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Summary Table

Feature	Details
Risk Factors	Children (minimal change disease), diabetes mellitus, SLE, amyloidosis, chronic infections (HIV, Hepatitis B/C), NSAID use, malignancies (membranous nephropathy in adults)
Etiology	Podocyte injury leading to disruption of the glomerular filtration barrier with resultant proteinuria
Patient Presentation	Periorbital and peripheral edema (worse in the morning), foamy urine, weight gain, fatigue
Classic Physical Exam	Periorbital edema, pitting edema of lower extremities, ascites, pleural effusion, anasarca in severe cases
Key Diagnostic Results	Proteinuria >3.5 g/day (or >40 mg/m$^2$/hour in children), hypoalbuminemia (<2.5 g/dL), hyperlipidemia, lipiduria (oval fat bodies, "Maltese cross" under polarized light), fatty casts
Management	Treat underlying cause; ACE inhibitors/ARBs for proteinuria reduction; corticosteroids (especially in minimal change disease); diuretics for edema; statins for hyperlipidemia; anticoagulation if thrombotic complications arise
Keywords	"Foamy urine," "periorbital edema," "oval fat bodies," "Maltese cross," "nephrotic-range proteinuria," "hypoalbuminemia with hyperlipidemia"

1. Pathophysiology

Nephrotic syndrome arises from damage to the glomerular filtration barrier, which consists of three layers: the fenestrated endothelium, the glomerular basement membrane (GBM), and the podocyte foot processes with their slit diaphragms. The podocyte layer is the final gatekeeper that prevents large proteins from crossing into the urine. When podocytes are injured, whether by immune complex deposition, metabolic damage, or cytokine-mediated effacement, the slit diaphragms lose their integrity and albumin freely passes into the filtrate.

The hallmark consequence is heavy proteinuria (>3.5 g/day), which directly drives the remaining features of the syndrome. As albumin is lost in the urine, serum albumin drops, reducing plasma oncotic pressure. This causes fluid to shift from the intravascular compartment into the interstitial space, producing edema. The liver responds to low oncotic pressure by ramping up protein synthesis broadly, which includes not only albumin but also lipoproteins, leading to hyperlipidemia. Since lipids are now elevated and filtered, they appear in the urine as lipiduria (oval fat bodies and fatty casts).

A critical and frequently tested consequence is hypercoagulability. The kidney loses antithrombin III in the urine (it is a relatively small protein that crosses the damaged barrier). Combined with elevated hepatic synthesis of clotting factors and hyperviscosity from hemoconcentration, patients are at high risk of venous thromboembolism, particularly renal vein thrombosis. Sudden-onset flank pain and hematuria in a nephrotic patient should immediately raise concern for this complication.

Another underappreciated consequence is increased susceptibility to infection. Loss of immunoglobulins (especially IgG) in the urine leaves patients vulnerable, particularly to encapsulated organisms such as Streptococcus pneumoniae. Spontaneous bacterial peritonitis is a well-recognized complication in nephrotic children with ascites. The Indonesian Pediatric Society (IDAI) consensus highlights that infection, cellulitis, and primary peritonitis are the leading infectious complications, with pneumonia and upper respiratory tract infections also frequently encountered.

2. Classification and Clinical Manifestation

Nephrotic vs. Nephritic Syndrome

Feature	Nephrotic Syndrome	Nephritic Syndrome
Core Mechanism	Podocyte injury causing disrupted filtration barrier	Inflammatory damage to glomerular capillaries
Proteinuria	>3.5 g/day (nephrotic-range)	<3.5 g/day (subnephrotic, but still present)
Hematuria	Absent or minimal	Present, often with dysmorphic RBCs
Urine Sediment	"Bland/fatty": oval fat bodies, fatty casts, Maltese cross	"Active": RBC casts (pathognomonic), WBC casts
Edema	Severe (periorbital, peripheral, anasarca) due to low oncotic pressure	Mild to moderate, due to salt/water retention
Hypoalbuminemia	Prominent (<2.5 g/dL)	Mild or absent
Hyperlipidemia	Present (compensatory hepatic synthesis)	Absent
Blood Pressure	Often normal early	Hypertension (due to fluid retention and RAAS activation)
Oliguria	Usually absent early	Present (reduced GFR from inflammation)
Complement Levels	Usually normal (except MPGN, membranous lupus)	Often low (post-infectious GN, lupus nephritis, MPGN)
Renal Function	Preserved early; slow decline	Rapid decline possible (RPGN if crescents present)
Hypercoagulability	Yes (loss of antithrombin III)	No
Infection Risk	Yes (loss of immunoglobulins, especially IgG)	No

Nephrotic Syndrome Spectrum

Subtype	Population	Histology / EM Finding	Key Clinical Feature
Minimal Change Disease	Children (most common cause in pediatric patients; ~80% of idiopathic nephrotic syndrome in children per IDAI data)	Podocyte foot process effacement on EM; normal on light microscopy	Highly responsive to corticosteroids; may follow URI or atopic episode
Focal Segmental Glomerulosclerosis (FSGS)	African Americans, HIV, obesity, heroin use; most common primary cause in adults	Focal and segmental sclerosis of glomeruli; foot process effacement on EM	Poor response to steroids (80-85% steroid-resistant); can recur in transplanted kidneys
Membranous Nephropathy	Adults (most common primary cause of nephrotic syndrome in White adults)	Diffuse GBM thickening with subepithelial "spike and dome" deposits	Strong association with malignancy (lung, colon), Hepatitis B, SLE (class V), and anti-PLA2R antibodies
Diabetic Nephropathy	Long-standing diabetes mellitus	Kimmelstiel-Wilson nodules (nodular glomerulosclerosis), GBM thickening	Most common cause of nephrotic syndrome overall in adults; progressive microalbuminuria preceding overt proteinuria
Amyloidosis	Chronic inflammatory conditions (AA type), multiple myeloma (AL type)	Apple-green birefringence under polarized light with Congo red stain	Nephrotic syndrome with involvement of other organs (heart, liver, tongue)
Membranoproliferative GN (MPGN)	Can present with mixed nephrotic/nephritic features	"Tram-track" or double-contour GBM on EM due to mesangial interposition	Associated with Hepatitis C, cryoglobulinemia; low complement levels

A point that test-writers frequently exploit: minimal change disease presents with nephrotic syndrome but has a normal-appearing glomerulus on light microscopy. The diagnosis requires EM to reveal foot process effacement. If the vignette describes a child with sudden-onset nephrotic syndrome and a biopsy that "appears normal," this is the answer.

Key Clinical Definitions (IDAI Consensus)

These definitions are essential for pediatric nephrology questions, because the classification of nephrotic syndrome in children is based on clinical response to steroid therapy rather than histopathology:

Term	Definition
Remission	Urine protein negative or trace (<4 mg/m$^2$/hour) for 3 consecutive days within 1 week
Relapse	Urine protein $\geq$2+ (>40 mg/m$^2$/hour) for 3 consecutive days within 1 week
Infrequent Relapse	<2 relapses within the first 6 months after initial response, or <4 relapses per year
Frequent Relapse	$\geq$2 relapses within the first 6 months after initial response, or $\geq$4 relapses per year
Steroid-Dependent	2 consecutive relapses occurring during steroid tapering (alternating dose) or within 14 days of stopping therapy
Steroid-Resistant	No remission after full-dose prednisone (2 mg/kg/day) for 4 weeks
Steroid-Sensitive	Remission achieved with full-dose prednisone within 4 weeks

The long-term prognosis of minimal change disease over 20 years of observation shows only 4-5% progress to end-stage renal disease. FSGS, by contrast, leads to end-stage renal disease in 25% within 5 years, with the majority experiencing progressive decline in renal function. This is why steroid response, rather than histology alone, is the stronger prognostic indicator in children.

3. Diagnostic Workup

Test	Purpose	Expected Finding
Urinalysis	Initial screening	Proteinuria (3+ or 4+), oval fat bodies, fatty casts, "Maltese cross" on polarized microscopy
24-hour urine protein or spot urine protein-to-creatinine ratio	Quantify proteinuria	>3.5 g/day or ratio >3.5 (in children: >40 mg/m$^2$/hour or spot ratio >2 mg/mg)
Serum albumin	Confirm hypoalbuminemia	<2.5 g/dL (IDAI threshold)
Lipid panel	Confirm hyperlipidemia	Total cholesterol >200 mg/dL, elevated LDL
Complete blood count	General evaluation	Hb, WBC with differential, platelets, hematocrit, ESR
Serum creatinine / BUN + creatinine clearance	Assess renal function	May be normal early; elevated in progressive disease. In children, use the Schwartz formula for creatinine clearance
Complement C3	Screen for secondary causes	Low in post-infectious GN, lupus nephritis, MPGN. If SLE is suspected, add C4, ANA, anti-dsDNA
Serologic workup	Identify secondary causes	HBsAg (Hep B), anti-HCV (Hep C), HIV, anti-PLA2R (membranous), HbA1c (diabetes)
Renal biopsy	Gold standard for determining etiology in adults	Varies by subtype (see classification table)

The best initial test when nephrotic syndrome is suspected is a urinalysis followed by quantification of proteinuria. The spot protein-to-creatinine ratio is increasingly favored over the 24-hour collection because it is faster and correlates well with the 24-hour value. A ratio exceeding 3.5 in adults (or >2 mg/mg in children) is diagnostic of nephrotic-range proteinuria.

Once nephrotic-range proteinuria is confirmed, the next step is to determine the cause. In children, the overwhelming likelihood is minimal change disease, and the standard approach is to start empiric corticosteroids without biopsy. A biopsy in a child is reserved for the following situations per the IDAI consensus: steroid-resistant cases; onset below age 1 or above age 16; persistent gross hematuria or persistent microscopic hematuria with low C3; sustained hypertension; declining renal function not attributable to hypovolemia; suspected secondary nephrotic syndrome; and before starting cyclosporine therapy.

In adults, a renal biopsy is almost always required because the differential is broader and treatment varies by subtype. Before performing the biopsy, a serologic workup should be sent to screen for secondary causes (SLE, hepatitis, HIV, diabetes, and malignancy screening in older adults with membranous nephropathy).

A classic exam trap involves lipiduria findings. Oval fat bodies are renal tubular epithelial cells that have absorbed filtered lipids. Under polarized light, the cholesterol esters within these cells produce the characteristic "Maltese cross" pattern, which is pathognomonic for nephrotic syndrome. If a vignette describes this finding on urinalysis, the diagnosis is essentially confirmed.

Before initiating steroid therapy in children, the IDAI consensus mandates a set of preliminary steps: measurement of weight and height, blood pressure check, physical examination for signs of systemic disease (SLE, Henoch-Schonlein purpura), screening for foci of infection (dental, ear, intestinal parasites), and a Mantoux test. If the Mantoux is positive, INH prophylaxis for 6 months must be given alongside steroids; if active tuberculosis is found, full anti-TB therapy is required before steroids begin. These steps often appear as "most appropriate next step" questions.

4. Management and Treatment

General Measures

Intervention	Indication	Details
Hospitalization	First episode in children	Accelerates evaluation, dietary adjustment, edema management, steroid initiation, and parent education
Dietary sodium restriction	All patients with edema	1-2 g/day while edema persists
Dietary protein	All patients	Normal intake per RDA (1.5-2 g/kg/day in children). High-protein diets are contraindicated because they increase glomerular hyperfiltration and promote sclerosis. Low-protein diets risk protein-energy malnutrition
ACE inhibitor or ARB	Frequent relapse, steroid-dependent, or steroid-resistant disease	Reduces intraglomerular pressure and proteinuria; renoprotecter via TGF-$\beta$1 and PAI-1 suppression. Captopril 0.3 mg/kg TID, enalapril 0.5 mg/kg/day divided BID, lisinopril 0.1 mg/kg once daily, losartan 0.75 mg/kg once daily. Combined ACEI+ARB produces greater proteinuria reduction
Statins	Hyperlipidemia in steroid-resistant disease	In steroid-sensitive nephrotic syndrome, lipid elevations are transient and dietary fat reduction suffices. In steroid-resistant disease, maintain normal weight and consider HMG-CoA reductase inhibitors
Calcium + Vitamin D	Long-term steroid therapy (>3 months)	Calcium 250-500 mg/day + Vitamin D 125-250 IU to prevent osteoporosis and osteopenia

Diuretic Algorithm (Stepwise Escalation per IDAI)

Before giving diuretics, always rule out hypovolemia first. This is a common exam trap: a nephrotic patient can be hypovolemic despite appearing edematous, because the fluid is in the interstitial space rather than the intravascular compartment. Monitor electrolytes (potassium and sodium) if diuretics are used for more than 1-2 weeks.

Step 1: Furosemide 1-3 mg/kg/day + spironolactone 2-4 mg/kg/day.
If no response (no weight loss or diuresis within 48 hours), proceed to Step 2.
Step 2: Double the furosemide dose (maximum 4-6 mg/kg/day).
If no response, proceed to Step 3.
Step 3: Add hydrochlorothiazide 1-2 mg/kg/day.
If no response, proceed to Step 4.
Step 4: IV furosemide bolus 1-3 mg/kg/dose, or continuous infusion at 0.1-1 mg/kg/hour.
If no response, proceed to Step 5.
Step 5: IV albumin 20% at 1 g/kg infused over 2-4 hours, followed immediately by IV furosemide 1-2 mg/kg.

The rationale for Step 5 is a critical exam pearl. Nephrotic patients may be diuretic-resistant because albumin is needed to transport furosemide to its site of action in the loop of Henle. In severe hypoalbuminemia ($\leq$1 g/dL), co-administration of IV albumin with IV furosemide overcomes this resistance by restoring the drug's delivery mechanism. If albumin is not affordable (a real consideration in resource-limited settings), plasma at 20 mL/kg/day infused slowly (10 drops/minute) is an alternative, with care to prevent cardiac decompensation. Albumin infusions can be given on alternate days to allow fluid redistribution and prevent volume overload. If ascites is severe enough to impair respiration, repeated paracentesis may be necessary.

Immunization in Nephrotic Syndrome

Patients receiving corticosteroids at >2 mg/kg/day or a total of >20 mg/day for more than 14 days are considered immunocompromised. During this period and for 6 weeks after stopping the medication, only killed-virus vaccines (such as IPV) are permitted. After 6 weeks off prednisone, live-virus vaccines (oral polio, measles, MMR, varicella) can be given. All children with nephrotic syndrome are strongly recommended to receive vaccination against pneumococcal infection and varicella.

Corticosteroid Protocols

Initial Therapy (IDAI Protocol)

Phase	Dose	Duration
Full Dose (FD)	Prednisone 60 mg/m$^2$/day or 2 mg/kg/day (max 80 mg/day), divided doses	4 weeks
Alternating Dose (AD)	40 mg/m$^2$/day or 1.5 mg/kg/day, single dose every other day, given after breakfast	4 weeks

Prednisone dosing is calculated using ideal body weight (weight for height). If remission occurs within the first 4 weeks, the patient transitions to the alternating phase. If no remission occurs after 4 weeks of full-dose therapy, the patient is classified as steroid-resistant.

Relapse Therapy

Full-dose prednisone daily until remission (maximum 4 weeks), then alternating-dose prednisone at 40 mg/m$^2$/day for 4 weeks.

A critical teaching point from the IDAI consensus: if proteinuria returns ($\geq$2+) without edema in a patient who was previously in remission, do not immediately treat as a relapse. First search for an infectious trigger (most commonly an upper respiratory tract infection). Give antibiotics for 5-7 days. If proteinuria resolves after treating the infection, no relapse therapy is needed. Only when proteinuria $\geq$2+ is accompanied by edema from the outset, or persists after treating the infection, should you initiate relapse-protocol steroids.

Frequent Relapse or Steroid-Dependent Disease

There are four escalating options:

Option 1: Long-term low-dose steroid. After achieving remission with full-dose prednisone, continue alternating-dose at 1.5 mg/kg. Taper by 0.2 mg/kg every 2 weeks until the threshold dose is reached (the lowest alternating dose that does not trigger relapse, typically 0.1-0.5 mg/kg). Maintain this dose for 6-12 months, then attempt discontinuation. School-age children generally tolerate 0.5 mg/kg alternating; preschool children may tolerate up to 1 mg/kg alternating.
Option 2: Levamisole. Given at 2.5 mg/kg as a single dose every other day for 4-12 months. It functions as a steroid-sparing agent. Side effects include nausea, vomiting, hepatotoxicity, vasculitic rash, and reversible neutropenia.
Option 3: Cyclophosphamide (CPA). Oral CPA at 2-3 mg/kg/day as a single dose for 8-12 weeks. Alternatively, pulse IV CPA at 500-750 mg/m$^2$ (dissolved in 250 mL normal saline, infused over 2 hours) given once monthly for 6 months (7 total doses). Monitoring of CBC (hemoglobin, WBC, platelets) every 1-2 weeks is mandatory. Hold the drug if WBC falls below 3,000/$\mu$L, Hb below 8 g/dL, or platelets below 100,000/$\mu$L; resume when WBC recovers above 5,000/$\mu$L. Cumulative gonadal toxicity and malignancy risk appear at total doses $\geq$200-300 mg/kg. A standard 3-month oral course delivers approximately 180 mg/kg, which is within the safe range.
Option 4: Cyclosporine (CyA) or Mycophenolate Mofetil (MMF). CyA at 4-5 mg/kg/day (100-150 mg/m$^2$), maintaining trough levels of 150-250 ng/mL. CyA can induce and maintain remission, allowing steroid reduction or discontinuation, but patients often become cyclosporine-dependent (relapse upon CyA cessation). CyA requires monitoring of drug levels, serum creatinine, and renal biopsy every 2 years due to nephrotoxicity (tubulointerstitial lesions). MMF at 800-1200 mg/m$^2$ or 25-30 mg/kg/day, given alongside steroid taper for 12-24 months, is reserved for cases unresponsive to levamisole or cytostatic agents. MMF side effects include abdominal pain, diarrhea, and leukopenia.

Steroid Contraindication

When steroids are contraindicated (hypertension, elevated urea/creatinine, severe infection), proceed directly to CPA: either oral (2-3 mg/kg/day for 8 weeks) or pulse IV (500-750 mg/m$^2$ monthly for 6 months).

Steroid-Resistant Nephrotic Syndrome (SRNS)

Before starting treatment, always perform a renal biopsy, because histopathology dictates prognosis.

CPA: Oral 2-3 mg/kg/day for 3-6 months with alternating-dose prednisone, followed by a 2-month taper (1 mg/kg/day for 1 month, then 0.5 mg/kg/day for 1 month). If CPA achieves remission but subsequent relapse occurs, try steroids again since previously resistant patients can become steroid-sensitive after CPA.

Cyclosporine: Reported to produce complete remission in 20% and partial remission in 13% of SRNS patients, but limited by cost in many settings.

Methylprednisolone Pulse (Mendoza Protocol):

Week	Methylprednisolone (30 mg/kg, max 1000 mg)	Number of Doses	Oral Prednisone
1-2	3 times/week	6	None
3-10	Once/week	8	2 mg/kg/day, single dose
11-18	Every 2 weeks	4	With or without taper
19-50	Every 4 weeks	8	Slow taper
51-82	Every 8 weeks	4	Slow taper

CPA (2-2.5 mg/kg/day) or chlorambucil (0.18-0.22 mg/kg/day) for 8-12 weeks can be added if proteinuria persists after 10 weeks of methylprednisolone.

Management of Complications

Complication	Presentation	Management
Primary Peritonitis	Fever, abdominal pain, ascites (Gram-negative organisms, S. pneumoniae)	Parenteral penicillin + third-generation cephalosporin (cefotaxime or ceftriaxone) for 10-14 days
Varicella Exposure	Contact with varicella patient	Varicella-zoster immunoglobulin within 96 hours; if unavailable, single-dose IVIG (400 mg/kg)
Active Varicella	Vesicular rash in immunocompromised patient	IV acyclovir 1500 mg/m$^2$/day divided TID, or oral acyclovir 80 mg/kg/day divided QID for 7-10 days; temporarily stop steroids
Renal Vein Thrombosis	Sudden flank pain, hematuria, worsening proteinuria	Subcutaneous heparin, then warfarin for $\geq$6 months. Low-dose aspirin prophylaxis is not recommended
Hypovolemia	Hypotension, tachycardia, cold extremities, abdominal pain (often despite edema)	Rapid IV normal saline 15-20 mL/kg over 20-30 minutes, followed by albumin 1 g/kg or plasma 20 mL/kg (slow drip). After volume restoration, if oliguria persists: furosemide 1-2 mg/kg IV
Hypocalcemia / Tetany	Long-term steroid use; vitamin D metabolite loss	Supplementation: calcium 250-500 mg/day + vitamin D 125-250 IU. If tetany: 10% calcium gluconate 0.5 mL/kg IV
Hypertension	At onset or from steroid toxicity	ACE inhibitor, ARB, calcium channel blocker, or beta-blocker; target below the 90th percentile

Long-Term Steroid Side Effect Monitoring

Prolonged steroid use causes increased appetite, growth impairment, behavioral changes, increased infection risk, salt and water retention, hypertension, and bone demineralization. All nephrotic syndrome patients on steroids require monitoring for Cushingoid features, blood pressure measurement, weight and height every 6 months, and annual cataract evaluation.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Nephritic syndrome	Both present with edema and abnormal urinalysis	Nephritic features hematuria with RBC casts, hypertension, and oliguria; proteinuria is typically <3.5 g/day. Nephrotic has heavy proteinuria, hypoalbuminemia, and hyperlipidemia with a bland sediment
Heart failure	Peripheral edema, possible pleural effusion, fatigue	Urinalysis is bland (no proteinuria); elevated BNP/NT-proBNP; JVD, S3 gallop, pulmonary crackles
Liver cirrhosis	Ascites, edema, hypoalbuminemia	Albumin is low due to decreased hepatic synthesis, not urinary loss. Urinalysis shows no nephrotic-range proteinuria. Stigmata of liver disease (spider angiomata, palmar erythema, jaundice)
Protein-losing enteropathy	Hypoalbuminemia with edema	Albumin loss is via the GI tract, not the kidney. Urinalysis is normal. Diarrhea and malabsorption are present
Mixed nephritic-nephrotic picture (MPGN, diffuse proliferative lupus nephritis)	Nephrotic-range proteinuria AND hematuria/RBC casts	Low complement levels and active urine sediment alongside heavy proteinuria. These straddle both categories

6. Traps and High-Yield Pearls

The single most common way students lose points on nephrotic syndrome questions is by confusing it with nephritic syndrome. Vignettes are deliberately written to blur the line. The key is to focus on two things: the degree of proteinuria and the urine sediment. If proteinuria exceeds 3.5 g/day with a bland sediment, it is nephrotic. If there are RBC casts and active sediment with moderate proteinuria, it is nephritic. If both features coexist, think MPGN or lupus nephritis (class IV progressing to class V).

Another frequent trap is the management of nephrotic syndrome in children versus adults. In a child with new-onset nephrotic syndrome, the answer is almost always "start corticosteroids" without biopsy, because minimal change disease is overwhelmingly likely (~80% of cases). In an adult, the answer is almost always "perform renal biopsy" because the differential is much broader. Getting this distinction wrong is a high-frequency error.

Test-writers also love to exploit complications. A nephrotic patient who suddenly develops flank pain and hematuria has renal vein thrombosis until proven otherwise. A nephrotic patient with acute dyspnea and pleuritic chest pain likely has a pulmonary embolism from the hypercoagulable state. A nephrotic child with fever and abdominal pain in the setting of ascites should raise concern for spontaneous bacterial peritonitis from immunoglobulin loss. Membranous nephropathy carries the highest thrombosis risk among the nephrotic subtypes, and prophylactic anticoagulation is considered when serum albumin falls below 2-2.5 g/dL.

A subtle but frequently tested point: proteinuria without edema in a previously remitted child does not automatically constitute a relapse. Per the IDAI protocol, you must first search for an infectious trigger (typically an upper respiratory infection), treat it, and reassess. Only if proteinuria persists with edema should relapse therapy be initiated. This "look before you leap" principle is a favorite exam question.

The "Maltese cross" under polarized light is pathognomonic for nephrotic syndrome and instantly confirms lipiduria. If a vignette mentions this finding, the diagnosis is locked in regardless of other confusing details in the stem.

Finally, be aware of the hypovolemia-edema paradox. Nephrotic patients can present with signs of intravascular volume depletion (hypotension, tachycardia, cold extremities, abdominal pain) even while appearing grossly edematous. Administering aggressive diuretics to a hypovolemic nephrotic patient is dangerous and can precipitate shock. Abdominal pain in a nephrotic child is a red flag for either peritonitis or hypovolemia, and the distinction must be made before choosing between antibiotics and volume resuscitation.

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