When compared with controls, the diets of kidney stone patients were found
to contain less vitamin C and more alcohol. Fellstrom B et al: Dietary habits
in renal stone patients compared with healthy subjeects. Br J Urol
63(6):575-580, 1989.
Compared with controls, the diet of 88 kidney stone patients was found to
be lower in dietary fibre, magnesium and vitamin B1. Griffith HM et al: A
case-control study of dietary intake of renal stone patients. II Urine
biochemistry and stone analysis. Urol Res 14(2):75-82, 1986.
There is evidence that one third of the population shows increased risk
factors for kidney stone disease after consuming sugar. These effects of sugar
consumption are thought to be due to the increased secretion of insulin, which
results in increased calcium excretion by the kidneys. Blacklock NJ et al:
Sucrose and idiopathic renal stone. Nutr Health 5(1):9-17, 1987.
Sugar may cause harmful changes to kidney tissue. Ten kidney stone patients
and 10 normal controls received 250 grams of sucrose daily for one week. In
both groups sucrose ingestion caused a rise in levels of urinary
N-acetyl-B-glucosaminidase (NAG), a marker of kidney tubular cell damage. NAG
was already at higher levels in the patients than the controls before the
study began. Li MK et al: Does sucrose damage kidneys? Br J Urol
58(4):353-7, 1986.
8 kidney stone patients were given diets either low or high in animal
protein for 8 weeks. There was increased urinary supersaturation and risk of
forming uric acid crystals on the high protein diet. Fellstrom B et al:
Dietary animal protein and urinary supersaturation in renal stone disease.
Proc Eur Dial Transplant Assoc 20:411-6, 1983.
In a study investigating the effects of diet on calcium kidney stone
patients, it was found that a high intake of carbohydrate and fat and a low
intake of calcium was associated with a higher rate of urinary oxalate
excretion, which is a risk indicator for this type of kidney stone. Masai M
et al: Effect of dietary intake on urinary oxalate excretion in calcium renal
stone formers. Br J Urol 76(6):692-6, 1995.
In a study investigating the differences in diet between 102 recurrent
calcium kidney stone patients and 146 controls, it was found that the patient
group had a significantly higher consumption of animal and vegetable protein.
A link between the protein content of the diet and urinary calcium levels was
confirmed but protein intake had little effect on oxalate excretion. Trinchieri
A et al: The influence of diet on urinary risk factors for stones in healthy
subjects. Br J Urol 67(3):230-6, 1991.
Coppersmiths exposed to chronic cadmium poisoning were found to have a 40%
incidence of kidney stones. Scott R et al: The importance of cadmium as a
factor in calcified upper urinary tract stone disease - a prospective 7-year
study. Br J Urol 54(6):584-9, 1982.
Lead interacts with kidney membranes and enzymes and disrupts energy
production , calcium metabolism, glucose homoeostasis and several other
functions. Lead damage to kidney function is irreversible. Nolan CV et al:
Lead nephrotoxicity and associataed disorders: biochemical mechanisms.
Toxicology 73(2):127-46, 1992.
Mercury, which is a kidney toxic, was found at autopsy to have accumulated
in the kidney cortex of 7 individuals with amalgam tooth fillings, at levels
significantly higher than in 5 amalgam-free individuals. Nylander M et al:
Mercury concentrations in the human brain and kidneys in relation to exposure
from dental amalgam fillings. Swed Dent J 11(5):179-87, 1987.
Eleven healthy volunteers were given increasing amounts of supplementary
selenium (up to 700 ug per day). Mean creatinine clearance increased
significantly, concomitantly with a reduction of serum creatinine levels. This
suggested that kidney function was positively influenced by selenium. Guidi
GC et al: Selenium supplementation increases renal glomerular filtration rate. J
Trace Elem Electrolytes Health Dis 4(3):157-161, 1990.
In 16 kidney stone sufferers supplemented with magnesium and vitamin B6,
there was a significant decline in the excretion of oxalate, leading to a
significant decrease in kidney stone risk index after 120 days of treatment.
Rattan V et al: Effect of combined supplementation of magnesium oxide and
pyridoxine in calcium-oxalate stone formers. Urol Res 22(3):161-5, 1994.
Urinary oxalate excretion was significantly reduced in 12 kidney stone
patients administered vitamin B6 supplements in doses of 250-500 mg daily. Mitwalli
A et al: Control of hyperoxaluria with large doses of pyridoxine in patients
with kidney stones. Int Urol Nephrol 20(4):353-9, 1988.
Urinary excretion levels of magnesium are abnormally low in 25% of kidney
stone patients. Supplementation with magnesium corrects this and effectively
prevents the recurrence of stones. Labeeuw M et al: Role of magnesium in the
physiopathology and treatment of calcium renal lithiasis (in French). Presse Med
16(1):25-7, 1987.
Dietary advice given to 392 kidney stone patients to increase dietary fibre
and reduce sugar, refined carbohydrates and animal protein resulted in a
significant reduction in the urinary excretion of calcium, oxalate and uric
acid. Rao PN et al: Dietary management of urinary risk factors in renal stone
formers. Br J Urol 54(6):578-83, 1982.
A meta-analysis of randomized, controlled studies using protein-restricted
diets in humans with chronic kidney disease found that such diets significantly
reduce the risk (by more than 30%) of kidney failure or death, effectively
slowing down the progression of kidney failure. Pedrini MT et al: The effect of
dietary protein restriction on the progression of diabetic and nondiabetic renal
diseases: a meta-analysis. Ann Intern Med 124(7):627-32, 1996.
106 patients with IgA nephropathy were randomized to receive either 12 g per
day of fish oil or placebo for two years. 10 per cent of the fish oil group died
or developed end-stage kidney disease, compared with 10 per cent in the placebo
group. Serum creatinine concentrations rose significantly more slowly in the
fish oil group. The investigators conclude that in patients with IgA nephopathy
treatment with fish oil retards the rate of loss of kidney function. Donadio JV
Jr et al: A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology
Collaborative Group. N Engl J Med 331(18):1194-9, 1994.
Eleven healthy volunteers were given increasing amounts of supplementary
selenium (up to 700 ug per day). Mean creatinine clearance increased
significantly, concomitantly with a reduction of serum creatinine levels. This
suggested that kidney function was positively influenced by selenium. Guidi
GC et al: Selenium supplementation increases renal glomerular filtration rate. J
Trace Elem Electrolytes Health Dis 4(3):157-161, 1990.
In 16 kidney stone sufferers supplemented with magnesium and vitamin B6,
there was a significant decline in the excretion of oxalate, leading to a
significant decrease in kidney stone risk index after 120 days of treatment.
Rattan V et al: Effect of combined supplementation of magnesium oxide and
pyridoxine in calcium-oxalate stone formers. Urol Res 22(3):161-5, 1994.
Urinary oxalate excretion was significantly reduced in 12 kidney stone
patients administered vitamin B6 supplements in doses of 250-500 mg daily. Mitwalli
A et al: Control of hyperoxaluria with large doses of pyridoxine in patients
with kidney stones. Int Urol Nephrol 20(4):353-9, 1988.
Urinary excretion levels of magnesium are abnormally low in 25% of kidney
stone patients. Supplementation with magnesium corrects this and effectively
prevents the recurrence of stones. Labeeuw M et al: Role of magnesium in the
physiopathology and treatment of calcium renal lithiasis (in French). Presse Med
16(1):25-7, 1987.
Dietary advice given to 392 kidney stone patients to increase dietary fibre
and reduce sugar, refined carbohydrates and animal protein resulted in a
significant reduction in the urinary excretion of calcium, oxalate and uric
acid. Rao PN et al: Dietary management of urinary risk factors in renal stone
formers. Br J Urol 54(6):578-83, 1982.
A meta-analysis of randomized, controlled studies using protein-restricted
diets in humans with chronic kidney disease found that such diets significantly
reduce the risk (by more than 30%) of kidney failure or death, effectively
slowing down the progression of kidney failure. Pedrini MT et al: The effect of
dietary protein restriction on the progression of diabetic and nondiabetic renal
diseases: a meta-analysis. Ann Intern Med 124(7):627-32, 1996.
106 patients with IgA nephropathy were randomized to receive either 12 g per
day of fish oil or placebo for two years. 10 per cent of the fish oil group died
or developed end-stage kidney disease, compared with 10 per cent in the placebo
group. Serum creatinine concentrations rose significantly more slowly in the
fish oil group. The investigators conclude that in patients with IgA nephopathy
treatment with fish oil retards the rate of loss of kidney function. Donadio JV
Jr et al: A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology
Collaborative Group. N Engl J Med 331(18):1194-9, 1994.
Eleven healthy volunteers were given increasing amounts of supplementary
selenium (up to 700 ug per day). Mean creatinine clearance increased
significantly, concomitantly with a reduction of serum creatinine levels. This
suggested that kidney function was positively influenced by selenium. Guidi
GC et al: Selenium supplementation increases renal glomerular filtration rate. J
Trace Elem Electrolytes Health Dis 4(3):157-161, 1990.
In 16 kidney stone sufferers supplemented with magnesium and vitamin B6,
there was a significant decline in the excretion of oxalate, leading to a
significant decrease in kidney stone risk index after 120 days of treatment.
Rattan V et al: Effect of combined supplementation of magnesium oxide and
pyridoxine in calcium-oxalate stone formers. Urol Res 22(3):161-5, 1994.
Urinary oxalate excretion was significantly reduced in 12 kidney stone
patients administered vitamin B6 supplements in doses of 250-500 mg daily. Mitwalli
A et al: Control of hyperoxaluria with large doses of pyridoxine in patients
with kidney stones. Int Urol Nephrol 20(4):353-9, 1988.
Urinary excretion levels of magnesium are abnormally low in 25% of kidney
stone patients. Supplementation with magnesium corrects this and effectively
prevents the recurrence of stones. Labeeuw M et al: Role of magnesium in the
physiopathology and treatment of calcium renal lithiasis (in French). Presse Med
16(1):25-7, 1987.
Dietary advice given to 392 kidney stone patients to increase dietary fibre
and reduce sugar, refined carbohydrates and animal protein resulted in a
significant reduction in the urinary excretion of calcium, oxalate and uric
acid. Rao PN et al: Dietary management of urinary risk factors in renal stone
formers. Br J Urol 54(6):578-83, 1982.
A meta-analysis of randomized, controlled studies using protein-restricted
diets in humans with chronic kidney disease found that such diets significantly
reduce the risk (by more than 30%) of kidney failure or death, effectively
slowing down the progression of kidney failure. Pedrini MT et al: The effect of
dietary protein restriction on the progression of diabetic and nondiabetic renal
diseases: a meta-analysis. Ann Intern Med 124(7):627-32, 1996.
106 patients with IgA nephropathy were randomized to receive either 12 g per
day of fish oil or placebo for two years. 10 per cent of the fish oil group died
or developed end-stage kidney disease, compared with 10 per cent in the placebo
group. Serum creatinine concentrations rose significantly more slowly in the
fish oil group. The investigators conclude that in patients with IgA nephopathy
treatment with fish oil retards the rate of loss of kidney function. Donadio JV
Jr et al: A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology
Collaborative Group. N Engl J Med 331(18):1194-9, 1994.
