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Stones are very hard formations resembling small pebbles of varying sizes.

The smaller formations, more similar to sand, are called gravel (or renal sand).

Stones and renal sand form from crystals, that is, clusters of salts (calcium oxalate in 70% of cases, uric acid in 10%, struvite in 10%, cystine in 2%, and other salts in the remaining 8%). These crystals tend to aggregate and form stones or sand in the presence of favorable conditions:

  • poor hydration
  • decrease in urinary components that inhibit crystallization
  • increased excretion of the salts that form them
  • alteration of urinary pH

 

 

The symptoms of kidney stones

What are the symptoms of kidney stones?

The extent of the damage and related symptoms is proportional to the size of the stone and its location. Crystals and renal sand, carried by the urinary flow, scratch the bladder wall and urethral mucosa, causing pain and difficulty emptying. Stones, on the other hand, do not cause symptoms until they grow excessively large or begin to move, damaging the mucosa they encounter along their path or blocking the passage itself.
If the stone obstructs the normal flow of urine at the urethral level, bladder retention occurs (resulting in cystitis), pain, difficulty emptying, frequency, intermittent urination, hematuria, urethral dribbling, and urethrocele (dilation of the urethra).
If the stone is located in the kidney tissue, in case of obstruction urine cannot pass and will accumulate in the renal calyces (the funnels where urine collects before passing into the ureters), causing excessive dilation (hydronephrosis) and therefore kidney colic, characterized by sharp, cramp-like pain in the lower back or lower abdomen, which can extend to the groin or cause nausea and vomiting. The onset of fever is generally a sign of infectious complication (pyelonephritis).

 Deep dive: The structure of the bladder

 

Stones and Cystitis

Are kidney stones linked to Cystitis?

Stones and renal sand are both a cause and a consequence of cystitis. This is due to the fact that tissue damaged by scratches is more prone to infections, and also because urine retention caused by obstruction from a stone (or parts of it) lodged in the urethra. Furthermore, in cases of lithiasis (stone disease), the bacteria responsible for the infection are very difficult to eradicate because the stone provides a perfect refuge. The stone is devoid of blood vessels, so antibiotics, macrophages, antibodies, and all our immune cells (all transported by the blood) cannot reach the bacteria nestled inside it. Therefore, the stone becomes a bacterial reservoir and at the same time a protective bunker for these germs, which continue to reproduce undisturbed and cause cyclic infections.

Deep dive: Sympoms of Cystitis

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The same organic residues produced by the infection accumulate on the stone, further increasing its size. This leads to greater blockage, increased urine retention, and the establishment of a vicious cycle that is unlikely to end until the stones are removed, the renal sand is eliminated, and the crystals are reduced.

However, it is not uncommon for symptoms caused by the presence of crystals, renal sand, or small stones to be mistaken for cystitis, even in the absence of bacteria.

Deep dive: How to manage acute Cystitis

 

The diagnosis

How is the diagnosis of kidney stones made?

To avoid confusing kidney stones with cystitis, it would be enough to analyze the urinary sediment with a simple urine test, which would reveal crystalluria, that is, the presence of crystals in the urine. Crystalluria, besides causing symptoms similar to cystitis, is a good indicator of the presence of stones or renal sand, or the risk of developing them in the future. A negative urine culture combined with a positive sediment analysis for crystals should always raise suspicion of a tendency to form stones.

Kidney stones can be detected through:

  • abdominal ultrasound
  • x-ray
  • contrast-enhanced urography
  • CT scan

 

The treatment of kidney stones

How are kidney stones treated?

It is now ingrained in the collective imagination (both popular and medical) that the best therapy to expel kidney stones is massive hydration with oligomineral or minimally mineralized water to avoid overloading the body with minerals, and that to prevent their formation a low-calcium diet and urinary acidification are necessary.

Nothing could be more wrong!

The most recent studies have shown that the old guidelines were wrong and have been replaced with the following:

  1. no massive hydration in case of renal colic (deep dive)
  2. low-calcium waters and diets do not help reduce or prevent kidney stones. A diet limiting protein, salt and oxalates is much more effective (deep dive)
  3. calcium, phytates (elements found in flours and whole grains), magnesium, zinc, and potassium prevent the formation of kidney stones (deep dive)
  4. vitamin C promotes the formation of oxalate stones (deep dive)
  5. the intake of citrates is a very effective aid in the fight against kidney stones (deep dive)
  6. urinary acidification promotes the formation of stones, while alkalinization hinders it (except in rare cases) (deep dive)

If all these measures are not sufficient to expel the stone, lithotripsy (shock waves that break the stone into smaller pieces to facilitate elimination), ureteroscopy (the endoscope passes through the urethra into the bladder, ureters, and kidneys to reach, break, and remove the stone), or percutaneous treatment (the endoscope reaches the stone through a small incision in the skin) will be used.

 

Deep dive: therapeutic guidelines

  1.  Renal colic occurs because the stone obstructs the renal ducts; pressure upstream increases, dilates these pathways, and causes pain. According to Dr. P. Piana (head of the Urinary Stone Center at A.S. Città della Salute e della Scienza in Turin), increasing water intake can only worsen symptoms rather than stop them, while anti-inflammatory drugs and muscle relaxants are much more effective in facilitating the passage and expulsion of the stone. Therefore, massive hydration seems to be recommended mainly for prevention rather than treatment. However, it is important to spread fluid intake evenly throughout the day. Drinking a lot in a short time would dilate the renal calyces upstream of the stone, causing hydronephrosis and kidney pain. A limited but constant intake throughout the day allows for renal flushing without overload.

  2.  It has been observed that hard waters (rich in calcium) paradoxically prevent the formation of calcium stones. Loris Borghi from the University Clinic of Parma demonstrated through a study on 120 patients that administering a diet without calcium restrictions, but with limited intake of salt (sodium), oxalates, and animal proteins, reduces stone formation much more than a diet that limits calcium. In fact, calcium bound to oxalates cannot pass through the intestinal wall, so it does not enter the bloodstream and is eliminated with the feces. If calcium is lacking, however, oxalate is fully absorbed, enters the bloodstream, and reaches the kidneys, where it forms crystals, precursors of stones.
    Sodium, on the other hand, competes with calcium. Therefore, at the renal level (where most of the minerals that arrive are reabsorbed and reintroduced into circulation), the renal tubule (the part of the kidney that "decides" which mineral to reabsorb) favors sodium, leaving calcium in the kidneys as waste to be eliminated along with excess fluids. Oxalates and calcium meet, leading to the formation of calcium oxalate stones.

  3.  For the reasons just explained, a calcium supplement taken with meals has been shown to reduce the presence of oxalates in the urine and thus the formation of stones. The same effect is achieved with a supplement of magnesium, potassium, zinc, and phytates.

  4. Vitamin C (ascorbic acid), in addition to acidifying the urine, is a direct precursor of oxalic acid, which precipitates to form oxalates. According to a study conducted at the Karolinska Institute in Stockholm, taking high doses (about 1 g per day) of ascorbic acid (vitamin C) doubles the risk of developing oxalate kidney stones. Twenty different vitamins were administered to 48,850 men over 11 years to evaluate their influence on stone formation. During these 11 years of study, 436 new cases of nephrolithiasis (kidney stones) occurred, most of which were in patients treated with ascorbic acid (double the risk compared to those who took other vitamins, which proved to have no effect on stone formation).

  5.  Citrate is a powerful inhibitor of stones. Numerous studies indicate that patients with nephrolithiasis have low levels of citrate in their urine (hypocitraturia). Citrate inhibits (in an alkaline environment) the aggregation of salts that are precursors of stones: phosphates, oxalates, calcium, uric acid, etc. Citrates inhibit both the initial phase of stone nucleus formation and the subsequent growth phase by progressive deposition of other salts. Additionally, citrate facilitates the elimination of residual stone fragments after lithotripsy (the disintegration of stones by shock waves).
    Citrates also play an important role in chronic prostatitis: the alkalinization of the prostatic secretion achieved with citrates would favor the diffusion of the antibiotic into the prostatic acinus.
    Citrates can also be taken to relieve burning sensations associated with inflammation of the urinary tract.

  6.  The formation of most stones is favored by an acidic pH. Acidity reduces both the amount of citrate in the urine and the effectiveness of the Tamm Horsfall protein, another powerful inhibitor of stones, thereby facilitating the aggregation of crystals of uric acid, calcium oxalate, amorphous urates (calcium, magnesium, sodium, and potassium), cystine, leucine, tyrosine, cholesterol, bilirubin, and xanthine.
    However, the Tamm Horsfall protein (pTH) tends to aggregate in an acidic environment, contributing to stone formation and reducing its bacterial adhesion surface (thus losing its antibacterial function). Conversely, an alkaline environment increases renal production of pTH, which remain non-aggregated. It has also been observed that the more sialic acid the pTH contain, the less they cause calcium oxalate aggregation. Therefore, not only the quantity of these proteins but also the pH of the solution they are in and the amount of sialic acid present are important.
    Among the alkalinizers useful for preventing crystallization are the very inexpensive sodium bicarbonate and the classic over-the-counter alkalinizers. The use of alkalinizers containing minerals in citrate form, such as magnesium citrate, is extremely useful.

      However, alkalinization does not always prevent stones. There are stones that form in an alkaline environment. This is the case for struvite stones, amorphous phosphate, calcium carbonate, calcium phosphate, ammonium acid urate, and calcium sulfate stones. Urease-positive bacteria (Proteus, Pseudomonas, Staphylococcus saprophyticus, Providencia, Morganella) can transform urea in the urine into ammonia. This makes the urine very alkaline, raising the urinary pH above 7.5. Excessive alkalinization reduces the solubility of phosphates, magnesium, and ammonium, which instead of dissolving accumulate and aggregate into crystals that will form struvite stones. Only in these cases is urinary acidification indicated to hinder crystal and stone formation. To acidify, specific supplements based on methionine (Acidif) and Chanca Piedra can be used.
    It is therefore important to know the composition of the stone or crystals in order to undertake a therapy suitable for their disintegration and prevention.

Testimonials

“I was ten years old. Having recurrent episodes, my pediatrician suspected the presence of kidney stones (due to family history, as I actually suffer from them).”
Scrat's story 09/03/2011 (Cistite.info forum)
“Believe it or not, I also suspected I had renal sand, in fact my sister was diagnosed with it years ago after repeated cystitis episodes.”
Comment by Viviana 03/14/2012 (Cistite.info forum)
“I am mainly affected by two different types of cystitis.
The first, which I believe I will have to live with forever, affects me when my poor kidneys start producing renal sand. The little grains irritate the bladder, and I become as irritable as mayonnaise with too much oil.
The second one appears shortly after feeling pain during sexual intercourse. I’m not talking about pain that makes you scream; even just a little discomfort is enough (a thousand factors, you know: awkward position, low lubrication, intercourse lasting too long…) and that’s it.
These days, I’m as polite as a truck driver whose radio has been stolen.
Facendo l’urinocultura, le colonie di batteri appaiono solo nel secondo caso”
Relm’s story 01/10/2012 (Cistite.info forum)

 

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Benefits: Agreements for members

 

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