Disturbances in mineral and bone metabolism occur early in the course of chronic kidney disease (CKD). Without prevention or treatment these disturbances progress to renal osteodystrophy encompassing varying combinations and degrees of high- and low-turnover bone disorders.

Although a broad body of literature indicates that load-bearing exercise has favorable effects on bone metabolism in the adult and aged skeleton [1, 2], there are no studies on the impact of exercise on bone in chronic or end stage renal disease (ESRD). However, much of what is known regarding the effects of exercise on bone, particularly in osteoporosis, may be helpful in the preservation of bone strength in these populations. This may be especially relevant due to the contribution of age-associated osteoporosis as the average age of CKD and ESRD patients increases.

While high impact activity is especially osteogenic [3], moderate intensity walking results in modest increases in lumbar bone mineral density (BMD) [4], indicating that low-impact activities can have a beneficial effect. This is an important consideration for individuals with kidney disease since they are prone to fatigue and generally have low exercise capacity [5]. Further, renal osteodystrophy carries increased risk for spontaneous tendon rupture, and low impact exercise is a safer choice. In the walking study, BMD increased due to suppression of bone turnover. Though suppression of bone turnover may be a concern in low-turnover disease, a recent report shows that active ESRD patients with adynamic bone disease have greater mineralized bone volume due to minimodeling compared to less active patients [6]. This suggests that bone formation can continue on a limited basis via this process that appears to be enhanced by physical activity.

Studies in humans including hemodialysis patients [7] show a positive correlation between muscle strength and BMD. This is because mechanical loading applied to the bone by muscle is directly responsible for bone formation and remodeling [8]. Although the effects of strength training on BMD have been equivocal in healthy populations [2], strength and muscle mass do increase in response to strength training in ESRD [9], and thus may benefit bone.

While there is no direct information to support beneficial effects of exercise on the bone disorders in kidney disease, existing information is suggestive of such effects. Because the literature suggests that both low-impact weight bearing exercise such as walking and resistance exercise (strength training) are beneficial to bone, patients with kidney disease should be encouraged to find ways to add these types of physical activity to their daily life. Easy suggestions to encourage more walking include; finding a walking buddy to take walks in the neighborhood, walking the dog, joining a local mall walking program, walking up a flight of stairs instead of taking the elevator, and parking the car further from the store. Local community centers often offer low impact exercise classes, and low to moderate intensity resistance exercise classes, as do many gyms. There are two very good illustrated resistance exercise program guides that patients can download from the National Institute of Aging (www.niapublications.org/exercisebook/index.asp) and from Life Options (www.lifeoptions.org ), another organization that helps educate people with CKD. The NKF also has good information about exercise for people with CKD on its Web site, www.kidney.org. Finally, the overall benefit of physical activity in decreasing the risks of comorbidities and preserving physical function cannot be overlooked, and the recommendation and encouragement of physical activity should be a priority for this population; see www.imakenews.com/ckdupdate/e_article000466465.cfm?x=b11,0,w .

Reference:

1. Wolff I, van Croonenborg JJ, Kemper HCG, Kostense PJ, Twisk JWR: The Effect of Exercise Training Programs on Bone Mass: A Meta-analysis of Published Controlled Trials in Pre- and Postmenopausal Women. Osteoporosis International 9:1-12, 1999
2. Wallace BA, Cumming RG: Systematic Review of Randomized Trials of the Effect of Exercise on Bone Mass in Pre- and Postmenopausal Women. Calcified Tissue International 67:10-18, 2000
3. Heinonen A, Oja P, Kannus P, Sievanen H, Haapasalo H, Manttari A, Vuori I: Bone mineral density in female athletes respresenting sports with different loading characteristics. Bone 17:197-203, 1995
4. Yamazaki S, Ichimura S, Iwamoto J, Takeda T, Toyama Y: Effect of walking exercise on bone metabolism in postmenopausal women with osteopenia/osteoporosis. Journal of Bone and Mineral Metabolism 22:500-508, 2004
5. Johansen KL: Physical functioning and exercise capacity in patients on dialysis. Advances in Renal Replacement Therapy 6:141-148, 1999
6. Ubara Y, Tagami T, Nakanishi S, Sawa N, Hoshino J, Suwabe T, Katori H, Takemoto F, Hara S, Takaichi K: Significance of minimodeling in dialysis patients with adynamic bone disease. Kidney International 68:833-839, 2005
7. Spindler A, Paz S, Berman A, Lucero E, Contino N, enalba A, Tirado S, Santana M, Zeballos A: Muscular strength and bone mineral density in haemodialysis patients. Nephrol. Dial. Transplant. 12:128-132, 1997
8. Chamay A, Tschantz P: Mechanical influences in bone remodeling. Journal of Biomechanics 5:173-180, 1972
9. Kouidi E, Albani M, Konstantinos N, Megalopoulos A, Gigis P, Guiba-Tziampiri O, Tourkantonis A, Deligiannis A: The effects of exercise training on muscle atrophy in haemodialysis patients. Nephrology Dialysis Transplantation 13:685-699, 199

I suggest you that the best way is carrying out the preventive measures. One most important measure is drinking much good quality water. You could read my post regarding my story with the kidney stones.

I got explanation from his family that during his teenage up to his death he had unhealthy lifestyle. As a student, he accustomed to drink instant energy drink and to consume instant noodle almost everyday. As we know that both kind of modern-processed food are rich of artificial food additives, such as MSG and artificial colorings and sweeteners. I hope you could learn from this tragic case: never consume too much food containing artificial food additives.

Many people who have chronic kidney disease don’t know it, because the early signs can be very subtle. It can take many years to go from chronic kidney disease (CKD) to kidney failure. Some people with CKD live out their lives without ever reaching kidney failure.

However, for people at any stage of kidney disease, knowledge is power. Knowing the symptoms of kidney disease can help you get the treatment you need to feel your best. If you or someone you know has one or more of the following symptoms of kidney disease, or you are worried about kidney problems, see a doctor for blood and urine tests. Remember, many of the symptoms can be due to reasons other than kidney disease. The only way to know the cause of your symptoms is to see your doctor.

Symptom 1:

Changes in Urination

Kidneys make urine, so when the kidneys are failing, the urine may change. How?

• You may have to get up at night to urinate.
• Your urine may be foamy or bubbly.
• You may urinate more often, or in greater amounts than usual, with pale urine.
• You may urinate less often, or in smaller amounts than usual with dark colored urine.
• Your urine may contain blood.
• You may feel pressure or have difficulty urinating.

What patients said:

“When you go to use the restroom, you couldn’t get it all out. And it would still feel just like tightness down there, there was so much pressure.”

“My urine is what I had started noticing. Then I was frequently going to the bathroom, and when I got there, nothing’s happening.”

“I was passing blood in my urine. It was so dark. And when I went to the hospital they thought I was lying about what color it was.”

Symptom 2:

Swelling

Failing kidneys don’t remove extra fluid, which builds up in your body causing swelling in the legs, ankles, feet, face, and/or hands.

What patients said:

“I remember a lot of swelling in my ankles. My ankles were so big I couldn’t get my shoes on.”

“My sister, her hair started to fall out, she was losing weight, but her face was really puffy, you know, and everything like that, before she found out what was going on with her.”

“Going to work one morning, my left ankle was swollen, real swollen, and I was very exhausted just walking to the bus stop. And I knew then that I had to see a doctor.”

Symptom 3:

Fatigue

Healthy kidneys make a hormone called erythropoietin (a-rith’-ro-po’-uh-tin) that tells your body to make oxygen-carrying red blood cells. As the kidneys fail, they make less erythropoietin. With fewer red blood cells to carry oxygen, your muscles and brain become tired very quickly. This condition is called anemia, and it can be treated.

What patients said:

“I was constantly exhausted and didn’t have any pep or anything.”

“I would sleep a lot. I’d come home from work and get right in that bed.”

“It’s just like when you’re extremely tired all the time. Fatigued, and you’re just drained, even if you didn’t do anything, just totally drained.”

Symptom 4:

Skin Rash/Itching

Kidneys remove wastes from the bloodstream. When the kidneys fail, the buildup of wastes in your blood can cause severe itching.

What patients said:

“It’s not really a skin itch or anything, it’s just right down to the bone. I had to get a brush and dig. My back was just bloody from scratching it so much.”

“My skin had broke out, I was itching and scratching a lot.”

Symptom 5:

Metallic Taste in Mouth/Ammonia Breath

A buildup of wastes in the blood (called uremia) can make food taste different and cause bad breath. You may also notice that you stop liking to eat meat, or that you are losing weight because you just don’t feel like eating.

What patients said:

“Foul taste in your mouth. Almost like you’re drinking iron.”

“You don’t have the appetite you used to have.”

“Before I started dialysis, I must have lost around about 10 pounds.”

Symptom 6:

Nausea and Vomiting

A severe buildup of wastes in the blood (uremia) can also cause nausea and vomiting. Loss of appetite can lead to weight loss.

What patients said:

“I had a lot of itching, and I was nauseated, throwing up all the time. I couldn’t keep anything down in my stomach.”

“When I got the nausea, I couldn’t eat and I had a hard time taking my blood pressure pills.”

Symptom 7:

Shortness of Breath

Trouble catching your breath can be related to the kidneys in two ways. First, extra fluid in the body can build up in the lungs. And second, anemia (a shortage of oxygen-carrying red blood cells) can leave your body oxygen-starved and short of breath.

What patients said:

“At the times when I get the shortness of breath, it’s alarming to me. It just fears me. I think maybe I might fall or something so I usually go sit down for awhile.”

“I couldn’t sleep at night. I couldn’t catch my breath, like I was drowning or something. And, the bloating, can’t breathe, can’t walk anywhere. It was bad.”

“You go up a set of stairs and you’re out of breath, or you do work and you get tired and you have to stop.”

Symptom 8:

Feeling Cold

Anemia can make you feel cold all the time, even in a warm room.

What patients said:

“I notice sometimes I get really cold, I get chills.”

“Sometimes I get really, really cold. It could be hot, and I’d be cold.”

Symptom 9:

Dizziness and Trouble Concentrating

Anemia related to kidney failure means that your brain is not getting enough oxygen. This can lead to memory problems, trouble with concentration, and dizziness.

What patients said:

“I know I mentioned to my wife that my memory—I couldn’t remember what I did last week, or maybe what I had 2 days ago. I couldn’t really concentrate, because I like to work crossword puzzles and read a lot.”

“I was always tired and dizzy.”

“It got to the point, like, I used to be at work, and all of the sudden I’d start getting dizzy. So I was thinking maybe it was my blood pressure or else diabetes was going bad. That’s what was on my mind.”

Symptom 10:

Leg/Flank Pain

Some people with kidney problems may have pain in the back or side related to the affected kidney. Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys and sometimes the liver, can cause pain.

What patients said:

“About 2 years ago, I was constantly going to the bathroom all the time, the lower part of my back was always hurting and I was wondering why…and they diagnosed that kidney problem.”

“And then you’re having to get up all time through the night, and then you have the side ache, a backache, and you can’t move.”

“At night, I would get a pain in my side. It was worse than labor pain. And I’d be crying and my husband would get up, everybody, rubbing my legs.”

Vitamin C, also known as ascorbic acid, is a water-soluble vitamin. Unlike most mammals and other animals, humans do not have the ability to make their own vitamin C. Therefore, we must obtain vitamin C through our diet.

Function

Vitamin C is required for the synthesis of collagen, an important structural component of blood vessels, tendons, ligaments, and bone. Vitamin C also plays an important role in the synthesis of the neurotransmitter, norepinephrine. Neurotransmitters are critical to brain function and are known to affect mood. In addition, vitamin C is required for the synthesis of carnitine, a small molecule that is essential for the transport of fat into cellular organelles called mitochondria, where the fat is converted to energy (1). Research also suggests that vitamin C is involved in the metabolism of cholesterol to bile acids, which may have implications for blood cholesterol levels and the incidence of gallstones (2).

Vitamin C is also a highly effective antioxidant. Even in small amounts vitamin C can protect indispensable molecules in the body, such as proteins, lipids (fats), carbohydrates, and nucleic acids (DNA and RNA), from damage by free radicals and reactive oxygen species that can be generated during normal metabolism as well as through exposure to toxins and pollutants (e.g., cigarette smoke). Vitamin C may also be able to regenerate other antioxidants such as vitamin E (1). One recent study of cigarette smokers found that vitamin C regenerated vitamin E from its oxidized form (3).

Role in Immunity

Vitamin C affects several components of the human immune system; for example, vitamin C has been shown to stimulate both the production  and function  of leukocytes (white blood cells), especially neutrophils, lymphocytes, and phagocytes. Specific measures of functions stimulated by vitamin C include cellular motility,   chemotaxis , and phagocytosis.  Neutrophils, which attack foreign bacteria and viruses, seem to be the primary cell type stimulated by vitamin C, but lymphocytes and other phagocytes are also affected ). Additionally, several studies have shown that supplemental vitamin C increases serum levels of antibodies  and C1q complement proteins  guinea pigs, which—like humans—cannot synthesize vitamin C and hence depend on dietary vitamin C. However, some studies have reported no beneficial changes in leukocyte production or function with vitamin C treatment. Vitamin C may also protect the integrity of immune cells. Neutrophils, mononuclear phagocytes, and lymphocytes accumulate vitamin C  to high concentrations, which can protect these cell types from oxidative damage.  In response to invading microorganisms, phagocytic leukocytes release non-specific toxins, such as superoxide radicals, hypochlorous acid (“bleach”), and peroxynitrite; these reactive oxygen species kill pathogens and, in the process, can damage the leukocytes themselves. Vitamin C, through its antioxidant functions, has been shown to protect leukocytes from such effects of autooxidation. Phagocytic leukocytes also produce and release cytokines, including interferons, which have antiviral activity. Vitamin C has been shown to increase interferon levels in vitro.

It is widely thought by the general public that vitamin C boosts the function of the immune system, and accordingly, may protect against viral infections and perhaps other diseases. While some studies suggest the biological plausibility of vitamin C as an immune enhancer, human studies published to date are conflicting. Further, controlled clinical trials of appropriate statistical power would be necessary to determine if supplemental vitamin C boosts the immune system.

Food Sources of Vitamin C

As shown in the table below, different fruits and vegetables vary in their vitamin C content, but five servings (2½ cups) of fruits and vegetables should average out to about 200 mg of vitamin C. If you wish to check foods for their nutrient content, search the USDA food composition database.

Food                                     Serving                 Vitamin C (mg)
Orange juice                  ¾ cup (6 ounces)                62-93
Grapefruit juice              ¾ cup (6 ounces)                62-70
Orange                              1 medium                           70
Grapefruit                        ½ medium                             38
Strawberries                   1 cup, whole                          85
Tomato                             1 medium                             16
Sweet red pepper         ½ cup, raw chopped               95
Broccoli                            ½ cup, cooked                       51
Potato                               1 medium, baked                 17

Vitamin C Supplements

Vitamin C (L-ascorbic acid) is available in many forms, but there is little scientific evidence that any one form is better absorbed or more effective than another. Most experimental and clinical research uses ascorbic acid or sodium ascorbate.

Natural vs. synthetic vitamin C

Natural and synthetic L-ascorbic acid are chemically identical and there are no known differences in their biological activities or bioavailabilities

Kidney Stones

Because oxalate is a metabolite of vitamin C, there is some concern that high vitamin C intake could increase the risk of oxalate kidney stones. Some, but not all, studies have reported that supplemental vitamin C increases urinary oxalate levels. Whether any increase in oxalate levels would translate to an elevation in risk for kidney stones has been examined in epidemiological studies. Two large prospective studies, one following 45,251 men for six years and the other following 85,557 women for 14 years, reported that consumption of ≥1,500 mg of vitamin C daily did not increase the risk of kidney stone formation compared to those consuming <250 mg daily. However, a more recent prospective study that followed 45,619 men for 14 years found that those who consumed ≥1,000 mg/day of vitamin C had a 41% higher risk of kidney stones compared to men consuming <90 mg of vitamin C daily—the current recommended dietary allowance (see RDA). In this study, low intakes (90-249 mg/day) of vitamin C (primarily from the diet) were also associated with a significantly elevated risk. Supplemental vitamin C intake was only weakly associated with increased risk of kidney stones in this study. Despite conflicting results, it may be prudent for individuals predisposed to oxalate kidney stone formation to avoid high-dose vitamin C supplementation.

Linus Pauling Institute Recommendations

For healthy men and women, the Linus Pauling Institute recommends a vitamin C intake of at least 400 mg daily—the amount that has been found to fully saturate plasma and circulating cells with vitamin C in young, healthy nonsmokers. Consuming at least five servings (2½ cups) of fruits and vegetables daily provides about 200 mg of vitamin C. Most multivitamin supplements provide 60 mg of vitamin C. To make sure you meet the Institute’s recommendation, supplemental vitamin C in two separate 250-mg doses taken in the morning and evening is recommended.

Older adults (65 years and older)

Although it is not yet known with certainty whether older adults have higher requirements for vitamin C than younger people, some older populations have been found to have vitamin C intakes considerably below the RDA of 75 and 90 mg/day for women and men, respectively. A vitamin C intake of at least 400 mg daily may be particularly important for older adults who are at higher risk for chronic diseases. In addition, a meta-analysis of 36 publications examining the relationship between vitamin C intake and plasma concentrations of vitamin C concluded that older adults (age 60-96 years) have considerably lower plasma levels of vitamin C following a certain intake of vitamin C compared with younger individuals (age 15-65 years), suggesting that older adults may have higher vitamin C requirements. Studies conducted at the National Institutes of Health indicated that plasma and circulating cells in healthy, young subjects attain maximal concentrations of vitamin C at a dose of about 400 mg/day—a dose much higher than the current RDA. Pharmacokinetic studies in older adults have not yet been conducted, but evidence suggests that the efficiency of one of the molecular mechanisms for the cellular uptake of vitamin C declines with age. Because maximizing blood levels of vitamin C may be important in protection against oxidative damage to cells and biological molecules, a vitamin C intake of at least 400 mg daily is particularly important for older adults who are at higher risk for chronic diseases caused, in part, by oxidative damage, such as heart disease, stroke, certain cancers, and cataract.

References:

1.  Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Am J Clin Nutr. 1999;69(6):1086-1107.

2.  Simon JA, Hudes ES. Serum ascorbic acid and gallbladder disease prevalence among US adults: the Third National Health and Nutrition Examination Survey (NHANES III). Arch Intern Med. 2000;160(7):931-936.

3.  Bruno RS, Leonard SW, Atkinson J, et al. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radic Biol Med. 2006;40(4):689-697.

4. Kennes B, Dumont I, Brohee D, Hubert C, Neve P. Effect of vitamin C supplements on cell-mediated immunity in old people. Gerontology. 1983;29(5):305-310

5.   U.S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Release 22. 2009. Available at: http://www.nal.usda.gov/fnic/foodcomp/search/. Accessed 11/7/09.

6.  Michels AJ, Joisher N, Hagen TM. Age-related decline of sodium-dependent ascorbic acid transport in isolated rat hepatocytes. Arch Biochem Biophys. 2003;410(1):112-120

The kidneys need stable fats both for their cushioning and as their energy source. We know that the kidney fat normally has a higher concentration of the important saturated fatty acids than are found in any of the other fat depots. These saturated fatty acids are myristic acid (the 14-carbon saturate), palmitic acid (the 16-carbon saturate), and stearic acid (the 18-carbon saturate). When we consume various polyunsaturated fatty acids in large amounts, they are incorporated into kidney tissues, usually at the expense of oleic acid, because the normal high level of saturated fatty acids in the kidney fat does not change.¹

A species of rat known to be prone to strokes and to spontaneously develop hypertension (high blood pressure) has been used to evaluate effects of different lipids such as plant sterols or cholesterol, and also fatty acids such as omega-3 or omega-6 fatty acids in the finely tuned functions of the kidney. These animals are very sensitive to dietary cholesterol manipulations and a deficiency of cholesterol in their membranes makes their membranes weak and fragile. When plant sterols found in vegetable oils are substituted for cholesterol in their diets, these animals have a shortened life span.² Also, these animals are reported to need a proper omega-6 to omega-3 ratio in the kidney phospholipids. It was further reported that feeding oils high in omega-6 fatty acids without omega-3 fatty acids resulted in renal injury, and that feeding oils rich in the omega-3 fatty acids such as fish oil, perilla oil, and flaxseed oil prolonged the survival time of this animal.³

The omega-3 fatty acids are recognized as being important, and the conversion of the flax oil-type omega-3 fatty acid (alpha-linolenic acid) to the fish oil-type omega-3 fatty acids (EPA and DHA) is enhanced when the diet contains saturated fat such as coconut oil. This conversion is hindered when there is extra omega-6 oils in the diet.⁴ Injury to the kidney from immune dysfunction (IgA nephropathy) responds to omega-3 fats (both flax oil-type omega-3 and fish oil-type omega-3).⁵ As noted, adding the saturated fats, especially coconut oil, improves the body’s use of omega-3 fatty acids.

Another reason that coconut oil enhances kidney function is because it supplies myristic acid, the 14-carbon saturated fatty acid.⁶ Myristic acid is involved in the signalling from cell membrane receptors through G proteins and their attachment to membranes. These signalling proteins require a lipid such as myristic acid to be added to one end of the protein, a process called myristolation.⁷

Thus, the fats that we recommend for general good health, namely various saturated animal fats and tropical oils, along with a supplement of flax oil, are also specifically helpful for kidney function. Products containing high omega-6 oils and trans fatty acids should be avoided.

References:

1. Suarez et al, Lipids 1996;31:345; Taugbol and Saarem, Acta Vet Scand 1995;36:93
2. Ratnayake, et al, J Nutrition 2000;130:1166
3. Miyazaki et al, Biochim Biophys Acta 2000;1483:101
4. Gerster, Int J Vitam Nutr Res 1998;68:159
5. Kelley, ISSFAL, 2000;7:6
6. Monserrat et al, Res Exp Med (Berl) 2000;199:195
7. Busconi and Denker, Biochem J 1997;328:23

I experienced suffering kidney stones two times in my life. The first one I’ve got in 1994 (when I was 28). Suddenly my urine became red and there was pain (renal colic) at waist area. I didn’t want to undertake any surgery to take out nor other measure to destroy the stone. I chose the moderate way, i.e.  to pass  the stone out of my body through urinary tract by drinking plenty of water and with the help from specific medicines formulated to ease the stone pass out of my body through  the urinary tract. Four month later, the stone with size of  one inch went out while I was urinating.

The second kidney stone attacked me 13 years later, in 2007. I got two times severe pain (renal colic)  around waist area (so pain that I felt like I would die). Based on the first experience,   I decided only applying the natural method of therapy in order to make the stone out of my body. Even though at  that time I didn’t know exactly what kind of therapy should be. I would like to tell the story  of the natural healing I’ve carried out to overcome the second time kidney stone, but  in the next special article.

The Science of Kidney Stones

The formation of kidney stones commonly occurs during the middle years, and in many cases, it is a consequence of some other condition. Other terms for the disorder are renal calculus, urinary calculus, kidney gravel, urolithiasis, and nephrolithiasis. The stones may occur in quantity and in a size as tiny as pinhead, on there may be a single stone as large as a walnut.

Causes

Kidney and urinary tract stones develop when calcium salts, uric acid, and other substances begin to crystallize and form masses that interfere with the body’s drainage process. They may be caused by an increased output of uric acid resulting from medicine used in treating gout; by a diet that is heavy in milk such as one that might be prescribed for the treatment of peptic ulcers; by a hyperparathyroid condition in which calcium levels  in blood and urine are increased; or by self-medication with overdoses of vitamin D. Kidney stones may also develop because of faulty metabolism that seems to run in particular families. Studies of 30 years a go already  indicated that a prime cause in the formation of urinary tract stones may be a tny organism known as mycoplasmas. These organism, halfway in size between viruses and bacteria, are known to inhabit the urinary tract of many people. They are now suspected of serving as the nucleus and part of the matrix of the obstructive stones.

Symptoms

The first symptom of kidney stones may be a urinary infection resulting from the obstruction of the urinary tract, and may possibly be signaled by nausea, vomiting, chills, and fever. Pain anyplace in this part of the body from the loin to the urethra – called renal colic – and blood in the urine are other signs of kidney stones.

Complications

Treatment

At yet there are no drugs that can safely dissolve kidney stones and therefore patent medicines that claim to do so should be avoided. Medications known as urinary solvents are not in general use because of their toxic side effects. Effective treatment for stones depends on the underlying cause and the severity of the symptoms. If some other disorder causing the stones can be identified and eliminated, further stone formation is usually prevented. Small stones of the gravel type are sometimes excreted without discomfort when the victim is placed on a regimen of high fluid intake. When a urinary infection is present, antibiotics are prescribed  at the same time that instruments may be used to remove the obstructive stone, such as catheter inserted through the urethra to ease out any stones  in the ureter. The doctor also uses a cystoscope in order to see the interior of the bladder and to find out whether stones have become so imbedded in tissue that removal by surgery is the only possible treatment. In case the size of kidney stones are too large to pass through (see Fig. 4 below), an ultrasound shock waves method should be used to crush the kidney stones, and as the result, the smaller pieces can easily pass out of body in urine. To ensure the existence (the position, number, and size) of the stones in kidney and in urinary tract, a  intravenous pyelogram (IVP) procedure  should be carried out (see Fig. 3 below).

• 
  
  Fig. 3. Intravenous Pyelogram (IVP):

Fig. 4. Lithotripsy Procedure:

Why You Need to Drink Water

Your body is estimated to be about 60% to 70% water. Blood is mostly water, and your muscles, lungs, and brain all contain a lot of water. Your body needs water to regulate body temperature and to provide the means for nutrients to travel to all your organs. Water also transports oxygen to your cells, removes waste, and protects your joints and organs.

Signs of Dehydration

You lose water through urination, respiration, and by sweating. If you are very active, you lose more water than if you are sedentary. Diuretics such as caffeine pills and alcohol result in the need to drink more water because they trick your body into thinking you have more water than we need.

Symptoms of mild dehydration include chronic pains in joints and muscles,lower back pain, headaches and constipation. A strong odor to your urine, along with a yellow or amber color indicates that you may not be getting enough water. Note that riboflavin, a B Vitamin, will make your urine bright yellow. Thirst is an obvious sign of dehydration and in fact, you need water long before you feel thirsty.

How Much Water do You Need to Drink?

A good estimate is to take your body weight in pounds and divide that number in half. That gives you the number of ounces of water per day that you need to drink. For example, if you weigh 140 pounds, you should drink at least 70 ounces of water per day (in SI unit, weight 70 kg should drink 2.072 liter of water). If you exercise you should drink another eight ounce glass of water for every 20 minutes you are active. If you drink alcohol, you should drink at least an equal amount of water. When you are traveling on an airplane, it is good to drink eight ounces of water for every hour you are on board the plane. If you live in an arid climate, you should add another two servings per day. As you can see, your daily need for water can add up to quite a lot.

Twenty percent of your water need will come from the foods you eat. The rest of your water need should come from the beverages you drink. Water is the best choice. Sodas have a lot of sugar in them, so if you drink sodas, you may take in more calories than you need. Herbal teas that aren’t diuretic are fine. Sports drinks contain electrolytes and may be beneficial, just look out for added sugar and calories that you don’t need. Juices are good because they have vitamins and nutrients.

Caffeinated beverages will also add to your daily water need. Even though caffeine is a diuretic, if you regularly consume caffeine, your body will regulate itself to that diuretic effect.

Water and Your Kidney

I  experienced suffering kidney stone disease two times in span of 13 years. One essential cause, among others, of that kidney disorder is lack of drinking water (less than 2 liter  a  day). The natural healing process to overcome the stone is by drinking plenty of water, more than 3 liter a day. The best preventive measure of kidney stone is drinking plenty of water, at least 2 liter (about 8 cups) a day. You have no choice. Kidney stone can lead to more severe kidney disorder like kidney failure, in which you have to undertake dialysis.

Drink Enough Water

It may be difficult to drink enough water on a busy day. Be sure you have water handy at all times by keeping a bottle for water with you when you are working, traveling, or exercising. If you get bored with plain water, add a bit of lemon or lime for a touch of flavor. There are some brands of flavored water available, but watch for extra calories.

_Sources:

_{Spigt MG, Kuijper EC, Schayck CP, Troost J, Knipschild PG, Linssen VM, Knottnerus JA. “Increasing the daily water intake for the prophylactic treatment of headache: a pilot trial.” Eur J Neurol. 2005 Sep;12(9):715-8.}

_{Armstrong LE, Pumerantz AC, Roti MW, Judelson DA, Watson G, Dias JC, Sokmen B, Casa DJ, Maresh CM, Lieberman H, Kellogg M. “Fluid, electrolyte, and renal indices of hydration during 11 days of controlled caffeine consumption.” Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):252-65.}

Over the past 10 years, major progress has been made in the pathogenesis of uric acid and calcium stones. These advances have led to our further understanding of a pathogenetic link between uric acid nephrolithiasis and the metabolic syndrome, the role of Oxalobacter formigenes in calcium oxalate stone formation, oxalate transport in Slc26a6-null mice, the potential pathogenetic role of Randall’s plaque as a precursor for calcium oxalate nephrolithiasis, and the role of renal tubular crystal retention. With these advances, we may target the development of novel drugs including:

1. insulin sensitizers;
2. probiotic therapy with O. formigenes, recombinant enzymes, or engineered bacteria;
3. treatments that involve the upregulation of intestinal luminal oxalate secretion by increasing anion transporter activity (Slc26a6), luminally active nonabsorbed agents, or oxalate binders; and
4. drugs that prevent the formation of Randall’s plaque and/or renal tubular crystal adhesions.

Introduction

Calcium oxalate is the most prevalent type of kidney stone disease in the United States and has been shown to occur in 70-80% of the kidney stone population.^[1] The prevalence of recurrent calcium oxalate stones has progressively increased in untreated subjects, approaching a 50% recurrence rate over 10 years.^[2] The lifetime risk for kidney stone disease currently exceeds 6-12% in the general population.^[3,4] In the final quarter of the twenty-first century, the prevalence of kidney stone disease increased in both gender and ethnicity.^[4] Although kidney stone nephrolithiasis is perceived as an acute illness, there has been growing evidence that nephrolithiasis is a systemic disorder that leads to end-stage renal disease.^[5-7] It is also associated with an increased risk of hypertension,^[8-12] coronary artery disease,^[13,14] the metabolic syndrome (MS),^[15-20] and diabetes mellitus.^[19-24] Nephrolithiasis without medical treatment is a recurrent illness with a prevalence of 50% over 10 years.^[2] Nephrolithiasis has remained a prominent issue that imposes a significant burden on human health and is a considerable financial expenditure for the nation. In 2005, based on inpatient and outpatient claims, this condition was estimated to cost over $2.1 billion.^[25] A novel strategy for the development of new drugs has been hampered largely by the complexity of this disease’s pathogenetic mechanism and its molecular genetic basis. Our further understanding of these underlying pathophysiologic mechanisms will be the key step in developing more effective preventive and therapeutic measures.

Ethiologic Mechanisms of Uric Acid Stone Formation

Three major factors for the development of uric acid (UA) stones are low urine volume, acidic urine pH, and hyperuricosuria. However, abnormally acidic urine is the principal determinate in UA crystallization. The etiologic mechanisms for UA stone formation are diverse, and include congenital, acquired, and idiopathic causes.^[26] The most prevalent cause of UA nephrolithiasis is idiopathic. In its initial description, the term ‘gouty diathesis’ was coined.^[27] The clinical and biochemical presentation of idiopathic UA nephrolithiasis (IUAN) cannot be attributed to an inborn error of metabolism ^[26,28,29] or secondary causes such as chronic diarrhea,^[30] strenuous physical exercise,^[31] and a high purine diet.^[32]

Calcium Oxalate Nephrolithiasis

Although it affects both genders, calcium oxalate nephrolithiasis generally tends to occur in more men than women. In the calcium oxalate stone former, urinary oxalate and urinary calcium are equally conducive in raising urinary calcium oxalate supersaturation.^[75] Hyperoxaluria is encountered in 8-50% of kidney stone formers.^[76-78] The main etiologic causes of hyperoxaluria can be classified into three groups: (1) increased oxalate production as a result of an inborn error in metabolism of the oxalate synthetic pathway, (2) increased substrate provision from dietary oxalate-rich foods or other oxalate precursors, and (3) increased intestinal oxalate absorption.^[1] With the study of Oxalobacter formigenes (OF)^[79,80] and the role of putative anion transporter Slc26a6^[81] as potential tools in the treatment of primary hyperoxaluria, our knowledge of the pathophysiologic mechanisms of oxalate metabolism has advanced significantly over the past decade.^[82]

Please find related articles in this blog and  for more information regarding kidney stone / nephrolithiasis, visit a special blog: www.blogofhealth.co.co

Source:   www.medscape.com

Summary

The incidence of kidney stone disease, particularly calcium oxalate nephrolithiasis in the US and other countries  has been increasing throughout the past three decades. Biopsy studies show that both calcium oxalate nephrolithiasis and nephrocalcinosis probably occur by different mechanisms in different subsets of patients. Before more-effective medical therapies can be developed for these conditions, we must understand the mechanisms governing the transport and excretion of oxalate and the interactions of the ion in general and renal physiology. Blood oxalate derives from diet, degradation of ascorbate, and production by the liver and erythrocytes. In mammals, oxalate is a terminal metabolite that must be excreted or sequestered. The kidneys are the primary route of excretion and the site of oxalate’s only known function. Oxalate stimulates the uptake of chloride, water, and sodium by the proximal tubule through the exchange of oxalate for sulfate or chloride via the solute carrier SLC26A6. Fecal excretion of oxalate is stimulated by hyperoxalemia in rodents, but no similar phenomenon has been observed in humans. Studies in which rats were treated with C-oxalate have shown that less than 2% of a chronic oxalate load accumulates in the internal organs, plasma, and skeleton. These studies have also demonstrated that there is interindividual variability in the accumulation of oxalate, especially by the kidney. This Review summarizes the transport and function of oxalate in mammalian physiology and the ion’s potential roles in nephrolithiasis and nephrocalcinosis.

Introduction

In the 1980s, the introduction of extracorporeal shockwave lithotripsy and percutaneous procedures revolutionized the treatment of kidney stones that were too big to pass spontaneously. Although this development greatly reduced the morbidity and mortality associated with nephrolithiasis, it did not reduce the incidence of this condition. On the contrary, the incidence of nephrolithiasis continues to increase in the US, particularly in women.^[1,2] The quality of life of stone formers has not been well studied, but casual conversations reveal dissatisfaction with the status quo, and especially with the lack of effective prevention.

Evidence is accumulating that nephrolithiasis is associated with decreased renal function. Two large studies reported that stone formers have slightly, but significantly, lower glomerular filtration rates and creatinine clearances than those who are not stone formers.^[3,4] Moreover, nephrolithiasis and shockwave lithotripsy might increase the risk of chronic kidney disease and hypertension.^[5,6] The relative contributions of nephrolithiasis, its treatment and its underlying predispositions to these conditions are unknown.^[7]

The prime factors that predispose an individual to the development of nephrolithiasis — stone-promoting urine chemistries, Randall’s plaques, and defects in the crystallization-inhibiting system — almost certainly have variable relative importance in the pathophysiology of calcium oxalate nephrolithiasis within subsets of patients. Given the heterogeneity of the clinical presentation of calcium oxalate nephrolithiasis, it is unlikely that any one defect can explain the development of this condition in the majority of cases.

Renal biopsies and Fourier transform infrared microspectroscopy show that idiopathic stone formers with mild hyperoxaluria (40-50 mg/day [444-556 µmol/day]) have interstitial nephrocalcinosis that is localized primarily to the loops of Henle and consists of hydroxyapatite (calcium phosphate) crystals.^[8] Calcium oxalate nephroliths in these individuals are often attached to Randall’s plaques.^[9,10] The formation or attachment of calcium oxalate crystals on these plaques is probably critical for the growth of nephroliths over extended periods, especially in stone formers whose urine is only sporadically conducive to crystal formation and attachment. Marked, persistent hyperoxaluria (60-83 mg/day [667-922 µmol/day]) is common following modern-day bariatric surgery^[11,12] and is characterized by intraluminal calcium phosphate nephrocalcinosis localized to the inner medullary collecting ducts.^[10] In this setting, nephroliths are typically free within the renal pelvis and are composed solely of calcium oxalate crystals. Following older forms of bariatric surgery, severe hyperoxaluria (100-200 mg/day [1.1-2.2 mmol/day]) was common and renal failure and intraluminal calcium oxalate nephrocalcinosis localized to the medullary collecting ducts were occasionally reported.^[13,14] These clinical observations demonstrate that different forms of hyperoxaluria promote nephrolithiasis by different mechanisms and are, thus, likely to require different interventions.

For many years, oxalate has been viewed as a metabolic waste product, a counter ion in transport studies, or an experimentally useful chelator of calcium, and it has not been considered worthy of detailed study. However, as discussed below, neither the excretion of oxalate nor the regulation of its transport are as investigators had expected, and evidence is mounting that oxalate affects normal physiology, especially in the kidney. This Review summarizes what is known of the role and transport of oxalate and also suggests mechanisms by which oxalate might promote nephrolithiasis.

Source of  Oxalate

Blood oxalate derives from erythrocytes, diet, the liver, and the metabolism of ascorbate . The plasma oxalate level is elevated in patients with extreme hyperoxaluria but is generally normal (1-5 µmol/l) in patients with idiopathic calcium oxalate nephrolithiasis.^[15,16]

Conclusions

Traditionally, oxalate has been relegated to the status of a metabolic by-product, the role of which in stone disease is limited to the physical chemistry of crystallization. Recent investigations indicate, however, that oxalate can increase chloride, water, and sodium reabsorption in the proximal tubule and activate multiple signaling pathways in renal epithelial cells. By contrast, little is known about the partitioning of oxalate between urinary excretion, fecal excretion, and accumulation in tissues and organs. Until the factors that control this partitioning are understood, preventive medical therapies will elude patients with idiopathic hyperoxaluria, or with hyperoxaluria secondary to bariatric surgery or cystic fibrosis.

Please find related articles in this blog and  for more information regarding kidney stone / nephrolithiasis, visit a special blog: www.blogofhealth.co.co

Source:   www.medscape.com