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Pyuria

Pyuria is a medical condition defined as the presence of an elevated number of , or leukocytes, in the , also known as leukocyturia, often appearing as —a thick fluid composed of dead cells, tissue debris, and —which can make the cloudy or discolored. It is typically diagnosed when there are at least 10 per high-power field or per cubic millimeter in a urine sample, and it serves as a key indicator of inflammation or infection in the urinary tract. While most cases are linked to bacterial infections such as urinary tract infections (UTIs), pyuria can occur without detectable , a phenomenon known as sterile pyuria. Sterile pyuria, which occurs in about 14% of females and 2.6% of males, may result from non-bacterial infections, STIs, or non-infectious conditions, and requires further evaluation to identify the underlying cause. Prompt medical attention is essential, as untreated pyuria can lead to serious complications.

Definition and Terminology

Definition

Pyuria is the abnormal presence of , or leukocytes, in the , typically defined as at least 10 leukocytes per on microscopic examination of centrifuged , or at least 10 leukocytes per cubic millimeter in uncentrifuged . This condition indicates an inflammatory response in the urinary tract, where pus-forming cells accumulate and are excreted. The term is often used interchangeably with leukocyturia, referring to the detection of leukocytes in samples. In healthy individuals, urine normally contains few or no leukocytes, with a typical range of 0 to 5 per , signifying the absence of pathological processes such as or . Exceeding these thresholds suggests pyuria, prompting further clinical evaluation to distinguish it from normal variations or . The word "pyuria" originates from the Greek "pyon," meaning , and "ouron," meaning , entering medical literature in the late as a descriptor for pus-laden . It gained prominence in 19th-century clinical descriptions of urinary disorders. Pyuria frequently accompanies urinary tract infections, which have an annual incidence of approximately 10% to 20% among women, with elevated rates in vulnerable groups such as those using indwelling urinary catheters. Leukocyturia is the primary for pyuria and is frequently used interchangeably in clinical contexts to describe the presence of (leukocytes) in the , at least 10 per on microscopic examination. This equivalence arises because pyuria fundamentally involves leukocytes or , which consists mainly of these cells along with debris, making the terms overlap in diagnostic reporting for urinary tract conditions. Pyuria must be distinguished from , which denotes the presence of red blood cells in the indicating potential bleeding or vascular issues, and from , characterized by excessive protein excretion often signaling glomerular dysfunction. While all three are abnormal findings, pyuria specifically highlights an inflammatory or infectious response involving , whereas hematuria and proteinuria point to hemorrhagic or renal filtration abnormalities, respectively. Colloquial or outdated expressions like " in the " or "leukocytes in " refer to the same condition but lack the precision of modern terminology, often appearing in older texts or lay descriptions before standardized microscopic criteria were established. The term pyuria derives etymologically from the Greek "pyon," meaning , and "ouron," meaning , with its first recorded medical use dating to in Latin . Leukocyturia, in contrast, stems from "leukos" (), "kytos" (), and "ouron" (), reflecting a later 19th-century shift toward cellular specificity as advanced in . In and , terminology has evolved from broad descriptive phrases like "pus in " in early observations to pyuria in the 18th and 19th centuries, and increasingly to leukocyturia in contemporary practice for its alignment with quantitative sediment analysis and avoidance of implying gross suppuration. This progression emphasizes diagnostic accuracy in identifying sterile or infectious leukocyturia without conflating it with visible purulent discharge.

Pathophysiology

Mechanisms of White Blood Cell Presence

Pyuria arises from the accumulation of white blood cells (WBCs), primarily neutrophils, in the urine as part of the inflammatory response in the urinary tract. This process begins with the activation of local tissues by irritants or pathogens, triggering the release of pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), which upregulate endothelial expression of adhesion molecules on nearby blood vessels. These molecules facilitate the initial tethering and rolling of circulating leukocytes along the vascular endothelium, marking the onset of leukocyte extravasation into the perivascular space. Leukocyte recruitment to the urothelium involves a multi-step cascade governed by and specific interactions. , including interleukin-8 (IL-8), are secreted by epithelial cells and resident immune cells in response to , creating a that directs migration from the bloodstream through the and toward the urothelial lining. molecules play a critical role: selectins (e.g., ) mediate initial loose binding, while (e.g., LFA-1 binding to ) enable firm and subsequent diapedesis, allowing leukocytes to traverse the vessel wall and enter the interstitial space. Once in the tissue, continued chemotactic signaling propels these cells toward the luminal side of the urothelium, where they are shed into the urine. Epithelial damage in the urinary tract further promotes leukocyte passage into the by compromising barrier integrity. In cases of urothelial or injury, disrupted tight junctions and desquamated epithelial cells create pathways for interstitial leukocytes to access the urinary directly. The origin of these leukocytes differs based on the site of : glomerular sources are less common and typically involve damage to the , permitting rare passage of WBCs into Bowman's space and downstream tubules, often alongside red cells in glomerular diseases. In contrast, and origins predominate in most pyuria cases, where leukocytes accumulate in the renal or collecting ducts due to tubulointerstitial , then enter the via disrupted without breaching the glomerular filtration barrier. The severity of urinary tract correlates quantitatively with leukocyte counts in the , serving as a marker of the extent of involvement. Elevated concentrations, often exceeding 10 cells per , reflect intense influx and ongoing cytokine-driven recruitment, with higher counts indicating more severe or widespread . In renal parenchymal involvement, this can lead to the formation of casts, where aggregated leukocytes mold within distal tubules or collecting ducts amid proteinaceous material, signifying intratubular and potential progression to damage.

Types of Pyuria

Pyuria can be classified into several types based on the presence or absence of bacteria, the source of leukocytes, and specific cellular composition. These distinctions aid in differentiating infectious from non-infectious etiologies and identifying potential contaminants or rare variants. Sterile pyuria refers to the presence of white blood cells in the urine without detectable bacterial growth on standard quantitative urine culture, typically defined as fewer than 10^5 colony-forming units per milliliter. It is diagnosed when pyuria—generally more than 10 leukocytes per cubic millimeter or greater than 3 leukocytes per high-power field in unspun urine—is accompanied by a negative culture result, often confirmed by dipstick showing positive leukocyte esterase but negative nitrites. This type accounts for a notable proportion of pyuria cases, with prevalence reported up to 13.9% in females and 2.6% in males in general population studies, though rates can reach 70% or higher in specific contexts like chronic kidney disease. In contrast, septic pyuria, also known as non-sterile pyuria, involves both elevated and significant bacterial growth in the , commonly signifying an active bacterial . This type is characterized by the same pyuria thresholds but with positive urine culture results identifying pathogens such as or other uropathogens, often correlating with symptoms like or fever. It represents the majority of infectious pyuria instances, particularly in acute settings where bacterial invasion triggers leukocyte recruitment. Pyuria is further distinguished as true or false based on whether the leukocytes originate from genuine urinary tract or external . True pyuria arises from actual pathophysiological processes in the , such as , , or tissue damage leading to leukocyte migration into the . False pyuria, however, results from specimen , often by vaginal secretions containing squamous epithelial cells and leukocytes or urethral during improper collection, which can mimic pyuria on but lacks clinical correlation with urinary . Midstream clean-catch techniques are recommended to minimize false positives. Eosinophilic pyuria is a rare subtype defined by the predominance of among urinary leukocytes, typically identified through Hansel's stain or specialized showing more than 1% eosinophils relative to total . It is particularly associated with allergic or drug-induced acute , where reactions cause infiltration into the renal and eventual urinary excretion. This form occurs infrequently, and its presence supports targeted evaluation for allergic over bacterial causes.

Causes

Infectious Causes

Infectious causes of pyuria primarily involve microbial invasion of the urinary tract, leading to an inflammatory response with accumulation in the urine. Bacterial infections are the most frequent etiology, accounting for the majority of cases, particularly through ascending infections from the periurethral area. Among bacterial pathogens, is the predominant cause, responsible for 70-95% of uncomplicated urinary tract infections (UTIs) that result in pyuria. This gram-negative bacterium adheres to uroepithelial cells via fimbriae, facilitating colonization and ascent from the to the kidneys in complicated cases. Other common bacterial contributors include species, , and species, which together comprise 10-20% of UTI-related pyuria and often occur in patients with risk factors such as indwelling catheters or structural abnormalities. Septic pyuria, a severe form involving systemic bacteremia, is typically associated with these pathogens in hospitalized or immunocompromised individuals. Viral infections contribute to pyuria less commonly but are significant in immunocompromised hosts. Adenovirus, particularly serotypes 11 and 21, can cause acute with pyuria due to direct epithelial cell infection and inflammation in the bladder. Similarly, BK polyomavirus reactivation in transplant recipients leads to pyuria through in urothelial cells, often manifesting as with leukocyte shedding. Fungal and parasitic agents are rarer causes, typically affecting vulnerable populations. Candida species, especially C. albicans, induce pyuria in diabetics, catheterized patients, or those on broad-spectrum antibiotics by forming biofilms and invading the urinary mucosa. Parasitic infections like in endemic regions of and the provoke eosinophilic pyuria through oviposition in the bladder wall, triggering granulomatous inflammation. Sexually transmitted infections often present with pyuria due to in sexually active individuals. Chlamydia trachomatis and are key culprits, causing nongonococcal and gonococcal urethritis, respectively, with inflammatory containing polymorphonuclear leukocytes that appear in urine sediment. These infections may lead to sterile pyuria on standard bacterial culture if not specifically tested.

Non-Infectious Causes

Non-infectious causes of pyuria encompass a range of inflammatory, structural, systemic, and iatrogenic factors that lead to the presence of in the without detectable microbial growth on standard cultures, often manifesting as sterile pyuria. These etiologies arise from mechanical irritation, immune-mediated responses, or direct tissue injury, and they require differentiation from infectious processes through targeted diagnostic evaluation. Inflammatory conditions frequently contribute to pyuria through tubulointerstitial damage or autoimmune mechanisms. Drug-induced , for instance, results from reactions to medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics like penicillins, or proton pump inhibitors, leading to leukocyte infiltration in the renal and subsequent pyuria. Autoimmune diseases, including systemic lupus erythematosus (SLE) in which approximately 23% of patients exhibit sterile pyuria due to immune complex deposition in the kidneys. Structural abnormalities in the urinary tract can provoke pyuria via chronic irritation or obstruction, promoting leukocyte shedding into the urine. Urinary stones (nephrolithiasis) cause mechanical trauma to the urothelium, resulting in and pyuria, particularly with staghorn calculi or recurrent calculi. Tumors, such as those in the , , or , similarly induce sterile pyuria through local tissue disruption and may serve as a marker for recurrence in . Indwelling catheters or stents exacerbate this by fostering formation and epithelial irritation without bacterial colonization. Systemic diseases extend beyond the urinary tract to indirectly cause pyuria through widespread inflammatory or vasculitic processes. , a medium-vessel primarily affecting children, is linked to sterile pyuria alongside and due to renal endothelial involvement. Other systemic contributors include , which triggers granulomatous inflammation in the kidneys, and renal , where immune-mediated allograft injury leads to leukocyte . Iatrogenic factors often stem from medical interventions that disrupt the urinary . Post-instrumentation pyuria commonly follows procedures like or nephroscopy, where transient trauma induces a sterile inflammatory response. Radiation cystitis from pelvic radiotherapy and contrast-induced nephropathy from dyes also provoke pyuria through direct mucosal damage or acute tubular injury.

Diagnosis

Urinalysis Methods

Proper collection of urine samples is essential for accurate detection of pyuria to minimize contamination from external sources such as . The preferred method is the midstream clean-catch technique, where the patient cleanses the genital area and discards the initial urine stream before collecting a midstream sample in a sterile container. This approach is non-invasive and suitable for most adults and older children. In cases where clean-catch collection is not feasible, such as in infants or immobilized patients, catheterization may be used, though it carries a risk of introducing and is reserved for necessary situations. First morning urine is often recommended due to its higher concentration of solutes and cells accumulated overnight, enhancing detection sensitivity; samples should be analyzed within two hours or refrigerated to prevent cell degradation. Dipstick urinalysis provides a rapid, point-of-care screening for pyuria through detection of , an enzyme released by (WBCs) that hydrolyzes a on the test strip, producing a color change. This indicates the presence of WBCs but can yield false negatives in conditions like high urinary specific gravity, , or ascorbic acid interference, and false positives with certain medications or vaginal contamination. The test demonstrates a of 72-97% and specificity of 41-86% for identifying pyuria associated with urinary tract s, making it a useful initial tool despite its limitations in confirming etiology. In older adults, pooled data show a of approximately 90% and specificity of 56% for bacteriuria detection via . Microscopic examination of urine sediment remains a cornerstone for confirming pyuria, involving centrifugation of 10-15 mL of well-mixed urine at 1,500-3,000 rpm for five minutes, followed by resuspension of the sediment and viewing under high-power field (HPF) magnification. Pyuria is typically defined as 10 or more WBCs per HPF (> approximately 25 WBCs/mm³) in the sediment or >10 WBCs/μL in uncentrifuged urine, though thresholds may vary slightly by gender, with normal ranges under 2 WBCs/HPF for men and under 5 WBCs/HPF for women. This method allows visualization of WBC morphology and associated findings like bacteria or casts, but it is labor-intensive and subject to inter-observer variability. Automated has emerged as an objective alternative in modern laboratories, using instruments like the Sysmex UF-500i to quantify leukocytes through laser-based detection of cell fluorescence and light scatter in uncentrifuged samples. This technique reduces subjectivity compared to , provides rapid results within minutes, and screens out a significant proportion of culture-negative samples (up to 64.5%), thereby streamlining workflows. Cutoff values, such as 10-17 WBCs/μL adjusted for age and gender, offer high negative predictive value (around 99%) for ruling out significant pyuria.

Confirmatory Tests

Confirmatory tests for pyuria aim to identify the underlying , distinguishing between infectious and non-infectious causes after initial detects in the . Urine culture remains the gold standard for confirming bacterial infections responsible for pyuria, particularly in suspected urinary tract infections (UTIs). This test involves inoculating a sample onto culture media to identify and quantify , with a (CFU) count exceeding 10^5 CFU/mL in a clean-catch specimen typically indicating significant diagnostic of UTI. In cases of sterile pyuria, where no is detected despite pyuria, culture helps rule out common bacterial pathogens and guides further investigation into atypical or non-bacterial causes. For sterile pyuria or when standard cultures are negative, (PCR) and other molecular tests provide rapid detection of atypical pathogens such as Chlamydia trachomatis or Mycoplasma genitalium, which may not grow on routine media. amplification tests (NAATs), including PCR, offer high sensitivity (25%-93%) and specificity (95%-100%) for these organisms, making them particularly useful in sexually active patients or those with persistent pyuria. In suspected genitourinary tuberculosis, PCR on three consecutive morning samples can detect Mycobacterium tuberculosis with improved sensitivity (up to 80%-90%) when combined with acid-fast bacilli staining and culture, aiding in the diagnosis of this rare but serious cause of sterile pyuria. Imaging modalities are employed to evaluate structural abnormalities contributing to pyuria, such as urinary stones, obstructions, or malignancies, especially in recurrent or complicated cases. Renal and serves as an initial non-invasive option to detect , calculi, or abscesses, while computed tomography () provides higher sensitivity for identifying renal calcifications (40%-70% in genitourinary TB) or ureteral strictures. allows direct visualization of the mucosa for evaluation of , tumors, or foreign bodies, and is particularly indicated when suggests intravesical pathology. Blood tests complement urinary evaluations by assessing systemic involvement or inflammation associated with pyuria. A complete blood count (CBC) may reveal leukocytosis, indicating an active infection or inflammatory process, while elevated C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) levels support the presence of ongoing inflammation. Specific serologic tests, such as interferon-gamma release assays (e.g., QuantiFERON-TB Gold) for tuberculosis or antinuclear antibody (ANA) testing for autoimmune conditions like systemic lupus erythematosus, help identify non-infectious etiologies when clinical suspicion is high.

Clinical Presentation

Symptoms and Signs

Pyuria, characterized by the presence of in the , often manifests through symptoms related to underlying urinary tract or , with (painful ), urinary frequency, and urgency serving as hallmark features in the majority of symptomatic cases. These are common in women with acute uncomplicated cystitis, a common cause of pyuria, reflecting irritation of the mucosa. Suprapubic discomfort may accompany these, further indicating localized . Visible signs of pyuria include cloudy urine due to the accumulation of and , which can alter the 's appearance and sometimes lead to a foul odor. , or blood in the , may occur concurrently in up to 30% of cases associated with pyuria, presenting as pink, red, or cola-colored . In cases involving the upper urinary tract, such as , additional signs emerge, including fever (often exceeding 38°C), chills, and flank pain radiating to the , signaling renal involvement. Asymptomatic pyuria, where are present without overt symptoms, is frequently detected incidentally through routine and is particularly common in certain populations. In elderly individuals, asymptomatic (often accompanied by pyuria) has a prevalence reaching 25-50% in institutional settings, linked to age-related changes in urinary tract mechanisms. Among diabetics, asymptomatic pyuria occurs in 10-30% of cases, with higher rates in women (up to 21%) compared to non-diabetics (around 9%), attributed to impaired immune responses and promoting bacterial growth. In pediatric patients, especially infants, pyuria presentations are often nonspecific due to limited verbal communication. Common signs include , poor feeding, , and , which may mimic other childhood illnesses; fever is a key indicator, as urinary tract infections account for approximately 5-7% of fevers in infants younger than 24 months. Older children may exhibit more classic symptoms like or , but early detection relies on recognizing these subtle cues in younger age groups.

Associated Conditions

Pyuria is frequently observed as a secondary finding in patients with (CKD), where it occurs in approximately 30-50% of cases due to recurrent urinary tract infections or underlying renal parenchymal such as . Studies indicate that the prevalence of pyuria, including sterile forms, is approximately 22% in CKD populations, with higher rates in advanced stages or among those on , reflecting impaired urinary tract defenses and increased susceptibility to . This association underscores the need for vigilant monitoring in CKD management, as persistent pyuria may signal ongoing renal injury independent of active infection. In pregnancy, pyuria is linked to physiological changes such as urinary and hormonal alterations that heighten the risk of ascending infections, affecting 5-10% of pregnancies through associated urinary tract infections. pyuria, in particular, has been reported in up to 21% of first-trimester cases, often preceding symptomatic cystitis or if untreated. These changes predispose pregnant individuals to bacterial ascension from the lower to upper urinary tract, making routine screening essential to mitigate maternal and fetal risks. Immunosuppressed patients, including those with or post-transplant status, exhibit a higher incidence of pyuria owing to opportunistic infections and reduced immune surveillance of the urinary tract. In untreated patients, pyuria is present in about 13% of cases, frequently tied to viral or atypical pathogens like that evade standard cultures. Among kidney transplant recipients, urinary tract infections—often manifesting as pyuria—affect up to 74% within the first year, driven by surgical factors, indwelling catheters, and immunosuppressive regimens that facilitate bacterial and fungal colonization. This elevated risk highlights the role of pyuria as an early indicator of infection in these vulnerable groups, necessitating tailored diagnostic approaches. Malignancies, particularly , are commonly associated with sterile pyuria in approximately 20% of cases, where tumor-related or obstruction leads to leukocyte infiltration without detectable . Preoperative pyuria in bladder tumor patients correlates with high-grade disease and advanced pathologic stages, serving as a potential for tumor aggressiveness and intravesical recurrence risk. This non-infectious emphasizes the importance of investigating persistent pyuria in the context of genitourinary neoplasms to avoid misdiagnosis as routine .

Treatment and Management

Management of Infectious Pyuria

The management of infectious pyuria focuses on eradicating the underlying bacterial infection, typically a urinary tract infection (UTI) caused by pathogens such as Escherichia coli. Initial treatment employs empiric antibiotic therapy, with first-line options for uncomplicated lower UTI including nitrofurantoin (100 mg orally twice daily for 5-7 days) or trimethoprim-sulfamethoxazole (160/800 mg orally twice daily for 3 days), provided local resistance rates to trimethoprim-sulfamethoxazole are below 20%. In cases of suspected resistance or complicated infections, urine culture and susceptibility testing guide targeted therapy, potentially involving alternatives like fosfomycin (3 g single oral dose) or beta-lactams such as cephalexin. Treatment duration varies by site and severity: 3-7 days for uncomplicated cystitis and 5-7 days for or other complicated upper tract infections, with durations guided by clinical response to minimize use. Supportive measures include increasing fluid intake to promote urinary flushing, use of analgesics like phenazopyridine (200 mg orally three times daily for up to 2 days) to alleviate , and avoidance of bladder irritants such as and . Follow-up involves repeat urinalysis 1-2 weeks post-treatment to verify clearance of pyuria and absence of persistent , with if symptoms recur or in high-risk patients.

Management of Sterile Pyuria

Management of sterile pyuria requires a targeted approach focused on identifying and addressing the underlying etiology, which may be infectious (e.g., non-bacterial pathogens such as those causing or sexually transmitted infections) or non-infectious, as empiric antibiotics are ineffective and may promote resistance. Initial evaluation involves a thorough history and to assess for potential causes such as medication use, autoimmune disorders, or structural abnormalities, followed by repeat with proper midstream clean-catch technique to confirm persistent pyuria without bacterial growth. For drug-induced sterile pyuria, the primary intervention is prompt discontinuation of the offending agent, such as nonsteroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), or antibiotics like , which often leads to resolution of symptoms and pyuria within weeks. In cases of genitourinary tuberculosis (GU-TB), confirmed through acid-fast bacilli (AFB) staining, culture, or () on three consecutive first-morning voided urine samples, standard anti-TB therapy with a regimen including isoniazid, rifampin, pyrazinamide, and ethambutol for 6–9 months is recommended, with monitoring for response via serial imaging and . Anti-inflammatory treatments are tailored to the specific cause; for autoimmune conditions like or , corticosteroids such as (initial dose 0.5–1 mg/kg/day) may be initiated to reduce inflammation and resolve pyuria, often in conjunction with immunosuppressive therapy if needed. For irritation from urinary stones, analgesics like acetaminophen or NSAIDs provide symptomatic relief, while definitive management involves stone removal via or ureteroscopy to eliminate the mechanical stimulus for leukocyte recruitment. In patients, close monitoring with serial every 4–6 weeks is preferred over immediate to track resolution without unnecessary antibiotics, particularly if the remains unclear after initial . For structural issues such as ureteral obstruction or indwelling causing pyuria, targeted interventions like stent placement or are indicated to restore urinary flow and reduce , guided by imaging such as or computed tomography (). A multidisciplinary approach is essential, with referral to for suspected structural or neoplastic causes (e.g., evaluation via ) or to for autoimmune etiologies, ensuring comprehensive care and preventing delays in . Ongoing collaboration among , infectious disease specialists, and allied health professionals facilitates holistic , especially in or cases.

Prognosis and Complications

Prognosis

The prognosis of pyuria is generally favorable when promptly identified and managed according to its underlying cause, with outcomes varying significantly between infectious and sterile forms. In uncomplicated infectious pyuria, typically associated with bacterial urinary tract infections (UTIs), appropriate antibiotic therapy leads to resolution in the majority of cases, often within 5 to 7 days. Clinical success rates exceed 80%, with symptoms and pyuria resolving in most patients without progression to complicated disease. Sterile pyuria presents more variable outcomes, depending on the etiology such as non-bacterial , inflammatory conditions, or medications. Resolution occurs following targeted of the underlying cause, though persistence is common in chronic conditions like renal , where anti-tubercular therapy may take months to clear leukocytes from the . Poor prognostic factors include , advanced age, , and delayed diagnosis, which can elevate recurrence rates to 20% to 30% by allowing progression to upper tract involvement or chronic inflammation. Long-term, pyuria carries a low mortality risk of less than 1% in uncomplicated scenarios, but untreated cases may contribute to through repeated or parenchymal damage.

Potential Complications

Untreated pyuria resulting from infectious urinary tract infections (UTIs) can progress to ascending infections, leading to in vulnerable populations such as the elderly, where complicated UTIs account for approximately 10% to 30% of all cases. This risk is heightened in older adults due to factors like impaired immune responses and comorbidities, with urosepsis representing about 25% of adult instances overall. Early is critical, as from pyuria-associated UTIs can result in high mortality rates if not addressed promptly. In cases of , a common infectious cause of pyuria, renal scarring develops in approximately 15% of affected children, based on meta-analyses of post-infection imaging. This scarring can lead to long-term in 10% to 30% of children and young adults with such damage, as well as contribute to renal insufficiency over time. The risk is particularly elevated in younger children with or recurrent episodes, potentially progressing to if scarring is extensive. Persistent sterile pyuria arising from structural abnormalities, such as urinary tract , may cause due to ongoing and irritation in the . For instance, conditions like urogenital or genitourinary can manifest as sterile pyuria with structural complications, including fistula formation, which exacerbates and leads to issues like abscesses or recurrent leakage. These sequelae often require surgical correction to alleviate symptoms and prevent further deterioration. Misdiagnosis of pyuria as a bacterial UTI frequently results in unnecessary antibiotic prescriptions, fostering among uropathogens. This overuse, particularly in or sterile cases, contributes to broader patterns of resistance. Such practices not only elevate individual risks of resistant infections but also amplify global challenges in treating common UTIs.

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