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Leonardo R. Reyes Rabanal, MD.

Instituto de Nefrología, Havana, Cuba.



Kidney stones have afflicted humankind since antiquity. The prevalence of urinary tract stone disease is estimated to be 2% to 15%. Urolithiasis is an entity, which has high morbidity and socio-economical impact, and low mortality.

Urinary stones were a major health problem in developed countries until the 1980s, with a significant proportion of patients requiring extensive surgical procedures and a sizeable minority losing a kidney. One study showed that about 20% of patients with recurrent stone disease who underwent surgery for obstruction and infection went on to develop mild renal insufficiency 1. The advent of extracorporeal techniques for stone destruction and the refinements in endoscopic surgery, however, have greatly decreased the morbidity associated with stone surgery, and the disorder is changing from a major health problem to a major nuisance. One unfortunate result of this technologic success is that advances in medical management of stone disease and research in prevention have languished. Surgical procedures treat stones but do not prevent them; however, as anyone who has passed a kidney stone can tell, this may be what the majority of patients with stone disease needs.

The management of urinary lithiasis requires co-operation between some specialists, for example nephrologist and urologist. Critical to the selection of proper therapy is knowledge of both medical and surgical methods of treating urinary stone disease.

Epidemiologic Aspects

Urolithiasis is a common clinical disorder. Its frequency has risen with the development of humanity and varies with the country, geographic area, etc.

Its world prevalence is estimated between 1 to 5%, in developed countries 2-13% (with a great variation among them), and in developing countries 0.5-1% 1,2,3,4. The overall probability of forming stones differs in various parts of the world: 1-5% in Asia, 5-9% in Europe, 13% in North America, 20% in Saudi Arabia 2,3,4. Lifetime prevalences in the USA and Europe range between 8 and 15%, annual incidences of kidney stones are about 0.1-0.4% of the population and the likelihood that a white man will develop stone disease by age 70 years is about 1 in 8 5. The prevalence among elderly men over 65 is 4.7% in Italy 6. On the other hand, silent kidney stone, which can be a presentation of urolithiasis, could have prevalence around 3% as has been found in Pakistan 7.

Stone in the upper urinary tract appear to relate to the life-style, being more frequent among affluent people, living in developed countries, with high animal protein consumption. Bladder stones are nowadays mainly seen in the Third World, on account of very poor socio-economic conditions 2. The later has been decreasing in most countries in the so-called endemic bladder stone belt with gradual improvements in levels of nutrition, especially in proteins. However, as living standards increase, particularly in the urban areas of the more affluent developing countries, so the incidence of upper urinary tract stones in adults is increasing.

The stone problem in the tropics is compounded by low urine volumes resulting in some areas from poor drinking water, which causes chronic diarrhoea, and in others from the hot climate and fluid losses through the skin. As nutrition improves in these countries, the formation of bladder stones gives way to upper urinary tract stones consisting of calcium oxalate, often mixed with calcium phosphate or uric acid, such as are formed in most Western countries.

Intrinsic Risk Factors


Numerous observers have noted that urinary calculi are relatively rare in Native Americans, blacks of Africa and America, and native-born Israelis. Conversely, the incidence of stone disease is highest in some of the colder temperate areas of the world, populated primarily by Asians and whites. Although the incidence of bladder stones seems to be related primarily to dietary habits and malnutrition in underdeveloped and primitive countries, dietary improvement over the years has resulted in a change of composition and the site of occurrence of urinary calculi from bladder to kidney 8.

About 25% of patients with kidney stones have a family history of kidney stones. 9. Genetic studies concluded that urolithiasis may be the result of a polygenic defect with partial penetrance 10,11. White, however, cautioned against accepting familial or hereditary theories of stone formation too readily 12. He noted that urinary calcium excretion was significantly higher in spouses of patients who were stone formers than in spouses of persons who did not form stones. White postulated that household diet as well as familial tendencies must be considered in theories of etiology of urinary lithiasis. Curhan found that kidney stones developed more frequently in men with a family history of kidney stones than in those without a family history 9. In a longitudinal follow-up study of 37,999 male health professionals, a family history of stones was more than three times higher in men with kidney stones than in non–stone formers. The relative risk of stone formation remained high even after adjusting for a variety of risk factors such as calcium intake and urinary metabolite excretion.

In pediatric patients with nephrolithiasis, 73% had family history of kidney stones in at least one first-order or second-order relative, as opposed to a prevalence of 22% in a control population of pediatric renal and urologic patients 13. Of the patients with hypercalciuria, the prevalence of nephrolithiasis in the family history was 69% 13.

In a population-based study of 1309 women with kidney stones, was found that renal stone formation was not associated with community of residence, high-oxalate or high-calcium diet, or high-energy intake 14. The lack of identifiable environmental correlates suggests that there are genetic components to kidney stone formation.

Several disorders that cause renal stones are hereditary. Familial renal tubular acidosis (RTA) is associated with nephrolithiasis and nephrocalcinosis in almost 70% of patients 15. Cystinuria is a homozygous recessive disease, and the genes that cause it have been cloned. Similarly, xanthinuria and dihydroxyadeninuria are rare hereditary disorders that cause renal stones. Coe et al. found a strong inheritance pattern in patients with nephrolithiasis that they conjectured was autosomal dominant 16. Human diseases in which up-regulation of intestinal calcium absorption is clearly the primary lesion are rare 17. However, hypersensitivity to 1.25(OH)2D3 or its metabolites can lead to increased intestinal absorption 18. Scott et al. 19 have found linkage of idiopathic hypercalciuria with an apparent absorptive component to microsatellite markers near the VDR locus. Genetic phosphate wasting leads to hypophosphatemia and increase in 1.25(OH)2 D3 , resulting in excess calcium absorption as in hereditary hypophosphatemic rickects with hypercalciuria 20. Mutations in the CLCN5 gene, coding for a chloride channel, have been seen in patients with the X-linked hypercalciuric kidney stone syndromes Dent's disease, X-linked recessive nephrolithiasis, and X-linked recessive hypophosphatemic rickets 21. Calcium-sensing receptor (CaSR) gene could be a component of the complex genetic background regulating Ca excretion. Arg990Gly polymorphism could facilitate activation of CaSR and increase Ca excretion and susceptibility to idiopathic hypercalciuria 22. In heterozigotic individuals no affected by familial hypomagnesemia with hypercalciuria and nephrocalcinosis with hypercalciuria and nephrolithiasis have been suggested a partial defect in paracellular calcium transport (gene dosage effect)23. Finally, a genetic primary bone resorption defect is suspected according the evidence of epidemiological and experimental animal studies where have been demonstrated that 45% or more of nephrolithiasis patients have osteopenia (low bone mineral density) independent of the bone volume 24,25,26,27,28 and increased sensitivity to 1.25(OH)2D3 may be due to augmented vitamin D receptor number in rat osteablasts 29,30

Age and Gender

The peak incidence of urinary calculi is from the twenties to the forties 31;32;33,34. Most patients, however, report onset of disease in their teens. However, the prevalence of urolithiasis in children has been reported for various studies as low. Most of the urinary stone diseases were diagnosed at the fifth decade 3.

A slightly higher rate of renal stone disease is reported in males than in females 2, about three males are afflicted for every female. In a systematically assessed epidemiologic survey about the rate of urolithiasis in Korea, 6.0% of korean men and 1.8% of women are expected to experience urinary stone disease during their lifetime 3. Another extensive study in Taiwan, men were more prone to nephrolithiasis than women with an age-adjusted prevalence of 12.2% in men and 3.1% in women 4. A greater proportion of upper urinary tract calculus disease is caused by chronic urinary tract infections or defects, such as cystinuria or hyperparathyroidism, in women than in men 35. Several investigators have commented on the apparently equal tendency toward urinary lithiasis in males and females during childhood 36;37. This observation, coupled with reports that increased serum testosterone levels resulted in increased endogenous oxalate production by the liver 38, led Finlayson to postulate that lower serum testosterone levels may contribute to the protection women and children have against oxalate stone disease 39. A study has found that men have mean higher oxalate concentrations than women 40. In other study was concluded that androgens increase whereas estrogens decrease urinary oxalate excretion, plasma oxalate concentration, and kidney calcium oxalate crystal deposition 41. Yet, was found that the urinary testosterone concentration of patients who were stone formers was lower than that of control 42. Some other authors demonstrated increased urinary citrate concentrations in the urine of women 43. They postulated that this finding might aid in protecting women from calcium urolithiasis. Further, others observed that women with recurrent stones have a higher prevalence of hypocitraturia than do women with first-time stones 44. The lower risk of stone formation in women may be due to the lower urinary saturation of stone forming salts. Estrogen treatment may decrease the risk of stone recurrence in postmenopausal women by lowering urinary calcium and calcium oxalate saturation 45. A study shown that male patients with stones also had a significantly lower mean glucosaminoglicans concentration than did the female patients.

Race / ethnicity

A slightly higher rate of renal stone disease has been reported in white Caucasians than in Blacks 2. Renal handling of dietary calcium and oxalate in South African black and white subjects is different and may explain the different stone incidence in both race groups 46. Factors which are conventionally used to assess stone risk (pH, oxaluria, citraturia, relative supersaturation) are not helpful in identifying why South African blacks are relatively immune to stones. We suggest that relatively lower oxalate absorption rates may be a physiological feature of this racial group 47.

Extrinsic Risk Factors


The prevalence of urinary calculi is higher in those who live in mountainous, desert, or tropical areas.

Urolithiasis is a problem that is generally increasing in the tropics as it is in most Western countries. There are 2 main types of the disorder-bladder stones in children, a form of the disorder that disappeared from Europe in the late 19th and early 20th centuries, and upper urinary tract stones in adults. The former has been decreasing in most countries in the so-called endemic bladder stone belt with gradual improvements in levels of nutrition. However, as living standards increase, particularly in the urban areas of the more affluent developing countries, so the incidence of upper urinary tract stones in adults is increasing. The types of stones formed depend mainly on the composition of urine, which, in turn, reflects the type of diet consumed in the countries concerned 48.

Finlayson reviewed several world-wide geographic surveys and stated that the incidence of urinary calculus disease in the United States is relatively high for its population 39. Other high-incidence areas are the British Isles, Scandinavian countries, Mediterranean countries, northern India and Pakistan, northern Australia, central Europe, portions of the Malayan peninsula, and China. Low-incidence areas include Central and South America, most of Africa, and those areas of Australia populated by aborigines. Several studies have noted that stones from Great Britain, Scotland, and Sudan are composed primarily of a mixture of calcium oxalate and calcium phosphate 49,50,51,52. Upper urinary tract calculi composed of uric acid tend to be more common in Israel 53. Prevalence rate was recently estimated to be 3.5% in South Korea 3, and the overall prevalence in Taiwan was 9.6% 4.

Extensive studies of the incidence of calculus disease in the United States have demostrated that hospitals in the southeastern United States showed an increased discharge rate, but only for calcium oxalate stones and the eastern seaboard had a higher rate of uric acid lithiasis. However, it has been observed that the stone discharge rate had not changed significantly in the preceding 3 decades despite advances in urolithiasis research 54,55,56.

The prevalence of nephrolithiasis has showed considerable differences in different geographic areas of Italy; the rate is higher in southern Italy and islands, within the average values in central regions, and much lower in northern Italy (about half of the south) 6.

Geography influences the incidence of urinary calculi and the types of calculi that occur within a given area. The capability of individuals to transport intrinsic genetic tendencies of urinary stone formation from area to area, however, makes it likely that the major tendencies contributing to urinary lithiasis reside in the individual. Geography represents just one aspect of the environmental factors—such as dietary habits, temperature, and humidity—superimposed on the intrinsic factors that predispose to stone formation.

Climatic and Seasonal Factors

The effect of geography on the prevalence of stone disease may be indirect, through its effect on temperature. Several workers show a relationship between environmental temperature and seasonal incidence of urinary stone disease. They found that the incidence of urinary calculi was higher during the summer months. Prince made a prospective analysis of 922 occurrences of ureteral stones 36,57. Once again, the peak incidence occurred in July, August, and September. The highest incidence of urinary calculi appeared to occur 1 to 2 months after the achievement of maximal mean annual temperature in the study area.

Bateson reported on the incidence of upper urinary tract calculi in the area surrounding Perth in western Australia 58. The incidence of urinary calculi peaked from December through March. This coincided with the peak maximal summer temperatures in that geographic area. Another study observed no significant seasonal variation with calcium oxalate or calcium phosphate stones 35. The incidence of uric acid stones increased significantly during summer and autumn, and that of infectious stones decreased significantly during spring and summer.

High temperatures increase perspiration, which may result in concentrated urine. This promotes increased urinary crystallization. It has been showed that crystalluria is greater during summer months in patients who form stones 59. Patients with a tendency toward the formation of uric acid or cystine calculi have an additional risk. Concentrated urine tends to be acidic, and acidic urine holds much less uric acid or cystine in solution.

Some authors suggested that increased exposure to sunlight causes increased production of 1,25-dihydroxyvitamin D3 and increased urinary calcium excretion (see the section on hypercalciuria)60. This may cause a higher incidence of urolithiasis during the summer months.

The subtropical and tropical temperature and gradually higher socioeconomic standards of living may contribute to the high prevalence of urolithiasis.

Fluid Intake

One of the prevailing assumptions in the literature on urolithiasis is that increased water intake and increased urinary output decrease the incidence of urinary calculi in those patients who are predisposed to the disease. It is the oldest existing treatment for kidney stones, and, up until a few decades ago, it was the only preventive measure at the physician’s disposal for stone recurrence. Perhaps still the most powerful, and undoubtedly the most economical means of prevention today, it is often not used to advantage by the stone formers. Two factors involved in the relationship between water intake and urolithiasis are 1 the volume of water ingested as opposed to that lost by perspiration and respiration and 2 the mineral or trace element content of the water supply of the region.

In a survey of urolithiasis in the United States, urologists said their opinions of methods of preventing recurrence of urinary stone disease. "Forcing water" received the highest total number of positive responses, along with elimination of infection and elimination of urinary obstruction 61. Others reaffirmed this opinion in reviews 39,62. Although urine dilution by increased water intake may increase ion activity coefficients and, hence, urinary crystallization, water diuresis also reduces the average time of residence of free crystal particles in urine, dilutes the components of urine that may crystallize and does not reduce the activity of natural inhibitors. Finlayson concluded that the dilutional effects of water diuresis outweigh the changes in ion activity and, therefore, help prevent stone formation 39.

The epidemiologic aspects of occurrence of urinary lithiasis in Israeli communities has been investigated and was noted that the areas of highest incidence of urolithiasis were the warmer desert regions as opposed to the cooler mountain regions 63. Within desert areas, the incidence of calculi formation was highest in immigrants from Europe, lower in those from East and North Africa, and lowest in the native-born population of Israel.

A very well conducted 5-year randomized prospective study 64 involving first stone episode patients has shown lower rates of recurrence (12%) in those with a higher intake of water compared to those without (27%). It should be emphasized that patients received no drug therapy nor were submitted to any dietary change so that the unique efficacy of increasing urinary volume could be validated 64.

The mineral content of water also may contribute to the causes of stone disease. Some state that excessive water hardness (e.g., by sodium carbonate) causes a greater incidence of stone disease (Sierakowski et al, 1978). However, data are conflicting 65,66. A study offered a potential explanation for this conflict 67. These Italian investigators examined the effect of three different types of mineral water on urinary analytes in 22 idiopathic calcium oxalate stone formers. Ingestion of hard water caused a reciprocal decrease in oxalate excretion and/or an increase in citrate excretion. Thus, increasing fluid intake—even with a high calcium content—affected inhibitory power and lithogenic salt excretion, decreasing the tendency toward calcium oxalate crystallization. Frustratingly, other Italian investigators were not able to reproduce the Caudrella finding 68. They found no decrease in oxalate or increase in citrate excretion with the ingestion of hard water.

Thus to what extent the hardness and mineral composition of water affect stone risk remains controversial 69,70,71. As the calcium content of drinking water increases, calcium excretion increases but oxalate excretion falls 70,72. Water with a large amount of bicarbonate may increase citrate excretion 70 and magnesium content may favourably alter citrate and magnesium excretion 73. Based on these findings, there is still no definite evidence that hard water, rich in calcium and magnesium, is more lithogenic than soft water.

The presence or absence of certain trace elements in water has been implicated in the formation of urinary calculi. For example, zinc is an inhibitor of calcium crystallization 74. Low urinary levels of zinc, therefore, may increase the tendency toward stone formation. Yet, someone reported that thiazide treatment decreased stone recurrences in their patients, even though urinary zinc concentrations declined in most of them 75.

A very recent epidemiological study based on food-frequency questionnaires has examined the effects of particular beverages on risk of symptomatic kidney stones in women 76. Consumption of tea, caffeinated and decaffeinated coffee was associated with a reduction of risk of 8 to 10% , while wine decreased the risk by 59%. Conversely, grapefruit juice ingestion was associated with a 44% increased risk for stone formation. The authors speculated that the protective effects of coffee, tea and wine were caused by urinary dilution, determined by the ability of caffeine and alcohol to inhibit antidiuretic hormone. Therefore, the decreased risk for decaffeinated coffee might have been conferred by another mechanism. The adverse effects of grapefruit juice remained unexplained, since other citrus juices, like orange and lemon, may prevent 77,78 and not stimulate stone formation due to their high citrate content. In summary, these results must still be interpreted with caution until adequate long-term randomised trials of dietary interventions are performed.


The association between dietary factors and stone formation was first evidenced by the "stone boom", i.e., the dramatic increase in stone disease incidence in Western industrialised nations, after World War II compared to the period during the war when malnutrition was the rule. The "stone clinic effect", a phenomenon described by the Mayo Clinic years ago to explain the reduction of stone recurrence in two third of the patients after basic dietary advice, further reinforced the importance of such association 79.

Dietary intake of various foods and fluids that result in greater urinary excretion of substances that produce stones has a significant effect on incidence of urinary calculi. Ingestion of excessive amounts of purines 80, oxalates 62, calcium, phosphate, sodium, and other elements often results in excessive excretion of these components in urine. High protein intake of animal origin increases acid, calcium, phosphate, oxalate, and uric acid excretion and decreases the citrate excretion 81,82. On the other hand, ingestion of deficient amounts of calcium and potassium has also been noticed increase the occurrence of urolithiasis 83.

Lonsdale pointed out that patients who form stones might have exceptional dietary patterns 49. Dietary excesses may also occur, such as the use of large amounts of Worcestershire sauce with its high oxalate content 84 and the habitual excessive ingestion of milk products in the form of cheese or ice cream; a vegetarian diet may be associated with childhood urolithiasis. In contrast, in a study of more than 45,000 men, was found that the prevalence of stone disease was lowest in patients on a high-calcium diet 85. However, high calcium intake alone, without concomitant changes in the diet (unaltered urinary oxalate because of greater amounts of ingested fluid, potassium and phosphate) poses a modest risk for calcium stone formation 86. In a study from Brazil, hypercalciuric stone formers ingested a diet that was higher in sodium and lower in potassium than age-matched control 87. Epidemiologic studies have demonstrated an increased incidence of kidney stones in individuals with low calcium intake. More recently, a 5-year clinical study found the recurrence of kidney stones was higher in stone-formers on a low dietary calcium treatment 88.

A slight but significant increase of about 20% on oxalate excretion after a 2-fold increase in oxalate intake was observed. However, such an increase was no longer observed when an amount of calcium (430 mg) had been concomitantly ingested. Marshall et al 89 have studied the effects of either oxalate or calcium restriction alone, as well as double restriction in stone forming patients and controls. In patients, oxalate restriction almost did not alter calcium excretion and produced only a very mild decrease in urinary oxalate. CaOx activity was not altered that much. On the other hand, a severe calcium restriction (down to 250 mg/d) caused an important elevation of urinary oxalate only when the supply of dietary oxalate was normal. The combined restriction of calcium and oxalate was the only way to prevent such oxalate elevation, leading to an effective decrease of CaOx product activity far below the formation product 89.

Bataille evaluated the probability of stone formation after a combined restriction of calcium and oxalate, and observed that the combined restriction was not able to decrease the probability of stone formation in dietary-independent hypercalciuria patients, inasmuch as a concomitant increase in oxalate excretion was still evidenced in these patients 90. In summary, the idea that calcium and oxalate must be maintained in balance during meals is unquestionable, but more long-term controlled studies are still needed to answer to the question as to whether double or no restriction should be recommended. In addition, oxalate excretion also depends on oxalate degradation by anaerobic bacteria in the gastrointestinal tract. The absence of this bacterium from the gut increases the risk for hyperoxaluria 91.

An epidemiological study has reported that the lower the potassium intake, below 74 mEq/d, the higher the relative risk for stone formation 85. Such an effect can be ascribed to an increase in urinary calcium and a decrease in urinary citrate induced by a low potassium intake 92. As was commented before, a low-normal potassium intake and a higher NaCl intake were observed in stone formers when compared to healthy subjects. The overall effect was a significantly higher urine Na/K ratio 87, increasing the risk for stone formation, as previously suggested by Cirillo et al 93.

The effect of sodium chloride (NaCl) intake on increasing calcium excretion is well established. Every 100 mmol increase in dietary sodium results in a 25 mg rise in urinary calcium 94. The adverse effects of a high NaCl intake and the resultant higher calcium excretion have been extensively reported by many investigators 95,96,97. A high NaCl intake is expected to lower citrate excretion as well 98.

Not only the diet, but also its source, may be important. Identical vegetables grown in various parts of Thailand contain amounts of oxalate that differ by 50% or more 99. A careful dietary history is critical to the evaluation of every individual who forms stones.

The types of stones formed depend mainly on the composition of urine, which, in turn, reflects the type of diet consumed in the countries concerned.


It has been indicated that urinary calculi are much more likely to be found in individuals who have sedentary occupations 49. Blacklock reported that the incidence of urinary calculi was higher in administrative and sedentary personnel of the royal Navy than in manual workers 32. The highest incidences were found in cooks and engineering room personnel.

Other study has confirmed that professional and managerial groups had an incidence that was much higher than expected and manual workers had a much lower than expected frequency of urinary calculi 52. Whitson and colleagues examined physiologic changes of metabolic and environmental origin in astronauts spending time in the microgravity environment of space 100. The risk of calcium oxalate and uric acid stone formation increases after a space flight because of hypercalciuria, hypocitraturia, decreased pH, and lower urine volumes.

Robertson and colleagues performed extensive studies of the relationships among occupation, social class, and risk of stone formation 101. They confirmed that the risk of formation of calcareous urinary calculi was increased in the most affluent countries, regions, societies, and individuals. The inhabitants of such countries have more disposable income to spend on animal protein, which leads to increased urinary concentrations of calcium, oxalate, and uric acid. In fact, these investigators have suggested that recurrent calcium oxalate stone formers should become vegetarians 102. It becomes difficult to assess whether occupation is a primary factor in stone disease or whether it merely establishes other aspects of environment, such as diet, heat exposure, and water drinking. Alterations in these factors may be the actual instigators of urolithiasis.

Medications – Drugs

The effect of large doses of vitamin C in increasing urinary oxalate excretion is controversial 103,104 and is eventually accounted for by the conversion of vitamin C to oxalate during the analytical procedure 104. In a large epidemiological study, the intake of vitamin C was not associated with risk of kidney stones in women 105. Some others drugs have been related with the kidney stone.

Stress and Kidney Stones

Although it is intuitively apparent that kidney stones can cause stress, it is not widely known that stressful life events can be associated with kidney stones. A case-control study of 200 symptomatic stone patients and 200 controls tested this hypothesis 106. In this study, lower family income, mortgage problems, and emotional life events were significantly associated with stone disease.

Clinical aspects

A urinary calculus usually presents with an acute episode of renal or ureteral colic as the result of a stone obstructing the urinary tract. There are five locations where stones can be impacted in the urinary tract. Most impacted ureteral stones are found in the pelvic portion of the ureter.

Renal or ureteric colic is a symptom complex that is characteristic for the presence of obstructing urinary tract calculi. A typical episode occurs during the night or early morning hours, is abrupt in onset, and usually affects the patient while sedentary or at rest. A partially obstructing, continuously moving calculus appears to create the greatest amount of colic.

Some time urolithiasis is asymptomatic. Glowacki and associates evaluated the natural history of asymptomatic urolithiasis in 107 patients who were identified by radiographic or ultrasonographic techniques as having renal stones. In each patient, the stone was asymptomatic for at least 6 months after identification. Over a 32-month follow-up, 68% of the patients continued to be asymptomatic. Of the 32% who developed symptoms, half passed the stone spontaneously, whereas half required urologic procedures. The cumulative 5-year probability of a symptomatic event was close to 50% and correlated with the number of previous stones as well as the number of stones at identification.

Urinalysis in most patients with urinary lithiasis reveals the presence of microscopic or gross hematuria. In some instances, gross hematuria may be the only presenting complaint. Moderate pyuria may occur even in patients with uninfected urinary lithiasis.

On occasion, a patient who is in an active phase of urinary lithiasis has urine crystals of the same type that are creating the calculus. The observation of cystine, uric acid, or struvite crystals in the urine may be an indication of the type of calculus ultimately found.

Morbidity and comorbidity

The recurrence rate without treatment for calcium oxalate renal stones is about 10% at 1 year, 35% at 5 years, and 50% at 10 years 107. Others also report that the recurrence rate is high, reaching 52% within 10 years and 75% within 20 years, respectively 5.

The urinary tract infection (UTI) and urolithiasis are very close related. The UTI can be a cause of urolithiasis, as frequently happens in women, or the consequence of it.

An Italian epidemiological study found relation of the urolithiasis and arterial hypertension but not with diabetes mellitus 6 compared to the general population.

As it has commented above, a significant proportion of patients required extensive surgical procedures until 1980s in developed countries; however, this figures still in developing ones. Fortunately, a sizeable minority loses a kidney. The renal function may be affected and mild to moderate chronic renal failure is expected to develop in up to 20% of the patients 108. One study showed that about 20% of patients with recurrent stone disease who underwent surgery for obstruction and infection went on to develop mild renal insufficiency 1.

There is reference from a study in general populations that 44% of patients with renal lithiasis were admitted in hospitals 109.


The mortality secondary to urolithiasis is low in general. It has improved on the last years. In Italy, there were only 100 deaths related to nephrolithiasis per year in 1998 6.

Social and economical impact.

Kidney stones are not usually quiescent, typically causing patients considerable pain and suffering. The social and economical impact is represented by its sequelae of renal colic, loss of work, need of medical care, hospitalization and urological intervention. In addition, cost for the diagnosis and treatment of kidney stones is not trivial, resulting in a substantial financial burden.

In 1993, urolithiasis cost the American economy $1.7 billion, including indirect costs from loss of productivity. The higher incidence of urolithiasis is between 30 to 50 years old when is the higher productivity of any person 110.

In a United States financial study made at the Chicago University was calculated that the cost for diagnosis and treatment of patients with recurrent kidney stone disease have been around $4,453,000/1000 patients year. It took into account the cost of stone event, procedures (cystoscopies, ESWL and surgery) and hospitalization 111.

Coe and Parks reported that 20% to 40% of patients with stone attacks may need hospital admission 112. Twenty two percent of these patients could require surgical procedures 113.

In Italy, the number of patients with nephrolithiasis treated by the National Health Service had greatly increased: from 1988 to 1993. The number of patients admitted to the hospitals increased from 60 000 to 80 000 per year; 14% of the hospitalised patients (about 12 000 per year) had also undergone surgery, and the number of ESWL treatment had been estimated to be 50 000 per year. Based in this information the cost of hospitalisation and surgery could be estimated at 300 billion Italian lire per year in that moment 6.


An epidemiological study in rural and urban general population was made to know the frequency, the potential risk factors, morbidity, and social and economical impact of urolithiasis in our tropical country, Cuba.


A representative sample of 1,504 and 1,400 subjects were randomly selected from the general population of 15,591 inhabitants in the rural area and 19,538 inhabitants in the urban area using the two-stage and equal probability functions with 95% CI. Both populations are in the west of Cuba.

After informed consent was obtained, a survey was conducted to identify the subjects in the sample that had developed urolithiasis at some time or another. The surveys were made for the same general practitioner in each area. All subjects with a history of urolithiasis were included in a second survey to obtain the data required to complete the study. This survey was made for the same nephrologist.


From the 2904 selected subjects for the study were found 103 with history of urolithiasis, 65 in the urban area and 38 in the rural. The prevalence of urolithiasis for the taken sample and inferred for the general population is in Table I.

Table I. Prevalence of urolithiasis according studied population.

Type of Population





White Colour

Black-Brown Colour




3.46 e




2.53 a

3.2 b

1.8 c

3.2 c

1.5 c,e




2.7 d


2.72 e

Significant difference between urban and rural population: a = p<0.005, b = p<0.01, c = p<0.05.
Significant difference between gender and colour of skin: d = p<0.01, e = p<0.05.

As can be observed the global prevalence and the prevalence according gender and colour of skin were higher in the urban population. We did not find prevalence of urolithiasis in any population for individuals lower than 15 years old.

The retrospective incidence for period of 5 years changed between the last 35 years and the time before in the urban area (Table II). In the former changed between 0.07 and 0.79% with a media of 0.56% in contrast to 0.12% in the previous period of time (Table II).

Table II. Incidence of urolithiasis

Periods (years)

No. of cases


1930 - 34



1935 - 39



1940 - 44



1945 - 49



1950 - 54



1955 – 59






1960 - 64



1965 - 69



1970 - 74



1975 - 79



1980 - 84



1985 - 89



1990 - 94






The most frequent age of the first stone events was between 20 and 29 years for both areas following the group of 30-39 years (Figure 1)

Figure 1. Age at first stone event for population.

The most frequent family and personal history of urolithiasis and other diseases are shown in the Table III.

Table III. Prevalence of urolithiasis and other diseases according populations.



of Population

Prevalence of diseases (%)

Kidney Stone

UTI (Study)


Ischaemic Card




















































Significant difference between prevalence in the study and in general populations: a = p<0.0001
Symbols: UTI=Urinary Tract Infection, AHT=Arterial Hypertension, Ischaemic Card.=Ischaemic Cardiopathy, DM=Diabetes Mellitus.

There were not significant differences between both population and gender in relation to family history of urolithiasis (36.1% in male and 44.8% in women in urban area vs. 34.8% in male and 40% in women in rural area). While there were differences between the prevalence of personal history of some diseases (arterial hypertension, ischaemic cardiopathy and diabetes mellitus) in the patients of the study and in the general population (p<0.0001).

53.8% of subjects related the warmer weather with the stone events in the urban population and a 47.3% in the rural one. 35.4% did not referred any relation or could not precise it in the urban area and 44.7% in the rural (p>0.05).

The long-term use of medication among individuals that suffered urolithiasis was poor in both populations.

High intake of foods rich in oxalic acid was referred by 84.5% of subjects, 68% declared to have high consumption of carbohydrates, 61.2% of proteins-purines and 55.3% of milky. However, there were not differences in the intake of some groups of foods between the urban and the rural population as can be observed in the Table IV. Several of these habits were present in the same subjects.

Table IV. General dietetic habits referred from subjects with urolithiasis according population.

Group of


Subjects with history of urolithiasis

Urban Population (%)

Rural Population (%)

Global Population (%)

High intake of oxalic acid

52 (80.0)

35 (92.1)

87 (84.5)

High intake of carbohydrates

35 (53.8)

35 (92.1) a

70 (68.0)

High intake of proteins - purines

32 (49.2)

31 (81.6) b

63 (61.2)

High intake of


31 (47.7)

26 (68.4) c

57 (55.3)

Low intake of


37 (56.9)

16 (42.1)

53 (51.1)

High intake of


15 (23.1)

10 (26.3)

25 (24.3)

Significant difference between urban and rural population: a = p<0.0001, b = p<0.002, c = p<0.05.

Half of patients had frequent large sweeties in the urban area while only 23.7% of them had it in the rural population (p<0.02). 61.5% of subjects with urolithiasis developed moderate to intense physical activity in the urban population and only 34.2% of them in the rural area (p<0.01). The occupations of patients from both populations were very variable. The physical activities developed during the occupations were poor in the 50.8% and 65.8% of individuals with urolithiasis in the urban and rural population respectively (p>0.05).

14.6% of subjects with history of urolithiasis suffered one episode of renal or ureteral colic, 29.1% had 2 to 5 episodes, 45.6% suffered more than 5 episodes and only 10.7% did not had pain.

The recurrence of the urolithiasis was present in the 46.6% of the stone formers. 33.8% of these subjects from the urban population had recurrence and 68.4% from the rural area suffered it (p<0.001). 41.7% of all these individuals had one recurrence and 58.3% had more than one (Table V)

Table V. Number of recurrence in the stone formers according population.

Number of


Type of Population

Urban (%)

Rural (%)

Global (%)


10 (45.5)

10 (38.5)

20 (41.7)


3 (13.6)

4 (15.4)

7 (14.6)


4 (18.2)

5 (19.2)

9 (18.7)


3 (13.6)

3 (11.5)

6 (12.5)


2 (9.1)

4 (15.4)

6 (12.5)


22 (100)

26 (100)

48 (100)

Significant difference between both populations: (p>0.05).

The average time between the first stone and the first recurrence was 8.2 years in the urban population and 10.2 years in the rural.

The methods most used for diagnosis of kidney stone in the global population were the clinic and the conventional radiographic (49.5%)(Table VI). In general, the use images was more frequent in the urban population (75%) than in the rural area (53%)(p<0.02).

Table VI. Methods used for diagnosis of urolithiasis according populations.



Type of Population

Urban (%)

Rural (%)

Global (%)

Clinic - X ray

38 (58.5)

13 (34.2) a

51 (49.5)


16 (24.6)

18 (47.4) a

34 (33)

Clinic- Xray - US

7 (10.8)

3 (7.9)

10 (9.7)

Clinic - US

4 (6.1)

4 (10.5)

8 (7.8)


65 (100)

38 (100)

103 (100)

Significant difference between urban an rural population: a = p<0.02.
Symbols: Clinic = expulsion of stone, Clinic – X ray = Clinic and conventional radiographic, Clinic - US = Clinic and ultrasonographic, Clinic – X ray - US = Clinic- radiographic- ultrasonographic

The procedures used for treatment of the subjects with history of urolithiasis included 27.25 of them.

A 27.2% of the subjects with history of urolithiasis needed some procedures for their treatment. The surgery was the most used (17.5%)(Table VII). The individuals from the urban area (33.8%) needed more these procedures than those from the rural area (15.7%)(p<0.05).

Table VII. Procedures used in the treatment of patients according populations



Type of Population

Urban (%)

Rural (%)

Global (%)


14 (21.5)

4 (10.5)

18 (17.5)


5 (7.7)

1 (2.6)

6 (5.8)


3 (4.6)

1 (2.6)

4 (3.9)


43 (66.2)

32 (84.3)a

75 (72.8)


65 (100)

38 (100)

103 (100)

Significant difference between urban y rural population: a = p<0.05

40% and 42.1% of the stone formers from the urban and the rural population were admitted in one or more than one occasions with the average of 1.5 and 2.8 time/patients respectively. The average hospital stays for subjects with urolithiasis from the urban area were 36.6% and for subjects from rural area was 26.6%. 40% and 42.1% of the stone formers from the urban and rural population had a prescription of resting for 39 and 35.3 days respectively.


Kidney stone is a frequent disease with high morbidity and social and economical impact all over the world.

Its causes and risk factors are multiples. The relations of intrinsic or genetic and the extrinsic or environmental risk factors are essential on its genesis. Although the knowledge is growing up about the first, looks that the last determines more its increase frequency in the world.

The studies have demonstrated that geographical, climatic and seasonal factors have a roll in the lithogenesis due to kidney stones are more frequent in subtropical than in cool regions of different countries. In tropical countries all these risk factors are more adverse and have also been reported high frequency of renal lithiasis.

The majority or may be all tropical countries are developing countries. When the social and economical conditions of any of these improve it have been confirmed that the frequency of kidney stone increase.

Thus tropical areas influence the frequency and the impact of the urinary calculi but it represents an aspect of the environmental factors superimposed on the intrinsic factors.


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