The cause of crystal growth in the kidneys is urinary supersaturation. Supersaturation is unquestionably necessary for stone synthesis since it’s important for the initiation of the development of crystalline particles [25].

When a supersaturated solution changes from a state of fluid to a solid phase, the process is referred to as nucleation [26].

After the crystal’s nucleus approaches an appropriate dimension and comparative excessive saturation has passed, adding more crystal components causes the total free energy to decrease [27].

When minerals in the resolution work together to produce bigger particles, the process is termed agglomeration. According to several studies, crystal gathering is the critical stage in the production of stones. Although crystal development is undoubtedly a phase in the creation of CaOx renal stone, crystals develop at a sluggish rate.

Urine production should be at least 1/2 day; therefore, intake of fluids should be enough. Patients with moderate-to-severe stone disease should be the only ones who take medications. There is the various pharmacological treatments for kidney stones.

According to research, those who consume less than 1.5 L of fluids per day have a 50% higher chance of acquiring kidney stones than those who consume more than 2.5 L.

Two studies, one observational and one interventional, suggest that drinking plenty of water helps prevent kidney disease and lessen recurrence [71]. After a 5-year follow-up, the subsequent recurrence rate decreased by 27% reduced 12% and daily water intake rose from 1 to 2 L.

Although water is essential for avoiding nephrolithiasis, it is unknown if hard water with high divalent ion levels contains the same anti-lithogenic properties as fresh water and leaves little dry residue. Consider trace elements, including calcium, sodium, potassium, chloride, magnesium, iron, fluorine, iodine, zinc, among selenium when determining how much water you consume [72]. However, adopting oligomineral, low NaCl (sodium chloride) water appears to be a viable solution.

Drinks that boost pH, Citric acid along with volume, which includes freshly squeezed oranges with lemons, juices, green tea, and wine, can be a good substitute for water.

Beer prevents calcium stone disease but raises the hazard of urate stone disease due to its high purine-guanosine satisfied [73]. Cranberry juice may not prevent calcium nephrolithiasis, but it can help cure infected stones.

Tea and coffee enhance oxalate levels; however, adding milk can decrease this effect because calcium binds to oxalate and limits absorption. Some drinks, including grapefruit and apple juice, as well as cola, may stimulate lithogenesis through an unknown mechanism [74].

Low amount of urine, resulting from inadequate one of the most significant risk factors underlying kidney stone formation is excessive fluid consumption as well as loss. Many pharmacological and pathophysiological disorders can cause dehydration, which alters water requirements [75]. These causes include excessive perspiration as a result of temperature exposure, mental stress, and intense workout levels, and profession, as well as persistent diarrhoea as a result of fat malabsorption caused by various gastrointestinal illnesses.

An investigation of 100 steel manufacturing employees discovered that 16% exhibited a history of stone disease, and more exceeding half had urine osmolality levels more than 700 mOsm, suggesting dehydration. Health care workers who have limited access to potable water are furthermore at a higher risk of acquiring stones. A survey of workers revealed that physicians who worked in an operating theatre had the highest occurrence of nephrolithiasis (17.4% compared 9.7%), as well as higher stress levels, in addition to lower fluid consumption compared to workers working elsewhere [76]. Other occupations that can contribute to urolithiasis include professional drivers, aeroplane pilots, and schoolteachers.

The effect of tap versus mineral water concentrations on kidney stone formation is still debated. The composition of drinking water, notably the percentage of divalent cations including magnesium and calcium, varies substantially among geographic regions within the same country.

Hard tap water with a calcium carbonate level of more than 120 mg/L can contribute to the daily consumption of calcium. A study of 2295 individuals from two sites in the United States found that those who consume water from the faucet from a private well are more likely to acquire urinary stones. However, the cause of the higher risk among individual well users remains unknown. Numerous cohort studies demonstrated no relationship between the level of hardness of public water supply and urinary disease associated with stones [77].

Bicarbonate, like calcium, magnesium, and other ions, is a reasonable component of inorganic water, as opposed to tap water. Bicarbonate enhances the body’s buffering capacity and acts as a powerful alkalising agent. Water from minerals rich in bicarbonate might aid in alkalinisation treatment and contribute to urinary inhibitory potential by raising urinary pH affects citrate excretion. Another randomised crossover trial with healthy participants looked at how an equimolar acidic load, either a form of bicarbonate-rich mineral water or potassium citrate, affected the urinary risk profile towards calcium oxalate as well as uric acid stone development.

Consuming 2 L/day of mineral-enriched water with 1715 mg/L bicarbonate, either 2.55 g/day potassium citrate significantly increased urinary pH along with citrate excretion while decreased oxalate excretion [78].

Both categories had a significant reduction in the relative overabundance of calcium oxalate as well as uric acid. A study of healthy persons conducted under controlled dietary conditions discovered that consuming mineral water rich in bicarbonate, calcium, plus magnesium increased urine pH as well as the excretion of citrate and magnesium, which are urinary inhibitors against calcium oxalate stone formation. Calcium excretion rose considerably, although the corresponding supersaturation associated with calcium oxalate remained the same [79].

The impact of fruit juices on metabolism is largely influenced by their alkali citrate content. When consumed, dietary citrate is absorbed in the digestive system and transformed into bicarbonate, which can raise both urine pH and the amount of citrate excreted. Citrus juices like lemon, orange, and grapefruit are rich sources of citric acid and can serve as natural alternatives to medicinal alkalizing agents [80]. Among these, orange juice is one of the most commonly consumed worldwide. However, studies on how orange juice affects urine factors linked to kidney stone formation have shown mixed results.

Some large-scale cohort studies suggest that regularly drinking orange juice may lower the risk of developing kidney stones. Controlled trials under specific dietary conditions have shown that orange juice provides an alkaline effect, leading to higher urine pH and citrate output. Still, despite this alkalizing benefit, most studies found that orange juice did not significantly reduce the risk of forming calcium oxalate stones [81]. Although orange juice has a low oxalate content, two out of three studies reported a noticeable rise in urinary oxalate levels, possibly due to the conversion of vitamin C (ascorbic acid) into oxalate inside the body.

Because of concerns about the high sugar and calorie content of orange juice and its low fiber, health experts often recommend eating whole fruits instead. It’s advised to limit fruit juice to one serving a day and to dilute it with water when consumed [82]. In a small crossover trial involving 10 healthy individuals on a regular diet, researchers compared Crystal Light lemonade with two reduced-calorie orange juice drinks. They found that only the Kroger brand low-calorie orange juice had a notable effect, though changes in citrate levels, an important factor in preventing calcium oxalate stones, were not significantly different between the beverages [83].

Additionally, potential health risks from excessive juice consumption and concerns about additives like artificial colors, preservatives, sweeteners, and ingredients such as added ascorbic acid and calcium limit the suitability of these drinks for individuals prone to kidney stones.

In a large randomized controlled trial involving individuals who regularly consumed soft drinks (at least 160 mL per day), male participants were randomly assigned to either stop drinking soft drinks or continue their usual intake as part of the control group. The results showed that soft drink consumption, especially beverages containing phosphoric acid, was associated with a higher risk of repeated kidney stone formation [84].

Further evidence from large-scale studies, including the Health Professionals Follow-Up Study (HPFS) and Nurses’ Health Studies (NHS I and II), which tracked 194,095 participants over more than eight years, also found a strong link between the intake of sugar-sweetened cola and non-cola soft drinks and an increased risk of kidney stones.

Additionally, a cross-sectional analysis based on the Third National Health and Nutrition Examination Survey (NHANES-III) showed that people who consumed more sugar-sweetened soft drinks had higher levels of uric acid in their blood and were more likely to suffer from hyperuricemia. Long-term cohort studies have further supported this association, identifying a clear connection between sugary soft drink intake and a higher risk of developing gout, particularly in men [85].

One possible explanation for these findings is the high fructose content in sugary soft drinks. Fructose has been shown to raise the risk of kidney stone formation, likely due to its impact on uric acid metabolism and urinary composition.

Tea and coffee rank among the most commonly consumed beverages worldwide. According to comprehensive reviews and large population-based studies, regular consumption of tea and coffee may help reduce the risk of kidney stone formation. This protective effect is thought to be largely due to caffeine’s mild diuretic action, which may help offset the calcium loss in urine (hypercalciuria) often linked with stone development [86].

The European Food Safety Authority (EFSA) has deemed a daily caffeine intake of up to 400 mg, roughly the amount in four cups of brewed coffee, as safe for healthy adults, except pregnant women. In addition to caffeine’s diuretic effect, tea might offer further protective benefits by increasing overall fluid consumption and through the antioxidant activity of its natural compounds, such as polyphenols.

However, many of the cohort studies did not distinguish between different types of tea and coffee, such as black, green, herbal, or fruit tea, which limits the precision of their findings. Another concern is the oxalate content present in these beverages. While coffee contains relatively low levels of oxalate, black and green teas vary significantly in oxalate concentration, depending on factors like plant type, harvest timing, and processing methods [87]. Among the teas, black and green varieties tend to have the highest oxalate levels, whereas herbal and fruit teas are typically much lower.

Because of these variations, the exact role and mechanism by which black and green tea may help prevent kidney stones remain unclear and warrant further investigation.

When daily calcium intake increases from 400 mg to 1200 mg, urinary calcium excretion also rises from 120 mg to 180 mg in healthy individuals, and from 240 mg to 400 mg in those with hypercalciuria. Traditionally, people prone to kidney stones have been advised to reduce their intake of milk and dairy products [88]. However, current research does not support this recommendation for several reasons:

1. Cutting down on calcium reduces its binding with oxalate in the gut, which leads to greater oxalate absorption and a higher risk of stone formation.

2. Avoiding dairy may lead patients to increase their consumption of animal protein (such as meat, fish, and poultry), which can negatively affect kidney stone risk.

Studies suggest that consuming around 1000 mg of calcium per day can lower the risk of kidney stones by about 30% compared to those who take in less than 600 mg daily. A five-year randomized clinical trial involving male patients with high urinary calcium showed that a diet with normal calcium intake but reduced salt and animal protein was more effective in preventing stone recurrence than a low-calcium diet [89].

The calcium-excreting effect of table salt is believed to come from its sodium and chloride content, which may impair calcium reabsorption in the kidneys. This, along with the acid load from proteins, can increase the risk of stone formation. Moreover, excess acid and potassium deficiency may reduce urinary citrate levels, a natural inhibitor of kidney stone formation, thereby contributing further to the risk of stone development [90].

Citrate plays a key role in preventing the formation of calcium oxalate kidney stones by binding to free calcium ions in the urine. This reduces the saturation of calcium oxalate and prevents crystal formation. A condition known as hypocitraturia or low urinary citrate is commonly observed in people with calcium kidney stones, affecting approximately 19% to 63% of such individuals [91]. As a result, measuring urinary citrate has become a standard part of the metabolic evaluation in stone-forming patients. In many cases, hypocitraturia can be corrected through oral alkali therapy, even though not all tissues respond uniformly to alkali loading.

The most frequent cause of low urinary citrate is metabolic acidosis, which alters how citrate is processed in the kidneys. Under acidic conditions, more citrate converts to its divalent form in the proximal tubules, where it is readily reabsorbed through the Sodium-dependent dicarboxylate transporter 1 (NADC-1) transporter, a protein also found in the small intestine and colon [92]. Research has linked NADC-1 deficiency to an increased risk of kidney stone formation in both human and animal studies. Acidic body conditions tend to lower urinary citrate levels.

A diet low in fruits and vegetables can contribute to hypocitraturia because these foods supply dietary alkali. Their absence leads to a more acidic internal environment, which encourages the kidneys to reabsorb more citrate rather than excrete it. Including more fruits and vegetables in the diet helps increase citrate levels in the urine by lowering hydrogen ion (H⁺) concentration, raising urinary pH, and reducing citrate reabsorption.

For individuals with low citrate levels, a diet rich in fruits and vegetables is recommended. Such a diet not only boosts urinary volume and citrate levels but also provides beneficial alkaline minerals like potassium and magnesium. This dietary approach typically involves reducing animal protein and salt intake as well [93]. Adherence to a DASH (Dietary Approaches to Stop Hypertension) diet significantly increased urinary output, even without increased fluid intake. The high water content and alkaline nature of fruits and vegetables likely account for the observed rise in urine citrate and volume. Multiple studies suggest that the stone-preventing effects of vegetables are due to these beneficial metabolic changes.

For adults, the recommended protein intake is about 0.8 to 1.0 grams per kilogram of ideal body weight per day. Consuming excessive protein has been linked to changes in urine composition that may raise the risk of kidney stone formation. A high-protein diet increases the body’s acid load, which can lead to higher urinary calcium levels, lower urine pH, and reduced citrate excretion, all of which are known risk factors for stone development [94].

In one study involving 18 patients with hypercalciuria and kidney stones, reducing protein intake to 0.8 g/kg of body weight per day resulted in lower urinary calcium and uric acid levels, along with an increase in urinary citrate excretion. However, systematic reviews have provided mixed results regarding the link between dietary protein and stone risk. For example, a review by Pedersen included two large cohort studies that found no significant association between protein intake and kidney stone development. On the other hand, one well-designed study did report that higher protein intake was associated with increased urinary calcium levels, which could promote calcium stone formation [95].

In healthy individuals, supplementation with 1.5 grams of L-methionine daily had no effect on calcium excretion, but increasing the dose to 3 grams per day resulted in a calcium excretion increase of about 1 mmol per day. So far, no randomized controlled trial has directly compared high versus low protein intake in relation to kidney stone formation risk.

Although the precise relationship between protein consumption and stone risk remains uncertain, large observational studies have shown that a higher dietary acid load, primarily from protein-rich foods, is linked with increased risk of stone formation [96]. Importantly, the balance of protein with alkaline foods like fruits and vegetables may be more predictive of stone risk than protein alone. These plant-based foods help neutralize the acid load from proteins and support higher urine pH and citrate excretion.

In patients with low urinary citrate, adding more fruits and vegetables to the diet has been shown to raise urinary pH, boost citrate levels, and reduce the relative supersaturation of both calcium oxalate and uric acid. Since a highly acidic diet lowers both urinary pH and citrate two important defenses against stone formation, maintaining a diet rich in alkalizing foods is beneficial [97]. Higher urine pH not only promotes the excretion of stone-inhibiting citrate but also enhances calcium binding in the urine, thereby lowering the risk of crystal formation.

Research exploring the relationship between carbohydrate intake and kidney stone risk has produced mixed findings. Some studies reported that individuals with kidney stones consumed similar amounts of carbohydrates as healthy controls, while others observed higher carbohydrate intake among stone formers. A major limitation of these studies is their failure to differentiate between types of carbohydrates, especially the common disaccharide sucrose and its components, glucose and fructose [98].

Prospective cohort studies have shown that higher sucrose intake is associated with an increased risk of kidney stone formation in women, though no such link was observed in men. Earlier research revealed that consuming 100 grams of glucose or sucrose increased urinary calcium excretion in both healthy individuals and calcium oxalate stone formers with the latter group showing a more pronounced effect. This rise in urinary calcium was believed to result from enhanced calcium absorption in the intestines and reduced reabsorption in the kidney tubules following a glucose load [99].

It has been suggested that this effect may be partly driven by elevated insulin levels in response to sugar intake. However, a controlled study involving calcium stone patients with idiopathic hypercalciuria and healthy participants on a fixed diet found that high insulin levels (hyperinsulinemia) are unlikely to play a major role in the stone formation process in these patients.

Fructose consumption has increased significantly in recent decades due to its widespread use as a sweetener in processed foods and beverages, often replacing glucose or sucrose [100]. A systematic review and meta-analysis found a positive association between fructose intake and kidney stone risk, although the exact biological mechanisms remain unclear. Fructose may contribute to stone formation by influencing the urinary excretion of calcium, oxalate, and uric acid, altering urine pH, and affecting uric acid metabolism.

Furthermore, a cohort study involving male participants linked higher fructose intake to an increased risk of developing gout, a condition closely tied to elevated uric acid levels [101]. To fully understand how sugars like sucrose, glucose, and fructose affect stone formation, more controlled studies using fixed metabolic diets are needed. Such studies could clarify how these sugars influence urinary chemistry and the risk of forming uric acid or calcium oxalate stones [102].

The connection between dietary fat intake and the risk of developing kidney stones remains unclear and poorly studied. Some research found no significant difference in fat consumption between individuals with kidney stones and healthy controls, while other studies reported higher fat intake among stone formers.

Emerging evidence suggests that the type of fat consumed, particularly the balance between omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFAs), may play a role in calcium oxalate stone formation through complex biological pathways [103]. For instance, individuals with idiopathic calcium oxalate stones have been found to have elevated levels of arachidonic acid (C20:4n-6) in their blood plasma and red blood cell membrane phospholipids compared to healthy people.

Arachidonic acid, stored in cell membrane phospholipids, can be released by phospholipase enzymes and converted into prostaglandin E2 (PGE2), a compound linked to increased urinary calcium loss. PGE2 may promote calcium stone formation by enhancing calcium absorption in the intestines, stimulating bone calcium release, and reducing the kidneys’ ability to reabsorb calcium [104]. High levels of arachidonic acid might also contribute to elevated urinary oxalate by enhancing oxalate transport across the intestinal and renal membranes through activation of anion transporters.

In a small study involving 20 healthy participants, supplementation with omega-3 fatty acids, specifically DHA (docosahexaenoic acid, 22:6n-3) and EPA (eicosapentaenoic acid, 20:5n-3) led to their incorporation into cell membrane phospholipids, replacing some of the arachidonic acid content [105]. This dietary shift in fatty acid composition is believed to help reduce the urinary excretion of both calcium and oxalate, potentially lowering the risk of stone formation.

Making changes to the diet is one of the most effective strategies to lower urinary risk factors associated with kidney stone formation, particularly calcium oxalate stones, which are the most common type. However, dietary recommendations should be personalized based on each patient’s specific biochemical and dietary risk profile [106]. Conducting a comprehensive nutritional assessment is an essential part of evaluating patients who form stones and is fundamental to providing effective dietary guidance.

Among the tools available, seven-day dietary records are considered the most reliable for assessing typical eating habits and identifying nutritional patterns linked to stone risk [107]. Multiple dietary factors, such as fluid intake, protein, carbohydrate, oxalate, calcium, and sodium chloride consumption, significantly impact urine composition and influence the likelihood of kidney stone development. Table 7 outlines detailed dietary guidelines tailored for individuals prone to calcium oxalate stones, helping to modify these key dietary elements to reduce stone recurrence and improve overall urinary health [108, 109, 110].

Green tea (Camellia sinensis) has been widely used as a traditional remedy due to its rich content of polyphenols, which give it strong antioxidant properties. Although green tea naturally contains oxalates and may not be ideal for individuals prone to calcium oxalate kidney stones, it has still attracted considerable interest as a dietary supplement for those with kidney stone issues. This is because of its potential anti-stone (antilithogenic), heart-protective (anti-atherosclerotic), and antioxidant effects [116].

Key compounds in green tea, known as catechins such as epigallocatechin gallate (EGCG), epicatechin gallate (ECG), epigallocatechin (EGC), and epicatechin (EC), have been found to guard the kidneys against oxalate damage. Experimental studies in rats showed that green tea intake reduced the supersaturation of brushite (a type of calcium phosphate), lowered the expression of osteopontin (OPN) and superoxide dismutase (SOD), improved the Bcl-2 protein levels, and reduced kidney cell death (apoptosis) [117].

Overall, these findings suggest that green tea, because of its antioxidant components, may help lower the formation of calcium-based kidney stones.

Raspberry (Rubus idaeus), a fruit from the Rosaceae family, is widely cultivated in parts of Europe and the Mediterranean region and has long been valued for its nutritional and medicinal benefits. Recent studies suggest that raspberries may help reduce the risk of kidney stones, even after short-term use [118].

Research has shown that raspberries are particularly effective against calcium oxalate stones the most common type of kidney stone. In animal studies, the aqueous extract of raspberry significantly reduced the buildup and crystallization of calcium oxalate in the kidneys. It also helped break down existing crystal matrices. Rats treated with raspberry extract showed lower levels of harmful markers such as malondialdehyde (MDA) and protein carbonyls, as well as decreased urinary calcium and phosphorus levels [119].

These findings suggest that raspberries may offer protective benefits against kidney stone formation through their antioxidant and crystal-inhibiting effects.

Rubia cordifolia, commonly known as madder or Indian madder, belongs to the Rubiaceae (coffee) family and has traditionally been used as a natural dye in foods. Phytochemical studies of R. cordifolia have shown that it contains several beneficial compounds, such as glycosides, triterpenoids, anthraquinones, saponins, quinones, and tannins. These bioactive components have made the plant useful in managing a wide range of health conditions, including jaundice, diabetic foot ulcers, and cardiovascular problems [120].

In addition to these benefits, R. cordifolia has shown potential in supporting kidney health and preventing the formation of urinary stones. Its extract helps reduce the development and accumulation of calcium oxalate crystals in the kidneys. This effect may be due to its ability to restore magnesium levels, reduce protein loss in urine (proteinuria), and lower uric acid excretion [121]. Its antioxidant properties likely contribute to its overall kidney-protective (nephroprotective) action.

Parsley (Petroselinum crispum), a versatile plant from the Umbelliferae family, is commonly used as an herb, spice, and vegetable across Western Asia, the Mediterranean, and Europe. Research has highlighted its numerous health benefits, including antioxidant, anti-inflammatory, diuretic, kidney-protective (nephroprotective), enzyme-regulating, and blood pressure-lowering effects [122]. These properties are largely attributed to its rich content of bioactive compounds such as flavonoids, carotenoids, coumarins, tocopherol (vitamin E), and ascorbic acid (vitamin C).

Parsley has also been recognized for its potential to help prevent kidney stones. In animal models of calcium oxalate stone formation, parsley extract significantly reduced the formation of calcium oxalate crystals, decreased urine supersaturation, and lowered protein excretion in urine [123]. Its high content of chlorophyll and magnesium is thought to reduce the risk of stone development by preventing oxalate overload and dehydration of crystals. Additionally, parsley helps maintain an optimal urine pH, which keeps calcium oxalate particles dispersed and easier to eliminate from the urinary system.

Pomegranate (Punica granatum) has a long history of use in traditional medicine and is often referred to as “a pharmacy in itself” due to its wide range of therapeutic compounds. The fruit is rich in powerful antioxidants such as polyphenols, anthocyanins, and alkaloids, which help neutralize harmful free radicals [124]. Almost every part of the plant, including its seeds, juice, peel, flowers, and seed oil, has been used for both preventive and therapeutic purposes.

In traditional practices, pomegranate seeds are used to ease urinary discomfort and burning sensations. Its juice and extracts have been employed to protect the kidneys from toxic damage, while the peel and flowers have shown potential in treating kidney dysfunction and supporting renal artery health. One of the most notable benefits of pomegranate is its ability to reduce excessive calcium levels in urine (anti-hypercalciuria) and prevent the formation of kidney stones (anti-urolithiasis), making it a valuable natural agent in the prevention of renal stone formation.

Ammi visnaga has been used for centuries in Egyptian traditional medicine, particularly in the form of herbal teas made from its fruits, to treat kidney stones. Research has shown that an aqueous extract from this plant can help speed up the breakdown of cystine stones.

Two of its primary active compounds, khellin and visnagin, have demonstrated beneficial effects in managing kidney stone formation caused by hyperoxaluria in experimental models. In male rats, these compounds helped reduce the build-up of calcium oxalate crystals, increased the excretion of citrate (a natural inhibitor of stone formation), and lowered the amount of oxalate excreted in urine [125]. These findings highlight Ammi visnaga as a promising natural approach to preventing and treating certain types of kidney stones.

Nigella sativa, commonly known as black seed, has been widely used in Iranian traditional medicine to help treat urinary stones. Scientific studies using ethylene glycol-induced kidney stone models in rats have shown that ethanolic extracts of Nigella sativa seeds significantly reduced the formation of calcium oxalate deposits in both the kidneys and the urine.

The herb’s main active compound, thymoquinone, displayed both preventive (prophylactic) and treatment (therapeutic) properties against kidney stone formation. In animal studies, thymoquinone effectively decreased the size and number of calcium oxalate crystals within the renal tubules, demonstrating its potential as a natural remedy for managing and preventing kidney calculi [126].

Hibiscus sabdariffa, widely recognized in traditional Thai medicine, has long been used for both the treatment and prevention of urinary stones. This medicinal plant is rich in active compounds, including polyphenols, anthocyanins, vitamin C (L-ascorbic acid), quercetin, and protocatechuic acid.

Experimental studies have demonstrated that aqueous extracts of Hibiscus sabdariffa exhibit strong antiurolithiatic effects. In animal models where kidney stones were induced using ethylene glycol, the extract significantly reduced the accumulation of stone-forming substances in the kidneys and blood serum [127]. Additionally, in rats fed a glycolate-enriched diet, the extract helped reduce oxalate retention time in the kidneys and promoted its excretion through urine, showing clear potential in limiting stone formation.

Origanum vulgare, commonly known as oregano, has been traditionally used as a lithotriptic (stone-dissolving agent), diuretic, antispasmodic, and culinary spice. Scientific studies have shown that a crude aqueous-methanolic extract of the aerial parts of this plant can inhibit the formation and clustering of calcium oxalate crystals in laboratory (in vitro) settings, significantly reducing crystal development in calcium oxalate supersaturated solutions [128].

Animal studies using ethylene glycol and ammonium chloride to induce kidney stones demonstrated that this extract exerted a strong antiurolithic effect, likely by preventing crystal growth, protecting kidney cells, and offering antioxidant and antispasmodic properties [129]. These protective actions are believed to stem from the plant’s diverse bioactive compounds, including flavonoids, terpenes, coumarins, saponins, alkaloids, sterols, and tannins.

ESWL is often preferred for treating small stones in the upper urinary tract, especially in children, because it is non-invasive, relatively simple, and effective. In the short term, the stone-free rate ranges from 57% to 97%, and in the long term, between 57% and 92%. ESWL works best for stones less than 20 mm located in the renal pelvis or calyces. Its effectiveness is lower for larger stones or those located in the distal ureters [134].

Possible short-term side effects include blood in urine (haematuria), pain, fever, stone fragments blocking the ureter (steinstrasse), and small internal bleeds (hematomas), although these are generally rare.

The long-term safety of ESWL in children remains unclear. Most studies show no lasting damage to kidney structure or function in children, but these studies are often limited by small participant numbers and short observation periods. Some recent data suggests a potential link to high blood pressure following ESWL, but further research is needed to fully understand this risk [135].

URS is another safe and effective method for treating kidney stones in infants and young patients, particularly for stones ≤20 mm in the mid or lower ureter. A systematic review of over 1700 procedures showed an average stone-free rate of 87.5%, with a 10.5% complication rate, mostly of mild to moderate severity (Clavien Grade I–III) [136].

However, for children under six, URS may require pre-stenting (inserting a tube before the procedure) due to the increased risk of complications or failure in younger patients.

PCNL is typically reserved for large stones, complex cases, blockages due to stones, or when other treatments do not succeed. It is especially useful for patients with high stone burden or persistent kidney infections caused by stones [137].

PCNL has a high success rate (around 90%), but it also carries more significant risks, such as bleeding requiring transfusion, injury to surrounding organs, and infection [138].

To reduce these risks, newer, minimally invasive forms of PCNL have been developed, such as mini-PCNL, ultramini-PCNL, and micro-PCNL. These techniques use smaller instruments, which help lower the chance of complications while still maintaining effective stone removal [139].