Urological footprint of chronic kidney disease: A nephrologist perspective on early detection and collaborative management

Abstract

Chronic kidney disease (CKD) is a multifactorial condition in which urological comorbidities including recurrent urinary tract infections, obstructive uropathy, nephrolithiasis, and voiding dysfunction play a critical but often overlooked role in disease onset and progression. This mini-review aims to highlight the prevalence, clinical relevance, and impact of urological disorders in CKD, advocating for their systematic recognition and management within nephrology practice. A narrative synthesis of published literature was conducted, focusing on epidemiological data, clinical studies, and expert consensus addressing the intersection of CKD and urological comorbidities. Evidence indicates that urological disorders are common among CKD patients, particularly in the presence of diabetes mellitus, hypertension, and persistent proteinuria. These conditions accelerate renal decline, increase complications, and impair quality of life. Early detection and timely intervention, coupled with interdisciplinary collaboration between nephrologists and urologists, can delay disease progression and optimize patient outcomes. Integrating urological insights into nephrology care is essential to address the multifactorial nature of CKD. Routine screening for urological comorbidities, proactive management strategies, and closer interdisciplinary collaboration is recommended. Future research should quantify the benefits of such integrative approaches and explore innovative models of care to improve long-term outcomes.

Key Words: Benign prostatic hyperplasia; Chronic kidney disease; Congenital anomalies of the kidney; End-stage kidney disease; Nephrolithiasis; Urological disorders

Core Tip: Chronic kidney disease is increasingly influenced by urological conditions such as recurrent urinary tract infections, obstructive uropathy, and nephrolithiasis are key contributors to chronic kidney disease progression but remain underrecognized in nephrology. To address this gap, nephrologists should embrace a comprehensive care model that actively incorporates urological evaluation, timely referrals, and integrated treatment planning. Enhancing collaboration between nephrology and urology is crucial for reducing kidney complications and delivering truly patient-centered care.

INTRODUCTION

Chronic kidney disease (CKD) has emerged as a pressing global health challenge, with its prevalence steadily increasing[1,2]. According to epidemiological data from the National Health and Nutrition Examination Survey III, CKD is estimated to affect approximately 10% of the global population[3]. In Pakistan, a recent literature review reported an overall CKD prevalence of 21.2% across all age groups[4]. Its spectrum spans from incipient kidney dysfunction to severe impairment, as delineated by the “Kidney Disease: Improving Global Outcomes” guidelines[5]. Historically, CKD has been approached predominantly through a nephrological framework, with clinical emphasis placed on metrics such as glomerular filtration rate (GFR), albuminuria, and disturbances in electrolyte balance. While these indicators remain pivotal for diagnosis and therapeutic monitoring, they capture only a fragment of the broader clinical landscape. Although diabetes mellitus and hypertension are firmly established as principal etiological factors[6], and considerable research has focused on cardiovascular complications and kidney replacement therapies, emerging evidence underscores the significant influence of urological determinants in both the initiation and progression of CKD in adults[7,8]. This facet, long overshadowed in conventional nephrological discourse, warrants deeper exploration and integration into clinical practice, transcending traditional diagnostic boundaries.

Urological complications, whether congenital or acquired, are intricately linked to the progression of CKD. Among the most prevalent are vesicoureteral reflux (VUR), recurrent urinary tract infections (UTIs), and various forms of urinary tract obstruction arising from both anatomical and functional anomalies, including ureteropelvic junction obstruction, bladder neck stricture, congenital urethral valves, urethral stenosis, kidney stones, malignancies, and benign prostatic hyperplasia (BPH). Overactive bladder, particularly in females, also plays a significant role in this complex interplay[9,10]. These disorders often manifest subtly and progress gradually, making early detection difficult. Despite their understated presentation, they can exert a profound influence on kidney and cardiovascular outcomes[11]. Rather than being incidental, such urological conditions frequently serve as underlying causes, aggravating factors, or complicating elements in CKD[12]. When overlooked, they may silently deteriorate kidney function, hinder timely therapeutic intervention, and undermine long-term management strategies. The growing elderly population, coupled with rising rates of diabetes and cardiovascular disease, has led to an increase in patients presenting with overlapping nephrological and urological pathologies[13]. This convergence underscores the need for a more integrated clinical approach, one that recognizes the interdependence of these systems and promotes collaborative care to optimize patient outcomes[14].

Moreover, CKD is frequently accompanied by a constellation of complications such as hypertension, proteinuria, diminished urine-concentrating capacity, hyperkalemia, metabolic acidosis, and focal segmental glomerulosclerosis, which bear significant long-term prognostic weight[15,16]. An important but underappreciated aspect is whether urological disorders act as primary causes of CKD or emerge as secondary consequences of renal impairment a distinction that directly informs clinical strategy. This distinction is not merely academic; it directly informs clinical strategy, determining whether management should focus on proactive intervention to halt disease initiation or on symptomatic treatment to mitigate complications of advanced CKD.

Drawing upon contemporary evidence and clinical experience, this narrative review advocates a paradigm shift, encouraging nephrologists to play a more proactive role in recognizing and managing urological comorbidities that may influence the trajectory of CKD. This mini-review aims to assess the prevalence and clinical significance of urological disorders across the stages of CKD, exploring their associations with diabetes, hypertension, recurrent infections, and proteinuria, while emphasizing the necessity of early detection and interdisciplinary collaboration. By bridging these domains, the review seeks to empower nephrologists with a more holistic understanding of CKD, one that moves beyond conventional frameworks and embraces the complexity of renal-urogenital interplay.

LITERATURE REVIEW

This study was conducted as a narrative mini-review. Literature published between January 2000 and January 2025 was identified through searches of PubMed, MEDLINE, Scopus, and Web of Science, using combinations of keywords related to CKD and urological comorbidities (e.g., obstructive uropathy, recurrent UTIs, nephrolithiasis, bladder dysfunction, BPH). A total of 66 references were included, consistent with the scope of a mini-review, aiming to provide a concise synthesis of current evidence rather than a systematic evaluation.

UROLOGICAL MANIFESTATIONS ACROSSCKD STAGES AND THEIR CLINICAL OUTCOMES

CKD can both result from and contribute to urological disorders. It presents a spectrum of urological manifestations that evolve as kidney function declines across its stages. In the early stages (CKD 1-2), patients are often asymptomatic; however, subtle urological signs, such as polyuria or nocturia, may emerge due to impaired tubular function and the reduced concentrating ability of the kidneys. These symptoms are frequently overlooked but may indicate underlying tubulointerstitial damage or early nephron loss. As CKD progresses into stages 3-4, structural and functional changes become more pronounced. Patients may experience lower urinary tract symptoms (LUTS) such as urgency, frequency, and incomplete bladder emptying, often exacerbated by comorbid conditions like diabetes or BPH. These urological issues can contribute to recurrent UTIs, which in turn accelerate kidney damage through inflammatory pathways and scarring. Supporting this, Kuo et al[17] examined 3226 patients with stage 3-5 CKD and demonstrated that recurrent pyuria or UTI episodes significantly heightened adverse kidney outcomes. Notably, patients experiencing more than one episode of pyuria within the first year (11.8%) exhibited markedly increased risks of progression to end-stage kidney disease (ESKD) [hazard ratio (HR) = 1.90, 95% confidence interval (CI): 1.58-2.28; P < 0.001], rapid decline in renal function (odds ratio = 1.49, 95%CI: 1.13-1.95; P = 0.001), and all-cause mortality (HR = 1.63, 95%CI: 1.29-2.05; P < 0.001), compared with those without pyuria[17].

In advanced (CKD stage 5) or ESKD, urological complications become more complex and clinically significant. Anatomical abnormalities such as hydronephrosis, ureteral strictures, and bladder dysfunction are common, especially in patients with longstanding obstruction or neurogenic bladder. Dialysis-dependent individuals frequently require catheterization, increasing the risk of infection and urosepsis. Cross-sectional studies have demonstrated that lower peak urinary flow rate is associated with increased odds of prevalent CKD[18-20], while higher post-void residual (PVR) has shown inconsistent associations with CKD[19,21]. Lee et al[19] further reported that maximal urinary flow rate correlated significantly with GFR in middle-aged men with moderate to severe LUTS (P < 0.001), reinforcing the link between urinary flow dynamics and kidney function. Similarly, Yamasaki et al[21] found that even small residual urine volumes (PVR ≥ 12 mL) were independently associated with CKD, highlighting the close interplay between bladder emptying efficiency and kidney health. Beyond voiding dysfunction, sexual complications are prevalent, with erectile dysfunction in men and menstrual irregularities in women arising from hormonal imbalances and uremic toxicity. Post-kidney transplant patients face unique urological challenges such as ureteral stenosis, VUR, and persistent LUTS, which require coordinated care between nephrologists and urologists[22,23]. Song et al[22] further evaluated clinical factors influencing bladder capacity and lower urinary tract dysfunction in ESKD patients following kidney transplantation. Their findings revealed that small bladder capacity was significantly associated with long-term dialysis, VUR, and PVR (P < 0.001, P = 0.004, P = 0.003). After kidney transplantation, 31 patients (4.9%) required treatment for lower urinary tract dysfunction, with age, VUR, and PVR emerging as significant predictors of its development (P = 0.001, P = 0.034, P < 0.001). These results emphasize that both pre-transplant factors and post-transplant complications contribute to persistent urological morbidity, reinforcing the need for vigilant monitoring and individualized management strategies in this patient population[22]. Overall, the interplay between CKD progression and urological health underscores the importance of early detection, routine urological evaluation, and multidisciplinary management to mitigate complications and preserve quality of life as summarized in Table 1. Many of these manifestations, such as LUTS in dialysis, bladder dysfunction, and recurrent UTIs represent secondary consequences of established CKD.

Table 1 Urological manifestations across chronic kidney disease stages and their clinical outcomes.

CKD stage	Urological manifestations	Impact on CKD outcomes	Clinical implications
Stage 1-2 (early CKD)	Polyuria, nocturia	Early signs of tubulointerstitial damage; often missed, delaying diagnosis	Need for early screening and symptom recognition
Stage 3-4 (moderate CKD)	LUTS (urgency, frequency, hesitancy), recurrent UTIs	UTIs accelerate nephron loss; LUTS complicate fluid balance	Routine urological evaluation; manage comorbidities like diabetes/BPH
Stage 5 (ESKD, pre-dialysis)	Bladder dysfunction (DU, BO), anuria, incontinence	Disuse atrophy, fibrosis, increased infection risk, poor dialysis outcomes	Multidisciplinary care; monitor bladder function and infection risk
Dialysis-dependent	Reduced bladder capacity, poor sensation, persistent LUTS	LUTS persist despite anuria; linked to lower QoL	Use of validated questionnaires; targeted symptom management
Post-transplant	Ureteral stenosis, VUR, persistent LUTS	Surgical complications and persistent symptoms affect graft function	Coordinated nephrology-urology follow-up

CKD: Chronic kidney disease; ESKD: End-stage kidney disease; LUTS: Lower urinary tract symptoms; DU: Detrusor underactivity; BO: Bladder oversensitivity; VUR: Vesicoureteral reflux; UTI: Urinary tract infection; QoL: Quality of life; BPH: Benign prostatic hyperplasia.

LUTS and decreased urine output patterns

LUTS and decreased urine output are common and clinically significant manifestations in patients with CKD, particularly as the disease progresses toward ESKD. LUTS encompasses a spectrum of symptoms related to bladder storage and voiding, including urinary frequency, urgency, nocturia, hesitancy, weak stream, straining, and a sensation of incomplete bladder emptying. These symptoms are often underreported by patients but can substantially impair quality of life and complicate CKD management.

Global prevalence estimates for LUTS range from 20% to 40% in adults, with higher rates in older populations and those with comorbid conditions like diabetes and CKD[24]. In specific cohorts, such as female nurses, prevalence has been reported as high as 68.9%[25]. As summarized in Table 2, LUTS and urine output patterns vary by CKD stage and carry important prognostic implications. In early CKD (stages 1-2), symptoms such as mild frequency or nocturia may occur despite preserved or increased urine output due to impaired concentrating ability. While subtle, these early LUTS can signal underlying tubular dysfunction and should prompt closer monitoring, as they may precede progressive renal decline. In moderate CKD (stages 3-4), LUTS become more prevalent due to structural and functional urinary tract changes. Nocturia, urgency, hesitancy, and incontinence are common, and declining urine output with nocturnal polyuria reflects worsening renal reserve. These symptoms are clinically significant because they increase infection risk, impair quality of life, and often predict faster CKD progression. Diabetic nephropathy further exacerbates LUTS through autonomic neuropathy, leading to detrusor underactivity (DU) or overactivity, which can accelerate bladder dysfunction and renal deterioration. In advanced CKD and ESKD (stage 5), urine output declines markedly, with many patients progressing to oliguria or anuria. Severe LUTS, poor bladder sensation, and incontinence persist despite minimal urine production. The study by Wu et al[26] found that LUTS are common among dialysis patients, with a significant proportion experiencing issues such as frequency, urgency, and nocturia. These symptoms remain prevalent and are strongly correlated with poorer quality of life scores. These symptoms also predispose to urinary stasis, infection, and bladder wall remodeling, all of which contribute to morbidity and complicate CKD management.

Table 2 Lower urinary tract symptoms and urine output pattern by chronic kidney disease stage.

CKD stage	LUTS	Urine output pattern
Stage 1 eGFR (> 90)	Mild frequency, possible urgency in glomerular disease	Normal or slightly increased (polyuria in some cases)
Stage 2 eGFR (60-89)	Nocturia, mild urgency/frequency	Normal or mildly reduced
Stage 3 eGFR (30-59)	Nocturia, urgency, incontinence, hesitancy	May show reduced concentration ability, nocturnal polyuria
Stage 4 eGFR (15-29)	Urinary retention, overflow incontinence, weak stream	Marked reduction in output (oliguria)
Stage 5 eGFR (< 15 or ESKD)	Severe LUTS, incontinence, poor bladder sensation	Severely reduced or absent (anuria), dialysis-dependent

CKD: Chronic kidney disease; eGFR: Estimated glomerular filtration rate; ESKD: End-stage kidney disease; LUTS: Lower urinary tract symptoms.

Functional bladder capacity further influences symptom development. In CKD stages IIIb-V, reduced diuresis and altered bladder compliance can manifest as either overactive bladder symptoms or retention-related issues. A clinical investigation using the International Consultation on Incontinence Modular Questionnaire-LUTS (International Consultation on Incontinence) questionnaire confirmed that LUTS was significantly associated with reduced bladder capacity and minimal urine output, particularly in dialysis-dependent individuals[27]. These findings highlight the importance of routine assessment of LUTS in CKD patients, as the observed patterns provide valuable clinical context for anticipating symptom progression and tailoring management strategies.

Bladder dysfunction in dialysis patients

Bladder dysfunction in dialysis patients is a multifactorial condition that arises primarily from the progressive decline in kidney function and the physiological changes induced by chronic CKD and its treatment. As patients transition into ESKD and begin maintenance dialysis, urine output often diminishes significantly, leading to oliguria or even anuria. This reduction in urinary flow results in decreased bladder distension and activity, which, overtime, causes the bladder to lose its functional capacity and compliance. Structural remodeling of the bladder wall, including fibrosis and thinning, further contributes to symptoms such as urgency, frequency, and incontinence, even in the absence of significant urine production.

As summarized in Table 3, the most common bladder dysfunctions observed in dialysis patients include DU, bladder oversensitivity (BO), overflow incontinence, loss of bladder sensation, and reduced bladder capacity. These abnormalities reflect the combined effects of disuse, altered bladder compliance, and urothelial injury, and each carries important clinical consequences. DU leads to incomplete bladder emptying, which predisposes patients to recurrent UTIs and further renal stress. BO manifests as urgency despite low urine volume, contributing to reduced quality of life and increased risk of infection from frequent voiding attempts. Long-term anuria and disuse result in markedly reduced bladder capacity, which complicates future renal transplantation by limiting graft function and increasing postoperative morbidity. Loss of bladder sensation and overflow incontinence further exacerbate infection risk, impair patient dignity, and worsen overall prognosis. Recognizing these dysfunctions is therefore critical, as they not only affect symptom burden but also influence CKD progression, transplant outcomes, and patient survival.

Table 3 Common bladder dysfunction types in dialysis patients.

Type of dysfunction	Description	Prevalence
DU	Weak bladder muscle contraction; leads to incomplete emptying	Common in long-term dialysis patients, may coexist with sensory deficits
BO	Heightened sensation despite low urine volume; causes urgency	Frequently reported; often overlaps with other dysfunctions
Overflow incontinence	Bladder overfills due to poor emptying; leaks involuntarily	Less common but clinically significant; may result from DU
Loss of bladder sensation	Patients may not feel the need to urinate, even when bladder is full	Often underdiagnosed; contributes to silent retention and overflow
Small bladder capacity	Due to long-term anuria and disuse, bladder shrinks in volume	Very common in anuric patients; reversible with restored urine output
Mixed dysfunction	Combination of two or more dysfunction types	Frequently observed; requires individualized assessment and management

DU: Detrusor underactivity; BO: Bladder oversensitivity.

Clinical studies support these observations. Abushamma et al[28] from Palestine reported that, out of 145 patients, 87% of hemodialysis patients experienced at least one storage symptom and 85% at least one voiding symptom, although their study was prospective and multicenter study among hemodialysis patients but it was limited by reliance on questionnaires rather than objective urodynamic testing. Similarly, Chen et al[29] demonstrated that cystometric bladder capacity and compliance decreased with longer dialysis duration (76.2 ± 9.71 months), and patients with anuria (41.9%) had significantly smaller bladder capacities than those without anuria (102 ± 12.0 mL vs 237 ± 17.5 mL; P = 0.002). More than two-thirds of patients also showed abnormal video urodynamic findings[29]. These findings align with the dysfunction types such as DU, BO, and reduced bladder capacity. Additionally, VUR was observed in 110 out of 622 patients (17.5%), and elevated PVR urine volumes were reported in 83 out of 622 ESKD patients (13.6%), requiring kidney transplantation[22].

Pathophysiological mechanisms further explain these dysfunctions. Chronic inflammation and urothelial dysfunction in ESKD patients are associated with increased mast cell infiltration, elevated apoptosis of urothelial cells, and reduced expression of tight junction proteins such as zonula occludens-1 and adhesion molecules like E-cadherin. These changes compromise the urothelial barrier, heightening bladder sensation and reducing capacity[30,31]. Cheng et al[32] confirmed that reduced zonula occludens-1 and E-cadherin expression correlated with increased bladder sensation and smaller bladder capacity, particularly in patients with DU.

Additionally, the long-term effects of uremic toxins, autonomic neuropathy (especially in diabetic patients), and repeated instrumentation such as catheterization further exacerbate bladder dysfunction[32]. Hemodialysis itself does not restore normal urinary physiology, and the absence of regular voiding can lead to disuse atrophy of the bladder. Observational studies have confirmed that LUTS are prevalent in dialysis populations and are independently associated with impaired quality of life, underscoring the need for routine urological assessment and targeted interventions[26].

Impact on quality of life: LUTS significantly impair quality of life in dialysis patients. Dysfunctions such as BO and DU contribute to urgency, incomplete emptying, and incontinence, which are linked to poorer sleep, increased anxiety, and reduced social engagement. Longer dialysis duration correlates with greater bladder dysfunction and lower quality of life scores[33].

Clinical recommendations:Table 4 summarizes the proposed clinical recommendations for assessing and managing bladder dysfunction in dialysis patients. Early detection is essential, as untreated dysfunction can worsen infection risk, impair bladder compliance, and complicate future transplant outcomes. Tools such as uroflowmetry[34] and validated questionnaires[35,36] (e.g., the International Prostate Symptom Score Overactive Bladder Symptom Score) not only facilitate timely identification of dysfunction but also allow clinicians to anticipate complications that may accelerate CKD progression or reduce quality of life. Integrating these strategies into routine care ensures that bladder dysfunction is recognized before it contributes to recurrent infections, obstructive uropathy, or poor transplant candidacy. Interventions such as bladder training, fluid management, and targeted pharmacotherapy do more than alleviate symptoms - they help preserve residual renal function, reduce morbidity, and improve long-term patient prognosis. Thus, urological assessment should be considered a core component of comprehensive dialysis management, directly influencing outcomes beyond symptom control.

Table 4 Clinical recommendations for bladder dysfunction in dialysis patients.

Recommendation	Evidence grade	Practical notes/applicability
Use validated questionnaires (e.g., IPSS, OABSS) for early detection of LUTS in dialysis patients	2B	Low-cost, feasible in most clinical settings; useful for screening but limited by patient self-reporting bias
Perform uroflowmetry and PVR measurement in symptomatic patients	1B	Provides objective assessment; requires equipment and trained staff, may be less feasible in resource-limited centers
Refer dialysis patients with persistent LUTS to urology for further evaluation (urodynamics, cystoscopy if indicated)	1C	Strong recommendation despite limited trial data; referral may be challenging in rural/Low-resource areas
Implement bladder training and fluid management strategies to improve storage/voiding symptoms	2C	Non-invasive, low-cost, but requires patient adherence and education
Consider pharmacological therapy (e.g., antimuscarinics for BO, alpha-blockers for voiding dysfunction) when conservative measures fail	2B	Evidence mainly extrapolated from non-CKD populations; careful monitoring needed due to altered drug clearance in ESKD
Incorporate routine LUTS/QoL assessment into dialysis care protocols	1C	Improves holistic patient management; feasible with minimal resources if integrated into dialysis unit workflow

Where 1 = strong recommendation, 2 = weak; A = high-quality evidence, B = moderate, C = low. IPSS: International Prostate Symptom Score; OABSS: Overactive Bladder Symptom Score; LUTS: Lower urinary tract symptoms; BO: Bladder oversensitivity; QoL: Quality of life; CKD: Chronic kidney disease; ESKD: End-stage kidney disease.

Increased risk of UTIs and their sequelae

Patients with CKD secondary to urological etiologies such as urinary tract obstruction, structural abnormalities, or neurogenic bladder face a heightened risk of developing UTIs across all stages of CKD. As summarized in Table 5, this risk increases progressively with advancing CKD stage, and the clinical consequences become more severe. In early CKD (stages 1-2), UTI risk is mild to moderate, often linked to incomplete bladder emptying or structural abnormalities. Even occasional pyuria or mild renal inflammation can accelerate tubular injury if left untreated. Early detection and urological management are therefore critical to prevent progression and preserve renal reserve. In moderate CKD (stage 3) reduced renal clearance and recurrent infections make UTIs clinically significant at this stage. Recurrent infections not only accelerate GFR decline but also increase the likelihood of antibiotic resistance, complicating long-term management. Close monitoring and tailored antimicrobial therapy are essential to slow disease progression and reduce hospitalization risk. Shankar et al[37] studied 129 CKD patients and reported that 76.2% were male and 23.8% female, with the highest prevalence of UTI in patients aged 61-70 years (25.6%), followed by those aged 51-60 years (19.3%).

Table 5 Risk of urinary tract infections and their sequelae across different stages of chronic kidney disease in patients with urological causes.

CKD stage	Risk of UTI	Contributing factors	Common sequelae	Clinical implications
Stage 1-2	Mild to moderate	(1) Structural abnormalities; and (2) Incomplete bladder emptying	(1) Occasional pyuria; and (2) Mild renal inflammation	Early detection and urological management can prevent progression
Stage 3	Moderate	(1) Reduced renal clearance; and (2) Recurrent infections	(1) Accelerated GFR decline; and (2) Onset of antibiotic resistance	Close monitoring and tailored antimicrobial therapy are essential to slow progression
Stage 4	High	(1) Impaired immune response; and (2) Chronic colonization	(1) Frequent hospitalizations; and (2) Risk of systemic infection	Repeated or resistant infections can hasten CKD progression; aggressive infection control is needed
Stage 5 (ESKD)	Very high	(1) Dialysis-related risks; and (2) Severe urinary tract dysfunction	(1) Sepsis; and (2) Multidrug-resistant organisms	Multidisciplinary care essential; infection prevention is critical

CKD: Chronic kidney disease; ESKD: End-stage kidney disease; UTI: Urinary tract infection.

In advanced CKD (stage 4), UTI risk becomes high due to impaired immune responses and chronic bacterial colonization. Frequent hospitalizations and systemic infections at this stage contribute to morbidity and hasten renal decline. Aggressive infection control measures and strategies to preserve residual kidney function are vital to improving prognosis. In ESKD (stage 5), patients face a very high UTI risk, compounded by dialysis-related factors and severe urinary tract dysfunction. Vulnerability to sepsis and multidrug-resistant organisms significantly increases mortality risk. Yang et al[38] demonstrated that CKD patients admitted for UTI experienced a significantly faster decline in estimated GFR (P < 0.0001), underscoring the profound impact of infection on disease progression.

Recurrent UTIs in CKD exacerbate renal inflammation, accelerate GFR decline, and worsen prognosis. In patients with urological causes of CKD, anatomical and functional disruptions further predispose to bacterial colonization and impaired clearance, making vigilant monitoring and stage-specific interventions essential. Understanding how infection risk evolves with CKD progression is crucial for guiding preventive strategies and tailoring therapy to improve long-term renal and systemic outcomes.

SYSTEMIC DISEASES AND UROLOGICAL SEQUELAE

While the direct urological manifestations of CKD highlight the local impact of declining kidney function on the urinary tract, systemic diseases that commonly coexist with CKD such as diabetes, lupus, and hypertension further amplify these sequelae. Diabetes may lead to cystopathy with incomplete bladder emptying and recurrent infections; lupus can cause cystitis with urgency, frequency, and obstructive complications; and hypertension contributes to detrusor dysfunction and nocturia through vascular injury. These manifestations are best understood as secondary consequences of systemic disease acting on the urinary tract in the context of CKD, and recognizing them is critical for comprehensive patient care.

Diabetic cystopathy

As the leading cause of CKD worldwide, diabetes not only drives renal decline but also exerts profound effects on bladder and urinary tract function. Diabetic cystopathy is a common and yet often underrecognized urological complication of diabetes mellitus, primarily resulting from chronic hyperglycemia and its damaging effects on the autonomic and somatic nervous systems. This condition manifests as progressive bladder dysfunction, beginning with impaired bladder sensation and leading to increased bladder capacity, reduced detrusor contractility, and ultimately urinary retention[39]. Patients may experience a wide spectrum of symptoms, ranging from overactive bladder such as urgency and frequency to underactive bladder with incomplete emptying and PVR[40]. The insidious nature of diabetic cystopathy means many individuals remain asymptomatic for years, only presenting when complications like recurrent UTIs or overflow incontinence arise. Urodynamic studies often reveal diminished bladder sensation and poor contractility, and treatment outcomes are frequently limited due to irreversible neuropathic changes.

Importantly, Cho et al[40] demonstrated that in type 2 diabetes, increased PVR is independently associated with faster renal function deterioration, with mean PVR of 69.8 ± 96.3 mL and 17.7% of patients showing PVR > 100 mL. Those with PVR > 100 mL had a 2.8-fold higher risk of greater estimated GFR decline over one year (95%CI: 1.1-6.8, P = 0.03). As diabetes prevalence continues to rise globally, early recognition and management of diabetic cystopathy are essential to prevent long-term urological sequelae and preserve quality of life.

Lupus and interstitial cystitis

Autoimmune conditions that damage the kidneys also predispose patients to urological complications, either directly through inflammation or indirectly via immunosuppressive therapy. Lupus and interstitial cystitis (IC) represent a complex interplay between autoimmune dysfunction and chronic bladder inflammation. Systemic lupus erythematosus, a multisystem autoimmune disease, can affect the urinary tract in various ways, including the bladder. In rare cases, lupus leads to a condition known as lupus cystitis, characterized by bladder wall inflammation, urgency, frequency, dysuria, and suprapubic pain. Although the exact pathophysiological mechanism remains uncertain, immune complex deposition causing small vessel vasculitis is considered central to bladder inflammation. Wen et al[41] conducted the first population-based cohort study showing a significantly higher incidence of IC in patients with systemic lupus erythematosus, with a 2.45-fold increased risk (adjusted HR = 2.45, 95%CI: 1.57-3.27, P < 0.05), supporting its concordance with autoimmune diseases and temporal association in systemic lupus erythematosus.

IC also known as painful bladder syndrome, is a chronic condition characterized by bladder pain, pressure, and urinary frequency lasting more than 6 weeks without identifiable infection or other causes[42]. The Society for Urodynamics and Female Urology convened international experts and reached substantial agreement on this definition[42]. While IC and lupus are distinct entities, research suggests that individuals with lupus may be more susceptible to developing IC-like symptoms due to shared inflammatory pathways and immune dysregulation. The overlap in symptoms such as pelvic pain and urinary urgency can make diagnosis challenging, often requiring cystoscopy or bladder biopsy to differentiate between the two.

Managing these conditions concurrently involves a multidisciplinary approach. Although no clinical guidelines exist, case reports suggest that pulses of methylprednisolone and cyclophosphamide, similar to lupus nephritis regimens, may be used for lupus cystitis, while IC treatment focuses on symptom relief through bladder instillations, dietary modifications, and pain management. Recognizing the potential link between lupus and IC is crucial for timely diagnosis and personalized care, especially in patients presenting with persistent bladder symptoms and a known history of autoimmune disease[43]. Lupus cystitis, though rare, can lead to obstructive complications and kidney damage, resulting in increased morbidity and mortality.

Hypertensive nephrosclerosis and associated voiding symptoms

Hypertension, both a cause and consequence of CKD, contributes to urological dysfunction through its effects on bladder dynamics and nocturnal urine production. Hypertensive nephrosclerosis is a form of chronic kidney damage caused by long-standing, poorly controlled high blood pressure. It leads to progressive sclerosis of the renal arterioles and glomeruli, resulting in reduced renal perfusion and gradual loss of kidney function[44]. While the primary manifestations are renal, this condition can also be associated with LUTS, especially in advanced stages. Patients may experience nocturia, urgency, and frequency, which are often attributed to impaired renal concentrating ability and altered fluid handling. Additionally, hypertensive nephrosclerosis may coexist with bladder dysfunction, particularly in older adults, where vascular changes and autonomic dysregulation contribute to detrusor overactivity or underactivity. These voiding symptoms can significantly impact quality of life and may be mistaken for primary urological disorders[45]. Therefore, a comprehensive evaluation of both renal and urinary tract function is essential in hypertensive patients presenting with LUTS, as early detection and blood pressure control can help mitigate progression and improve symptom management.

Shared pathophysiological mechanisms linking systemic disease to urological dysfunction: The systemic diseases discussed above, diabetes, lupus, and hypertension, not only affect kidney function directly but also share overlapping pathophysiological mechanisms that drive urological sequelae.

Vascular injury: Microvascular damage from chronic hyperglycemia, hypertension, or autoimmune vasculitis impairs perfusion in both renal and bladder tissues, contributing to nephrosclerosis and detrusor dysfunction. Strict blood pressure and glycemic control, along with vasculitis-targeted immunosuppression, may help preserve bladder and renal perfusion.

Oxidative stress: Elevated reactive oxygen species damage renal tubular cells and bladder innervation, exacerbating diabetic cystopathy and accelerating CKD progression. Antioxidant strategies, lifestyle modification, and tight metabolic control could mitigate progression.

Crystal injury: Disordered mineral metabolism in CKD leads to crystal deposition in renal and bladder tissues, promoting inflammation and fibrosis. Regulation of mineral metabolism through dietary measures and phosphate binders can reduce crystal burden.

Inflammation: Systemic inflammation, whether from autoimmune disease or metabolic syndrome, affects both kidney and bladder function. In lupus, immune complex deposition and cytokine release contribute to nephritis and cystitis. Immunosuppressive therapy in lupus or anti-inflammatory interventions in metabolic syndrome may protect both kidney and bladder.

Gut-kidney axis disruption: CKD-associated dysbiosis and increased gut permeability allow endotoxins to enter circulation, fueling systemic inflammation and potentially sensitizing bladder afferents. Dietary interventions, probiotics, or microbiome-targeted therapies could reduce endotoxin load and improve systemic inflammation.

Recognizing these shared mechanisms is essential for a holistic understanding of CKD-related urological dysfunction. It underscores the need for integrated care approaches that address both systemic disease control and local urological symptom management.

RECURRENT UTIS AND OBSTRUCTIVE UROPATHY

Recurrent UTIs and obstructive uropathy form a vicious cycle that directly contributes to CKD initiation and progression. Obstruction promotes infection through urinary stasis and impaired clearance, while infections particularly with urease-producing organisms exacerbate obstruction via edema, stricture formation, and stone development. These conditions should be emphasized as primary causes of CKD, not incidental findings, because they can initiate renal injury and accelerate decline in GFR. Examples include neurogenic bladder, VUR, prostatic enlargement, ureteral strictures, and recurrent stone disease, all of which predispose patients to both obstruction and infection. Breaking this cycle requires timely decompression of the urinary tract, targeted antimicrobial therapy, and preventive strategies that address both urinary tract mechanics and microbial persistence. Importantly, patients with CKD have a 2-4 times higher risk of UTIs compared to the general population, due to impaired immune function, urinary stasis, and frequent instrumentation[46].

Mechanism, consequences, and co-management strategies

Obstructive uropathy promotes urinary stasis and elevated intratubular pressure, compromising host defenses and fostering bacterial persistence. It is a reversible cause of both acute and CKD. However, delayed intervention risks irreversible damage. While exact global prevalence is variable, obstructive uropathy accounts for approximately 10%-15% of acute kidney injury cases in hospital settings. In CKD populations, structural causes like BPH and ureteral strictures contribute significantly to disease progression, especially in older males[47]. Acute management begins with urgent decompression, which is critical when obstruction is accompanied by infection, acute kidney injury, or severe pain. The primary goal is to relieve pressure and restore urinary flow through temporizing drainage methods such as urethral catheterization, percutaneous nephrostomy, or ureteral stenting, depending on the site and severity of the obstruction. This intervention is often the most decisive factor in improving kidney outcomes. Alongside decompression, targeted antibiotic therapy plays a vital role. Ideally, urine cultures should be obtained before initiating treatment, allowing for empiric coverage that reflects local resistance patterns, followed by de-escalation based on sensitivity results to minimize unnecessary exposure and resistance development[48]. Post-obstructive diuresis, a common physiological response after relief of obstruction, requires close monitoring of fluid balance, electrolytes, and hemodynamic status. Careful replacement of fluids is essential to prevent complications such as hypovolemia and electrolyte imbalances, particularly hyponatremia or hypernatremia[47]. Together, these strategies form a comprehensive approach to stabilizing the patient, preserving kidney function, and reducing infectious burden.

Chronic prevention and stabilization of recurrent UTIs in the context of obstructive uropathy requires a comprehensive and individualized approach. The cornerstone of management is addressing the underlying cause of obstruction, whether it be stones, strictures, BPH, or neurogenic bladder, through definitive urologic correction or durable drainage to ensure low-pressure, complete bladder emptying and reduce the risk of infection. Differentiating between relapse and reinfection is essential; if the same bacterial species recurs, clinicians should investigate for persistent sources such as infected stones, unilateral remnants, or anatomical anomalies using imaging and endoscopic evaluation[46]. Antibiotic stewardship plays a critical role in long-term management, aiming to balance symptom control with the reduction of unnecessary antimicrobial exposure. Guidelines emphasize minimizing overuse, incorporating patient-centered preventive strategies, and reserving suppressive antibiotics for select cases. In persistent infections, tailored antimicrobial regimens that target intracellular bacteria and biofilm-associated communities are often necessary[46]. Ongoing follow-up is vital to reassess residual urine volumes, recurrence patterns, renal function, and any adverse effects from treatment. Prevention strategies should be adjusted iteratively to maintain low recurrence rates while minimizing drug burden and preserving quality of life[48].

Risk of infection-related graft loss in transplant settings

Infection-related graft loss remains a significant concern in kidney transplant settings, where immunosuppression and surgical complexity create a vulnerable environment for infectious complications. Post-transplant infections, particularly sepsis, UTIs, and viral reactivations like BK virus and cytomegalovirus can directly impair graft function and increase the risk of graft failure[49]. Post-operative UTI rates can reach 30%-50% within the first year, with infection-related graft loss occurring in up to 10%-15% of cases depending on severity and pathogen type. A prospective study found that sepsis significantly worsened both patient and graft survival, with kidney replacement therapy and prolonged mechanical ventilation emerging as key predictors of graft loss[50]. Similarly, a retrospective analysis revealed that BK virus and coronavirus disease 2019 infections were strongly associated with increased graft loss, underscoring the impact of viral pathogens in immunocompromised recipients[51].

The mechanisms behind infection-related graft loss include direct cytopathic effects on kidney tissue, immune-mediated injury triggered by infection, and nephrotoxic consequences of antimicrobial therapy. Moreover, infections can precipitate acute rejection episodes or necessitate reductions in immunosuppression, both of which compromise graft integrity. Co-management strategies emphasize early detection, aggressive treatment of infections, and careful modulation of immunosuppressive regimens to balance infection control with graft preservation.

Impact of delayed or inappropriate management on CKD progression

Delayed or inappropriate management of recurrent UTIs and obstructive uropathy can significantly accelerate CKD progression and worsen patient prognosis. Persistent obstruction leads to sustained intrarenal pressure, ischemia, and tubular damage, which may become irreversible if not promptly relieved[52]. Similarly, recurrent infections especially when inadequately treated can cause chronic inflammation, scarring, and pyelonephritis, further compromising kidney function.

In transplant recipients, delayed recognition or mismanagement of infections increases the risk of graft dysfunction and loss. Infections may trigger acute rejection episodes or necessitate reductions in immunosuppression, both of which jeopardize graft survival. Moreover, inappropriate antimicrobial use can promote resistance, complicate future treatment and increasing the risk of sepsis.

These risks underscore the importance of early decompression, accurate microbial identification, and tailored therapy. A proactive, multidisciplinary approach is essential to break the cycle of obstruction and infection, preserve renal function, and improve long-term outcomes.

NEPHROLITHIASIS: THE OVERLAP

CKD and nephrolithiasis share a complex, bidirectional relationship. Stones can act as a primary cause of CKD by inducing obstruction, recurrent infections, and parenchymal scarring. At the same time, CKD itself predisposes to stone formation due to altered calcium-phosphate metabolism, hypocitraturia, and changes in urinary pH. This interplay creates a vicious cycle in which stones accelerate renal decline, while progressive CKD increases the likelihood of recurrent stone disease.

CKD as a risk factor for stones

CKD is increasingly recognized as a risk factor for nephrolithiasis due to altered urinary composition and impaired renal function. Patients with CKD often exhibit reduced urine volume, hypocitraturia, and acid-base disturbances, all of which contribute to stone formation. Moreover, metabolic derangements such as hyperparathyroidism, hyperphosphatemia, and calcium imbalance, common in CKD, further predispose individuals to calcium-based stones[53]. In CKD patients, stone disease must be identified early because obstruction or infection can accelerate renal decline. Management requires balancing stone clearance with preservation of remaining renal function, often prioritizing fewer invasive approaches and close monitoring.

Metabolic considerations and recurrence prevention

Metabolic abnormalities play a central role in the pathogenesis and recurrence of nephrolithiasis. Common contributors include hypercalciuria, hyperoxaluria, hypocitraturia, and hyperuricosuria, each of which alters urinary solubility and promotes crystal formation. Identifying these disturbances through a comprehensive metabolic evaluation including 24-hour urine analysis is essential for targeted prevention. Dietary modifications such as increased fluid intake, reduced sodium and animal protein consumption, and adequate calcium intake can significantly lower recurrence risk. Pharmacologic interventions, including thiazide diuretics for hypercalciuria, potassium citrate for hypocitraturia, and allopurinol for hyperuricosuria, may be warranted based on individual profiles. For example, aggressive fluid intake may risk volume overload, thiazides can worsen electrolyte imbalances, and citrate therapy requires caution in advanced CKD due to acidosis risk. Thus, recurrence prevention must be tailored to renal stage and metabolic profile[54].

Unique considerations in transplant patients

Nephrolithiasis in kidney transplant recipients presents distinct challenges due to altered anatomy, immunosuppression, and graft vulnerability. Stones may form in the native kidneys or the transplanted graft, often going undetected due to denervation and atypical symptoms. Immunosuppressive therapy can exacerbate metabolic risk factors such as hyperuricosuria and hypocitraturia while also increasing susceptibility to infection[55]. In transplant patients, management must prioritize graft preservation. Imaging should minimize nephrotoxicity, and interventions should be carefully selected to avoid jeopardizing graft function. Preventive strategies require multidisciplinary coordination, balancing metabolic correction with immunosuppressive stability.

Influence of prevention and surgical interventions on kidney function

Preventive strategies (hydration, diet, pharmacologic correction) reduce recurrence and protect renal function. However, in CKD patients, these must be carefully adapted: Fluid loading risks overload, and medications require close monitoring[56]. Surgical interventions, including ureteroscopy, percutaneous nephrolithotomy, or shockwave lithotripsy, are often necessary for stone removal. While these procedures can restore urinary flow and prevent further kidney damage, they also carry risks particularly in patients with reduced kidney reserve. Potential complications include bleeding, infection, and transient or permanent loss of kidney function, especially if the procedure involves the solitary kidney or transplanted graft[56]. Surgical choices in CKD must balance urgency of stone clearance with renal reserve. Multidisciplinary planning, preoperative optimization, and postoperative monitoring are essential to ensure that interventions improve, rather than compromise, kidney outcomes[57].

THE ROLE OF THE NEPHROLOGIST IN EARLY DETECTION

Tailoring detection strategies depending on whether the disorder is causal (requiring early intervention) or consequential (requiring complication management) is essential.

Clinical vigilance: History, physical exam, and targeted testing

Clinical vigilance is the cornerstone of early detection and effective management in nephrology and urology, requiring a disciplined approach to history-taking, physical examination, and targeted testing. A detailed patient history should explore urinary symptoms such as frequency, urgency, dysuria, hematuria, and nocturia, as well as systemic signs like fatigue, edema, or hypertension that may signal renal involvement. Past medical events especially recurrent infections, stone disease, or urological surgeries can offer critical clues. The physical exam complements this by assessing for signs like costovertebral angle tenderness, bladder distension, or peripheral edema, which may indicate obstructive or inflammatory processes. Targeted testing then sharpens diagnostic accuracy: Serum creatinine and GFR assess renal function, urinalysis detects proteinuria or hematuria, and imaging studies such as renal ultrasound or computed tomography scans reveal structural abnormalities. Together, these elements form a vigilant clinical framework that enables timely intervention and collaborative care[58].

Biomarkers and imaging strategies

The nephrologist plays a critical role in the early detection of kidney disease, particularly when subtle or atypical presentations mask underlying pathology. Traditional markers like serum creatinine and estimated GFR often lag behind actual renal injury, prompting the need for more sensitive and specific biomarkers. Emerging tools such as neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and cystatin C offer earlier insights into tubular damage and filtration deficits, often before irreversible changes occur. Inflammatory markers like interleukin-18 and monocyte chemotactic protein-1 further enhance diagnostic precision by reflecting ongoing injury and repair processes[59]. Imaging strategies complement biomarker data by revealing structural and functional abnormalities. Renal ultrasound remains a first-line modality for assessing kidney size, echogenicity, and obstruction. Advanced imaging such as computed tomography urography or magnetic resonance imaging can detect subtle anatomical changes, vascular compromise, or masses. In cases of contrast-induced nephropathy, imaging must be paired with biomarker-driven risk stratification to minimize harm[60]. By integrating these diagnostic tools, nephrologists can identify kidney dysfunction at its earliest stages, tailor interventions, and collaborate effectively with other specialties to preserve kidney health.

Red flags requiring urology referral

In the early detection of kidney dysfunction, nephrologists must remain alert to specific red flags that warrant timely referral to urology for specialized evaluation and intervention. These red flags often signal underlying structural or malignant urological conditions that may contribute to or mimic CKD (Figure 1). Nephrologists serve as gatekeepers in identifying these warning signs and ensuring swift collaboration with urologists. This interdisciplinary approach is vital to prevent irreversible renal damage and to address potentially life-threatening conditions at an early stage.

Figure 1 Red flags for urology referral. UTI: Urinary tract infection; PSA: Prostate-specific antigen; DRE: Digital rectal examination.

COLLABORATIVE MANAGEMENT FRAMEWORK

Effective management of CKD requires integration of nephrological and urological care, since urinary tract complications can both initiate and accelerate renal decline. Table 6 outlines a stage-based nephron-urological management pathway, highlighting routine screening, referral triggers, and co-management goals across the CKD spectrum.

Table 6 Stage-based nephro-urological management pathway in chronic kidney disease.

CKD stage	Routine urological screening	Referral triggers	Co-management goals
Stage 1-2 (early CKD)	(1) Urinalysis (proteinuria, hematuria); (2) Kidney/bladder ultrasound; and (3) History of LUTS, recurrent UTIs, stone disease	(1) Recurrent UTIs; (2) Hematuria not explained by nephrology; and (3) Suspected obstruction (hydronephrosis, poor bladder emptying)	(1) Identify and treat reversible urological causes early; and (2) Prevent progression of CKD
Stage 3-4 (moderate CKD)	(1) Post-void residual measurement Uroflowmetry if LUTS present; and (2) Stone risk assessment (metabolic work-up)	(1) Persistent LUTS despite medical therapy; and (2) Recurrent stones Obstructive uropathy on imaging	(1) Slow CKD progression; (2) Prevent recurrent infections and obstruction; and (3) Optimize bladder function
Stage 5 (ESKD, pre-dialysis)	(1) Focused urological history and exam; and (2) Imaging for obstruction if symptoms/signs present	(1) Hydronephrosis or ureteral stricture; and (2) Severe LUTS impacting quality of life	(1) Prepare for renal replacement therapy; and (2) Ensure unobstructed urinary tract before transplant
Dialysis-dependent	(1) Catheter/vascular access infection surveillance; and (2) Bladder function assessment in long-term dialysis	(1) Recurrent UTIs or urosepsis; and (2) Catheter-related complications	(1) Prevent infection; (2) Manage bladder dysfunction; and (3) Maintain quality of life

CKD: Chronic kidney disease; ESKD: End-stage kidney disease; LUTS: Lower urinary tract symptoms; UTI: Urinary tract infection.

Case-based nephro-urology collaborations

Case-based discussions have highlighted the value of such partnerships, where timely interdisciplinary coordination has led to successful interventions[61]. For instance, in a case of xanthogranulomatous pyelonephritis, a rare and aggressive renal infection, nephrologists identified atypical renal dysfunction, and referred the patient for surgical evaluation, leading to a life-saving nephrectomy. Another case involved a pediatric patient with steroid-resistant nephrotic syndrome and an alpha-actinin-4 variant, where joint management enabled successful transplantation. These examples show how shared decision-making and integrated planning improve outcomes.

Integrated care models

Hospital-based models include multidisciplinary rounds and co-managed units for conditions like obstructive uropathy and post-surgical acute kidney injury. Shared electronic health records and rapid referrals streamline care. Outpatient joint clinics address overlapping issues like CKD with BPH or recurrent UTIs, while telemedicine ensures continuity for remote patients. These models enhance efficiency, accuracy, and patient-centered care.

Patient education and shared decision-making

Patient education and shared decision-making are foundational to high-quality care in both nephrology and urology, empowering individuals to actively participate in decisions that affect their health outcomes. In CKD, for example, patients may face complex choices between dialysis modalities, conservative management, or transplantation decisions that carry profound lifestyle implications. Similarly, in urology, shared decision-making is critical when discussing prostate cancer screening, surgical interventions, or managing recurrent infections. Studies show that patients engaged in shared decision-making report greater satisfaction, improved adherence, and better alignment between treatment plans and personal goals[62]. By prioritizing education and dialogue, clinicians can move beyond paternalistic models and create partnerships that honor the patient’s voice at every stage of care.

Challenges and barriers to interdisciplinary implementation

While collaborative nephro-urology care offers clear benefits, its implementation faces several real-world challenges. Structural barriers such as fragmented healthcare systems, siloed specialties, and inconsistent referral pathways often hinder timely coordination. Resource limitations, including staffing shortages, lack of dedicated joint clinics, and limited access to advanced diagnostics or telemedicine infrastructure, further constrain integration. Cultural and professional boundaries may also impede collaboration. Differences in clinical priorities, communication styles, and decision-making frameworks between nephrologists and urologists can lead to misalignment or delays. Variability in electronic health record systems and data-sharing protocols can obstruct seamless information exchange. From the patient perspective, limited health literacy, financial constraints, and geographic barriers may reduce engagement in shared decision-making or access to multidisciplinary care. In transplant settings, balancing immunosuppression with infection risk adds complexity to joint management.

Addressing these barriers requires systemic reform, including incentivizing interdisciplinary models, investing in shared infrastructure, and fostering a culture of collaboration through joint training and communication protocols. By acknowledging these limitations, clinicians and policymakers can work toward more equitable and effective care delivery.

CONCLUSION

CKD is inseparably linked with urological comorbidities such as obstructive uropathy, recurrent UTIs, nephrolithiasis, and bladder dysfunction. These conditions are not incidental but integral to CKD progression and outcomes. Nephrologists must adopt a proactive approach that includes routine screening for urological risk factors, timely referrals, and close collaboration with urologists. Such interdisciplinary synergy is essential to prevent kidney injury, delay disease progression, and deliver comprehensive, patient-centered care.

From a practice standpoint, nephrologists should integrate structured urological assessments into CKD management, while urologists should remain vigilant about renal implications of their interventions. Joint guidelines from nephrology and urology societies are urgently needed to standardize care pathways, reduce fragmentation, and promote collaborative management[63].

From a research perspective, systematic reviews have shown that artificial intelligence and remote monitoring technologies can enhance diagnostic accuracy, predict CKD progression, and improve patient engagement[64-66]. However, most studies remain exploratory or single-center, underscoring the need for multicenter trials and meta-analyses to validate these tools in diverse populations. Future research should also evaluate the long-term impact of integrated nephro-urological care models on patient outcomes, quality of life, and healthcare costs.

Ultimately, the convergence of nephrology and urology represents a critical frontier in CKD care. By embracing interdisciplinary collaboration, evidence-based guidelines, and technological innovation, clinicians can reshape management strategies to meet the growing global burden of CKD.