Pediatric Nephrology Ultimate Exam Guide

L1: Introduction to Pediatric Nephrology

Kidney Functions & Glomerular Filtration Rate (GFR)

• Homeostasis & Endocrine roles: Generates energy via gluconeogenesis, produces renin, vitamin D metabolites, and erythropoietin.
• Glomerular Filtration Rate (GFR): The best measure of kidney function.
• Filtration Barrier: Filters all plasma substances EXCEPT proteins having a molecular weight of ≥68 kDa (e.g., albumin and globulins).
• Filtration Forces: Promoted by glomerular capillary hydrostatic pressure (systemic Blood Pressure (BP) modified by afferent and efferent arterioles tone). Opposed by glomerular capillary oncotic pressure (gradient between plasma proteins and protein-free Bowman’s space).

GFR in Children & Creatinine Measurement

• Fetal vs Postnatal: Kidney function is not necessary for intrauterine homeostasis because the placenta is the major fetal excretory organ.
• Maturation: GFR reaches adult values (100 to 120 mL/min/1.73 m²) rapidly during the first 2 years of life.
• Serum Creatinine (Cr): Derived from muscle mass metabolism. It is an insensitive measure of early acute renal failure because it does not rise above normal until GFR falls by 30-40%. Must be evaluated under steady-state conditions.
• Schwartz Formula for GFR: GFR = 0.413 × Height (cm) / Serum Creatinine (mg/dL).
• Clearance: Precise measurement requires clearance of a substance that is freely filtered, neither reabsorbed nor secreted.

🔥 Exam Hints & Pearls (L1)

• 1. A neonate with abnormal kidneys can survive in utero because the placenta clears waste.
• 2. 68 kDa is the magic number for the filtration barrier; anything larger (like Albumin) cannot pass normally.
• 3. Normal GFR (100-120 mL/min/1.73 m²) is achieved by 2 years of age.
• 4. Serum creatinine is a late indicator of AKI (requires 30-40% GFR drop to rise).
• 5. In the Schwartz formula, height MUST be in centimeters (cm).

L2: Hemolytic-Uremic Syndrome (HUS)

Definition, Triad & Etiology

• Classic Triad: Microangiopathic hemolytic anemia, Thrombocytopenia, and Kidney insufficiency.
• Most common cause: Shiga toxin–producing Escherichia coli (STEC). Serotype O157:H7 is most common in Americas/Europe. Causes Diarrhea-associated (Typical) HUS (90% of cases).
• Transmission: Undercooked meat, raw milk, unpasteurized apple cider, contaminated pools.
• Atypical HUS / Pneumococcal HUS: Neuraminidase cleaves sialic acid to expose the cryptic Thomsen-Friedenreich (T) antigen on RBCs/platelets, triggering endogenous IgM. Thus, it has a Positive direct Coombs test (Unlike STEC-HUS which is Coombs negative).

Pathogenesis & Clinical Manifestations

• Pathogenesis: Shiga toxin / verotoxin binds endothelial cells causing damage. Swelling and accumulation of fibrillar material narrows lumen. Mechanical injury to Red Blood Cells (RBCs) causes nonimmune anemia (negative Coombs).
• Prodrome: Onset 5-7 days after gastroenteritis (often bloody diarrhea). Followed by sudden pallor, weakness, and lethargy.
• Volume Status: Can present with severe dehydration or volume overload (masked oliguria by ongoing diarrhea).
• CNS Involvement: Severe in ≤20% of cases (Seizures, encephalopathy). Large strokes are rare.
• Other Complications: Hyperkalemia, pericarditis, myocardial dysfunction, intussusception, pancreatitis.

Diagnosis & Management

• Diagnosis: Schistocytes (fragmented RBCs), platelets 20,000-100,000/mm³, NORMAL PT/PTT, negative Coombs (except pneumo-HUS). Microscopic hematuria. Leukocytosis is often present and significant.
• Treatment is Supportive: Volume expansion early is nephroprotective. Red cell transfusions required. 50% require dialysis.
• Pneumococcal HUS specific: Must use Washed RBCs for transfusion to remove residual plasma (contains IgM against T-antigen). Plasmapheresis is specifically contraindicated.
• CONTRAINDICATIONS (DO NOT USE): Antibiotic therapy (increases Shiga toxin release), Platelet transfusions (rapidly consumed, worsens thrombosis), and Anticoagulation/Fibrinolytics (risk of hemorrhage).
• Atypical HUS Rx: Eculizumab (anti-C5 antibody targeting complement).

🔥 Exam Hints & Pearls (L2)

• 1. Triad: Hemolytic anemia + Thrombocytopenia + AKI.
• 2. Coombs Test: Negative in typical STEC-HUS; Positive in Pneumococcal HUS.
• 3. Strict Contraindications: NO Antibiotics, NO Platelets, NO Anticoagulants in STEC-HUS.
• 4. Washed RBCs MUST be used if transfusing a patient with Pneumococcal-HUS.
• 5. Eculizumab is the specific treatment for Atypical HUS (Complement inhibitor).

L3: Acute Poststreptococcal Glomerulonephritis (APSGN)

Etiology, Pathology & Pathogenesis

• Etiology: Follows infection by Nephritogenic strains of Group A β-hemolytic streptococci (GABHS). Pharyngitis (winter) or Pyoderma/Skin (summer).
• Pathology (Light Microscopy): Diffuse mesangial cell proliferation.
• Pathology (Immunofluorescence): Lumpy-bumpy deposits of immunoglobulin (IgG) and complement (C3).
• Pathology (Electron Microscopy): Electron-dense subepithelial "humps".
• Pathogenesis: Immune complex mediated. Possible molecular mimicry or in situ immune complex formation. Result is Depression of serum C3.

Clinical Manifestations & Diagnosis

• Demographics & Timing: Common in ages 5-12 years. Occurs 1-2 weeks after Pharyngitis, or 3-6 weeks after Pyoderma (Skin).
• Acute Nephritic Syndrome: Sudden onset of Gross Hematuria (cola-colored urine), Edema, Hypertension, and Oliguria.
• Complications: Hypertensive Encephalopathy (blurred vision, severe headaches, seizures) and Heart Failure (pulmonary edema, volume overload).
• Laboratory Diagnosis: Red Blood Cell (RBC) Casts. Significantly reduced C3 level (>90% of patients) that returns to normal in 8-10 weeks. C4 is typically NORMAL.
• Antibody Titers: Elevated ASO (Antistreptolysin O) for throat. Elevated Anti-DNase B (antideoxyribonuclease B) for skin infections. Streptozyme screen is highly valuable.
• Differential Diagnosis: Must consider systemic lupus erythematosus, endocarditis, and membranoproliferative GN.

Treatment, Prevention & Prognosis

• Biopsy Indications: Only if Acute Kidney Failure, Nephrotic syndrome, Normal complement levels, or if low C3 persists >2 months.
• Treatment: 10-day Penicillin (Does NOT affect the natural history/course of APSGN, only limits bacterial spread). Manage HTN with Salt/fluid restriction, Loop Diuretics, and calcium channel antagonists or ACE inhibitors.
• Prognosis: Excellent. >95% complete recovery. Recurrences are extremely rare.

🔥 Exam Hints & Pearls (L3)

• 1. Timing: Throat = 1-2 weeks. Skin (Pyoderma) = 3-6 weeks.
• 2. Complement Levels: C3 is extremely LOW, while C4 is NORMAL.
• 3. Antibodies: ASO titer for throat; Anti-DNase B is best for skin.
• 4. Antibiotics: Penicillin prevents spread to family members but does NOT change the renal course of the patient.
• 5. Biopsy rule: Do NOT biopsy unless presentation is atypical (e.g., normal C3, or low C3 persisting >2 months).

L4: Nephrotic Syndrome

Definition & Pathogenesis

• Classic Triad: Nephrotic-range proteinuria / Heavy proteinuria (>3.5 g/24 hr or Urine Protein:Creatinine ratio >2), Hypoalbuminemia (≤2.5 g/dL), and Hyperlipidemia (Cholesterol >200 mg/dL). Edema is the most common presenting symptom.
• Podocyte Role: The core defect is effacement of the epithelial cell (podocyte) foot processes and altered slit diaphragm integrity, leading to massive protein leak.
• Edema Hypotheses:
  • Underfill: Proteinuria -> low oncotic pressure -> fluid leaks to interstitium -> low volume stimulates RAAS, vasopressin, and atrial natriuretic factor.
  • Overfill: Primary sodium retention at distal tubule -> volume expansion.
• Hyperlipidemia: Increased hepatic synthesis and decreased catabolism of lipids. Includes increase in low-density lipoproteins and VLDL.

Clinical Consequences & Complications

• Infections: Susceptible due to Urinary loss of IgG and Alternative complement factors (Factor B and D). Highest risk for encapsulated bacteria (Pneumococcus).
• Spontaneous Bacterial Peritonitis (SBP): Fever, abdominal pain. Diagnosis is highly suggested by Peritoneal leukocyte count >250 cells/μL. Treat empirically with 3rd-generation Cephalosporin.
• Hypercoagulability: Risk of DVT, Renal Vein Thrombosis. Due to Urinary loss of Antithrombin III and Protein S, hemoconcentration, and increased hepatic synthesis of fibrinogen.

Types, Pathology & Treatment

• Histologic Types: Minimal change nephrotic syndrome (MCNS) (85%), Focal segmental glomerulosclerosis (FSGS) (most common in adolescents), Membranous nephropathy, Membranoproliferative glomerulonephritis.
• MCNS triggers: May occur after viral infections, allergen challenges, or associated with Hodgkin lymphoma.
• MCNS Presentation: Ages 2 to 6 years. Absence of gross hematuria, hypertension, or renal failure. Normal C3/C4. May have pleural effusions, ascites, genital edema, and intravascular volume depletion.
• Diagnosis: Spot urine protein:creatinine ratio is the simplest method. First morning sample preferred.
• Pre-treatment screening: Must rule out Tuberculosis with purified protein derivative skin test or interferongamma release assay.
• Indications for Biopsy (DO NOT treat blindly if): Age <1 year or >12 years, Gross hematuria, Sustained HTN, Low C3, or Steroid Resistance.
• Treatment: Corticosteroids (Prednisone/Prednisolone) 2 mg/kg/day (Max 60 mg/day) for 4-6 weeks, then alternate days. 80-90% respond.
• Relapse: Defined as Protein:Creatinine ratio >2 or ≥3+ protein on dipstick for 3 consecutive days. Triggered by URTI.
• Steroid Resistance: Failure to achieve remission after 4 weeks of corticosteroid therapy.
• Side effects of long-term steroids: Cushingoid appearance, cataracts, growth failure, hypertension.
• Immunizations: Give Pneumococcal and annual Influenza. Live virus vaccines are CONTRAINDICATED during high-dose steroid or immunosuppressive therapy. If exposed to Varicella, give varicella-zoster immune globulin.

🔥 Exam Hints & Pearls (L4)

• 1. Triad + 1: Heavy Proteinuria (>3.5g) + Hypoalbuminemia (<2.5) + Hyperlipidemia + Edema.
• 2. Infection Risk: High risk of Pneumococcal SBP (Diagnostic tap: >250 WBCs/μL).
• 3. Thrombosis Risk: Due to loss of Antithrombin III and Protein S in urine.
• 4. Steroid Resistance definition: Still having proteinuria after 4 weeks of maximum steroid therapy.
• 5. Live Vaccines: Absolutely contraindicated while on high-dose immunosuppressives. Give VZIG if exposed to chickenpox.

L5: Acute Kidney Injury (AKI)

Definition & Classification

• Diagnostic Criteria: Increase in Serum Cr by ≥0.3 mg/dL within 48 hours, OR Increase to ≥1.5 times baseline within 7 days, OR Urine volume ≤0.5 mL/kg/hr for 6 hours.
• Prerenal AKI / prerenal azotemia: Diminished effective circulating volume (Dehydration, sepsis, hemorrhage). Reversible if corrected.
• Intrinsic renal AKI: Structural damage (Acute Tubular Necrosis (ATN), Glomerulonephritis, HUS).
• Postrenal AKI: Obstruction. Most common in neonates: Posterior Urethral Valves (PUV) or bilateral ureteropelvic junction obstruction. Must be Bilateral in a patient with two functioning kidneys to cause AKI.

Diagnosis & Urinary Indices

• Prerenal Indices: Urine Specific Gravity >1.020, Urine Osmolality >500 mOsm/kg, Urine Na <20 mEq/L, and Fractional Excretion of Sodium (FENa) <1%.
• Intrinsic Indices: Urine Specific Gravity <1.010, Urine Osmolality <350 mOsm/kg, Urine Na >40 mEq/L, and FENa >2%.
• Urine Microscopy: RBC/Granular casts = Intrinsic/Glomerular/ATN. WBC casts = Tubulointerstitial. Urinary Eosinophils = Drug-induced Acute Interstitial Nephritis (AIN).

Management of AKI & Complications

• Fluid Management: For hypovolemia, give isotonic saline 20 mL/kg over 30 mins. Once euvolemic but oliguric, STRICT fluid restriction: 400 mL/m²/24 hr (insensible losses) + Urine Output. Diuretics and dopamine may be used but lack strong prevention evidence.
• Life-Threatening Hyperkalemia (>6 mEq/L):
  • ECG: Peaked T waves -> Wide QRS -> Arrest.
  • Cardioprotection (First step for severe ECG changes): 10% Calcium Gluconate (Stabilizes myocardium, does NOT lower K+ levels).
  • Shift K+ intracellularly: Sodium bicarbonate, Regular insulin + Glucose, Beta-agonists.
  • Remove K+ from body: Sodium polystyrene sulfonate (Kayexalate) or Dialysis.
• Acidosis: Treat with IV Bicarb only if severe (pH <7.15). Danger: Rapid correction of acidosis reduces Ionized Calcium, precipitating Tetany.
• Hypocalcemia: Treat by lowering phosphorus using Phosphate Binders (sevelamer, calcium carbonate). Do NOT give IV calcium unless symptomatic tetany (risk of tissue deposition).
• Hypertension Management: Rapid reduction with isradipine, nicardipine, sodium nitroprusside.
• Dialysis Indications: Anuria with Fluid Overload (Pulmonary Edema) refractory to diuretics, Persistent Hyperkalemia, Severe Metabolic Acidosis, Uremic Encephalopathy/Pericarditis.

🔥 Exam Hints & Pearls (L5)

• 1. Prerenal vs Intrinsic: FENa <1% in Prerenal; >2% in Intrinsic ATN.
• 2. Postrenal Rule: Obstruction MUST be bilateral to cause AKI in a child with two kidneys.
• 3. ECG Changes in Hyperkalemia: Peaked T-waves is the earliest sign.
• 4. Hyperkalemia Treatment: Calcium Gluconate protects the heart but DOES NOT lower Potassium! Insulin/Glucose lowers it.
• 5. Acidosis danger: Correcting acidosis too rapidly drops Ionized Calcium and causes Tetany.

L6: Chronic Renal Failure (CKD)

Definition, Causes & Staging

• Definition: Structural or functional abnormalities OR Glomerular Filtration Rate (GFR) < 60 ml/min/1.73 m² for ≥ 3 months. Associated with loss of erythropoietin and Vit D metabolism.
• Etiology (< 5 years): Congenital abnormalities (Renal hypoplasia, dysplasia, Obstructive uropathy, Congenital Nephrotic Syndrome).
• Etiology (> 5 years): Acquired diseases (Glomerulonephritis), Inherited (Alport syndrome), Metabolic (Cystinosis).
• Stages (by GFR): Stage 1 (>90), Stage 2 (60-90), Stage 3 (30-60), Stage 4 (15-30), Stage 5 (< 15 or on dialysis - ESRD).
• GFR Equation: k × Height (cm) / Serum Creatinine (mg/dL). k=0.55 for children/adolescent females, 0.70 for adolescent males. Note: Inulin clearance is gold standard but difficult.

Complications & Medical Management

• Nutrition: Protein restriction is GENERALLY NOT recommended for children (due to growth adverse effects). Give 2.5 g/kg/24 hr of high biologic value protein.
• Anemia: Due to Decreased Erythropoietin (EPO). Treat when Hb <10 g/dL with Recombinant Human Erythropoietin (rHuEPO) SC + Iron. Goal is Hb 12-13. Side effects: Hypertension, seizures.
• Growth Failure: Have high Growth Hormone (GH) but Decreased IGF-1 and IGF-BP (GH resistance). Treat with exogenous rHuGH (0.05 mg/kg/day SC) until reaching 50th percentile height or renal transplant.
• Renal Osteodystrophy: Due to decreased 1,25-Vit D, hyperphosphatemia, hypocalcemia -> Secondary Hyperparathyroidism. X-ray shows Osteitis Fibrosa Cystica.
  • Treatment: Phosphate Binders. Active Vitamin D (Calcitriol).
  • MUST maintain Calcium × Phosphorus product < 55 to prevent metastatic tissue calcification.
• Hypertension & Proteinuria: Use ACE Inhibitors or Angiotensin II Receptor Blockers (ARBs) to decrease proteinuria and slow CKD progression.
• End-Stage Renal Disease (ESRD): Requires Renal Replacement Therapy (Hemodialysis, Peritoneal Dialysis, or renal transplantation - which is the definitive treatment).

🔥 Exam Hints & Pearls (L6)

• 1. Time Criteria: CKD requires abnormalities persisting for ≥ 3 months.
• 2. Protein Intake: Unlike adults, DO NOT restrict protein in children with CKD (due to growth requirements).
• 3. Anemia: Treat with EPO when Hb drops below 10 g/dL. (Watch out for HTN as a side effect).
• 4. Bone Disease: Keep Calcium × Phosphorus product < 55 to avoid ectopic tissue calcification.
• 5. Proteinuria control: ACE Inhibitors / ARBs are the drugs of choice to slow CKD progression by reducing proteinuria.

L7: Renal Tubular Acidosis (RTA)

Overview & Proximal (Type II) RTA

• Definition: Characterized by Non-Anion Gap (Hyperchloremic) Metabolic Acidosis with NORMAL Glomerular Filtration Rate.
• Proximal (type II) RTA: Due to Impaired Bicarbonate Reabsorption in the proximal tubule.
• Fanconi Syndrome: Global proximal tubule dysfunction. Features: Proximal RTA + Low-molecular-weight proteinuria, Glycosuria, Phosphaturia, Aminoaciduria.
• Cystinosis: Most common systemic cause of Fanconi. Autosomal recessive defect causing cystine crystal accumulation.
  • Diagnosis: cystine crystals in cornea (slit lamp), increased leukocyte cystine.
  • Treatment: cysteamine (converts cystine to cysteine) orally + eyedrops. Delays ESRD.
• Urine pH in Proximal RTA: Because distal acidification is intact, urine pH can drop to < 5.5 when serum bicarb is very low.
• Treatment for Type II: Requires Massive doses of Bicarbonate (up to 20 mEq/kg/24 hr) because giving bicarb simply leads to massive spilling in urine. Phosphate supplementation for rickets.

Distal (Type I) RTA

• Pathogenesis: Failure of the distal (type I) RTA tubule to Secrete Hydrogen (H+) ions.
• Key Features: Urine pH is ALWAYS > 5.5 (cannot acidify urine). Causes Hypokalemia (K+ is secreted instead of H+).
• Complications: Hypercalciuria, nephrocalcinosis, nephrolithiasis (Kidney Stones). This is worsened by hypocitraturia (Citrate prevents stones, but is absorbed excessively in acidosis). Also causes Bone Demineralization / Rickets because bone buffers the retained H+.
• Treatment for Type I: Only requires small base replacement: Bicarbonate 2-4 mEq/kg/24 hr. Thiazide diuretics if hypercalciuria is symptomatic. Correction of acidosis heals bone dissolution and hypercalciuria.

🔥 Exam Hints & Pearls (L7)

• 1. Type I (Distal) RTA: Cannot excrete H+. Urine pH is ALWAYS > 5.5.
• 2. Type II (Proximal) RTA: Cannot reabsorb Bicarb. Requires MASSIVE Bicarb replacement (up to 20 mEq/kg/day).
• 3. Stones vs Bones: Type I (Distal) commonly causes Kidney Stones (Nephrocalcinosis). Type II is associated with Rickets (Fanconi syndrome).
• 4. Fanconi Syndrome: Think global proximal failure = Glucose, Amino Acids, Phosphate, and Bicarb all lost in urine.
• 5. Cystinosis: The classic cause of Fanconi. Look for corneal crystals; treat with Cysteamine.

L8: Urinary Tract Infections (UTI)

Epidemiology & Etiology

• Epidemiology: Below 1 year, Male:Female is 4:1 (especially uncircumcised males). After 1 year, striking female preponderance (1:10).
• Etiology: Escherichia coli (E. coli) is the most common colonic bacteria causing UTI.
• Pathogenesis: Virtually all are Ascending infections from perineal flora. Hematogenous spread is rare (neonates). Risk factors: VUR, uncircumcised males, constipation, labial adhesions.

Clinical Types & Diagnosis

• Types:
  • Asymptomatic Bacteriuria: Positive culture, no symptoms. Common in girls.
  • Cystitis (Lower UTI): Dysuria, urgency, suprapubic pain. No fever. Adenovirus can cause Acute Hemorrhagic Cystitis.
  • Pyelonephritis (Upper UTI): Fever, flank pain, systemic symptoms (vomiting). Xanthogranulomatous pyelonephritis is a rare granulomatous form. Can lead to renal scarring.
• Diagnosis:
  • sterile pyuria Causes: Partially treated bacterial UTI, Viral infection, Renal Tuberculosis (TB), Appendicitis.
  • Urine Culture Gold Standard: >50,000 colonies of a single pathogen (catheterization or clean catch).
  • Sample Storage: Must culture promptly. If delayed, Refrigeration prevents false overgrowth of contaminants.

Imaging & Management

• Imaging Guidelines:
  • Renal Ultrasound (US): Indicated for ALL infants with UTI, febrile UTIs, recurrent UTIs.
  • Voiding Cystourethrogram (VCUG): Ordered if US is abnormal, detects Vesicoureteral Reflux (VUR).
  • DMSA Scan: Best test to detect renal scars after severe/recurrent pyelonephritis.
• Treatment (Cystitis): Oral TMP-SMZ, Nitrofurantoin, or Amoxicillin for 3-5 days.
• Treatment (Pyelonephritis / Febrile UTI):
  • Admit if: Age ≤1 month, severe dehydration, unable to drink.
  • IV Antibiotics: Ceftriaxone or Ampicillin + Gentamicin.
  • WARNING: Nitrofurantoin should NEVER be used in febrile UTI (Pyelonephritis) because it does NOT achieve significant renal tissue levels.
• Prophylaxis: Indicated for recurrent UTI, Neurogenic bladder, severe VUR. Use 1/3 of therapeutic dose of TMP-SMZ or Nitrofurantoin daily.

🔥 Exam Hints & Pearls (L8)

• 1. Gender Shift: Males dominate < 1 year (due to foreskin/congenital anomalies). Females dominate > 1 year.
• 2. Cystitis vs Pyelo: Fever and Flank Pain point directly to Pyelonephritis (Upper UTI).
• 3. Nitrofurantoin Trap: Excellent for Cystitis, but USELESS in Pyelonephritis because it doesn't reach therapeutic levels in renal tissue.
• 4. Sterile Pyuria: Think Partially treated UTI, Renal TB, or Appendicitis.
• 5. Imaging: DMSA scan is the gold standard for detecting renal scars. Ultrasound is the first initial test for all infants.

Ultimate Exam Comparisons

1. Prerenal vs. Intrinsic AKI Indices

Parameter	Prerenal AKI (Volume Depletion)	Intrinsic AKI (ATN/Glomerular)
Urine Specific Gravity	> 1.020 (Concentrated)	< 1.010 (Dilute)
Urine Osmolality	> 500 mOsm/kg	< 350 mOsm/kg
Urine Sodium (UNa)	< 20 mEq/L (Kidney retaining Na)	> 40 mEq/L (Tubules damaged)
FENa (Fractional Excretion Na)	< 1%	> 2%
Urine Casts	Hyaline casts / Normal	RBC Casts (Glomerular) / Granular (ATN)

2. Proximal (Type II) vs. Distal (Type I) RTA

Feature	Proximal (Type II) RTA	Distal (Type I) RTA
Defect Location	Proximal Tubule (Cannot reabsorb HCO3)	Distal Tubule (Cannot secrete H+)
Urine pH	Can drop < 5.5 (Distal acidification intact)	ALWAYS > 5.5
Potassium (K+)	Hypokalemia	Hypokalemia
Bicarbonate Rx Dose	Massive (up to 20 mEq/kg/day)	Small (2-4 mEq/kg/day)
Complications	Fanconi Syndrome, Rickets	Nephrocalcinosis (Kidney stones)

3. Typical (STEC) vs. Atypical (Pneumococcal) HUS

Feature	Typical HUS (Diarrhea-associated)	Atypical / Pneumococcal HUS
Cause	Shiga-toxin E. coli (O157:H7)	Neuraminidase exposing T-antigen
Direct Coombs Test	Negative	Positive
Prodrome	Bloody Diarrhea (5-7 days prior)	Pneumonia / Meningitis
Transfusion Rule	Standard PRBCs (avoid platelets)	MUST use Washed RBCs (to remove IgM)
Specific Rx / Avoidance	Avoid Antibiotics & Anticoagulants	Treat with Eculizumab. Avoid Plasmapheresis

4. Poststreptococcal GN: Pharyngitis vs. Pyoderma

Feature	Throat Infection (Pharyngitis)	Skin Infection (Pyoderma)
Season	Cold-weather months (Winter)	Warm-weather months (Summer)
Serotypes	M1, M4, M25, M12	M49
Latent Period	1 to 2 weeks	3 to 6 weeks
Best Antibody Test	ASO (Antistreptolysin O)	Anti-DNase B

5. Nephrotic Edema: Underfill vs. Overfill Hypothesis

Theory	Primary Mechanism	Blood Volume Status
Underfill Hypothesis	Proteinuria → ↓ Oncotic Pressure → Fluid leaks to interstitium → Stimulates RAAS	Intravascular Volume Depletion (Hypotension, Tachycardia)
Overfill Hypothesis	Primary Sodium Retention at the distal tubule	Intravascular Volume Expansion (Overload)

6. Lower UTI (Cystitis) vs. Upper UTI (Pyelonephritis)

Feature	Cystitis (Lower UTI)	Pyelonephritis (Upper UTI)
Symptoms	Dysuria, urgency, suprapubic pain	Fever, flank pain, vomiting, malaise
Fever	Absent	Present (Hallmark)
Renal Injury Risk	No renal scarring	High risk of permanent Renal Scarring
Nitrofurantoin Use	Effective (First line)	CONTRAINDICATED (poor tissue levels)

7. CKD Etiology by Age

Age Group	Most Common Causes	Examples
Children < 5 years	Congenital Abnormalities	Renal hypoplasia, dysplasia, Obstructive uropathy, Congenital Nephrotic Syndrome, PUV.
Children > 5 years	Acquired, Inherited, Metabolic	Glomerulonephritis, Alport syndrome, Cystinosis.

8. Methods to Quantify Proteinuria

Method	Normal Range	Comments
Dipstick	Negative/Trace	False positive if alkaline pH >8 or specific gravity >1.025
Spot Urine (Pr/Cr Ratio)	< 0.2 mg/mg (>2 yr old)	Simplest method; preferred on first morning specimen.
24-hr Urine Collection	< 150 mg/m²/24 hr	Most accurate but inconvenient.