Kidney Stones (Nephrolithiasis): A Pain In My… Flank?

Kidney stones, or nephrolithiasis, come in different types. There are calcium, struvite, uric acid, and cystine stones. They all form under different conditions with some being more common than others. In addition, when urine is analyzed under a microscope the crystals form unique shapes that help identify one type of stone from another.

Calcium Kidney Stone
Struvite Stone
Uric Acid Stones
Cystine Stones
Calcium stones are the most common. They are composed of either calcium phosphate or calcium oxalate. They form under conditions of hypercalciuria (ie: high calcium in the urine). There are many reasons why someone would have elevated urinary calcium levels. Some examples include hyperparathyroidism (an overactive parathyroid gland), vitamin D toxicity, cancer, and the milk alkali syndrome. In many patients the reason for the elevated urinary calcium is never discovered.

Calcium stones are also associated with hyperoxaluria (ie: too much oxalate in the urine), as well as hyperuricosuria (ie: too much uric acid in urine), and hypocitraturia (ie: too little citrate in the urine).

The second most common type of stone is a struvite stone. A struvite stone is composed of magnesium, ammonium, and phosphate. They form during kidney infections when the "bug" responsible for the infection is a urease spliting bacteria such as proteus vulgaris. These bacteria are capable of producing ammonium from urea. In large enough quantities the ammonium can combine with magnesium and phosphate to form a struvite stone. These stones can be large and in the shape of the draining system of the kidney (ie: calyces); when the have this appearance they are referred to as "staghorn calculi".

Uric acid stones are produced under conditions of high amounts of uric acid in the blood and urine (ie: gout or conditions where cell death is high such as in leukemias and other cancers). Some patients lack elevated levels of uric acid in the blood or urine. However, they are still capable of forming uric acid stones, especially if their urine is acidic. This is because urate precipitates in acidic environments.

Finally, cystine stones form because of certain genetic conditions. The cells that line the urinary tract are normally able to re-absorb amino acids like cysteine. However, certain genetic mutations cause abnormalities in the ability of these cells to transport cysteine from the urine back into the blood. The resultant increase in cysteine in the urine can cause cystine stones to form.

Signs and Symptoms

A fair number of kidney stones are asymptomatic. However, occasionally a stone will pass from the kidney to the bladder through a narrow tube called the ureter. This can produce excruciating pain that is located in the flank region. Sometimes the pain can be referred to the scrotum in males, or labia majora in women.

In addition, sometimes the urine will have blood in it from irritation of the urinary tract. If there is enough blood, the urine will turn pink; although, microscopic hematuria (ie: blood in the urine that can only be picked up by lab testing) can also occur.


There are several worrisome complications of kidney stones. They include hydronephrosis and pyelonephritis. Hydronephrosis refers to dilation of the urinary tract secondary to blocked urine and increased pressures. The increased pressure is reverberated all the way to the filtration unit of the kidney, the glomerulus. If high enough pressures are reached, irreversible kidney damage can occur leading to chronic kidney disease and renal failure.

Pyelonephritis is a fancy term for an infected kidney. The irritation caused by the stones provides a suitable environment for bacteria to proliferate. These infections can be life threatening, and like hydronephrosis, can lead to irreversible kidney damage and renal failure.


Diagnosis of kidney stones is made by looking at urine under the microscope. This is known as urine microscopy. Different types of stones have different appearances (see images above), but more importantly also have different treatments.

In addition, a urine analysis is often performed in order to determine the pH. Urine electrolytes including calcium, magnesium, sodium, etc. are also sent, and can be helpful in determining the type of stone.

Imaging studies are also commonly done. The quickest, cheapest, and most readily available is an ultrasound of the kidney. If stones are present they can cast shadows (similar to the ones gallstones cast), which are picked up by the ultrasound machine. CT scans of the kidney can also show stones. Occasionally a procedure known as intravenous pyelography (IVP) is done. In IVP, radio-opaque dye is injected into the veins. It ultimately gets filtered and excreted by the kidneys, at which point an X-ray is taken; the X-ray can provide information about stones if they are present.

CT of Kidney Stones


The treatment of kidney stones depends in part on the size of the stone, as well as the type. Stones that contain large amounts of calcium cannot be dissolved with current medicines available; uric acid and cysteine stones can. Medical therapy is designed to either (a) dissolve the stone, or (b) get it to pass with minimal amounts of discomfort.

Expulsive therapy involves using medications to relax the smooth muscles around the "tubes" (ie: ureter, urethra) of the urinary tract. Commonly used medications that do this include:

(1) Alpha-blockers (ie: tamsulosin, terazosin, etc.)
(2) Calcium channel blockers (ie: nifedipine)

These medications help stones pass, especially when they are larger than 3mm in size. In addition, medications for controlling pain associated with kidney stones are paramount to ensuring stone expulsion.

Stones that are larger than 8mm in diameter usually do not pass on their own, even with medical expulsive therapies. These stones must be managed through mechanical or surgical means.

The first approach is to break the stones into smaller fragments using a technology called extracorporeal shockwave lithotripsy. This is a non-invasive method that delivers powerful waves through the body designed to fragment the stone. The second, and more invasive, procedure is ureteroscopy. This refers to placing a tiny camera into the urethra, bladder, and ultimately into the ureter in order to directly visualize the stone. It is then removed with small forceps.

Staghorn calculi larger than 4 cm diameter require a procedure known as percutaneous nephrolithotomy. In essence, a tube is placed through the skin into the kidney. From there the stone can be directly visualized and removed.

Preventing stones from re-forming is also important. Adequate hydration is critical in preventing all stone types, and is probably the single most important preventative measure! Hydration ensures that urine output is high enough to prevent precipitation of minerals that commonly cause stones.

Prevention includes:
(1) adequate hydration
(2) low sodium diet
(3) low protein diet
(4) low oxalate diet
(5) normal or high
       calcium diet
In addition, dietary modifications are also recommended. Paradoxically, excess restriction of calcium from the diet can actually lead to stone formation. This is believed to be due to oxalate being absorbed from the GI tract instead of calcium. The excess absorption of oxalate leads to increased calcium oxalate stone formation in the tubules of the kidneys. Therefore, people with calcium stones should eat a diet that is high in calcium (1 to 4 grams/day); however, supplementing the diet with calcium tablets is not recommended. Diets high in oxalate should be avoided. Avoidance of diets high in salt and protein are also generally recommended.

Treatment for specific types of stones are also given. To prevent the re-formation of uric acid stones, potassium citrate is commonly given to make the urine less acidic (more alkaline). This increases the solubility of urate and keeps it from precipitating into a stone.


Kidney stones come in different shapes and sizes. The most common type are calcium stones. Many patients are asymptomatic although flank pain that radiates into the scrotum and labia majora are common. Blood tinged urine may also be seen. Diagnosis is based on urine microscopy, kidney ultrasound, CT scan, and urinalysis. Treatment for all kidney stones consists of adequate hydration and analgesics. Stones larger than 8mm often need to be broken up or removed via mechanical means.

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References and Resources

Too Much Pee! Understanding Diabetes Insipidus

In order to understand diabetes insipidus we have to understand a little about how the kidneys reabsorb water. Water absorption in the kidney is dictated by a hormone known as vasopressin (aka: antidiuretic hormone). This hormone is synthesized in the hypothalamus of the brain, transported down the pituitary stalk, and excreted into the blood stream by the posterior portion of the pituitary gland.

Once in the blood stream vasopressin goes to the kidney where it binds to receptors on cells in the collecting ducts of the nephron. This interaction sets off a series of reactions that allows the kidney to reabsorb water from urine. The end result is that the body retains water and the urine becomes more concentrated (“Look mom my pee is yellow!”).

With this background, we can now discuss diabetes insipidus (DI). Diabetes insipidus occurs when the hypothalamus, or pituitary gland fail to communicate effectively with the kidneys. This can happen in one of two ways: the hypothalamus or pituitary can fail to send a signal (ie: vasopressin) to the kidney, or the kidney can fail to respond to that signal. The first case is known as “central” diabetes insipidus, and the second case is known as “nephrogenic” diabetes insipidus.

In either case, the kidney fails to reabsorb water. The end result is dehydration and a steadily rising blood sodium level, which can cause numerous signs and symptoms.

Signs and Symptoms

Patients with diabetes insipidus pee like crazy! This is because the kidney is unable to reabsorb water. Patients can urinate over a liter of fluid per hour! Because of this, the serum sodium level can increase precipitously. The resulting hypernatremia (ie: elevated sodium level) can cause seizures, altered mental status, and coma if not recognized and treated aggressively.

In addition, patients with diabetes insipidus are usually very thirsty. They typically ask for “ice water”, and will drink large volumes in an attempt to keep up with their urinary losses.


Diagnosis is based on several clinical markers. Urine output greater than 250 mL/hour in the setting of a low urine osmolarity (50-150 mOsm/L) or specific gravity (1.001-1.005), a high normal or above normal blood sodium concentration, and a higher than normal blood osmolarity are indicators of diabetes insipidus.

Often times the diagnosis may still be difficult to make when only one, or a few of the above are present. If this is the case, a “water deprivation test” can be performed. This test is exactly what it sounds like: don’t allow the patient to receive any form of fluid (either intravenous or oral). You must monitor their condition carefully!

Under conditions of water deprivation, a normal person’s kidneys will start to retain water, and because of this, the urine will become more concentrated (usually to greater than 600 mOsm/L). However, in patients with diabetes insipidus the kidneys are unable to absorb water and the urine osmolality remains lower than expected (ie: the urine remains dilute).

If the water deprivation test is positive then the next step is to determine if central or nephrogenic diabetes insipidus is present. The easiest way to do this is to provide synthetic vasopressin (“thank god for the pharmaceutical companies!”). If the patient has central DI then the urine output will decrease, and the urine concentration will increase; in other words, the kidney is responding to the synthetic vasopressin.

However, in nephrogenic diabetes insipidus the patient will continue to have increased urine output and the urine concentration will fail to increase. In other words the kidney is unable to respond to vasopressin either in natural, or synthetic form.


Treatment is dependent on what form of diabetes insipidus is present and how severe it is. Some patients with DI are capable of drinking enough water to compensate for their urinary losses and therefore require no specific intervention.

However, other patients may not be able to drink enough to keep up with their losses. This can occur in patients who are urinating so much that they can not possibly keep up orally, or in patients who are unable to drink for other reasons (ie: coma, swallowing problems, etc.). If this is the case, then a patient with central diabetes should be given artificial vasopressin, also known as desmopressin (DDAVP).

Patients with nephrogenic diabetes insipidus are treated with a combination of medications depending on the severity of their disease. Thiazide diuretics such as hydrochlorothiazide can decrease the urine output. Interestingly, non-steroidal anti-inflammatory medications like ibuprofen and indomethacin can decrease urine output by blocking the formation of prostaglandins, which normally inhibit the effects of vasopressin.


Diabetes insipidus occurs when the kidney fails to respond to vasopressin, either because vasopressin is not secreted by the pituitary, or because of an intrinsic defect in the kidney’s ability to sense vasopressin.

In either situation the kidney fails to reabsorb water, which causes dehydration and hypernatremia (ie: elevated sodium level in the blood). If the patient is unable to drink enough fluids the condition can be fatal. If oral rehydration is not enough, then patients with central diabetes insipidus can be treated with synthetic vasopressin analogues. In patients with nephrogenic diabetes insipidus diuretics such as hydrochlorothiazide and non-steroidal anti-inflammatory medications may  help decrease urine output. 

References and Resources

  • Trepiccione F, Christensen BM. Lithium-induced nephrogenic diabetes insipidus: new clinical and experimental findings. J Nephrol. 2010 Nov-Dec;23 Suppl 16:S43-8. Review.
  • Noda Y, Sohara E, Ohta E, et al. Aquaporins in kidney pathophysiology. Nat Rev Nephrol. 2010 Mar;6(3):168-78. Epub 2010 Jan 26. Review.
  • Ranadive SA, Rosenthal SM. Pediatric disorders of water balance. Endocrinol Metab Clin North Am. 2009 Dec;38(4):663-72.
  • Knepper MA, Verbalis JG, Nielsen S. Role of aquaporins in water balance disorders. Curr Opin Nephrol Hypertens. 1997 Jul;6(4):367-71.
  • Robertson GL. Regulation of arginine vasopressin in the syndrome of inappropriate antidiuresis. Am J Med. 2006 Jul;119(7 Suppl 1):S36-42.