kidney stones in men
Francesco P. Cappuccio1, Alfonso Siani2,3, Gianvincenzo Barba2,3,
Maria Cristina Mellone4, Luigina Russo2, Eduardo Farinaro5,
Maurizio Trevisan6, Mario Mancini2 and Pasquale Strazzullo2
Although naturally occurring urolithiasis is rare in animals, spontaneously hypertensive rats are prone to develop kidney stones . In humans, the ®rst report of an association between hypertension and kidney stones can be traced back to 1761  when Giovan Battista Morgagni described a patient with clinical and anatomical ®ndings suggestive of long-standing hypertension and the presence of kidney stones. More recently, cross-sectional epidemiological surveys have described an independent association between hypertension and a history of kidney stone disease [3±6]. However, given the retrospective nature of the assessment of urolithiasis, the time sequence of events is unclear, and, in particular, the possibility that hypertension may result from renal damage caused by kidney stones could not be ruled out. Prospective investigations are therefore needed to establish whether hypertension precedes the development of kidney stones and may therefore be considered as a possible cause of this condition.
Madore et al.  have recently reported prospective analyses of the Health Professionals Follow-up Study suggesting that prior occurrence of kidney stones increases the risk of subsequent hypertension. We report
the results of a prospective study of middle-aged men without evidence of urolithiasis at the baseline and followed-up for 8 years to establish the incidence of kidney stone disease and its relation to hypertension. The present study assesses both exposure and outcome by direct measurement and veri®cation and is based on the `a priori' hypothesis that hypertension would precede the development of kidney stones. It also provides measures of renal function and other potential confounders.
countries are renal stones . Men were classi®ed as incident cases of kidney stones if, within the period of follow-up, they experienced any of the following: spontaneous passage of one or more stones, X-ray or
echographic evidence of one or more stones in the upper urinary tract, lithotripsy or surgical removal of stones from kidney or ureter. The self-reported occurrence of kidney stones was checked against available
This research through a prospective cohort study to examine whether hypertension predicts the incidence of kidney stone disease in men or not. Based on this study have five hundred and three male workers, aged 21 to 68 years, with no evidence of kidney stone disease at baseline. To endorse these preventive strategies, however, we need to confirm the cost-effectiveness of such early diagnosis and the beneficial effect of sodium restriction not only on the reduction of urinary calcium excretion but on the overall reduction of the incidence of kidney stones or their recurrence rate using a randomized controlled clinical trial at the Olivetti factory in Southern Italy. During research time we use sphygmomanometer, Anthropometer, Weight instrument measure our participants, the outcome of measures are Anthropometry, blood pressure, biochemistry and history of kidney stone disease were evaluated at the baseline examination. Occurrence of kidney stone disease was evaluated again in recent year. Hypertension was defined as systolic blood pressure > 160 or diastolic blood pressure, > 95 mmHg or both, or being on drug therapy for hypertension. Occurrence of kidney stone disease was defined as radiological or echo graphic evidence of calculi or documented passage of one or more stones.
Hypertensive men had a greater risk of developing kidney stones than normotensive ones (RR 1.96; 95% confidence interval 1.16±3.32). The risk was unaffected by the exclusion of treated hypertensive’s (2.01; 1.13±3.59) and after adjustment for age (1.89; 1.12±3.18), body weight (1.78; 1.05±3.00) or height (2.00; 1.19±3.38).
Hypertension in middle-aged men is a significant predictor of kidney stone disease rather than a consequence of renal damage caused by the kidney stones.
In humans, the first report of an association between hypertension and kidney stones can be traced back to 1761 when Giovan Battista Morgagni described a patient with clinical and anatomical ®ndings suggestive of long-standing hypertension and the presence of kidney stones. More recently, cross-sectional epidemiological surveys have described an independent association between hypertension and a history of kidney stone disease.
Within the United States, about 10–15% of adults will be diagnosed with a kidney stone, and the total cost for treating this condition was US$2 billion in 2003. The incidence rate increases to 20–25% in the Middle East, because of increased risk of dehydration in hot climates. (The typical Arabian diet is also 50% lower in calcium and 250% higher in oxalates compared to Western diets, increasing the net risk.)Recurrence rates are estimated at about 10% per year, totaling 50% over a 5–10 year period and 75% over 20 years. Men are affected approximately 4 times more often than women. Recent evidence has shown an increase in pediatric cases.
Based on this study, the incidence of kidney stones is increasing worldwide [29±33]. It is estimated that 12±15% of the population will develop kidney stones over their life-time [29,30]. Moreover, stone-formers are at a much greater risk of recurrence (as high as 80%) . Although kidney stone disease is seldom fatal, it does lead to substantial morbidity from pain, urinary tract infections and obstructive uropathy, with a considerable economic burden on healthcare provision for an effective treatment (mostly removal, fragmentation or extracorporeal shockwave lithotripsy) . Primary prevention and prevention of recurrence would therefore be an important aspect of the population approach to the overall control of urolithiasis. Despite early reports of cross-sectional associations between hypertension and kidney stones [3±5], very little attention has so far been paid to consideration of hypertension as a risk factor (or a marker of risk) for urolithiasis [28,35], nor has a reduction of the intake of sodium ± a major determinant of urinary calcium excretion ± been seriously implemented as a dietary approach to the management of hypercalciuria [28,35]. The present prospective study highlights the importance of hypertension as a marker of kidney stone risk.
1. Stone formation is inhibited by Citrate
2. Women have much higher levels of citrate than men
3. Low citrate levels are related to most stone forms
Kidney stone are crystalline mineral deposits that form in the kidney. They develop from microscopic crystals in the loop of Henle, the distal tubule, or the collecting duct, and they can enlarge to form visible fragments. The process of stone formation depends on urinary volume; concentrations of calcium, phosphate, oxalate, sodium, and uric acid ions; concentrations of natural calculus inhibitors; and urinary pH.4 High ion levels, low urinary volume, low pH, and low citrate levels favor calculus formation.
stones are classified into five categories based on their composition: calcium oxalate (70 percent), calcium phosphate (5 to 10 percent), uric acid (10 percent), struvite (15 to 20 percent) and cystine (1 percent). stones can be classified more broadly into calcareous stones and noncalcareous stones. Calcareous stones usually are visible on radiographic imaging (Figure 1), whereas noncalcareous stonesoften are radiolucent or poorly visualized on plain film radiography. Many calculi have a mixed composition, with one type of crystal becoming a nidus for heterogeneous crystallization.
Last edited by guomanman on Wed 01 Jul 2009, 9:29 am; edited 2 times in total