The Effect of Fasting During the Holy Month of Ramadan on the Risk of Calcium-Oxalate and Uric-Acid Stone Formation

Urolithiasis ◽  
1989 ◽  
pp. 761-761
Author(s):  
W. G. Robertson ◽  
W. Qunibi ◽  
S. Taher ◽  
V. R. Walker ◽  
H. Hughes ◽  
...  
2018 ◽  
Author(s):  
José Luiz Nishiura ◽  
Ita Pfeferman Heilberg

Nephrolithiasis is a highly prevalent condition, but its incidence varies depending on race, gender, and geographic location. Approximately half of patients form at least one recurrent stone within 10 years of the first episode. Renal stones are usually composed of calcium salts (calcium oxalate monohydrate or dihydrate, calcium phosphate), uric acid, or, less frequently, cystine and struvite (magnesium, ammonium, and phosphate). Calcium oxalate stones, the most commonly encountered ones, may result from urinary calcium oxalate precipitation on the Randall plaque, which is a hydroxyapatite deposit in the interstitium of the kidney medulla. Uric acid nephrolithiasis, which is common among patients with metabolic syndrome or diabetes mellitus, is caused by an excessively acidic urinary pH as a renal manifestation of insulin resistance. The medical evaluation of the kidney stone patient must be focused on identifying anatomic abnormalities of the urinary tract, associated systemic diseases, use of lithogenic drugs or supplements, and, mostly, urinary risk factors such as low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH that can be affected by dietary habits, environmental factors, and genetic traits. Metabolic evaluation requires a urinalysis, stone analysis (if available), serum chemistry, and urinary parameters, preferably obtained by two nonconsecutive 24-hour urine collections under a random diet. Targeted medication and dietary advice are effective to reduce the risk of recurrence. Clinical, radiologic, and laboratory follow-ups are needed to prevent stone growth and new stone formation, to assess treatment adherence or effectiveness to dietary recommendations, and to allow adjustment of pharmacologic treatment. This review contains 5 highly rendered figure, 3 tables, and 105 references.


1994 ◽  
pp. 581-586 ◽  
Author(s):  
W. G. Robertson ◽  
H. Hughes ◽  
I. Husain ◽  
S. Al-Faqih ◽  
A. Arafat ◽  
...  

2017 ◽  
Author(s):  
José Luiz Nishiura ◽  
Ita Pfeferman Heilberg

Nephrolithiasis is a highly prevalent condition, but its incidence varies depending on race, gender, and geographic location. Approximately half of patients form at least one recurrent stone within 10 years of the first episode. Renal stones are usually composed of calcium salts (calcium oxalate monohydrate or dihydrate, calcium phosphate), uric acid, or, less frequently, cystine and struvite (magnesium, ammonium, and phosphate). Calcium oxalate stones, the most commonly encountered ones, may result from urinary calcium oxalate precipitation on the Randall plaque, which is a hydroxyapatite deposit in the interstitium of the kidney medulla. Uric acid nephrolithiasis, which is common among patients with metabolic syndrome or diabetes mellitus, is caused by an excessively acidic urinary pH as a renal manifestation of insulin resistance. The medical evaluation of the kidney stone patient must be focused on identifying anatomic abnormalities of the urinary tract, associated systemic diseases, use of lithogenic drugs or supplements, and, mostly, urinary risk factors such as low urine volume, hypercalciuria, hyperuricosuria, hypocitraturia, hyperoxaluria, and abnormalities in urine pH that can be affected by dietary habits, environmental factors, and genetic traits. Metabolic evaluation requires a urinalysis, stone analysis (if available), serum chemistry, and urinary parameters, preferably obtained by two nonconsecutive 24-hour urine collections under a random diet. Targeted medication and dietary advice are effective to reduce the risk of recurrence. Clinical, radiologic, and laboratory follow-ups are needed to prevent stone growth and new stone formation, to assess treatment adherence or effectiveness to dietary recommendations, and to allow adjustment of pharmacologic treatment. This review contains 5 highly rendered figure, 3 tables, and 105 references.


Urolithiasis ◽  
2017 ◽  
Vol 46 (2) ◽  
pp. 167-172 ◽  
Author(s):  
Alberto Trinchieri ◽  
Emanuele Montanari

1988 ◽  
Vol 18 (4) ◽  
pp. 465-468 ◽  
Author(s):  
Tsuneo Fukushima ◽  
Akira Sugita ◽  
Shigeyuki Masuzawa ◽  
Yasunobu Yamazaki ◽  
Hiroshi Takemura ◽  
...  

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Steeve Doizi ◽  
Kathy Hill ◽  
John Poindexter ◽  
Margaret Pearle ◽  
Khashayar Sakhaee ◽  
...  

2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Bao-Song Gui ◽  
Rong Xie ◽  
Xiu-Qiong Yao ◽  
Mei-Ru Li ◽  
Jian-Ming Ouyang

The composition and morphology of nanocrystals in urines of healthy persons and lithogenic patients were comparatively investigated by means of X-ray diffraction (XRD) and transmission electron microscopy (TEM). It was shown that the main composition of urinary nanocrystals in healthy persons were calcium oxalate dihydrate (COD), uric acid, and ammonium magnesium phosphate (struvite). However, the main compositions of urinary nanocrystals in lithogenic patients were struvite,β-tricalcium phosphate, uric acid, COD, and calcium oxalate monohydrate (COM). According to the XRD data, the size of nanocrystals was calculated to be23∼72 nm in healthy urine and12∼118 nm in lithogenic urine by Scherer formula. TEM results showed that the nanocrystals in healthy urine were dispersive and uniform with a mean size of about 38 nm. In contrast, the nanocrystals in lithogenic urine were much aggregated with a mean size of about 55 nm. The results in this work indicated that the urinary stone formation may be prevented by diminishing the aggregation and the size differentiation of urinary nanocrystals by physical or chemical methods.


2018 ◽  
Vol 85 (3) ◽  
pp. 93-98 ◽  
Author(s):  
Elisa Cicerello

Uric acid nephrolithiasis appears to increase in prevalence. While a relationship between uric acid stones and low urinary pH has been for long known, additional association with various metabolic conditions and pathophysiological basis has recently been elucidated. Some conditions such as diabetes and metabolic syndrome disease, excessive dietary intake, and increased endogenous uric acid production and/or defect in ammoniagenesis are associated with low urinary pH. In addition, the phenomenon of global warming could result in an increase in areas with greater climate risk for uric acid stone formation. There are three therapeutic steps to be taken for management of uric acid stones: identification of urinary pH profiles, assessment of urinary volume status, and identification of disorders leading to excessive uric acid production. However, the most important factor for uric acid stone formation is acid urinary pH, which is a prerequisite for uric acid precipitation. This article reviews recent insights into the pathophysiology of uric acid stones and their management.


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