Are small (at the beginning), hard mineral deposits that form in the kidney. Urine contains dissolved salts and minerals. If the urine has high levels of this deposits, you can form kidney stones. Stones can stay in the kidney, but eventually can travel down to the ureter, bladder and urethra. If the stone blocks the ureter, it also blocks the urinary flow and can cause excruciating pain.
- How common are kidney stones?
The lifetime prevalence of having kidney stones is estimated at 1% to 15%. It varies according to race, age, gender and geographic location. Specifically, 114.3 per 100,000 people will have an episode of kidney stones. It is estimated that more than 500,000 people visit emergency departments for kidney stone disease.
- What are kidney stones made of?
Calcium stones (calcium oxalate by far is the most common) in 80% of cases. Uric acid stones 5-10%. Struvite 10% mostly related to urinary tract infections. Cystine less than 1% of cases.
- What are the risk factors for kidney stones?
Men are affected 2-3 times more than women. It is more common in whites, followed by hispanics, asians, and african-americans. It is uncommon before age 20 but peaks in the fourth to sixth decades of life. It has a higher prevalence in hot, arid, or dry climates (mountains, desert, or tropical areas). However, genetic factors and diet may influence this disease. Heat exposure and dehydration are occupational risk factors for kidney stone disease. Also overweight and high body mass index are directed related to kidney stone disease. Despite this risk factors, the most important risk factor is dehydration, so a high fluid intake can prevent urolithiasis.
Don’t miss PART II of this FAQ.
Kidney stones (nephrolithiasis or urolithiasis) affect approximately 12% of men and 5% of women during their lifetime. Nearly half of all first time stone formers will have another stone episode within the next four years.
Stones can form when calcium, oxalate, uric acid or cystineÂ are at high levels in the urine.
Uric acid stones represents 5 – 10% of all kidney stones. But they comprise 40% in areas with hot/arid climates where low urine volume and acid urine pH promote uric acid precipitation.
Prevalence: Â In patients with gout without antihyperuricemic treatment is 20%. Hundreds-fold greater than healthy adults.
Risk factors: It primarily occurs in patients without abnormality in uric acid metabolism such as: relatively high serum uric acid levels, comparatively low urinary pH, and low fractional excretion of urate. Clinical gout. Hyperuricosuria, chronic diarrhea (bicarbonate loss and dehydration). Â Diabetes, metabolic syndrome and overweight.
How it occurs?: Â Two major factors contribute uric acid precipitation
- a high concentration of uric acid in urine
- acid urine pH
Diagnosis: Is suggested from the acute onset of flank pain, a positive non-contrast-enhanced CT scan, and history of a predisposing disease (gout, cancer, etc). Plain X-ray is not helpful because these stones are not radiopaque. Confirmation of the diagnosis is best made by chemical analysis of a stone that has been passed.
- Maintenance of the urine output above 2 L/day to diminish the urine uric acid concentration
- alkalinization of the urine (increase the urine pH) with potassium bicarbonate or potassium citrate (cytra-k; polycitra-k; urocit-k; citro-k)Â can be given and this regimen can both dissolve preexisting stones and prevent the formation of new ones.
- Allopurinol (zyloprim; aloprim; atisuril)
- Reduction in dietary purine intake (protein)
Image courtesy of: Urocit-K