Multifaceted Perspectives on Kidney Stone Disease: Pathogenesis, Integrating Diet, Genetics, Management, and Emerging Global Challenges Across the Lifespan

Abstract

Kidney stone disease (KSD), or nephrolithiasis, is a growing global health concern characterized by the formation of crystalline calculi within the urinary tract. This review provides a comprehensive overview of the multifactorial etiology of KSD, encompassing metabolic abnormalities, genetic predisposition, dietary habits, microbial influences, and environmental factors. The pathogenesis involves urinary supersaturation, crystal nucleation, oxidative stress, inflammation, and biofilm formation, with a key role played by Randall’s plaques and immune responses. Genetic polymorphisms in calcium and phosphate transport genes further increase susceptibility. Risk factors such as inadequate hydration, high oxalate intake, and metabolic disorders are explored alongside age- and sex-specific variations. Global warming, occupational heat exposure, and urbanization are also linked to increased stone incidence. Diagnostic advances include low-dose and dual-energy CT, AI-based stone prediction models, and 24-hour urine analysis. Innovations in treatment, such as laser lithotripsy, robotic ureteroscopy, and mHealth tools, are enhancing outcomes. Preventive strategies—centered on dietary modifications, adequate fluid intake, and pharmacological agents like thiazides and citrate—play a pivotal role in reducing recurrence. The disease’s impact on renal function and quality of life emphasizes the need for early intervention and personalized care. This review underscores the importance of multidisciplinary approaches for effective KSD management.

Keywords

Kidney stone disease (KSD), Nephrolithiasis, Urolithiasis, Crystal nucleation and aggregation, Calcium oxalate, Thulium fibre laser

Introduction

Kidney stone disease (KSD), also known as urolithiasis or nephrolithiasis, is a prevalent and recurrent urological disorder characterized by the formation of crystalline calculi within the urinary tract, affecting approximately 12% of the global population during their lifetime ^[1]. With rising incidence in both developed and developing nations, KSD poses a significant public health burden due to its painful manifestations, recurrence tendency, and potential to impair renal function ^[2].  Nearly 80% of kidney stones are comprised of calcium-based salts, with calcium oxalate (CaOx) and calcium phosphate (CaP) representing the predominant mineral constituents. These types of calculi are the most frequently encountered in clinical cases of urolithiasis^[3]. The occurrence and frequency of kidney stones are gradually increasing worldwide, affecting individuals of all ages and ethnicities^[4-5] In recent years, the connection between kidney stones and various systemic diseases—including chronic kidney disease, osteopenia or osteoporosis, high blood pressure, type 2 diabetes mellitus (DM), metabolic syndrome, coronary artery disease, and more recently, ischemic stroke—has led to a shift in both the understanding and clinical approach to the condition.^[6-9] Nephrolithiasis is recognized as a chronic condition, with epidemiological data indicating that, in the absence of therapeutic intervention, the recurrence rate exceeds 50% over a ten-year period.^[10] The pathogenesis of kidney stone formation is multifactorial, involving supersaturation of urine with lithogenic substances, crystal nucleation, aggregation, and retention in the renal tubules ^[11]. Beyond genetic predisposition, multiple extrinsic factors such as dietary habits, fluid intake, and lifestyle changes have a direct influence on stone risk, with inadequate hydration, high oxalate consumption, and excessive animal protein intake being well-documented contributors ^[12]. Recent years have witnessed the emergence of innovative diagnostic modalities and management strategies for KSD, including advanced imaging techniques like dual-energy computed tomography (DECT) and non-invasive stone composition analysis ^[13]. Likewise, minimally invasive surgical technologies and robotic-assisted procedures have revolutionized treatment outcomes, especially in complex and recurrent cases ^[14]. The demographic shift toward an aging population has underscored the importance of understanding the nuances of KSD in elderly individuals, who often present with atypical symptoms and comorbidities that complicate diagnosis and management ^[15]. Additionally, the role of urinary tract infections, particularly those caused by urease-producing organisms, further complicates stone formation and recurrence ^[16]. Differences in stone composition between sexes have been observed. Men more commonly develop calcium oxalate and uric acid stones, whereas women are more prone to struvite stones, often associated with urinary tract infections. This distinction may be due to higher rates of urinary tract infections in women, which can alter urinary pH and promote struvite stone formation.^[17]. Pediatric urolithiasis is another growing concern, with rising cases attributed to changes in dietary patterns, reduced physical activity, and genetic susceptibility ^[18]. Genomic studies have begun to unravel the genetic underpinnings of stone disease, identifying mutations in genes regulating calcium, oxalate, and urate metabolism as key contributors ^[19]. Moreover, the intersection between KSD and climate change is drawing increasing attention, as rising global temperatures are linked to dehydration and heightened stone risk—particularly in tropical and subtropical regions ^[20]  Given the evolving landscape of KSD, this review comprehensively explores the dietary influences, pathogenesis, diagnostics, management, age- and sex-related variations, genetic determinants, environmental factors, and psychosocial impacts associated with this condition. Through this multidisciplinary lens, the article aims to provide a consolidated update on recent advances, existing challenges, and future directions in kidney stone disease research and clinical practice.

2.Pathogenesis of Kidney Stones:

Kidney stones, or nephrolithiasis, are a result of a complex interplay of metabolic, anatomical, dietary, microbial, and genetic factors. The pathogenesis begins with urinary supersaturation, progresses through crystal nucleation, growth, and aggregation, and culminates in inflammation, fibrosis, and recurrence.

2.1.Initiation: Supersaturation and Nucleation:

The initial trigger for stone formation is supersaturation of urine with lithogenic substances such as calcium, oxalate, phosphate, uric acid, and cystine. Supersaturation occurs due to dehydration, high dietary sodium or animal protein, and metabolic syndromes like obesity and diabetes .^[21-22] These conditions alter urine pH, reduce volume, and disturb solute balance, creating an environment conducive to crystal nucleation. Crystallization begins when solutes in urine exceed their solubility, leading to homogeneous nucleation or heterogeneous nucleation ^[23]. Inhibitors like citrate, magnesium, and glycoproteins normally prevent crystal formation and growth, but their deficiency promotes lithogenesis.

2.1.1.Growth, Aggregation, and Retention:

Once crystals are formed, they undergo growth and aggregation, especially in low-flow zones of the nephron. Aggregation is enhanced when crystal inhibitors are reduced and when urinary flow is sluggish. These crystals adhere to renal tubular epithelial cells and basement membranes, often leading to obstruction and injury .^[24]

A hallmark of calcium-based stones is the formation of Randall’s plaques, which are subepithelial calcium phosphate deposits located at the tips of renal papillae. These plaques originate in the basement membranes of the thin limbs of Henle’s loop and extend toward the papillary surface. They serve as anchors for the deposition of calcium oxalate crystals, thereby initiating stone formation .^[25-26]

2.2.Cellular Damage and Molecular Stress Responses

Crystals attached to tubular epithelium cause oxidative stress, releasing reactive oxygen species (ROS) that damage cells and reduce antioxidant capacity. Additionally, endoplasmic reticulum (ER) stress is triggered, marked by increased levels of GRP78 and CHOP proteins. This stress response contributes to cell apoptosis and renal fibrosis, exacerbating stone formation^.[27] Moreover, crystal-induced inflammation creates a self-perpetuating cycle of injury and repair, where damaged epithelial cells attract immune cells, release cytokines, and promote fibrosis, setting the stage for chronic disease.

2.3.Role of Micro-organisms and Biofilms

Certain kidney stones are classified as infection stones, particularly struvite stones, which are composed of magnesium ammonium phosphate. These stones form in the presence of urease-producing bacteria such as Proteus, Klebsiella, and Pseudomonas. These organisms hydrolyze urea, raising urine pH and favoring phosphate precipitation. ^[28] Interestingly, even non-urease-producing bacteria are implicated in calcium-based stone formation through biofilm production. Biofilms create a sticky matrix on the urothelium that promotes crystal adherence and aggregation.

2.4. Immune System Involvement

The immune system is increasingly recognized in stone pathogenesis. Macrophage polarization plays a dual role: pro-inflammatory M1 macrophages worsen tissue injury, while anti-inflammatory M2 macrophages aid in crystal phagocytosis and clearance. ^[28]  The significant role of IL-11 signaling in tubular epithelial cells (TECs) during impaired kidney repair and suggest that targeting IL-11 could help activate the body’s natural healing mechanisms in both chronic and acute kidney diseases. ^[29]

2.5.Genetic and Environmental Predisposition

A significant genetic component contributes to nephrolithiasis. Polymorphisms in genes such as CaSR, CLDN14, SLC34A1, and VDR are associated with altered calcium and phosphate handling, increasing stone risk. Family history also raises individual susceptibility by 2–3 times. ^[25] Environmental factors, including hot climates, sedentary lifestyle, and Westernized diets rich in salt, oxalate, and protein, amplify this genetic risk .^[22,21]

2.6.Final Outcomes and Recurrence

Without treatment, recurrence rates exceed 50% within 5 years, and chronic inflammation may progress to chronic kidney disease (CKD) and even end-stage renal disease (ESRD) ^[30-31].  Recurrent stones also increase the risk of hypertension and cardiovascular disease.

3.Risk Factors:

3.1.Genetic Basis of Kidney Stones:

Kidney stone disease (nephrolithiasis) is influenced by both environmental and genetic factors. Twin and family studies indicate heritability over 45% for nephrolithiasis and 50% for hypercalciuria, affirming a strong genetic component. ^[32]While some cases arise from monogenic disorders like primary hyperoxaluria, Dent disease, cystinuria, or APRT deficiency, most are idiopathic and linked to complex polygenic influences .^[33] These monogenic forms often manifest early and recur frequently. Several genes are implicated in stone formation through genome-wide association studies and candidate gene analyses. Notable among them are VDR, CASR, CLDN14, SLC34A1, TRPV5/6, and UMOD, which regulate calcium, phosphate, and oxalate transport in renal tubules. ^[32,34] Variants like rs1256328 in ALPL and polymorphisms in the osteopontin and urokinase genes increase risk, whereas Klotho gene variants may confer protection. ^[35] Ethnic differences also affect the distribution and impact of these SNPs. In summary, genetic evaluation is vital for recurrent and early-onset cases, offering potential for precise diagnosis, targeted treatment, and familial risk assessment ^[36]

4.Sexual Dimorphism:

Sexual dimorphism significantly influences kidney stone disease, with men exhibiting a higher incidence than women, though the gap narrows with age. This disparity is attributed to hormonal, metabolic, and environmental factors. Testosterone promotes, while estrogen inhibits, stone formation by modulating oxalate metabolism and oxidative stress. ^[37] Men have higher urinary supersaturation of stone-forming compounds and lower citrate excretion, increasing risk. ^[38] Risk in men peaks around age 53, while in women it rises steadily with age, likely due to hormonal shifts. ^[39] Environmental heat exacerbates risk more in men, suggesting sex-specific physiological responses to dehydration ^[40] Clinically, men often present with typical symptoms, whereas women may show atypical features, potentially delaying diagnosis. ^[41]

5.Impact of Global Warming in KS:

Global warming is emerging as a major contributor to the increasing global prevalence of kidney stone disease. Higher ambient temperatures lead to increased perspiration and decreased urine output, causing urine to become more concentrated—an important factor in stone formation Climate models predict that by 2095, 70% of the U.S. population will reside in high-risk zones for kidney stones, up from 40% in 2000, potentially adding over 2 million new cases and significantly raising healthcare costs.^[42] In Brazil, hospitalization rates for nephrolithiasis were found to be higher in tropical regions, with a strong positive correlation to temperature and a negative one to humidity ^[43]. On a global scale, regions with warm climates and specific geological features—like carbonate rocks and phosphate-rich soils—are more susceptible to kidney stone formation, with climate change expected to expand these high-risk zones ^[44]. Urbanization intensifies the issue through heat islands, where city temperatures exceed rural areas.^[45] Occupational exposure to heat is also a growing concern. ^[46]

6. Dietary influence on KS and Role of Nutritional Interventions:

Kidney stone disease (KSD), or nephrolithiasis, is a multifactorial condition characterized by the formation of crystalline aggregates in the renal tract, most commonly calcium oxalate stones. While genetic and environmental components contribute to pathogenesis, dietary factors are among the most modifiable risk elements. Several clinical and epidemiological studies have consistently demonstrated that specific dietary patterns influence both the incidence and recurrence of KSD. High intake of dietary oxalate, sodium, animal proteins, and added sugars is strongly associated with elevated urinary excretion of lithogenic substances such as calcium, oxalate, and uric acid. Simultaneously, these dietary habits may suppress protective factors like urinary citrate and magnesium. As outlined in ^[47-48], lifestyle changes including the adoption of low-sodium and low-fat diets, along with increased hydration, can significantly mitigate stone risk. Hydration is universally regarded as the most effective preventive measure, promoting urine dilution and reducing supersaturation of stone-forming solutes. Evidence from ^[49-50] supports daily fluid intake that maintains urine output above 2.5 liters as an essential preventive strategy. Moreover, balanced dietary calcium intake from natural sources is preferable over supplements, as low dietary calcium can enhance intestinal oxalate absorption and increase urinary oxalate excretion, a finding supported by ^[51] The inflammatory potential of diet also appears to influence stone risk. A cross-sectional study in ^[52] demonstrated that diets with higher inflammatory index scores are linked to increased odds of hypercalciuria, hyperuricosuria, hypocitraturia, and hypercreatininuria, all of which are established urinary risk factors for nephrolithiasis. This underscores the need to limit pro-inflammatory foods such as red meat, refined sugars, and saturated fats in stone-prone individuals. Beyond traditional risk factors, the evolving field of nutrigenomics reveals that dietary constituents can modulate gene expression via epigenetic pathways.^[53] describes how compounds such as acetic acid upregulate protective microRNAs that decrease calcium reabsorption and enhance urinary citrate, potentially preventing stone aggregation. These effects are mediated through histone acetylation and gene silencing mechanisms that regulate transport proteins like NaDC1 and CLDN14. An umbrella review further reinforces the dietary connection, identifying sodium, fructose, and low fluid intake as positively correlated with nephrolithiasis. Protective associations were observed with caffeine, alcohol, DASH-style diets, and dietary calcium. These findings support a multifaceted dietary approach emphasizing moderation and balance.  Plant-based diets, particularly vegetarian regimens rich in fruits, vegetables, and low-fat dairy, appear to reduce lithogenic risk when appropriately managed for calcium and oxalate balance. ^[54] Vegan diets must be supplemented with adequate calcium to prevent hyperoxaluria, well-balanced vegetarian diets are generally associated with reduced incidence of stones. ^[55] The beneficial effects of herbal compounds like parsley, green tea, and pomegranate which offer antispasmodic, diuretic, and antioxidant properties. ^[56]

6.1.Hydration and Fluid Intake in Kidney Stone Disease:

Insufficient fluid intake is a major modifiable risk factor in nephrolithiasis. It contributes to reduced urine volume and increased supersaturation of lithogenic solutes, thus promoting stone formation. A cross-sectional analysis from the NHANES 2009–2012 cycles found that higher total fluid intake and urine flow rate were associated with reduced kidney stone prevalence, while markers of dehydration significantly increased risk. ^[57] In adolescents, data from the Barriers to Water Intake study showed that each 1 L increase in daily water intake led to a 710 mL increase in 24-hour urine output. This supports fluid-targeted prescriptions to meet urine volume goals. ^[58] From the UK Biobank study, each additional 200 mL/day of total fluid intake reduced the risk of a first kidney stone by 13%. Interestingly, while tea, coffee, and alcohol showed protective effects, plain water did not show a significant association in this population. ^[59] Clinical recommendations emphasize maintaining at least 2.5 L/day of fluid intake  to achieve a urine output of ≥2–2.5 L/day. Water is the preferred fluid, while beverages high in fructose or phosphoric acid should be limited. ^[60]

7.Special Population:

7.1.Impact of KSD in the pediatric population:

Pediatric kidney stone disease is rising at an alarming rate of 5–10% annually, especially among adolescent females in the U.S. South and Midwest^[61-62]. Children commonly present with flank pain, hematuria, or vomiting, with renal stones seen in younger children and ureteral stones in older ones ^[63].Metabolic abnormalities such as hypercalciuria and hypocitraturia are found in 50–84%, significantly increasing recurrence risk ^[62]. Notably, 50% of children experience recurrence within three years, while 24-hour urine analysis can reduce this risk by 60% ^[64]. Ultrasound is the preferred imaging modality due to low radiation ^[65]. Long-term consequences include chronic kidney disease and cardiovascular risks, emphasizing the disease’s systemic nature ^[66]. Early diagnosis and metabolic evaluation are critical for effective pediatric management.

7.2.Impact of Age on Kidney Stone Disease:

Elderly individuals experience a notable delay in the clearance of urinary stones after procedures like ureteroscopic lithotripsy. This delay is primarily due to age-related reductions in ureteral peristalsis, decreased physical activity, and comorbidities that impair spontaneous stone passage. The decline in renal function with ageing further complicates stone management. ^[67] A study of elderly individuals revealed a significant association between nephrolithiasis and age under 75 years, particularly among males and those with high BMI. Interestingly, patients with nephrolithiasis were younger within the elderly cohort and exhibited higher uric acid levels, suggesting that age-related metabolic factors and body composition changes influence stone formation. ^[68]  Analysis of 1,495 stone cases showed that stone composition significantly varies with age. Younger and middle-aged individuals were more likely to develop calcium phosphate and magnesium ammonium phosphate stones, while simple calcium oxalate remained prevalent across all ages. These differences are influenced by age-dependent metabolic alterations and gender distribution. ^[69] Among aging Taiwanese males, metabolic syndrome (MetS) was found to be a significant risk factor for kidney stones. Components like hypertension and insulin resistance—conditions that become more common with age—were strongly associated with stone development. Abnormal blood pressure was identified as the most influential MetS component linked to nephrolithiasis. ^[70] In adults with calcium urolithiasis, osteoporosis was more prevalent in older individuals. Decreasing bone mineral density with age, especially in postmenopausal women, contributes to increased urinary calcium excretion. This calcium imbalance likely plays a role in the heightened incidence of calcium-based stones among the elderly. ^[71] Data from a large international ureteroscopy cohort indicated that the prevalence of diabetes, cardiovascular disease, and anticoagulation therapy increases with age. These age-associated comorbidities elevate the risk of complications after stone surgery and may indirectly contribute to stone formation through altered metabolic and vascular function. ^[72]

8.Clincal Implications:

8.1.Impact of Kidney Stone Disease on Renal Function:

Kidney stone disease (urolithiasis) has been increasingly recognized as both a cause and consequence of renal dysfunction. The obstruction caused by calculi, recurrent episodes of infection, and crystal-induced tubular injury collectively contribute to long-term renal damage. Over time, these events can lead to interstitial fibrosis, nephron loss, and a decline in glomerular filtration rate (GFR), particularly in patients with bilateral stones, recurrent episodes, or associated comorbidities such as diabetes or hypertension. Notably, stone types such as struvite and uric acid stones have a stronger association with renal impairment compared to calcium-based stones. ^[73]  In patients with calcium oxalate (CaOx) nephrolithiasis—the most prevalent stone type globally—renal function, often measured by creatinine clearance (CrCl), significantly influences urinary excretion profiles. A retrospective study analyzing 24-hour urine samples from 993 CaOx stone formers demonstrated that lower CrCl is independently associated with decreased excretion of key lithogenic factors such as urinary citrate, calcium, and oxalate. These changes suggest a diminished renal capacity to handle solute load and maintain urinary homeostasis, which may alter the risk of future stone formation. Additionally, aging and renal function exert independent and combined effects on urinary chemistry, underscoring the importance of considering both factors in the clinical evaluation and management of stone-forming individuals ^[74]

8.2.Effect of KSD on Quality of Life:

Patients with kidney stone disease (KSD) experience reduced quality of life (QoL), primarily due to pain, physical limitations, and psychological distress. Studies using tools like SF-36, WISQoL, and PROMIS-43 show significant impairment in domains such as bodily pain, physical function, general health, and emotional well-being ^[75-76]. Female and younger patients often report worse outcomes.^[77] Recurrence, multiple procedures, and ureteral stents further reduce QoL, with financial and occupational consequences .^[78] While interventions like ESWL and PNL initially reduce QoL postoperatively, recovery trends are favorable by three months^[79] These findings highlight the importance of incorporating patient-centered QoL assessments into KSD management.

9.Diagnostic Tools for Kidney Stone Detection:

The diagnosis of kidney stones employs a range of imaging, laboratory, and computational methods, each contributing unique advantages. The integration of traditional modalities with AI-based tools is advancing the accuracy and speed of diagnosis.

9.1.Imaging Modalities:

Non-Contrast Computed Tomography (CT): CT is the gold standard for detecting kidney stones due to its high sensitivity and specificity (~95–98%)  across all stone types and locations. Low-dose and dual-energy CT protocols reduce radiation exposure while enabling stone composition analysis.^[80]

Ultrasonography: As a radiation-free and cost-effective option, ultrasound is commonly used for initial evaluation, especially in pregnant women and children. Though less sensitive than CT, it effectively detects obstructive features and is favored for its safety and bedside availability. ^[81]

Plain X-Ray (KUB): Suitable for follow-up of known radiopaque stones, but limited for initial diagnosis due to low sensitivity and inability to detect radiolucent stones. ^[82]

Magnetic Resonance Imaging (MRI): Not routinely used due to limited visibility of calcifications, but beneficial in specific populations and in research involving multimodal diagnostics. ^[83]

Dual-energy CT: It enables in vivo stone composition analysis, aiding in treatment selection.Emerging tools include miniaturized scopes and enhanced intraoperative imaging, particularly in pediatric cases, where precision is critical ^[84]

9.1.2.Laboratory and Biochemical Evaluation :

Metabolic Work-up and Stone Analysis: Includes 24-hpurs urine collection and composition analysis of retrieved stones, Essential for identifying underlying metabolic disorders and preventing recurrence in high-risk individuals. ^[85]

9.1.3.Artificial Intelligence and Integrative Approaches:

Machine Learning for Stone Typing: Ensemble learning models predict stone composition with high accuracy based on clinical and urinary parameters. ^[86]

10.Preventive Stratergies for Recurrent Kidney Stone Disease:

Recurrent kidney stone disease (KSD) presents a significant clinical and economic burden, with recurrence rates ranging from 11% at 2 years to as high as 80% at 3 years depending on stone composition and patient risk profile. Preventive measures are essential to reduce recurrence and improve long-term outcomes.

10.1.Fluid Intake in Diuresis:

Adequate hydration is the cornerstone of prevention. A daily fluid intake of 2.5–3.0 liters with a urine output target of >2.0–2.5 liters helps dilute stone-forming solutes. A landmark randomized trial reported a 12% recurrence rate in high-fluid intake groups versus 27% in controls ^[87]. Guidelines now recommend this universally.

10.2. Dietary Modifications:

Limit sodium intake, oxalate-rich foods, and animal protein. Ensure adequate calcium intake. Increase intake of citrus fruits, which raise urinary citrate, a natural inhibitor of stone formation. Avoid vitamin C and D supplementation unless medically indicated.These strategies are summarized in recent nutritional reviews and meta-analyses ^[88]

10.3.Lifestyle Adjustments:

Obesity, smoking, and high-heat work environments increase stone risk. Recommendations include maintaining normal BMI, regular hydration in hot climates, and smoking cessation ^[89]. Personal and family history of stones, higher BMI, and prior surgical treatment also raise recurrence risk ^[90]

10.4. Pharmacological Prevention:

Thiazide diuretics reduce urinary calcium excretion—effective for hypercalciuric patients.

Citrate salts increase urinary citrate and pH—effective for calcium and uric acid stones.

Allopurinol helps prevent calcium stones in patients with hyperuricosuria.

These drugs are supported by both randomized and non-randomized studies^[91].

10.5.Monitoring and Follow-Up:

Structured follow-up involving 24-hour urine collections and metabolic evaluations is critical for high-risk patients. However, standardized protocols are still lacking in clinical practice. Imaging and urine tests tailored to patient risk can reduce recurrence^[92].

10.6. Risk Stratification by Stone Morphology:

Stone composition and morphology are strong predictors of recurrence. For example, certain calcium oxalate monohydrate (COM) morphologies are associated with recurrence rates over 80%, even though COM stones generally show lower recurrence overall. Morphological analysis enhances risk prediction beyond mineral composition alone^[93]

10.7..Early Biomarker-Guided Interventions:

Short-term changes in urinary supersaturation and excretion of citrate, potassium, and magnesium after diet modification can predict long-term recurrence risk. Monitoring these changes early  may help guide personalized prevention strategies ^[94].

11.Emerging Tech In KS:

11.1.Advances in Laser Lithotripsy:

Holmium:YAG Laser Enhancements: Modern Holmium:YAG lasers allow modulation of pulse energy, frequency, and width. Techniques such as dusting, fragmentation, and non-contact popcorn method have improved stone clearance rates.

Moses Technology: A pulse modulation method that reduces retropulsion and increases efficiency by delivering energy through an initial vapor bubble.^[95]

Thulium Fiber Laser (TFL): A newer, more efficient laser system with superior energy absorption and lower thermal damage. Ideal for finer dusting and may replace Holmium in future^[96]
11.1.2. Robotic and AI-based Innovations:

Robotic Ureteroscopy (RoboURS): Increases procedural precision, stability, and reduces fatigue. Emerging systems allow memory positioning and reduced fluoroscopy time.
Artificial Intelligence and 3D Simulation: Used for pre-surgical planning, training, and outcome prediction. Integrating VR and machine learning tools is becoming common. ^[97]
 

11.2. Minimally Invasive Techniques & New Devices:

11.2.1.Mini-PCNL and Suction-Assisted Sheaths: Miniaturized percutaneous nephrolithotomy reduces morbidity, especially for moderate-sized stones. Suction-enhanced access sheaths help clear debris and reduce intrarenal pressure. ^[97,98]

11.2.2.Single-Probe Dual-Energy (SPDE) Lithotripters: Devices combining ultrasonic and ballistic energy with suction are emerging as highly effective tools in large-volume stone removal.^[97]

11.2.3.Mobile Health & eHealth Integration:

Smart Water Bottles & Hydration Apps: Devices track and encourage fluid intake to prevent stone recurrence, with studies showing increased patient compliance.

Digital Stent Trackers: Mobile tools to prevent forgotten ureteral stents, improving post-op outcomes.
Virtual Clinics & Smartphone Endoscopy: Offer affordable diagnostic and follow-up care, particularly useful in resource-limited settings. ^[99]

11.2.4. Multi-Tract PCNL for Complex Kidney Stones:

Multiple-tract PCNL: For large or staghorn calculi, multiple-access PCNL provides better stone-free rates compared to single-tract or flexible methods. Though it has higher bleeding risks, it is safe when managed by experts. ^[98,100]

CONCLUSION:

Twenty years after the initial concerning report, kidney stone disease is on the rise globally, posing growing difficulties for both individuals and healthcare systems. The reasons behind this increase are still unclear. However, shifts in dietary habits and global climate changes, dimorphism, age difference may be contributing factors and should be prioritized in efforts to prevent the disease.

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