A look into the effect of dietary intake on patients with kidney stone disease.
At the helm of non-pharmacological preventative therapies for kidney stones; also known as renal calculi, nephrolithiasis, or urolothiasis (Mayoclinic.com, Kidney stones - Symptoms and causes, 2021), are dietary and lifestyle changes, as well as vitamin supplementation.
Kidney stones can be defined as hardened masses that consist of crystallised minerals and salts, generated by concentrated urine. Stones too large to pass through the urinary system require medical treatment or intervention. Kidney stone disease is a common finding in today’s society, Studies show that, “It is estimated that one in ten people will have a kidney stone at some point in their lives.”(Kidney.org, Kidney Stones, 2021)
Kidney stones form due to various factors such as; obesity, genetics, lifestyle and certain medical conditions. A multitude of studies and trials have proven the link between the increased/decreased consumption or the exclusion of certain minerals/nutrients, and the reduced risk of kidney stone formation.
This article is based on the publication by, Ita P. Heilberg and David S. Goldfarb, titled Optimum Nutrition for Kidney Stone Disease. The following summarises their writings on the impact of certain dietary intake (Calcium, Oxalate, Protein, Sodium, Citrate & Potassium, Beverages, Phytate, and Calories & Fructose) on the risk of kidney-stone formation. Sharing their notes on the impact of the aforementioned factors on specific stone types, being; Calcium Oxalate Stones, Calcium Phosphate Stones, Uric Acid Stones, Cystine Stones, and Struvite Stones.
Calcium (Ca) is one of the most important minerals required by the human body to maintain optimal performance of functions such as:
- Growth and maintenance of healthy, strong bones.
- Neurotransmission - maintaining healthy communication throughout the body.
- Muscle movement.
- Cardiovascular movement.
According to Heilberg and Goldfarb, calcium over-saturation of the urine is one of the biggest risk factors for calcium nephrolithiasis (Heilberg and Goldfarb, 2013). Calcium based stones account for up to 65-70% of kidney stones.
High levels of calcium present in the urine is referred to as hypercalciuria, and occurs in secondary and idiopathic incidences.
- Secondary: Resulting as a side effect of another condition that causes excessive levels of calcium in the bloodstream.
- Idiopathic: Occurring on its own, with normal levels of calcium present in the bloodstream. A complex primary metabolic alteration. At least half of calcium based stone formers are found to have idiopathic hypercalciuria.
- An increase in active calcium transport by the intestines is observed in individuals with idiopathic hypercalciuria (IH). Seeing as; regardless of calcium intake, absorption of calcim is higher in IH patients.
Commonly observed in IH patients:
- A decrease in bone mineral density
- High bone reabsorption
- Reduced bone formation
- Patients with IH excrete more calcium than was previously ingested when confronted with low calcium intake. The source of the excess calcium is most likely derived from bone.
- Therefore, the entirety of effects decreasing calcium intake in IH stone forming patients has not yet been established.
- Adversely to IH stone formers; decreasing dietary calcium intake in all other incident stone formers, reduces the risk of stone formation.
- However, it has been widely observed that low calcium intake in young men, and younger and older women; can result in a 34% higher risk of developing kidney stones.
- Milk, cheese, cream and other dairy products.
- Certain vareties of beans and lentils
- Leafy vegetables
Such as spinach or kale
- Fortified flours
Such as sesame, poppy, chia and celery
- Soya products, particularly those with added calcium.
Oxalate is a naturally occurring byproduct of metabolic activity, and derives from dietary sources. Excess urinary oxalate has the potential to collect in the kidneys and combine with other minerals present - leading to stone formation.
- Urinary oxalate absorption is also dependant on calcium intake.
- The malabsorption of fat is also responsible for increasing intestinal absorption of oxalate in conditions whereby reducing dietary fat might be considered.
- It has been observed that in comparison to reducing oxalate intake, a more effective way of reducing urinary oxalate excretion is to increase calcium intake, especially if initial regular calcium intake is low.
- The colonisation of Oxalobacter formigenes is another variable to factor into the consideration of the importance of dietary oxalate. Oxalobacter formigenes are obligate oxalate-degrading anaerobes [bacterium], found within the normal microbiome.
- It's presence in the colon is linked to a lower urinary oxalate excretion.
- The significance of dietary oxalate restriction is yet to be determined in the overall prevention of stone formation. The exception being conditions such as bariatric surgery.
- However, probiotic ingestion in patients characterised by high oxalate absorption resulted in the highest expectancy to experience clinically significant reductions in urinary oxalate.
Which suggests that dietary oxalate plays a key role as a determinant of urinary oxalate excretion in response to the use of probiotic.
- Black tea
- Cocoa powder
- Fizzy drinks/Soda
- Green leafy vegetables
eg. Almonds and cashews
- Soy beans & milk
- Stevia sweetener
- Sweet potato
- Wheat bran
Protein is a fundamentally essential nutrient the body requires. Two of the most important roles played by protein are; providing the body with a source of fuel; and facilitating healing and growth, as protein is one of the main constituents for the formation of bodily tissue. However, sources of protein derived from animals has been proven to have a prevalent effect on many urinary variables that lead to stone formation.
- The combination of a low-calcium diet with a high-animal-protein diet induces a negative calcium balance which is exceptionally harmful.
- High animal-protein intake places one at risk of developing calcium based stones as it is a contributing factor to hyperuricosuria.
- Hyperuricosuria - excessive amounts of uric acid present in the urine.
Hyperuricosuria can in turn lead to hypocitraturia
- Hypocitraturia - abnormally low urinary citrate excretion.
- The induction of hypercalciuria by animal-protein intake occurs as a result of higher bone resorption (The removal of calcium from the bones) and lower tubular calcium reabsorption (A higher loss of calcium in the urine because the kidneys reclaim less calcium from the urine.).
Although, it has been established that the acid load accompanying high animal-protein intake is not responsible for hypercalciuria.
- In patients with nephrolithiasis, a short-term reduction of animal-protein intake, for up to approximately two weeks has yielded a significant increase in citrate excretion and a reduction of urinary excretion of calcium, phosphate, hydroxyproline, uric acid, and oxalate.
- In spite of the significant role increased animal-protein intake plays in adverse fluctuations in urine chemistry; thus increasing the risk of kidney stones - the only diet restricting animal-protein intake to effectively reduce stone risk, entailed higher calcium intake and a reduction of sodium intake.
- Animal products
Beef, pork, poultry and fish/seafood
- Animal byproducts
Dairy products and eggs etc.
In order for our bodies to function properly and optimally, we require a relatively low intake of sodium (Na). Sodium is both mineral and electrolyte, playing roles in:
- The regulation of the body's water and electrolyte balances
- Muscle function
- Nerve function
- Electrical impulses throughout the body
- Regulation of blood pressure and volume
- A diet consisting of high sodium intake in patients with reduced proximal sodium reabsorption, will lead to decreased kidney tubular calcium reabsorption. (The kidney's ability to remove calcium from the urine.)
- Considerable changes to dietary sodium intake reflected direct variations in daily urinary calcium excretion.
- Stone-formation have been observed to experience a deleterious effect on calcium and bone loss.
- It's been observed that a higher calcium, and reduced sodium intake is linked to the reduction of calciuria.
Calciuria: calcium presence in the urine.
- Cured meats
- Foods containing vegetable preservatives and additives
- Multi-ingredient meals
Such as; pizza, filled sandwiches, macaroni and cheese, and frozen meals
- Salad dressing
- Processed/refined snacks
Such as crisps/chips
Citrate & Potassium
Citrate: is a key component of metabolism. Derived from the three carboxy groups of citric acid (Pubchem, 2021). Essentially, citrate is the salt form of citric acid. Citric acid/citrate play important roles throughout the body; however, in context of kidney function and stone disease - urinary citrate inhibits the growth of calcium oxalate stones, and increases the solubility of calcium salts in the kidneys.
Potassium: is a naturally occurring mineral the human body requires. Potassium is also classified as an electrolyte; due to the reaction that takes place when introduced to water, which is the production of positively charged ions. Potassium weighs in as one of the top three most abundant minerals found in the human body. Playing roles in:
- Fluid regulation
- Regulation of muscle contraction and function
The health benefits of a potassium-rich diet have been proven to be significant; potentially reducing blood pressure and alleviating water retention; also aiding in the prevention of stroke, osteoperosis and kidney stones.
- Multiple factors plays a role in the regulation of kidney citrate excretion; however, acid-base variables were found to have the biggest impact.
Acid-base: refers to the reaction that takes place between an acid (low pH) and a base (high pH), which results in a salt (neutral pH)
- Acid-loads and acidosis aid in reducing ones risk of uric acid and cystine-based calculi. Both increase urinary citrate excretion by increasing kidney tubule reabsorption of citrate. Thus, reducing calciuria.
- Stone formers with increased/high animal protein intake, are encouraged to substitute this intake with fruits and vegetables.
- An alternative nonpharmacological therapy to potassium citrate is an increased intake of citrus fruits such as:
- Certain tangerines
Being sources of natural dietary citrate, the intake of these citrus fruits may aid the management of hypocitraturia and/or uric acid and cystine stones.
- Citrate found in both orange and grapefruit have been noted to increase urinary pH.
- Drinking freshly squeezed citrus fruit juice delivers a similar amount of dietary citrate whilst also increasing fluid intake and output. However, it is not advised to cosnume processed, commercial fruit juice in high quantities due to their often high; caloric, fructose and/or carbohydrate content.
- However, it has been observed that orange juice is an exception, as it has no significant effect on the risk of stone formation.
- Increased fluid intake = increased fluid output
By increasing ones fluid intake and in turn output, urine supersaturation is reduced. Thereby, reducing the risk of kidney stones.
- Another alternate non-pharmacological therapy for hypocitraturic stone formers is the increased intake of non-citrus alkaline fruits such as melon.
Various melons provide high loads of; potassium, malate and citrate. The consumption of which can result in an increase of citrate excretion.
- In contrast, observational studies indicated that a higher potassium intake is linked to incident stones in males and older women.
- Citrus fruits and juice
(Lemons and limes containing the most citric acid, followed by oranges and grapefruit.)
- Animal products
Beef, fish and poultry
- Certain fruit and vegetable juices
Such as bananas, oranges and apricots
Such as; cooked spinach/broccoli, mushrooms, zucchini, cucumber and peas
- Increasing water intake to ensure a urinary output volume of approximately 2.5 litres per day, is associated with reduced risk of stone reccurance.
- Although the previous point advocating the consumption of water in stone formers, is tried and true; certain variables may be reasons to be concerned about the, "effect of water hardness on kidney stone incidence." Consuming inordinate/excessive amounts of water can have adverse effects on the kidneys.
Water "hardness", merely refers to the mineral content of the water. Noteably calcium and magnesium. The "harder" the water, the higher this mineral content is.
- The ingestion of mineral waters that deliver loads of bicarbonate and magnesium may reduce ones risk of of uric acid percipitation as the minerals may result in;
- Favourable changes in urine pH.
- Favourable changes in magnesium and citrate excretion.
- Favourable changes to inhibitors of calcium oxalate stone formation.
- Favourable changes to counterbalancing increased calcium excretion.
- Caffeinated as well as decaffeinated tea and coffee have been observed to reduce the risk of stone formation.
- (In moderation) Alcohol (specifically beer) has been associated with the reduced risk of kidney stone formation. Possibly as a result of decreased urinary concentration due to alcohols ability to inhibit the secretion of antidiuretic hormone (ADH). Leading to an increased need to urinate.
- Many phytate rich foods (Such as; beans, cereal, whole grains and rice) are rich in oxalate content too.
- It is possible that phytate alleviates/nullifies oxalate content - "induced lithogenic potential."
- Although only roughly 5% of ingested phytate appears in urinary output (implying that phytate is mostly nonabsorpable), the increased consumption of dietary phytate is strongly associated with increases in urinary excretion. Thus decreasing ones risk of kidney stone formation.
Calories & Fructose
Fructose is a simple sugar that the liver converts into glucose, which is another main source of fuel for the body. Fructose makes up 50% of table sugar, which is why high fructose intake can result in abnormal metabolic activity.Vegetables and sweet fruits (and fruit in general) contain relatively low amounts of dietary fructose.
- Many observational and epidemiological studies link, obesity, weight gain, insulin resistance, metabolic syndrome and diabetes with an increased prevalence of kidney stones.
- A higher body mass index (BMI) is associated with:
- Lower urine pH and increased risk of uric acid stones.
- Increased excretion of urinary oxalate.
- Uric acid stone formers have been known to have an increased net-acid excretion and a decreased urine pH, compared to non-uric acid stone formers at any given level of urine sulphate excretion.
This in turn means that another nonpharmacological treatment known as a process called alkalinisation (the neutralisation of an acid) has been observed to fail in uric acid stone formers.
- Weight loss has been associated with reduced risk of formation of all compositions of stone.
- Stone formers are recommended to avoid diets that combine intakes of high animal-protein with low- carbohydrate, such as the Atkins diet. Due to the following:
- Reduced urine pH
- Reduced citrate excretion
- Increased uric acid excretion
- Instead, stone formers are encouraged to follow a DASH diet, which stands for Dietary Approaches to Stop Hypertension. A low calorie DASH-style diet is rich in fruits and vegetables.
- Although the consumption of fructose is not definitively linked to kidney stone formation, it has been observed that high fructose intake is associated with an increased risk of incident kidney stone formation.
THE TAKE AWAY
The following summary is directly quoted from the source document; Optimum Nutrition for Kidney Stone Disease, written by Ita P. Heilberg and David S. Goldfarb
Calcium Oxalate Stones
"Idiopathic oxalate stone-formers are advised to reduce animal protein, oxalate and sodium in their diets as well as maintain adequate intake of calcium and increasing their consumption of citrate and potassium."
Calcium Phosphate Stones
"Reduce their sodium intake to reduce calcium excretion."
Uric Acid Stones
"The mainstay of therapy is weight loss and urinary alkalinisation, provided by a more vegetarian diet, leading to an increase in urine citrate content and pH. Reduction in animal protein intake may further reduce purine ingestion and uric acid excretion."
"Restrict animal protein to reduce cystine methionine ingestion, and restrict sodium intake to further reduce excretion and supersaturation of cystine. Ingestion of vegetables high in content of organic anions, such as citrate, should be associated with higher urine pH."
"Because of their infectious origin, diet has no definitive role for Struvite stones."