I. Symptoms
Some people with kidney stones may not experience any symptom at all. Renal colic is
characterized by an excruciating intermittent pain, usually in the flank
(the area between the ribs and hip), that spreads across the abdomen,
often to the genital area and inner thigh. The pain tends to come in
waves, gradually increasing to a peak intensity, then fading, over about
20 to 60 minutes. The pain may radiate down the abdomen toward the
groin or testis or vulva.
Other symptoms include nausea and vomiting,
restlessness, sweating, and blood in the urine. A person may have an
urge to urinate frequently, particularly as a stone passes down the
ureter. Chills, fever, and abdominal distention sometimes occur.(1a)
Causes
1. Dehydration
Dehydration or strenuous exercise without adequate fluid can cause the forming of kidney stones as a result of low levels of urine pH (below 5.5)(1).
2. Ramadan fasting ( food restriction)
Ramadan fasting are associated with risk of kidney stones forming. In the study to evaluate the effects of fluid and food restriction in Ramadan fasting on urinary factors in kidney and urinary calculus formation, researchers at the Shahid Beheshti University of Medical Sciences, found that fasting during Ramadan has different effects on total excretion and concentrations of urinary precipitate and inhibitory factors contributing to calculus formation(2).
3. Rotavirus infection
There is a report of 4 patients with RV infection who developed postrenal renal failure induced by urinary tract obstruction with uroammoniac calculi or crystals... Uric acid stone formation was considered to have originated from the low pH caused by dehydration and the increase of urinary uric acid excretion from damaged cells(3).
4. Calcium
In the study to explore the relationship among intestinal fractional calcium absorption, calcium intake and nephrolithiasis in a prospective cohort of 9,704 postmenopausal women recruited from population based listings in 1986 and followed for more than 20 years, showed that fractional calcium absorption is higher in women with a history of nephrolithiasis. Higher intestinal fractional calcium absorption is associated with a greater risk of historical nephrolithiasis. Dietary and supplemental calcium decrease fractional calcium absorption, and may protect against nephrolithiasis(3a).
5. Gastrointestinal lipase inhibitor
Intestinal malabsorption can cause urinary stone disease via enteric hyperoxaluria. The use of lipase inhibitors, especially under a diet rich in oxalate alone or associated with fat, leads to a significant and marked increase in urinary oxalate and a slight reduction in uCa and uMg that, taken together, resulted in an increase in AP (CaOx) index(rat), elevating the risk of stone formation(3b).
6. High fat intake
A comparison of the dietary intake per kilogram body weight in each group was made using standard statistical procedures. None of the nutrient intakes showed a significant difference, but dietary fibre intake and the percentage of energy provided by carbohydrate were consistently higher in the control group, whereas the percentage of energy provided by fat was consistently higher in the renal stone group(3c).
7. Vitamins
In the study of a total of 1078 incident cases of kidney stones was documented during the 14-yr follow-up period. A high intake of vitamin B6 was inversely associated with risk of stone formation. After adjusting for other dietary factors, the relative risk of incident stone formation for women in the highest category of B6 intake (> or =40 mg/d) compared with the lowest category (<3 mg/d) was 0.66 (95% confidence interval, 0.44 to 0.98). In contrast, vitamin C intake was not associated with risk. The multivariate relative risk for women in the highest category of vitamin C intake (> or =1500 mg/d) compared with the lowest category (<250 mg/d) was 1.06 (95% confidence interval, 0.69 to 1.64). Large doses of vitamin B6 may reduce the risk of kidney stone formation in women. Routine restriction of vitamin C to prevent stone formation appears unwarranted(3d).
8. Etc.
1. Dehydration
Dehydration or strenuous exercise without adequate fluid can cause the forming of kidney stones as a result of low levels of urine pH (below 5.5)(1).
2. Ramadan fasting ( food restriction)
Ramadan fasting are associated with risk of kidney stones forming. In the study to evaluate the effects of fluid and food restriction in Ramadan fasting on urinary factors in kidney and urinary calculus formation, researchers at the Shahid Beheshti University of Medical Sciences, found that fasting during Ramadan has different effects on total excretion and concentrations of urinary precipitate and inhibitory factors contributing to calculus formation(2).
3. Rotavirus infection
There is a report of 4 patients with RV infection who developed postrenal renal failure induced by urinary tract obstruction with uroammoniac calculi or crystals... Uric acid stone formation was considered to have originated from the low pH caused by dehydration and the increase of urinary uric acid excretion from damaged cells(3).
4. Calcium
In the study to explore the relationship among intestinal fractional calcium absorption, calcium intake and nephrolithiasis in a prospective cohort of 9,704 postmenopausal women recruited from population based listings in 1986 and followed for more than 20 years, showed that fractional calcium absorption is higher in women with a history of nephrolithiasis. Higher intestinal fractional calcium absorption is associated with a greater risk of historical nephrolithiasis. Dietary and supplemental calcium decrease fractional calcium absorption, and may protect against nephrolithiasis(3a).
5. Gastrointestinal lipase inhibitor
Intestinal malabsorption can cause urinary stone disease via enteric hyperoxaluria. The use of lipase inhibitors, especially under a diet rich in oxalate alone or associated with fat, leads to a significant and marked increase in urinary oxalate and a slight reduction in uCa and uMg that, taken together, resulted in an increase in AP (CaOx) index(rat), elevating the risk of stone formation(3b).
6. High fat intake
A comparison of the dietary intake per kilogram body weight in each group was made using standard statistical procedures. None of the nutrient intakes showed a significant difference, but dietary fibre intake and the percentage of energy provided by carbohydrate were consistently higher in the control group, whereas the percentage of energy provided by fat was consistently higher in the renal stone group(3c).
7. Vitamins
In the study of a total of 1078 incident cases of kidney stones was documented during the 14-yr follow-up period. A high intake of vitamin B6 was inversely associated with risk of stone formation. After adjusting for other dietary factors, the relative risk of incident stone formation for women in the highest category of B6 intake (> or =40 mg/d) compared with the lowest category (<3 mg/d) was 0.66 (95% confidence interval, 0.44 to 0.98). In contrast, vitamin C intake was not associated with risk. The multivariate relative risk for women in the highest category of vitamin C intake (> or =1500 mg/d) compared with the lowest category (<250 mg/d) was 1.06 (95% confidence interval, 0.69 to 1.64). Large doses of vitamin B6 may reduce the risk of kidney stone formation in women. Routine restriction of vitamin C to prevent stone formation appears unwarranted(3d).
8. Etc.
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Use The Revolutionary Findings To Achieve
Optimal Health And Loose Weight
Super foods Library, Eat Yourself Healthy With The Best of the Best Nature Has to Offer
Back to General health http://kylejnorton.blogspot.ca/p/general-health.html
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/12649987
(1a) http://www.merckmanuals.com/home/kidney_and_urinary_tract_disorders/stones_in_the_urinary_tract/stones_in_the_urinary_tract.html?qt=&sc=&alt=
(2) http://www.ncbi.nlm.nih.gov/pubmed/22218117
(3) http://www.ncbi.nlm.nih.gov/pubmed/20420802
(3a) http://www.ncbi.nlm.nih.gov/pubmed/22341269
(3b) http://www.ncbi.nlm.nih.gov/pubmed/15253722
(3c) http://www.ncbi.nlm.nih.gov/pubmed/6269684
(3d) http://www.ncbi.nlm.nih.gov/pubmed/10203369
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