by Dr. Valerie Tan
Nephrolithiasis, or commonly known as kidney stones, is a common disease that affects 1 in 11 people in the United States, with incidence and prevalence rates increasing over the last several decades.
Men are more commonly affected than women, with a male-to-female ratio of 3:1, and having a family history of kidney stones further increases the risk.
Most stones develop in persons aged 20-49 years, with peak incidence among those aged 35-45 years, but it can occur in any age group.
Patients can have a single stone or multiple stones at the time of diagnosis. Kidney stones typically recur, and recurrence rates after the first stone episode are 14% at 1 year and up to 52% at 10 years.
The majority of kidney stones are made up of calcium, either in combination with other compounds like oxalate or phosphate, accounting for 75% of kidney stones.
The rest of the most common chemical types of kidney stones include struvite (magnesium ammonium phosphate) stones, uric acid stones, cystine stones and stones from precipitation of certain drugs or its metabolites.
Struvite stones account for 15% of stones and they are associated with chronic urinary tract infections (UTI) with certain kinds of bacteria. Uric acid stones account for 6% of kidney stones.
Approximately 25% of patients with uric acid stones have gout. Cystine stones account for 2% of stones, and they arise because of an intrinsic metabolic or genetic defect.
Drug-induced stones arise from the precipitation in the urine of drug components or metabolites.
The most common cause of kidney stones is low fluid intake, causing low volume of urine, which leads to high concentrations of stone-forming components in the urine.
This causes supersaturation of stone components like calcium, oxalate and uric acid in the urine, leading to crystal formation, which in turn becomes the nidus for further precipitation of the components, eventually forming a stone.
The stones first develop in the kidneys and then migrate to different parts of the urinary tract as they try to pass.
An acute kidney stone attack (renal colic) is described as excruciatingly painful, sometimes described as worse than childbirth. The stones cause symptoms when they become impacted within the ureter as they pass toward the bladder.
The colicky-type pain is primarily caused by the dilation, stretching, and spasm caused by the acute obstruction in the ureter.
It usually begins in the upper lateral mid back and then radiates down and to the front toward the groin.
Contrary to common belief, the severity of the pain depends on the degree and site of the obstruction, not on the size of the stone. Other symptoms can include blood in the urine or symptoms of urinary infection.
Approximately 80-85% of stones pass spontaneously, while about 15-20% of patients with an acute stone attack will require hospitalization due to unrelenting pain, inability to keep food or water down, inability to pass the stone, or worse, presence of severe kidney infection.
Obstruction of the ureter by a kidney stone, especially complete obstruction, can lead to damage to the affected kidney because blood flow to the affected kidney decreases to approximately 50% after 72 hours and down to 12% after 8 weeks.
As such, intervention within 4 weeks is recommended to avert permanent kidney damage.
Treatment for acute renal colic involves medical or surgical interventions or both.
Patients with uncomplicated ureteral stones that are 10 mm or less in diameter and are close to the bladder can be managed with aggressive medical measures with IV fluids and pain control.
Larger stones that seem unlikely to pass spontaneously require some type of surgical procedure and possibly hospitalization. However, most patients with acute renal colic can be treated on an outpatient basis.
Treatment of kidney stones does not end with the spontaneous passage or surgical removal of the stone.
Subsequent metabolic and medical evaluations for risk factors are indicated due to the high risk of recurrence, especially for those who present with multiple stones, who have a personal or family history of previous stones, are younger in age, or who have residual stones after treatment.
Metabolic evaluation for stone risk factors involves a 24-hour urine collection to evaluate for high concentrations in the urine of calcium, uric acid, or oxalate, or low concentrations of citrate.
Your medical provider can advise dietary changes or prescribe medications to alkalinize the urine to decrease the risk factors for further stone formation.
The most important aspect of medical therapy, however, is maintaining high fluid intake, which subsequently increases urine volume, effectively decreasing the risk of supersaturation of calcium, uric acid, and oxalate.
The goal is to increase fluid intake enough to achieve a 24-hour urine volume of at least 2.5 liters.
General dietary modifications include avoiding excessive intake of sodium (salt), animal protein, and high purine foods (eg, organ meats, legumes, fatty fish, meat extracts, gravies).
Although medical therapy and dietary changes generally do not completely stop the tendency for stone formation, it is, however, effective at delaying further stone formation.
Increased fluid intake and dietary modifications can cut the stone recurrence rate by 60%, which may be enough to decrease stone episodes in one’s lifetime.
DR. VALERIE TAN is a board-certified physician in Internal Medicine and Nephrology. She practices as a Nephrologist at Hawaii Nephrologists LLC.
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