Low carb diets fight back.

A diet rich in soy and whey protein, found in products such as soy milk and low-fat yogurt, has been shown to reduce breast cancer incidence in rats. (Photo credit: Wikipedia)

In a recent study published in the annals of internal medicine, researchers from Italy followed 215 patients who were overweight and found that a low carbohydrate diet (called the mediterranean diet which obtained less than 50% of calories from carbohydrates) was superior for the control of glucose levels in type 2 diabetics.

Unfortunately this study did not have an index of the degree of atherosclerosis present in both groups. This would have been helpful as low carbohydrate diets have recently been found to increases the risk of atherosclerosis despite improvements in cholesterol levels. This risk has been postulated to be based on inability to repair damage caused during the process of atherosclerosis. It seems that carbohydrates may be needed to jump start the repair process in normal people.

The finding however will directly impact patients with type 2 diabetes where glucose control is directly linked to retinal damage kidney damage, nerve damage and cardiovascular risk. Patients will also derive benefit from the weightloss which occurs which will directly result in reduced resistance to their own endogenous insulin levels.

Related articles

• Choosing A Low Carbohydrate Diet (answers.com)
• New Research Shows Type 2 Diabetes and Autism May Be Linked, as Reported by DiabeticLive.com (prweb.com)

Rituximab and FSGS.

Intermed. mag. Image: Focal segmental glomerulosclerosis - high mag.jpg (Photo credit: Wikipedia)

FSGS or focal and segmental glomerulosclerosis is the most common non diabetic cause of nephrotic syndrome in the world. This is particularly true among African Americans. The treatment of this disorder is frequently complicated by non response to the primary modality of treatment which is steroids. Combine this with the need for high doses to produce an effect, the known toxicity of steroids and we begin to see there is need for a better drug. Unfortunately many of the drugs attempted are also toxic or produce a situation of dependence where the disease may go into remission but it quickly relapses when the drug is discontinued. Rituximab is a drug that has had some success in lupus nephritis and now it is undergoing trials in patients with FSGS. The current study by investigators from spain, looked at a small cohort of 8 patients and found that rituximab was effective only in the minority of patients, only 3 patients had a favourable response to the drug. It is however interesting that in at least one patient that responded there was a durable massive reduction in proteinuria. The fact that this occurred should inspire some hope that the drug may be useful if an effective regimen capable of benefiting more patients can be elucidated.

Related articles

• Steroids and Kidney Disease (allkidney.com)
• New Treatments For FSGS -ASN Conference (allkidney.com)

Patient Education: What is the best form of dialysis.

Dialysis USA 3-2007 004 (Photo credit: jimforest)

This question is asked more times than can be counted. A patient is informed that they have stage 4 kidney disease and they need to make a choice as to what modality of dialysis they prefer while they await transplantation.

The patient is usually confused and unsure, already overwhelmed with dealing with the reality of having to receive organ replacement therapy in the first place. Usually the decision is made without enough information and reflects the personal bias of the physician with whom the patient has the most trust.

Rarely will a patient have a preconceived idea as to what form of dialysis would best fit their lifestyle and rarely still does one find a busy nephrologist with the patience to explain in the detail the pros and cons of all modalities without introducing personal and professional preference.

If we were to take a moment to answer this question we would realize that thinking about the answer in a vacuum without a patient involved is difficult. It is difficult because there are patient specific factors which influence the modality of choice. Therefore the best way would be to examine the pro's and cons of each separate modality, giving the patient the power of choice empowered by knowledge.

The most established modality is haemodialysis dating back to 1945, physicians therefore have a great deal of experience with this modality it has stood the test of time and advanced rapidly with greater understanding of the processes of diffusion and osmosis as well as the development of plastics. Understanding the complex equations which determine membrane transport characteristics and hence dialysis adequacy are a badge of pride for nephrologists.

Peritoneal dialysis could be considered to be the older dialysis modality. It was first attempted in humans in 1923 and was partially successful. Between 1923 and 1928 surgeons performed several procedures which prolonged the life of patients using peritoneal dialysis, however adoption of this method was slow and to some extent marginalized during the development of haemodialysis.

Modern haemodialysis and peritoneal dialysis can be considered equal means of renal replacement therapy they each have their strengths and weaknesses.

HAEMODIALYSIS

http://www.flickr.com/photos/nomadicentrepreneur/ / CC BY-NC 2.0

Pros

• Treatment is rapidly effective at clearing toxins from the blood stream.

• Dialysis adequacy can be increased easily to match the needs of the patient.

• Treatment failure and withdrawl from haemodialysis is less common.

Cons

• Dialysis occurs across an artificial membrane which may cause allergic reactions.

• Blood stream access is necessary and most be maintained.

• Haemodialysis is expensive

• Low blood pressure occurs during haemodialysis more frequently

• Higher risk of bleeding due to the use of blood thinners like heparin.

PERITONEAL DIALYSIS.

Peritoneal dialysis (Photo credit: Wikipedia)

Pros

• Uses a perfectly bio-compatible membrane, the bodies peritoneum.

• Dialysis is controlled by the patient.

• Dialysis can be done in a continuous manner.

• Low blood pressure is unlikely.

• Removal of excess body fluid is more easily accomplished in a gentle manner.

Cons.

• Although the peritoneum is biocompatible it was never meant to be used for dialysis. Hence it has a set life time during which it will function as a dialysis membrane and becomes progressively more inadequate for the purposes of dialysis.

• Higher chance of treatment failure.

• Not suitable for very obese patients, patients with intrabdominal masses or hernia's

• Risk of peritoneal infection and discontinuation of dialysis.

• Not all patients may be trained to perform their own dialysis.

In terms of patient related factors, for peritoneal dialysis to be effective the patient must be highly motivated and trainable with clean suitable surroundings in which to perform exchanges. Patients have an advantage on peritoneal dialysis if they have a high peritoneal surface area to body surface area. Patients may choose peritoneal dialysis for the independence that it grants. Patients who have had previous myocardial infarction stroke or poor vascular tone are less likely to have episodes of low blood pressure on peritoneal dialysis that may result in another stroke or myocardial infarction.

Dialysis is a continuously changing process recent advances in haemodialysis and peritoneal dialysis are closing the gaps between the two. In fact recent reports suggest that nocturnal daily haemodialysis may be the closest to full replacement of renal function that we have yet seen. While development of new solutions and cyclers for peritoneal dialysis have removed some of the inherent drawbacks of peritoneal dialysis increasing benefit to patients who were previously unlikely to do well in peritoneal dialysis.

Related articles

• Peritoneal Dialysis and Encapsulating Peritonitis (allkidney.com)
• Home-based Dialysis For Kidney Failure Gaining Popularity In Developing Countries (medicalnewstoday.com)
• Peritoneal Dialysis vs Hemodialysis (drjejsrf.wordpress.com)

Warfarin may cause increased risk of stroke in hemodialysis.

Previously aspirin and clopidogrel were found to having an increase risk of mortality in patients on haemodialysis. However warfarin is known to have a survival advantage in patients with atrial fibrillation as the drug prevents clot formation in the poorly contracting left atrium of the heart. Any reduction in clot formation results in a reduction in the chance of a clot passsing from the heart into the brain resulting in an ischemic stroke. The present study looked at warfarin use in an area where it has been established to be beneficial in other patient groups. However in this study of 1671 haemodialysis patients with atrial fibrillation warfarin was found to increase the risk of stroke in a dose dependent manner. In other words the risk of a stroke was highest in patients on the highest dose of warfarin. The study incidentally did not demonstrate an increased risk of stroke due to ASA and clopidogrel this time around. However aspirin and clopidogrel are not as effective as warfarin in the normal population for the prevention of stroke and have a mixed track record in the prevention of even access related clotting. The study did note that patients who had blood tests done regularly at the centre where they are dialysed to monitor the effectiveness of warfarin and appropirately adjust the dosage of the drug had the lower risk for stroke compared to the unattended use of warfarin.

http://www.flickr.com/photos/vitualis/ / CC BY-NC-SA 2.0

This finding is to be expected as many drugs and substances interact with warfarin making it very difficult to maintain a smooth level of the drug within the body.

I suspect that warfarin use in a highly monitored setting may have some use in patients with atrial fibrillation and further studies designed to tease out this relationship will likely show that benefit.

Related articles

• Warfarin Helps Cut Stroke Risk, Researchers Report (nlm.nih.gov)

Patient Education: Testing for kidney disease.

Physiology of Nephron (Photo credit: Wikipedia)

The kidney is a highly selective filter than receives a large supply of blood from the circulatory system. The entire blood volume passes through the kidney several times over per day. The kidney selectively removes toxins from the blood and in the process forms urine which leaves the body through the ureters bladder and urethra.

The Ultimate goal of the diverse functions of the kidney is to preserve a careful balance of electrolytes minerals and water in order to maintain the finely tuned processes which give rise to life. The ultimate result of kidney failure is break down of the myriad pathways which rely on this balance. Every organ system therefore relies to some extent on the daily functions of the kidney and the kidney relies on feedback from these systems to determine how well its doing its job. When the system works as it ought to there is a perfect balance between intake of nutrient and excretion of waste products.

The functions of the kidney are still being determined by scientists everyday. What has been learned so far is as follows:-

• The kidney detects the level of oxygen in the blood and stimulates the bone marrow to produce oxygen carrying blood cells as necessary to most efficiently maintain the oxygen level of the blood. It does this by producing a hormone known as erythropoeitin.

• The kidney receives and contributes critical information to important parts of the brain which determine if there is enough fluid within the body. If fluid is deemed to be in excess urine volume is increased and water is excreted to return the body to a state of fluid balance. If the body is dehydrated the kidney conserves water by decreasing urine formation to the minimum required to still excrete wastes.

• The kidney removes waste products by allowing them to filter into the urine and sometimes actively excreting them into the urine.

• The kidney constantly monitors urine that is being formed and reabsorbs from the urine anything that is still useful before it leaves the body.

• The kidney senses the flow through it and determines and instructs centers in the brain to increase or decrease blood pressure to maintain an appropriate flow rate to perform its function.

• The kidney removes acid from the body and is the most important source by which acidic compounds generated by daily activity is removed.

• The kidney plays an important role in bone formation as it is the last step in the synthesis of vitamin D.

Any test of kidney function should be able to to test individually these functions and determine if there is kidney disease present or not.

Some of these tests are as follows:-

• The ability of the kidney to filter is expressed by the term GFR or glomerular filtration rate. This is an index of all the fluid passing across the filter per minute of every day. This number can be determined by a series of calculations performed using the ratios of concentrations of various substances in the blood vs the urine.

1. This may be measured by a 24 hour collection of all urine passed. The GFR being calculated from the ratio of creatinine in the urine and blood.
2. A radioactive material may be injected and the rate of the excretion of the radioactive material in the urine determined using a collector or counter for radiation. This is termed a renal scan.
3. The concentration of a substance that is generated within the body, that we know should be promptly excreted by the kidney could be measured with a single blood test. This is the basis of the measurement of creatinine and blood urea nitrogen. When the kidney is functioning normally it should be within the normal range. Unfortunately these tests are not as accurate as the above more direct methods of determining GFR. They should really be considered markers of function vs dysfunction.
4. The GFR may be calculated based on a single test for creatinine by using a formula that takes into account the age, weight, gender and race of the subject. This is more reliable that relying on the BUN or creatinine alone.

• The ability of the kidney to detect and respond to the oxygen carrying content of the blood is determined by measuring the blood count on a routine blood test. But there are many causes for a low blood count. Only after excluding all the most common causes can we directly say that the kidney is the reason why the blood count is low and thus prompt a more thorough work up for kidney disease

• Regularly checking the blood pressure is a good way to detect kidney disease. As one of the functions of the kidney is blood pressure regulation patients with high blood pressure should have one of the above tests of kidney function done.

• Testing the urine for protein blood and any abnormal constituent of urine. There are substances that do not enter urine under normal circumstances because the kidney reabsorbs them during the process of forming urine or selectively does not allow the them to be filtered in the first place. The most important of these is protein, persistent levels of protein in the urine may imply damage to the filtration apparatus of the kidney. This is one area where early intervention is very important. This is why a dipstick of the urine is a standard procedure when you see your physician.

• Testing the level of acid in the blood or urine may draw attention to a previously unknown kidney disease.

• Low vitamin D levels or low calcium levels may be due to kidney disease.

• Testing the level of various electrolytes whose concentrations are determined by kidney function may also highlight previously unknown kidney disease

Low carbs diets....bad for you?

low carb (Photo credit: daBinsi)

Low carbohydrate diets are known for their ability to jump start weight loss. High protein diets such as the Atkin's diet have been associated with no increase in cholesterol and have been credited with higher initial weight loss than traditional caloric restriction.
Recently we have reported research that high protein diets are unexpectedly associated with increased risk of cardiovascular mortality.





The current study carried out in a mouse laboratory model has shown that when fed a low carbohydrate diet the mice developed more hardening of the arteries that led to restriction of blood flow to vital tissues. The mice fed on a low carbohydrate diet were also less likely to be able to compensate for interruption to blood flow to vital organs. This occurred despite the absence of an increase in serum cholesterol implying that these effects were modulated via mechanisms independent of traditional risk factors for atherosclerosis.

http://www.flickr.com/photos/su-lin/ / CC BY-NC-ND 2.0

The implications for patients on low carbohydrate diets could be unfortunate as this is the second study in a short period of time to bring to light a possible negative role of high protein diets which usually go hand in hand with low carbohydrate diets.

Related articles

• High Fat, Low Carbohydrate Diets May be Harmful to Diabetics (mizrhi.wordpress.com)
• High Protein Diets and Weight Loss - The Soy Connection - Health & Nutrition - United Soybean Board (soyconnection.com)
• Low-Carb Diet Referenced in BIDMC Study Not Related to Atkins (prweb.com)

Obesity and chronic kidney disease.

Almost every possible human ailment has been somehow linked to obesity. It is therefore no surprise that obese patients have significantly more risk of developing kidney disease. In fact there is a discrete entity that has been described which is known as obesity related glomerulopathy. Which is dysfunction of the filtering apparatus of the kidney as a result of obesity. The glomerulopathy is associated with distinct structural changes that can be seen on biopsy. The disease usually runs a mild course and rarely does it damage the kidneys sufficiently to require dialysis.

However population based studies have demonstrated that obesity puts you at increased risk of requiring dialysis when compared to the non obese. The mechanism acting here is unlikely to be due to obesity related glomerulopathy and is largely unknown.

However there are theories that fat cells have the ability to produce hormones that act on the kidney such as leptin, adiponectin and tumour necrosis factor. These agents are known to cause inflammation in various tissues of the body. They have also been implicated as playing a role in other diseases of the kidney. The risk of severe renal disease is higher with each additional condition present in addition to being obese. So in the obese and hypertensive with diabetes and low levels of the good cholesterol(HDL), the highest risk of developing end stage renal disease occurs.

http://www.flickr.com/photos/sdobie/ / CC BY-NC 2.0

The risk can be reduced by treating each associated disease. So good blood pressure control to the lowest possible blood pressure that does not result in dizzyness when you stand suddenly, blood sugar that is well controlled, increasing good cholesterol (HDL) and lowering bad cholesterol (LDL.) are all indicated to improve outcomes.

In terms of weight loss, a reduction of risk occurs for every point reduction in BMI achieved. Therefore ANY weight loss, no matter how small the amount will be beneficial, with the biggest losers gaining the most.

Related articles

• Obesity and cancer risk - guest post by Joleen Krupa (itsaguythingblog.wordpress.com)
• Higher birth weights in girls may predict obesity (cbc.ca)
• Insulin Resistance May Lead to Kidney Disease in the Elderly: Study (news.health.com)

Is Aspirin safe in Kidney disease?

Generic regular strength enteric coated 325mg aspirin tablets, distributed by Target Corporation. The orange tablets are imprinted in black with "L429". (Photo credit: Wikipedia)

Low dose aspirin is a well established means of prevention of a second heart attack or stroke also known as secondary prevention. The evidence is less compelling for patients who have never had a heart attack or stroke, with the preventative benefit competing with a steadily increasing risk of bleeding from the intestines over time. Under the latter circumstances in some studies aspirin will come out ahead and in others slightly behind.

Patients on hemodialysis are at increased risk of bleeding, yet one of the main reasons for the discontinuation of dialysis remains access complications related to thrombosis (clotting). The question of whether the survival of dialysis access can be prolonged by the prescription of agents to prevent clotting has been asked before. At that time low dose coumadin therapy was associated with an unacceptably high rate of bleeding complications.

Several small studies have shown that aspirin and clopidogrel (the two main antiplatelet drugs tested) increased the risk of bleeding in patients on hemodialysis.

An article published in the clinical journal of the american society of nephrology collected data from multiple studies by a technique known as metanalysis. By combining data from multiple smaller studies the investigators hoped to gain the kind of quality statistical information required to answer the question.

The current study analysed results for 40,676 patients and concluded that the use of a single drug such as clopidogrel does not increase the risk of bleeding in patients on dialysis, the use of aspirin by itself was associated with mixed results however. In fact in patients who used grafts as a form of dialysis access aspirin increased the risk of graft thrombosis. No agent was successful at increasing primary patency of AV fistula in patients at risk of thrombosis. While using two or more antiplatelet agents increased the risk of bleeding significantly.

The current study failed to show any benefit in terms of patency rates for vascular access and overall discourages the use of antiplatelet agents in general for any form of primary prevention in dialysis patients. The role of aspirin in terms of secondary prevention of cardiovascular disease in dialysis patients is yet to be resolved.

http://www.flickr.com/photos/jypsygen/ / CC BY-NC-ND 2.0

Related articles

• Preventing Bleeding (hematuria) in Polycystic Kidney Disease (allkidney.com)
• Cannulation Technique may Improve Fistula Survival (allkidney.com)
• Questions Raised About Antiplatelet Therapy in Chronic Kidney Disease (forbes.com)

What is Shock Wave Lithotripsy Treatment.

A lithotriptor machine in an operating room. Other equipment is seen in the background, including an anesthesia machine and a mobile fluoroscopic system (or "C-arm"). (Photo credit: Wikipedia)

So you just found out you have a kidney stone and the doctor told you that you need to have a procedure called lithotripsy and you have already started to panic. Well first things first, stop breathe and read....

Lithotripsy refers to a medical procedure that uses shockwaves to break up kidney stones. The kidney stones then pass naturally in the urine or through a tube that is inserted into the kidney called a nephrostomy tube.

The sound waves used for lithotripsy pass from the outside of the body to the inside of the body , hence a better name for the procedure would be outside of the body shockwave lithotripsy. In medical jargon this translates to extracorporeal (outside the body) shockwave lithotripsy or ESWL.

On the day of the procedure you will lie on a water filled cushion. The water will conduct the sound waves to the skin and hence to the stone after being sedated, because there may be discomfort a painkiller is also administered prior to the procedure.

In some cases a tube will need to be inserted to allow the stones to pass out of the kidney. With good planning your doctor will place this before hand if necessary, however circumstances sometime dictates that this be placed after the procedure. The procedure takes generally 1 hour and you may feel unusual sensations in the area of the stone as it absorbs the sound wave energy.

Because this is a noninvasive procedure it is generally safe, however you should be aware that the stone may be too large to break up entirely in one treatment. If the stone shatters within the kidney with sufficient energy there may be bleeding. If the kidney is damaged by the stone as it breaks up it may lead to a permanent loss of kidney function in some cases. The stones may be broken up reducing them to a size where they may now move into the narrower ureters (see diagram above) and obstruct the flow of urine leading to pain which may require another procedure. The procedure is also associated with a small risk of ulceration of the stomach and small intestine.

http://www.flickr.com/photos/kidneynotes/ / CC BY-NC-ND 2.0

Your chances of having one of these complications is low, however to minimize the risk one should inform the doctor before the procedure if you are on any medication including herbs that could increase bleeding such as aspirin, and other pain killers, green tea or ginko biloba.

You should have an empty stomach for the procedure and will receive specific instructions from your physicians about when to stop eating and when you will be able to eat again.

Study suggests protein intake linked to heart attack and stroke innormal people.

Most patients with chronic kidney disease will be referred to a dietician as part of their management. The standard of care has been to provide a normal protein diet of about 0.80 grams protein per kg of body weight. However some researchers believe that dietary protein intake be restricted even further as some studies suggested that decreased dietary protein intake would prolong the survival of the kidney in chronic kidney disease.

But is there an effect of higher protein intake on cardiovascular disease as well. The current study analyzed data from 8461 individuals and followed these people who incidentally did not have renal disease for about 6.4 years. The daily protein intake was scientifically measured based on the amount of protein breakdown products produced in the urine (this is one of the most accurate means of determining the actual protein intake of a patient). The data was then compared to determine if there was any relationship between protein intake and cardiovascular disease and renal function.















The study demonstrated that protein intake was associated with cardiovascular events (heart attack and stroke) but not associated with worsening of kidney disease.

The conclusion therefore is that in the general population high protein intake, such as promoted by many weight loss systems may increase your risk of heart attack and stroke, but does not increase your risk for kidney disease.

New Drugs: Pirfenidone a new hope in diabetic kidney disease.

Diabetic nephropathy may be slowed by several means, the standard of care is blood pressure control, prescription of drugs which reduce protein in the urine and dietary changes. However the condition is almost always progressive despite these interventions.

Pirfenidone is not a particularly new drug, it has been known as an antifibrotic agent in that it reduces the formation of the primary constituent of scar tissue. Scar tissue referred to as fibrosis at the microscopic level forms as a consequence of inflammation during the process of healing.

Diabetic kidney disease has been associated with a unique type of scarring which occurs in the portion of the kidney responsible for filtering the blood. Over time this delicate filter is destroyed by fibrosis.

http://www.chemblink.com/products/53179-13-8.htm

The current study found that pirfenidone when given to laboratory mice reduced the damage to their kidneys by reducing the precursors of inflammation that lead to scarring. This is exciting news as pirfenidone directly targets a pathway that was previously not directly influenced by current therapy. This would therefore be a valuable adjunctive medication to be used alongside established treatment should the drug live up to its promise.

New Drugs: Pirfenidone a new hope in diabetic kidney disease.

Diabetic nephropathy may be slowed by several means, the standard of care is blood pressure control, prescription of drugs which reduce protein in the urine and dietary changes. However the condition is almost always progressive despite these interventions.

Pirfenidone is not a particularly new drug, it has been known as an antifibrotic agent in that it reduces the formation of the primary constituent of scar tissue. Scar tissue referred to as fibrosis at the microscopic level forms as a consequence of inflammation during the process of healing.

Diabetic kidney disease has been associated with a unique type of scarring which occurs in the portion of the kidney responsible for filtering the blood. Over time this delicate filter is destroyed by fibrosis.

http://www.chemblink.com/products/53179-13-8.htm

The current study found that pirfenidone when given to laboratory mice reduced the damage to their kidneys by reducing the precursors of inflammation that lead to scarring. This is exciting news as pirfenidone directly targets a pathway that was previously not directly influenced by current therapy. This would therefore be a valuable adjunctive medication to be used alongside established treatment should the drug live up to its promise.

Gene for severe Polycystic Kidney Disease can be predicted.

Polycystic kidney disease is the third single most common cause of ESRD in the dialysis population based on US data. It is a disease charachterised by the development of cysts within the kidney which expand over time and damage the structure and function of the organ giving rise to chronic kidney disease then chronic renal failure. The rate of progression varies between patients, however sophisticated genetic tools are capable of distinguishing those who are likely to progress more slowly from those who are likely to need dialysis at a younger age.

The current study by Moumita et. al. published in the Journal of the association of nephrology (JASN) demonstrates that while sophisticated genetic tests are quite well and good, simply taking certain historical details from the patient at interview had a positive predictive value of 100% and sensitivity of 75% to detect the presence of the more severe type of polycystic kidney disease.

When interviewed, if patients had even one relative who had to be dialysed because of chronic kidney disease they were almost guaranteed to have the PKD1 gene. The PKD1 gene is the gene responsible for polycystic kidney disease in 85% of cases and has a median age of onset of kidney disease requiring dialysis at 53 years of age as opposed to PKD2 gene which has a median age of kidney disease requiring dialysis at 72.7 years of age.

This is a simple option for gaining prognostic information which is cheap and easily applied to all patients. However if there is insufficient clinical history then this criteria cannot be applied and gene testing is the way to go.

Related articles

• Preventing Bleeding (hematuria) in Polycystic Kidney Disease (allkidney.com)
• New Hope For Patients With Polycystic Kidney Disease (allkidney.com)
• Other problems in Polycystic Kidney Disease (allkidney.com)
• Sirolimus for Polycystic Kidney Disease (allkidney.com)

Patient Education: What causes kidney stones?

Patients may be at risk for kidney stones if:-

• High concentrations of calcium, oxalate or uric acid in the urine.


• Low pH (urine too acidic)


• Concentrated urine (poor fluid intake)


• Not eating enough calcium (you absorb too much oxalate if calcium is low)


• Eating too much calcium


• High sugar intake


• High protein intake.


• High sodium intake.

MEDICAL CONDITIONS MAY ALSO PREDISPOSE TO KIDNEY STONE FORMATION

Gout

Diabetes Mellitus

Obesity

Gastric bypass

Primary hyperparathyroidism.

Crohn's disease.

SOME QUICK FACTS.

If you have previously had a stone you are at increased risk for a new one.

Drinking high volumes of grapefruit juice has been linked to kidney stones.

Green tea and coffee lowers the risk

Beer and wine are ok.

A normal calcium intake may protect you from kidney stone formation

A high calcium intake causes stones as well as a low calcium intake too.

Dietary fibres such as wheat and cereal reduces risk.

Excessive vitamin C intake increases the risk

Kidney stone symptoms.

Related articles

• Too Little Calcium, Water Linked to Kidney Stones (nlm.nih.gov)
• Impact of Nutritional Factors on Incident Kidney Stone Formation: A Report From the WHI OS (dynamomelano.wordpress.com)

Patient Education: Having Pain in the Kidneys, It may be Kidney Stones.

These are some of the larger passed fragments of a 1-cm kidney stone that was blasted using lithotripsy. The stone was composed of calcium oxalate. (Photo credit: Wikipedia)

KIDNEY STONES IN THE NEWS.

OVERVIEW

• Kidney stones affect approximately 12 percent of men and 5 percent of women by age 70.


• Treatment is available to effectively manage most stones.


• Recurrence can occur at a rate of up to 5 percent per year.

FORMATION OF THE STONE

There are different types of kidney stones.

KUB stone (Photo credit: Wikipedia)

• calcium kidney stones.


• oxalate kidney stones.


• cystine kidney stones.


• uric acid kidney stones.

When these substances are at high levels in the urine they precipitate out of solution and become solid crystals which get stuck somewhere in the tract from the kidney to the ureter and bladder, the kidney stone then forms particularly at narrow points along the way.

Usually, the stone will be moved through the tract by the flow of urine until entering the bladder and eventually be expelled.

A larger kidney stone may cause the sensation of kidney pain as it moves and damage to the walls of the ureter or bladder thus causing blood in the urine.

If the kidney stone is too large it may not enter the ureter at all.

Instead it enlarges to fill the entire kidney outflow tract called the hilum. These kidney stones may take on a specific shape like the horns of a stag. They are termed staghorn kidney stones. They may cause kidney obstruction, kidney infection and kidney failure if untreated.

KIDNEY STONE RISK FACTORS

Patients may be at risk for kidney stones if:-

• High concentrations of calcium, oxalate or uric acid in the urine.


• Low pH (urine too acidic)


• Concentrated urine (poor fluid intake)


• Not eating enough calcium (you absorb too much oxalate if calcium is low)


• Eating too much calcium


• High sugar intake


• High protein intake.


• High sodium intake.

MEDICAL CONDITIONS MAY ALSO PREDISPOSE TO KIDNEY STONE FORMATION

• Gout


• Diabetes Mellitus


• Obesity


• Gastric bypass


• Primary hyperparathyroidism.


• Crohn's disease.

SOME QUICK FACTS.

If you have previously had a kidney stone you are at increased risk for a new kidney stone.

Drinking high volumes of grapefruit juice has been linked to kidney stones.

Green tea and coffee lowers the risk of kidney stones

Beer and wine are ok.

A normal calcium intake may protect you from kidney stone formation

A high calcium intake causes kidney stones as well as a low calcium intake too.

Dietary fibres such as wheat and cereal reduces risk of kidney stone formation.

Excessive vitamin C intake increases the risk of kidney stone formation.

KIDNEY STONE SYMPTOMS INCLUDE

KIDNEY PAIN

This can be very severe pain which is never quite relieved by changing position. Causing some amount of restlessness walking around or twisting and turning. The pain occurs in episodes of intensification followed by slightly reduced pain a phenomenon known as colic.

Kidney pain may be associated with vomiting or nausea.

Kidney pain is caused by obstruction of the ureters and stretching of the tissues around the kidney.

The passage of the stone through the urinary tract is associated with a downward moving of the pains which ultimately enter the flank and may even continue down to the groin. Classically described as loin to groin pain.

On the other hand..........

Some patients have large kidney stones for several years with only a dull ache or no symptoms at all. These kidney stones however can grow so large they cause a silent slowly evolving kidney failure. These kidney stones are associated with recurrent kidney infections which become more difficult to treat with time requiring removal of the kidney stone.

Blood in the urine.

Damage to the delicate tissues of the kidney and urinary tract is the cause of bleeding. Bleeding may discolour the urine making it red or near to red in the spectrum. However the bleeding may be invisible to the naked eye and require a dipstick test.

Gravel.

This refers to the passage of small kidney stones which have the consistency of gravel this is more common in uric acid kidney stones.

DIAGNOSIS OF KIDNEY STONES

Kidney Stones may be diagnosed by any of the following tests :-

A CT scan of Kidney Ureter and Bladder.

This is a non invasive test similar to an xray but more advanced. In which actual internal anatomy can be seen in 3d. Kidney stones show up easily with this test. It is also possible to learn if there is kidney obstruction or any obvious damage to the kidney at the same time. This test has a higher yield when the patient actually complains of kidney pain.

Ultrasonography of the kidney ureter and bladder.

This test is more dependent on the skill of the observer than the previous test. It is based on sound waves traveling through tissues. The kidney stone blocks the sound waves if large and can be seen as a shadow on the screen. Small kidney stones are frequently missed. This test avoids the use of radiation and may be the best choice in a pregnant patient complaining of kidney pain. Overall it is inferior to CT scan.

Plain Abdominal xray.

Moderately reliable for larger calcium containing kidney stones. Small uric acid kidney stones may be missed. This test is inferior to CT-SCAN

IVP

Dye that shows up white on xray is injected to the blood stream. It passes through the kidney and enters the urine. It outlines the areas of the urinary tract that can be filled by the dye. The kidney stone is seen as a filling defect. This test can assess to some degree function of the kidney and is the gold standard for determining if a small kidney stone is present.

Unfortunately the dye may cause a significant allergic reaction. This test is generally avoided in patients with a history of any allergies.

General testing to identify a metabolic problem as an underlying cause of kidney stones should also be done.

KIDNEY STONE TREATMENT

When kidney pain is severe the patient may have bouts of vomiting leading to

dehydration. If dehydration occurs the flow of blood through the kidney is reduced. The kidney creates urine from blood, so urine flow is further reduced this may prolong the passage of the kidney stone.

Fluid resuscitation via IV fluid should be commenced simultaneously as soon as possible. Sometimes giving lots of fluids into the vein will cause the kidney to produce more urine and flush the kidney stone out.

Kidney pain is frequently severe and is caused by muscle spasm, a muscle relaxing drug such as Baralgin, in combination with aspirin based pain killers such as Voltaren, Cataflam, Brufen should be used however strong painkillers may be required such as narcotics and if necessary given IV.

If vomiting occurs the patient is usally admitted to hospital. If the kidney stone is larger than 9 millimeters it is unlikely to pass from the kidney on its own.

If the patient passes urine it must be examined for the presence of any kidney stones by passing the collected urine through a strainer.

If the kidney stone is not passed out then a special procedure may be required such as:-

ESWL (sound waves)

- Depending on the density of the stone and postion and size the stone may be destroyed by sound waves targetted at the stone in a non invasive manner.

PNL- (microsurgery)

- Percutaneous nephrolithotomy. If the stone is very large microsurgery may be performed through small holes in the skin to break up the stone.

Ureteroscopy- (a scope is passed)

A fibreoptic scope is passed up the ureter, however it cannot reach all the way to the top of the kidney. So the stone has to be at least half way down for this to be effective.

KIDNEY STONE PREVENTION

To decrease the chances of another kidney stone:-

You need to determine the cause of the first stone and treat the problem. This is accomplished by analysing the stone to determine its primary component.

General measures such as increased fluid intake to dilute the urine and flush the kidney.

Making the urine more alkaline with lime juice or citric acid in select cases.

Dietary changes.

Surveillance with CT scan or IVP for new stones that have not yet caused a problem is possible. The smaller the stone the easier to treat.

Using the DASH diet.

Kidney News: Food additives can Kill

food sources of magnesium: bran muffins, pumpkin seeds, barley, buckwheat flour, low-fat vanilla yogurt, trail mix, halibut steaks, garbanzo beans, lima beans, soybeans, and spinach (Photo credit: Wikipedia)

A little known but important fact outside of the kidney care community is that phosphates are a major cause of disease in patients with kidney problems. The problem is particularly severe in patients who are on dialysis. Phosphate is present in many foods. However skilled dieticians are able to reduce the phosphate content of the diet through specifically tailored meal plans and procedures to prepare the food so that phosphate content is as low as possible.

Dietary advice aside the major means of removing toxins from the body in patients with kidney disease, which is dialysis is not particularly helpful in patients as phosphate is very slow to be removed by conventional dialysis. The only modality that seems to have a profound effect on phosphate removal is long nocturnal hemodialysis, the benefit here is that phosphate removal is primarily tied to the the length of time that you are dialysed.

So if phosphate is present in many foods and beverages, particularly sodas and conventional dialysis does not perform well in its removal, then we end up with phosphate accumulation in dialysis patients. Since not everyone has access to nocturnal hemodialysis the answer would seem to be reducing phosphate intake.

However even with dietary manipulation phosphate has been slowly creeping back into the diet of patients on dialysis through an unsuspected mechanism.

Food additives are substances added to food in order to preserve and give longer shelf life in most cases. Frequently the phosphate content of the food additive is not available to the dietician when planning the diet sheet of the dialysis patient and as such the dietary advice may have very little effect on overall phosphate intake. Proper labelling of foods would of course solve this problem but this is not yet a requirement.

But what exactly does high phosphate levels cause?

The problem with phosphate is that it is one of the substances that make up bone and as such it is regulated by a hormone known as PTH. High phosphate stimulates PTH levels, elevated PTH somehow affects the cardiovascular system contributing to increased stiffness of the blood vessels and increased risk of cardiovascular disease.

What can be done?

Focused education on the need to be aware of the phosphate content of food may result in lower phosphate intake if alternative preservative and additive food sources can be accurately identified. In other words educate, create the need and someone will provide the service of low phosphate food.

A recent review of the phosphate content of food is available here

Related articles

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• Latest Kidney News: Post ASN Round Up. (allkidney.com)
• Older Dialysis Patients May Not Derive Benefit from Dialysis (allkidney.com)