxalosis due to excess vitamin C in kidney transplant recipients can affect renal transplants and cause graft failure.
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Vitamin C and oxalate stones in kidney
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