Nephrotic Syndrome and Acute glomerulo nephritis and renal failure in Children

Renal Disorders in Children – Nursing Notes

Introduction to Pediatric Renal Disorders

Renal disorders in children present unique challenges for healthcare providers. This educational resource provides comprehensive information on three major pediatric renal conditions: nephrotic syndrome, acute glomerulonephritis, and renal failure. These notes integrate pathophysiology, clinical presentation, diagnostic approaches, and evidence-based management strategies essential for nursing care.

Key Points for Nursing Care:

Children with renal disorders require close monitoring of fluid balance, electrolytes, and vital signs
Growth and development assessment is crucial due to the impact of renal disease on pediatric growth
Medication administration requires precise dosing based on renal function and weight
Family education and emotional support are essential components of comprehensive care
Nutrition management is critical for preventing complications and supporting recovery

Comparison of Pediatric Renal Disorders

Feature	Nephrotic Syndrome	Acute Glomerulonephritis	Renal Failure
Definition	Group of symptoms including proteinuria, hypoalbuminemia, edema, and hyperlipidemia	Inflammation of the glomeruli causing hematuria, proteinuria, and azotemia	Temporary or permanent damage to kidneys with loss of normal function
Primary Pathophysiology	Altered glomerular permeability leading to massive protein loss	Immune-mediated damage to glomerular basement membrane	Acute: Sudden impairment of kidney function Chronic: Progressive loss of nephrons
Common Cause in Children	Minimal change disease (80-90% of cases)	Post-streptococcal infection	Acute: Dehydration, infection, obstruction Chronic: Congenital anomalies
Key Clinical Features	Periorbital edema, ascites, foamy urine	Hematuria, hypertension, oliguria	Acute: Oliguria, fluid overload Chronic: Growth failure, anemia
Diagnostic Findings	Proteinuria >40 mg/m²/hr Hypoalbuminemia Hyperlipidemia	Hematuria RBC casts Low C3 complement	Elevated BUN, creatinine Electrolyte imbalances Metabolic acidosis
Treatment Approach	Corticosteroids Sodium restriction Diuretics for edema	Antibiotics if infection present Supportive care BP management	Acute: Fluid management, dialysis if needed Chronic: Medication, dialysis, transplant
Prognosis	Good; most respond to steroids May have relapses	Usually resolves without permanent damage	Acute: Often reversible Chronic: Progressive decline

1. Nephrotic Syndrome in Children

Overview

Nephrotic syndrome is not a disease but a group of symptoms that indicate kidney dysfunction. It’s characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. In children, it most commonly affects those between 2-7 years of age, with a higher prevalence in boys.

Clinical Definition

Proteinuria >40 mg/m²/hr or protein/creatinine ratio >2.0 mg/mg
Hypoalbuminemia (serum albumin <2.5 g/dL)
Edema (often periorbital, progressing to generalized)
Hyperlipidemia (elevated cholesterol and triglycerides)

Epidemiology

Annual incidence: 2-7 cases per 100,000 children
Peak incidence: 2-7 years of age
Male to female ratio: 2:1
90% of cases in children are due to minimal change disease

Pathophysiology

Fig 1: Normal kidney anatomy showing glomeruli – the sites affected in nephrotic syndrome

The fundamental pathophysiologic event in nephrotic syndrome is increased permeability of the glomerular filtration barrier, which consists of:

Capillary Endothelium

First barrier with fenestrations that normally allow passage of water and small solutes but not larger proteins

Basement Membrane

Middle layer composed of type IV collagen, laminin, and proteoglycans that provides size and charge selectivity

Podocytes

Epithelial cells with foot processes and slit diaphragms that are crucial for preventing protein loss

Sequence of Events:

Podocyte injury → foot process effacement and loss of slit diaphragm integrity
Increased glomerular permeability → massive protein loss in urine (primarily albumin)
Hypoalbuminemia → decreased plasma oncotic pressure
Fluid shift from intravascular to interstitial space → edema formation
Compensatory hepatic protein synthesis → increased production of lipoproteins → hyperlipidemia
Activation of renin-angiotensin-aldosterone system → sodium and water retention → worsening edema

Key Concept: Podocyte Injury

In minimal change disease (most common in children), the podocyte injury is believed to be caused by a circulating factor, possibly released by T cells, that disrupts the actin cytoskeleton of podocytes, leading to foot process effacement.

Etiology and Classification

Primary (Idiopathic) Nephrotic Syndrome

Most common in children, with no identifiable cause. Histologic variants include:

Type	Frequency in Children	Pathologic Features	Steroid Response
Minimal Change Disease (MCD)	80-90%	Normal glomeruli on light microscopy; foot process effacement on electron microscopy	Usually responsive (90%)
Focal Segmental Glomerulosclerosis (FSGS)	5-10%	Segmental sclerosis in some glomeruli; foot process effacement	Often resistant
Membranous Nephropathy	1-5%	Thickened GBM with subepithelial immune deposits	Variable response
Membranoproliferative GN	Rare in children	Mesangial proliferation with thickening of GBM	Usually resistant

Secondary Nephrotic Syndrome

Less common in children, caused by:

Infections

Hepatitis B and C
HIV
Malaria
Syphilis

Systemic Diseases

Lupus nephritis
Henoch-Schönlein purpura
Diabetes mellitus
Amyloidosis

Drugs/Toxins

NSAIDs
Penicillamine
Gold
Bismuth

Genetic Causes

Congenital nephrotic syndrome (Finnish type)
Alport syndrome
NPHS1, NPHS2 mutations

Mnemonic: “NEPHROTIC”

To remember key features of nephrotic syndrome:

N – Numerous proteins lost in urine
E – Edema (periorbital, then generalized)
P – Proteinuria (>40 mg/m²/hr)
H – Hypoalbuminemia (<2.5 g/dL)
R – Risk of infections and thrombosis
O – Oncotic pressure decreased
T – Triglycerides elevated
I – Immune dysregulation (in MCD)
C – Cholesterol increased

Clinical Presentation

Cardinal Signs and Symptoms

Edema (Most Common Presenting Feature)

Periorbital edema (most noticeable in morning)
Progresses to dependent areas (feet, ankles, genitalia)
Can become generalized (anasarca) with ascites, pleural effusions

Urinary Findings

Foamy urine (due to proteinuria)
Normal or decreased urine output

General Symptoms

Fatigue and malaise
Poor appetite
Irritability

Complications

Infections

Increased susceptibility (loss of immunoglobulins)
Peritonitis (particularly pneumococcal)
Cellulitis, pneumonia, UTIs

Thromboembolism

Loss of anticoagulant factors in urine
Increased clotting factors (fibrinogen, factors V, VIII)
Risk of renal vein thrombosis, pulmonary emboli

Acute Kidney Injury

Due to hypovolemia
Renal vein thrombosis
Interstitial nephritis from medications

Clinical Pearls:

Morning periorbital edema that improves throughout the day is a classic initial presentation
Weight gain is often the first objective sign parents notice
Hypertension is uncommon in pure minimal change disease – its presence suggests alternative diagnosis
Gross hematuria is rare – if present, consider other diagnoses

Diagnostic Evaluation

Initial Laboratory Evaluation

Urinalysis

Proteinuria (3+ to 4+ on dipstick)
Hyaline casts
Absent or minimal hematuria

Urine Studies

24-hour urine protein (>40 mg/m²/hr or >1g/m²/day)
Spot urine protein/creatinine ratio (>2.0 mg/mg)
Urine protein electrophoresis (predominant albumin)

Blood Tests

Serum albumin (<2.5 g/dL)
Total protein (decreased)
Cholesterol and triglycerides (elevated)
BUN and creatinine (usually normal)
Electrolytes (may show hyponatremia)

Additional Investigations

Complement Studies

C3, C4 (typically normal in MCD)
Low complement suggests MPGN or lupus nephritis

Serologic Studies (for secondary causes)

ANA, anti-dsDNA (for lupus)
ANCA (for vasculitis)
Hepatitis B, C, HIV serology

Imaging

Renal ultrasound (normal size kidneys in MCD)
Chest X-ray (if respiratory symptoms present)

Renal Biopsy

Not routinely indicated initially in children with typical presentation. Indications include:

Age <1 year or >12 years
Steroid resistance or dependence
Atypical features (gross hematuria, hypertension)
Low complement levels
Persistent renal insufficiency

Diagnostic Criteria for Nephrotic Syndrome:

Proteinuria >40 mg/m²/hr or spot urine protein/creatinine ratio >2.0 mg/mg
Hypoalbuminemia (serum albumin <2.5 g/dL)
Edema
Hyperlipidemia (not required for diagnosis but typically present)

Management Approach

Pharmacological Management

Corticosteroids (First-line)

Initial therapy: Prednisone 60 mg/m²/day or 2 mg/kg/day (max 60 mg) for 4-6 weeks
Followed by: 40 mg/m²/day or 1.5 mg/kg/day on alternate days for 4-6 weeks, then taper
80-90% of children with MCD respond within 4 weeks

For Frequent Relapses or Steroid Dependence

Cyclophosphamide: 2-3 mg/kg/day for 8-12 weeks
Levamisole: 2.5 mg/kg on alternate days
Mycophenolate mofetil: 600-1200 mg/m²/day in 2 divided doses
Calcineurin inhibitors:
- Cyclosporine: 3-5 mg/kg/day in 2 divided doses
- Tacrolimus: 0.05-0.1 mg/kg/day in 2 divided doses
Rituximab: 375 mg/m² weekly for 1-4 doses (for difficult cases)

Symptomatic Management

Diuretics: For severe edema (furosemide 1-2 mg/kg/dose)
Albumin infusion: 25% albumin 0.5-1 g/kg followed by diuretic (for severe edema with hypovolemia)
ACE inhibitors: To reduce proteinuria in steroid-resistant cases
Statins: For persistent hyperlipidemia (rarely needed in children)

Supportive Management

Nutritional Management

Normal protein diet (1-2 g/kg/day)
Sodium restriction (1-2 g/day) during edematous phase
No routine fluid restriction unless hyponatremia present
Low cholesterol diet if hyperlipidemia persists

Infection Prevention

Pneumococcal vaccination
Prompt treatment of infections
Avoid unnecessary exposure to sick contacts

Thrombosis Prevention

Early mobilization when possible
Consider prophylactic anticoagulation in high-risk cases

Activity and Lifestyle

Return to school once edema resolves
No restriction of physical activity once in remission
Regular monitoring of urine protein at home

Response Definitions:

Remission: Urine protein negative or trace for 3 consecutive days
Relapse: Urine protein 3+ or 4+ for 3 consecutive days after having been in remission
Frequent relapses: ≥2 relapses within 6 months of initial response or ≥4 relapses in any 12-month period
Steroid dependence: Two consecutive relapses during steroid therapy or within 14 days of discontinuation
Steroid resistance: Failure to achieve remission after 8 weeks of daily prednisone

Nursing Considerations

Assessment

Initial Assessment

Comprehensive measurement of edema (location, pitting)
Accurate weight and vital signs (baseline)
Abdominal girth measurement (if ascites present)
Fluid balance assessment
Respiratory status (for pleural effusions)

Ongoing Monitoring

Daily weight (same time, clothing, scale)
Strict intake and output
BP monitoring (at least twice daily)
Daily urine dipstick for protein
Signs of steroid side effects
Signs of infection or thrombosis

Interventions

Medication Administration

Administer steroids with food to minimize GI effects
Give diuretics in morning to avoid nighttime diuresis
Monitor for medication side effects
Administer albumin infusions slowly (over 2-4 hours)

Edema Management

Elevate edematous extremities
Reposition frequently to prevent pressure areas
Gentle skin care for edematous areas
Monitor skin integrity, especially in skin folds

Family Education

Home urine dipstick monitoring
Recognition of relapse signs
Medication administration and side effects
Dietary sodium restriction
When to seek medical attention
Infection prevention strategies

Nursing Care Mind Map for Nephrotic Syndrome

                            NEPHROTIC SYNDROME NURSING CARE
                            ├── ASSESSMENT
                            │   ├── Daily Weight
                            │   ├── Edema Evaluation
                            │   ├── Vital Signs
                            │   ├── Intake & Output
                            │   └── Urine Protein Monitoring
                            │
                            ├── MANAGEMENT
                            │   ├── Medication Administration
                            │   │   ├── Corticosteroids
                            │   │   ├── Diuretics
                            │   │   └── Immunosuppressants
                            │   │
                            │   ├── Fluid & Electrolyte Balance
                            │   │   ├── Sodium Restriction
                            │   │   └── IV Albumin (if ordered)
                            │   │
                            │   └── Skin Care for Edematous Areas
                            │
                            ├── MONITORING
                            │   ├── Complications
                            │   │   ├── Infection
                            │   │   ├── Thrombosis
                            │   │   └── Steroid Side Effects
                            │   │
                            │   └── Laboratory Values
                            │       ├── Urine Protein
                            │       ├── Serum Albumin
                            │       └── Electrolytes
                            │
                            └── EDUCATION
                                ├── Disease Process
                                ├── Medication Information
                                ├── Home Monitoring
                                ├── Dietary Guidance
                                ├── Activity Recommendations
                                └── When to Seek Medical Care

2. Acute Glomerulonephritis

Overview

Acute glomerulonephritis (AGN) is inflammation of the glomeruli resulting in hematuria, proteinuria, decreased urine output, and often hypertension and edema. In children, it is most commonly post-infectious, particularly following group A beta-hemolytic streptococcal infection (post-streptococcal glomerulonephritis or PSGN).

Clinical Definition

Abrupt onset of hematuria (microscopic or gross)
Variable proteinuria (usually subnephrotic)
Decreased glomerular filtration rate
Edema and hypertension (nephritic syndrome)

Epidemiology

Most common between ages 5-12 years
Male:female ratio of 2:1
More common in developing countries
May occur sporadically or in epidemics
Incidence decreasing in developed countries

Pathophysiology

Fig 2: Histopathology of acute post-infectious glomerulonephritis showing hypercellularity and inflammatory infiltrate

Acute glomerulonephritis is primarily an immune-complex mediated disease where immune complexes deposit in the glomeruli, activating inflammatory pathways.

Pathogenesis of Post-Streptococcal Glomerulonephritis:

Streptococcal infection (typically pharyngitis or impetigo from “nephritogenic” strains)
Latent period (1-2 weeks after pharyngitis, 3-6 weeks after impetigo)
Formation of immune complexes (either in circulation or in situ within glomeruli)
Glomerular immune complex deposition (primarily in subepithelial location)
Complement activation (primarily via alternative pathway)
Inflammatory response with neutrophil and monocyte infiltration
Endothelial injury causing decreased glomerular filtration rate
Proliferation of mesangial and endothelial cells (giving “lumpy-bumpy” appearance)

Glomerular Changes

Enlarged, hypercellular glomeruli due to proliferation of endothelial and mesangial cells and infiltration of neutrophils

Immune Deposits

Granular deposits of IgG and C3 along the capillary walls and mesangium appearing as “lumpy-bumpy” pattern on immunofluorescence

Electron Microscopy

Subepithelial electron-dense deposits (“humps”) with effacement of podocyte foot processes

Functional Consequences:

Decreased glomerular filtration rate due to:
- Inflammatory narrowing of capillary lumina
- Structural damage to glomerular basement membrane
- Mesangial and endothelial cell proliferation
Hematuria from damage to glomerular filtration barrier
Proteinuria from altered capillary permeability
Sodium and water retention leading to edema and hypertension
Azotemia from reduced GFR and impaired waste elimination

Key Concept: Streptococcal Antigens in PSGN

Several streptococcal antigens have been implicated in PSGN pathogenesis, including:

Nephritis-associated plasmin receptor (NAPlr)
Streptococcal pyrogenic exotoxin B (SpeB)
Streptococcal M proteins (particularly M types 1, 4, 12, 49, 55, 57, 60)

These antigens may directly deposit in the glomeruli or form immune complexes that trigger inflammation.

Etiology and Classification

Post-Infectious Causes

The most common causes of AGN in children:

Pathogen	Specific Agents	Clinical Features
Bacterial	Group A β-hemolytic Streptococcus (most common) Staphylococcus Pneumococcus Meningococcus	Latent period between infection and nephritis; hypocomplementemia
Viral	Hepatitis B virus Epstein-Barr virus Cytomegalovirus HIV Parvovirus B19	Often concurrent infection and nephritis; variable complement levels
Parasitic	Plasmodium (malaria) Toxoplasma Schistosoma	More common in endemic regions; may have other system involvement

Non-Infectious Causes

Primary Glomerular Diseases

IgA nephropathy (Berger’s disease)
Membranoproliferative glomerulonephritis
Anti-glomerular basement membrane disease
C3 glomerulopathy

Systemic Diseases

Henoch-Schönlein purpura
Systemic lupus erythematosus
ANCA-associated vasculitis
Goodpasture syndrome

Classification by Histopathology

Diffuse Proliferative GN

Affects most/all glomeruli; characterized by endocapillary hypercellularity. Most common pattern in PSGN.

Focal Proliferative GN

Affects some but not all glomeruli; common in IgA nephropathy and Henoch-Schönlein purpura.

Crescentic GN

Characterized by crescent formation; indicates severe injury; associated with rapidly progressive GN.

Mnemonic: “NEPHRITIS”

To remember causes of acute glomerulonephritis in children:

N – Nephritogenic strep (Group A β-hemolytic streptococcus)
E – Endocarditis (infective)
P – Post-infectious causes (viral, bacterial)
H – Henoch-Schönlein purpura
R – Renal diseases (IgA nephropathy)
I – Immune complex diseases (lupus nephritis)
T – Toxin-mediated (heavy metals)
I – Infectious diseases (HBV, HCV, HIV)
S – Systemic diseases (vasculitis)

Clinical Presentation

Cardinal Signs and Symptoms

Urinary Findings

Hematuria (microscopic or gross “tea-colored” or “cola-colored” urine)
Proteinuria (usually non-nephrotic range)
RBC casts in urine sediment
Oliguria (reduced urine output)

Fluid Retention

Periorbital edema (typically most prominent in morning)
Peripheral edema (less prominent than in nephrotic syndrome)
Facial puffiness
Weight gain

Hypertension

Present in 60-80% of cases
Usually mild to moderate
Due to fluid retention and activation of renin-angiotensin system

Associated Symptoms

General Symptoms

Fatigue and malaise
Low-grade fever
Flank or abdominal pain
Anorexia

In Severe Cases

Acute kidney injury (elevated BUN and creatinine)
Pulmonary edema (dyspnea, crackles)
Hypertensive encephalopathy (headache, altered mental status, seizures)
Heart failure

Post-Streptococcal Specific

History of recent pharyngitis or impetigo
Latent period between infection and nephritis
May have persistent sore throat or skin lesions

Clinical Course of PSGN:

Onset typically 1-2 weeks after pharyngitis, 3-6 weeks after skin infection
Most children recover completely within 6-8 weeks
Urinary abnormalities may persist for several months
Microscopic hematuria may take up to 1-2 years to resolve
Less than 1% of children develop chronic kidney disease
Recurrence is rare in post-streptococcal glomerulonephritis

Diagnostic Evaluation

Initial Laboratory Evaluation

Urinalysis

Hematuria (RBCs >5/HPF)
RBC casts (pathognomonic of glomerular disease)
Proteinuria (1+ to 2+)
Dysmorphic RBCs (indicating glomerular origin)

Blood Tests

BUN and creatinine (may be elevated)
Electrolytes (may show hyponatremia)
Complete blood count (may show anemia)
Albumin (usually normal or slightly decreased)

Complement Studies

C3 levels (decreased in PSGN)
C4 levels (usually normal in PSGN)
CH50 (total complement, usually decreased)

Specific Tests for PSGN

Streptococcal Infection Markers

Anti-streptolysin O (ASO) titer (elevated in pharyngeal infections)
Anti-DNase B (elevated in both skin and pharyngeal infections)
Streptozyme test (combination of streptococcal antibodies)
Throat or skin culture (may be negative by time of nephritis)

Additional Investigations

Antinuclear antibodies (if suspecting lupus)
ANCA (if suspecting vasculitis)
Anti-GBM antibodies (if suspecting Goodpasture syndrome)
Viral studies (for hepatitis B, C, HIV if suspected)

Imaging

Renal ultrasound (normal or enlarged kidneys with increased echogenicity)
Chest X-ray (if pulmonary symptoms present)

Renal Biopsy

Not routinely indicated in typical post-streptococcal glomerulonephritis. Consider if:

Atypical presentation or course
Persistent low complement beyond 8 weeks
Rapidly progressive renal failure
Nephrotic range proteinuria
No evidence of streptococcal infection

Diagnostic Strategy for Acute Glomerulonephritis:

Establish the presence of glomerulonephritis (hematuria, proteinuria, RBC casts)
Assess renal function (BUN, creatinine, GFR)
Evaluate complement levels (low C3 suggests post-infectious or lupus)
Look for evidence of streptococcal infection (ASO, anti-DNase B)
Consider other etiologies if PSGN is unlikely based on history, exam, and labs
Reserve renal biopsy for atypical presentations or failure to improve

Management Approach

General Management Principles

Treatment of Underlying Cause

For PSGN: Antibiotic therapy if active streptococcal infection is present
- Penicillin V: 250-500 mg PO QID for 10 days
- Amoxicillin: 50 mg/kg/day in divided doses
- For penicillin allergy: Erythromycin or azithromycin
Note: Antibiotics don’t alter the course of nephritis once established but prevent spread of infection

Supportive Care

Fluid management:
- Monitor fluid balance closely
- Restrict fluids if edema or hypertension present
- Replacement based on urine output and insensible losses
Diet:
- Sodium restriction (1-2 g/day)
- Potassium restriction if hyperkalemic
- Moderate protein intake

Management of Complications

Hypertension Management

Mild to moderate hypertension:
- Sodium and fluid restriction
- Calcium channel blockers (e.g., amlodipine 0.1-0.6 mg/kg/day)
- Beta-blockers (e.g., metoprolol 1-2 mg/kg/day)
Severe hypertension:
- IV labetalol (0.2-1 mg/kg/dose)
- Nicardipine infusion (1-3 mcg/kg/min)
- Sodium nitroprusside (0.5-10 mcg/kg/min) for hypertensive emergency

Volume Overload/Edema

Loop diuretics (furosemide 1-2 mg/kg/dose)
Consider dialysis if severe/refractory

Acute Kidney Injury

Maintain fluid and electrolyte balance
Avoid nephrotoxic drugs
Dialysis indications:
- Severe hyperkalemia (K+ >6.5 mEq/L)
- Severe acidosis (pH <7.2)
- Uremic symptoms
- Refractory fluid overload

Monitoring and Follow-up:

Daily weight and vital signs during acute phase
Regular monitoring of urinalysis, BUN, creatinine, electrolytes
Follow complement levels until normalization
Monitor blood pressure until normalized
Follow-up visits:
- Weekly initially
- Then monthly until urine findings resolve
- Long-term follow-up for 1-2 years with periodic urinalysis

Nursing Considerations

Assessment

Initial Nursing Assessment

Comprehensive vital signs with accurate BP measurement
Careful assessment of volume status and edema
Urine appearance, output, and frequency
Neurological assessment (for hypertensive encephalopathy)
Respiratory assessment (for pulmonary edema)

Ongoing Monitoring

Strict intake and output monitoring
Daily weight measurements
Monitor BP every 4-6 hours or more frequently if elevated
Check urine for color, clarity, and presence of blood
Monitor for signs of worsening kidney function

Interventions

Fluid and Electrolyte Management

Implement prescribed fluid restrictions
Administer diuretics as ordered, monitor response
Educate on low-sodium diet adherence
Monitor for signs of electrolyte disturbances

Blood Pressure Management

Administer antihypertensive medications as prescribed
Ensure proper BP cuff size for accurate measurements
Monitor for signs of hypertensive emergency
Position patient with head elevated if hypertensive

Education and Support

Explain disease process and expected course
Teach importance of medication adherence
Instruct on home BP monitoring techniques
Provide guidance on dietary sodium restriction
Educate on when to seek medical attention

Nursing Care Mind Map for AGN

                            ACUTE GLOMERULONEPHRITIS NURSING CARE
                            ├── ASSESSMENT
                            │   ├── Vital Signs (Especially BP)
                            │   ├── Fluid Status
                            │   │   ├── Edema
                            │   │   ├── Daily Weight
                            │   │   └── Intake & Output
                            │   │
                            │   ├── Urine Characteristics
                            │   │   ├── Hematuria
                            │   │   └── Proteinuria
                            │   │
                            │   └── Symptoms of Complications
                            │       ├── Encephalopathy
                            │       └── Pulmonary Edema
                            │
                            ├── INTERVENTIONS
                            │   ├── Fluid Management
                            │   │   ├── Fluid Restriction
                            │   │   └── Diuretic Administration
                            │   │
                            │   ├── Hypertension Management
                            │   │   ├── Medication Administration
                            │   │   └── Position & Activity Adjustments
                            │   │
                            │   ├── Infection Prevention
                            │   │   ├── Antibiotic Administration
                            │   │   └── Hand Hygiene
                            │   │
                            │   └── Rest & Comfort Measures
                            │
                            └── EDUCATION
                                ├── Disease Process
                                ├── Medication Information
                                ├── Dietary Restrictions
                                ├── Activity Guidelines
                                └── Follow-up Schedule

3. Renal Failure in Children

Overview

Renal failure in children refers to the inability of kidneys to adequately filter waste products, concentrate urine, and maintain fluid and electrolyte balance. It is classified into acute kidney injury (AKI) and chronic kidney disease (CKD), each with distinct causes, presentations, and management approaches.

Acute Kidney Injury (AKI)

Sudden, potentially reversible decline in kidney function
Develops over hours to days
Results in accumulation of nitrogenous wastes and fluid imbalance
May be reversible with prompt intervention

Chronic Kidney Disease (CKD)

Progressive, irreversible loss of kidney function
Develops over months to years
Results in permanent kidney damage
Eventually leads to end-stage renal disease (ESRD) requiring dialysis or transplantation

Pathophysiology

Fig 3: Pathophysiological mechanisms of renal failure showing tubular injury and dysfunction

Acute Kidney Injury Pathophysiology

Mechanisms of Injury:

Prerenal: Decreased renal perfusion
- Hypovolemia (dehydration, hemorrhage)
- Decreased cardiac output
- Renal vasoconstriction
Intrinsic renal: Direct kidney damage
- Acute tubular necrosis (ischemic or toxic)
- Acute interstitial nephritis
- Glomerulonephritis
- Vascular disease
Postrenal: Urinary tract obstruction
- Congenital anomalies
- Stones
- Tumors
- Posterior urethral valves

Tubular Injury Process:

Reduced renal blood flow → decreased oxygen delivery
Tubular epithelial cell injury and death
Tubular obstruction from cellular debris
Backleak of filtrate through damaged tubules
Vasoconstriction from tubuloglomerular feedback
Reduced glomerular filtration rate (GFR)

Chronic Kidney Disease Pathophysiology

Progressive Nephron Loss:

Initial kidney injury (congenital or acquired)
Loss of functioning nephrons
Hyperfiltration of remaining nephrons
Compensatory hypertrophy
Secondary glomerulosclerosis
Further nephron loss in self-perpetuating cycle
Eventually, critical mass of nephrons lost

Systemic Complications:

Fluid and electrolyte imbalances: Inability to regulate sodium, potassium, acid-base balance
Metabolic bone disease: Abnormal vitamin D metabolism, phosphate retention, secondary hyperparathyroidism
Anemia: Reduced erythropoietin production
Growth retardation: Metabolic acidosis, malnutrition, resistance to growth hormone
Cardiovascular changes: Hypertension, left ventricular hypertrophy, vascular calcification

Uremic Toxins

Accumulation of nitrogenous waste products (urea, creatinine) and other uremic toxins leads to systemic manifestations and end-organ damage

Hormonal Dysregulation

Disruption of renin-angiotensin-aldosterone system, erythropoietin, vitamin D activation, and FGF-23/klotho axis

Growth Impact

Unique to pediatric patients: decreased linear growth, delayed puberty, and impaired cognitive development due to uremia and metabolic disturbances

Key Concept: Kidney Reserve

Children, like adults, have substantial renal reserve. Serum creatinine does not typically rise until 50% of nephrons are damaged. This results in “silent” progression of CKD until significant damage has occurred.

Etiology and Classification

Acute Kidney Injury Causes

Category	Common Causes	Pathophysiology
Prerenal (55%)	Dehydration/volume depletion Septic shock Cardiac failure Hepatorenal syndrome Medications affecting renal perfusion (NSAIDs, ACE inhibitors)	Decreased renal perfusion leading to reduced GFR; kidney function remains intact
Intrinsic Renal (40%)	Acute tubular necrosis Hemolytic uremic syndrome Acute glomerulonephritis Interstitial nephritis Nephrotoxins (antibiotics, contrast media) Tumor lysis syndrome Rhabdomyolysis	Direct damage to kidney parenchyma affecting glomeruli, tubules, interstitium, or blood vessels
Postrenal (5%)	Posterior urethral valves Ureteropelvic junction obstruction Neurogenic bladder Urolithiasis Tumor compression	Obstruction to urine flow leading to increased backward pressure and decreased GFR

Chronic Kidney Disease Causes

Causes vary by age group:

Age Group	Common Causes
Infants (0-1 years)	Congenital anomalies of kidney and urinary tract (CAKUT) Renal dysplasia/hypoplasia Polycystic kidney disease Obstructive uropathy Cortical necrosis
Young Children (1-5 years)	CAKUT Hemolytic uremic syndrome Nephrotic syndrome Renal vein thrombosis
Older Children (6-12 years)	Chronic glomerulonephritis Alport syndrome Chronic pyelonephritis Focal segmental glomerulosclerosis
Adolescents (13-18 years)	Lupus nephritis IgA nephropathy FSGS Diabetic nephropathy Reflux nephropathy

Classification of Acute Kidney Injury (KDIGO)

Stage	Serum Creatinine	Urine Output
1	1.5-1.9 times baseline OR ≥0.3 mg/dL increase	<0.5 mL/kg/hr for 6-12 hrs
2	2.0-2.9 times baseline	<0.5 mL/kg/hr for ≥12 hrs
3	3.0 times baseline OR Increase to ≥4.0 mg/dL OR Initiation of renal replacement OR GFR <35 mL/min/1.73m²	<0.3 mL/kg/hr for ≥24 hrs OR Anuria for ≥12 hrs

Classification of Chronic Kidney Disease

Stage	GFR (mL/min/1.73m²)	Description
1	≥90	Normal or high GFR with kidney damage*
2	60-89	Mildly decreased GFR with kidney damage*
3a	45-59	Mildly to moderately decreased GFR
3b	30-44	Moderately to severely decreased GFR
4	15-29	Severely decreased GFR
5	<15	Kidney failure (ESRD)

*Kidney damage defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies

Mnemonic: “RENAL FAILURE”

To remember common causes of renal failure in children:

R – Renal dysplasia/hypoplasia
E – Endocrine disorders (diabetes)
N – Nephrotic syndrome
A – Acute tubular necrosis
L – Lupus nephritis
F – Focal segmental glomerulosclerosis
A – Alport syndrome
I – Interstitial nephritis
L – Lower urinary tract obstruction
U – Urologic abnormalities (CAKUT)
R – Reflux nephropathy
E – Ehrlichia (Hemolytic uremic syndrome)

Clinical Presentation

Acute Kidney Injury Presentation

Urinary Findings

Oliguria (<0.5 mL/kg/hr) or anuria
May have polyuria in some cases
Hematuria (variable)
Proteinuria (variable)

Volume Status

Prerenal: Signs of dehydration (decreased skin turgor, dry mucous membranes)
Intrinsic: Variable, may have edema
Postrenal: May have bladder distention, flank tenderness

Systemic Features

Hypertension
Fluid overload (edema, pulmonary crackles)
Lethargy, confusion (from uremia or electrolyte disturbances)
Anorexia, nausea, vomiting
Features of underlying cause (rash, joint pain, etc.)

Chronic Kidney Disease Presentation

Early CKD (Often Asymptomatic)

Growth retardation (often first sign in children)
Mild hypertension
Polyuria/nocturia (concentrating defect)
Mild anemia
Subtle neurocognitive issues

Advanced CKD

Poor growth and delayed puberty
Moderate to severe hypertension
Bone deformities and pain
Pallor (anemia)
Uremic symptoms (fatigue, poor appetite, nausea)
Pruritus
Neurological symptoms (reduced concentration, poor school performance)

End-Stage Renal Disease

Severe growth failure
Uremic frost
Pericarditis
Encephalopathy
Peripheral neuropathy
Bleeding diathesis
Severe anemia

Special Considerations in Children:

Growth parameters: Linear growth impairment is often the earliest and most sensitive marker of CKD in children
Developmental milestones: May be delayed with significant renal dysfunction
Pubertal development: Often delayed in CKD stages 3-5
School performance: May decline due to anemia, subtle uremia, and frequent medical appointments
Psychosocial impact: Self-image concerns, depression, anxiety more common with visible signs of kidney disease

Diagnostic Evaluation

Laboratory Studies

Blood Tests

BUN and creatinine (elevated)
Electrolytes
- Potassium (often elevated)
- Sodium (variable)
- Calcium (decreased in CKD)
- Phosphorus (elevated in CKD)
Acid-base status (usually metabolic acidosis)
Complete blood count (anemia common in CKD)
Albumin (may be decreased)

Urine Studies

Urinalysis (for blood, protein, specific gravity)
Urine electrolytes (helps distinguish prerenal from intrinsic causes)
- Fractional excretion of sodium (FENa)
- Urine sodium
Protein/creatinine ratio
Urine output measurement

Additional Studies for CKD

Parathyroid hormone (elevated in CKD)
25-OH and 1,25-OH vitamin D levels
Alkaline phosphatase (bone metabolism)
Lipid profile
Iron studies
Glomerular filtration rate (GFR) estimation
- Schwartz formula for children
- Nuclear medicine studies (gold standard)

Imaging and Additional Tests

Imaging Studies

Renal ultrasound
- Kidney size and echogenicity
- Evidence of obstruction
- Congenital anomalies
Voiding cystourethrogram (for suspected reflux or obstruction)
CT scan (rarely needed)
MRI (for detailed anatomy or vascular issues)
Nuclear scans (for function assessment)

Specialized Testing

Kidney biopsy (for definitive diagnosis of intrinsic disease)
Genetic testing (for suspected hereditary conditions)
Complement studies (for glomerulonephritis)
Autoantibody studies (for autoimmune causes)

Monitoring in CKD

Growth parameters (height, weight, BMI)
Blood pressure monitoring
Bone age X-rays
Renal osteodystrophy evaluation
Developmental assessment
Cardiovascular risk assessment

Diagnostic Approach:

Confirm the presence of kidney dysfunction (elevated creatinine, abnormal GFR)
Determine acuity (acute vs. chronic) – history, previous labs, imaging, anemia, growth
In AKI, identify the mechanism (prerenal, intrinsic, postrenal)
In CKD, stage the disease based on GFR and identify underlying cause
Assess for complications of kidney failure
Evaluate growth and development in pediatric patients

Management Approach

Acute Kidney Injury Management

Initial Stabilization

Treat life-threatening complications
- Hyperkalemia
- Pulmonary edema
- Severe acidosis
- Uremic encephalopathy
Correct underlying cause
- Fluid resuscitation (for prerenal causes)
- Relief of obstruction (for postrenal causes)
- Discontinue nephrotoxic drugs
- Treat infections

Fluid and Electrolyte Management

Careful fluid management
- Replace ongoing losses
- Restrict fluids if oliguric
- Adjust maintenance based on output
Hyperkalemia management
- Calcium gluconate (for cardiac stabilization)
- Insulin and glucose
- Sodium bicarbonate
- Potassium-binding resins
Acidosis correction (sodium bicarbonate for severe acidosis)

Renal Replacement Therapy (RRT) Indications

Refractory hyperkalemia
Severe acidosis unresponsive to medical therapy
Volume overload causing respiratory compromise
Uremic symptoms (encephalopathy, pericarditis)
Certain toxin ingestions

RRT Modalities

Peritoneal dialysis (often first choice in small children)
Continuous renal replacement therapy (CRRT)
Intermittent hemodialysis

Chronic Kidney Disease Management

Slow Progression

Blood pressure control
- ACE inhibitors or ARBs preferred
- Target BP <90th percentile for age, height, and sex
Proteinuria reduction
Glycemic control (if diabetic)
Avoid nephrotoxins

Metabolic Complications Management

Anemia
- Erythropoiesis-stimulating agents
- Iron supplementation
Mineral bone disorder
- Phosphate binders