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The Kidney Stone Page |
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SUGAR
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ABSTRACT
Urol Int 1993;51(4):185-90
Glucose metabolism in renal stone patients.
Iguchi M, Umekawa T, Takamura C, Sugihara I, Nakamura K, Kohri K, Kurita T.
Department of Urology, Kaizuka Municipal Hospital, Osaka, Japan.
The calciuric response and the changes of plasma glucose and insulin produced by a 75-gram oral glucose tolerance test were determined in 27 male patients with idiopathic calcium renal stones (6 with dietary hypercalciuria, 5 with nondietary hypercalciuria and 16 with normocalciuria) and 22 healthy male subjects. The subjects were classified as obese (> or = 120% ideal weight) and nonobese. The incidence of an abnormal response to glucose loading was similar in the stone patients and the healthy subjects. In addition, the plasma glucose and insulin levels after oral glucose load did not differ between the stone patients and control subjects and were affected by the individual degree of obesity. Urinary calcium excretion increased significantly after glucose ingestion in both the stone patients and the control subjects. Urinary calcium excretion was greater in the stone patients than in the control subjects due to the presence of patients with nondietaryhypercalciuria, and the increment in urinary calcium excretion in the dietary hypercalciuric and normocalciuric stone patients was indistinguishable from that in the control subjects. The degree of obesity did not affect the increment in urinary calcium excretion. These results suggest that overconsumption of refined carbohydrates such as sugar-sweetened soft drinks, soda and cakes may be a risk factor for stone formation, especially in the patients with nondietary hypercalciuria.
PMID: 8266608, UI: 94090934
ABSTRACT
Ann Urol (Paris) 1991; 25(4):204-8
[Is sucrose a risk factor in calculus formation]? [Article in French]
Sakly R, Hdhili A, Achour A, Barkia A, Yaacoub M, Kallal Z, Mbazzaa A.
Institut National de Nutrition, Tunis.
The addition of sucrose to drinking water of rats at the rate of 2.5 or 5 grams per 100 ml, for one month, induced hypercalciuria which appeared to be dependent on the degree of supplementation. In spite of these disorders, calcium deposits were not observed
in treated animals. This protection against renal calculi was probably due to high urinary excretions of magnesium, phosphorus, zinc and copper. These lithogenesis inhibitors varied, like oxaluria and calciuria, in parallel with dietary sucrose intake.
PMID: 1746929, UI: 92082215
ABSTRACT
Nutr Health 1987;5(1-2):9-17
Sucrose and idiopathic renal stone.
Blacklock NJ University Hospital of South Manchester.
Idiopathic renal stone comprises more than 80 per cent of kidney stone disease. Whilst the incidence rate in the Western World is high, that in Africa south of the Sahara is very low. Epidemiological studies point to a dietary aetiology as the basis for stone
formation in the kidney. A number of dietary constituents increase the urinary risk factors for stone formation and one of these is sucrose. The sucrose effect is exaggerated when it is consumed in certain forms. There is also the evidence that a third of a normal population responds in an exaggerated manner in respect of an increased excretion of urinary risk factors when sucrose is consumed and this phenomenon has been noted in over 70 per cent of idiopathic stone formers. In studying the mechanism of this, insulin was found to influence distal renal tubular function to increased calcium excretion. Stone formers with an exaggerated urinary risk factor response to sucrose were found to have abnormally high and sustained blood levels of insulin following a standard glucose test meal. Where sucrose or sucrose products are in abundance, quite apart from its effect in increasing urinary risk factors in the population in general, there is particular vulnerability of a significant sub group within the population with this type of insulin response. Sucrose furthermore is known to induce nephrocalcinosis in the kidney of the rodent and similar calcific lesions have been found in the kidney substance of man and these have been observed to begin to appear within the first decade of life.
PMID: 3313140, UI: 88039791 Br J Urol 1986 Aug; 58(4): 353-7
ABSTRACT
Does sucrose damage kidneys?
Li MK, Kavanagh JP, Prendiville V, Buxton A, Moss DG.
Blacklock NJ
There is evidence to suggest that sucrose ingestion can cause renal parenchymal changes as well as increasing the urinary saturation index for calcium oxalate. Ten stone formers and 10 normal subjects received 250 gm of sucrose daily over a period of 7 days.
Observations on the risk factors for calcium stone formation and urinary N-acetyl-B-glucosaminidase (NAG), a marker of renal tubular cell damage, were made. Oxalate excretion increased. Urinary calcium levels were unchanged but the pattern of response was different between the two groups, as with magnesium and phosphate. NAG was spontaneously higher in the patient group and increased significantly after sucrose ingestion in both groups.
PMID: 3756399, UI: 87001082
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