Nephrology Flashcards

Question

What is focal segmental glomerulosclerosis (FSGS)?

Answer 1

FSGS is a histopathological pattern characterized by segmental sclerosis of some glomeruli. It may be primary (idiopathic) or secondary (e.g., reflux nephropathy, obesity). It typically presents with steroid-resistant nephrotic syndrome. Poor prognosis; often progresses to chronic kidney disease. Diagnosis requires renal biopsy.

Answer 2

• Edema: Periorbital (especially in the morning), scrotal/labial, ascites, pedal edema. • Weight gain: Due to fluid retention. • Oliguria: From renal sodium retention. • Fatigue and anorexia • Susceptibility to infection (e.g., spontaneous bacterial peritonitis) • Hypertension: Less common than in nephritic syndromes.

Answer 3

• Infections: SBP (Streptococcus pneumoniae), cellulitis, sepsis (due to loss of IgG, complement) • Thromboembolism: Loss of antithrombin III, protein S/C in urine • Hypovolemia: Decreased effective circulating volume • Acute kidney injury: Due to volume depletion or nephrotoxic drugs • Hyperlipidemia: Increased risk of atherosclerosis • Malnutrition: Loss of protein and anorexia

Answer 4

• Severe anasarca or respiratory compromise • Hypovolemia or shock • Infection (e.g., peritonitis, pneumonia) • Acute kidney injury • Need for intravenous albumin or diuretics • Poor oral intake, vomiting • Failure of outpatient steroid therapy or suspicion of steroid resistance

Answer 5

• Urinalysis: Proteinuria (3+ or 4+), microscopic hematuria • Spot urine protein/creatinine ratio (UPCR) • Serum albumin and total protein • Serum creatinine, urea, electrolytes • Lipid profile: Hypercholesterolemia, hypertriglyceridemia • CBC: Anemia, leukocytosis • Infection screening: Hepatitis B/C, HIV, ASO titers, PPD if risk present

Answer 6

• Selective proteinuria: Primarily albuminuria; characteristic of minimal change disease; better prognosis. • Non-selective proteinuria: Loss of a wide range of plasma proteins (e.g., IgG, transferrin); indicates glomerular basement membrane damage—seen in FSGS or membranous nephropathy; associated with poor steroid response.

Answer 7

Diagnostic criteria include: • Nephrotic-range proteinuria: >40 mg/m²/hr or spot urine protein/creatinine ratio >2 mg/mg • Serum albumin <2.5 g/dL • Edema: Generalized (anasarca), often first seen as periorbital • Hyperlipidemia: Serum cholesterol >200 mg/dL Exclusion of secondary causes (e.g., SLE, infections) is essential for diagnosis.

Answer 8

In typical pediatric cases, MCD is diagnosed clinically due to age (1–10 years), absence of hematuria or hypertension, and excellent steroid responsiveness. Renal biopsy is not required unless atypical features are present. If done, electron microscopy shows diffuse podocyte foot process effacement; light microscopy is normal.

Answer 9

First-line therapy is oral corticosteroids: • Prednisolone or prednisone at 2 mg/kg/day (maximum 60 mg/day) for 4–6 weeks. • Followed by 1.5 mg/kg on alternate days (maximum 40 mg) for 4–6 weeks. Monitor urine protein daily (dipstick) for response. Most children show complete remission within 2 weeks.

Answer 10

The standard regimen is: • Induction phase: Prednisolone 2 mg/kg/day (max 60 mg) for 4–6 weeks • Maintenance phase: 1.5 mg/kg (max 40 mg) on alternate days for 4–6 weeks, then taper • Total duration: Typically 12 weeks Longer courses are associated with fewer relapses but increased steroid toxicity.

Answer 11

Steroid resistance is defined as failure to achieve remission (urine protein nil/trace for 3 consecutive days) after 4 weeks of daily prednisolone therapy at 2 mg/kg/day. Common in FSGS and genetic forms of nephrotic syndrome. These patients have a poorer prognosis and require biopsy and second-line therapy.

Answer 12

Options include: • Calcineurin inhibitors: Cyclosporine or tacrolimus (mainstay) • Cyclophosphamide: Especially in frequent relapsers or steroid-dependent cases • Mycophenolate mofetil (MMF) • Rituximab: Anti-CD20 monoclonal antibody for refractory cases Choice depends on biopsy findings, comorbidities, and risk of toxicity.

Answer 13

Biopsy indications: • Steroid resistance • Age <1 year or >10 years at onset • Hematuria or hypertension • Low complement levels • Impaired renal function • Frequent relapses or dependence on high-dose steroids Biopsy helps determine underlying histopathology (MCD vs FSGS vs membranous nephropathy).

Answer 14

• Early recognition and treatment of infections (especially peritonitis) • Vaccination: Pneumococcal, influenza, varicella • Prophylactic antibiotics in high-risk settings • Hygiene and caregiver education • Avoiding contact with infected individuals during immunosuppression

Answer 15

• Pneumococcal vaccines: - PCV13 (conjugate) and PPSV23 (polysaccharide, ≥2 years old) • Influenza vaccine: Annual inactivated vaccine • Varicella vaccine: If not immune and not on high-dose steroids • Hepatitis B: If not vaccinated Live vaccines are contraindicated during high-dose steroid or immunosuppressive therapy.

Answer 16

Prognosis is excellent: • >90% achieve remission with corticosteroids • ~50–70% have relapses, especially in the first 6 months • Frequent relapsers may need alternative agents (e.g., cyclophosphamide, MMF) • No progression to chronic kidney disease in isolated MCD Long-term monitoring is essential for steroid side effects and relapse management.

Answer 17

AGN is a renal disorder characterized by immune-mediated inflammation of the glomeruli, leading to reduced filtration and leakage of blood and protein into the urine. Hallmark features include hematuria, proteinuria, edema, and hypertension. Common causes in children include post-infectious glomerulonephritis, IgA nephropathy, lupus nephritis, and membranoproliferative GN.

Answer 18

• Hematuria: Often gross (cola- or tea-colored urine) • Edema: Periorbital and peripheral, due to salt/water retention • Hypertension: Common and may be severe • Oliguria: Reduced urine output due to GFR reduction • Proteinuria: Usually non-nephrotic range • May have constitutional symptoms (fatigue, malaise, headache).

Answer 19

PSGN is the most common cause of AGN in children, typically occurring 1–3 weeks after a streptococcal infection (pharyngitis or impetigo). It results from immune complex deposition in glomeruli triggered by nephritogenic strains of group A beta-hemolytic Streptococcus. Classic findings include gross hematuria, edema, and hypertension.

Answer 20

• Gross hematuria: Brown or cola-colored urine • Periorbital edema, especially in the morning • Hypertension: May present with headache or seizures • Oliguria or anuria in severe cases • Systemic signs of recent streptococcal infection (e.g., sore throat, skin infection)

Answer 21

PSGN commonly affects children aged 5–12 years, with a male predominance (2:1). It is more frequent in low-resource settings and in the post-rainy season when streptococcal skin infections are more prevalent.

Answer 22

PSGN is caused by immune complex deposition in the glomerular basement membrane and mesangium. These complexes form in response to streptococcal antigens such as SpeB and nephritis-associated plasmin receptor. Complement activation, especially via the alternative pathway, results in inflammation, capillary damage, and reduced GFR.

Answer 23

• Urinalysis: RBCs (often dysmorphic), RBC casts, proteinuria (sub-nephrotic) • Serum C3: Low in >90% of cases, returns to normal within 6–8 weeks • ASO titer: Elevated if recent pharyngitis • Anti-DNase B: Positive if recent skin infection • Elevated BUN/creatinine in moderate-to-severe disease

Answer 24

Low serum C3 is a hallmark of PSGN and reflects activation of the alternative complement pathway. C3 levels usually normalize within 6–8 weeks. Persistent hypocomplementemia beyond this time should raise suspicion for lupus nephritis or membranoproliferative GN.

Answer 25

• Supportive care is the mainstay: - Manage fluid overload with diuretics (e.g., furosemide) - Antihypertensives (e.g., nifedipine) • Antibiotics (e.g., penicillin) if active streptococcal infection is present or recent • Sodium restriction, fluid restriction if edematous • Dialysis in rare cases of renal failure

Answer 26

Prognosis is excellent in children: • >95% achieve full recovery with normalization of renal function • Edema: Resolves within 1-2 weeks. • Hypertension: Typically resolves within 2-4 weeks but may persist in 5-10% of patients for up to 6-12 months. • Oliguria: Usually resolves within 1-2 weeks as renal function improves. • Gross Hematuria: Disappears within 1-4 weeks, often within the first 1-2 weeks. • Microscopic Hematuria: Can persist for 6-12 months and occasionally up to 2 years. • Proteinuria: Usually resolves within 6-12 months, but may persist longer in rare cases, sometimes up to 2 years. • Decreased Serum C3: Normalizes within 6-8 weeks, typically within 8-12 weeks. • Renal Function (Creatinine): Returns to normal within 1-3 weeks, typically within 2-3 weeks.

Answer 27

IgA nephropathy (Berger disease) is the most common primary glomerulonephritis worldwide, characterized by IgA immune complex deposition in the mesangium. It often follows mucosal infections (e.g., upper respiratory, GI). It may be isolated or part of Henoch-Schönlein purpura nephritis. Disease course is variable—some progress to ESRD.

Answer 28

• Recurrent gross hematuria, often within 1–2 days of an upper respiratory or GI infection (synpharyngitic hematuria) • May also present with asymptomatic microscopic hematuria ± proteinuria • Rarely presents with nephrotic syndrome or rapidly progressive GN • Blood pressure and renal function may remain normal in early stages

Answer 29

Definitive diagnosis requires renal biopsy, showing: • Mesangial proliferation on light microscopy • Mesangial IgA deposition on immunofluorescence Serologic markers are non-specific. Evaluate for secondary causes (e.g., liver disease, celiac disease). C3 is typically normal, distinguishing it from PSGN.

Answer 30

Biopsy is performed when: • Uncertain etiology (non-PSGN presentation) • Persistent low complement beyond 8 weeks • Rapidly deteriorating renal function • Nephrotic-range proteinuria • Suspected secondary GN (e.g., lupus, MPGN) It aids in diagnosis, prognosis, and guiding immunosuppressive therapy.

Answer 31

• Lupus nephritis • Membranoproliferative GN (MPGN) • Anti-GBM disease (Goodpasture’s syndrome) • ANCA-associated vasculitis (e.g., GPA, MPA) • Henoch-Schönlein purpura nephritis • Infective endocarditis-associated GN • C3 glomerulopathy These require serologic and histopathologic evaluation.

Answer 32

• Severe or malignant hypertension • Pulmonary edema or congestive heart failure • Oliguria or anuria • Hypertensive encephalopathy (seizures, altered mental status) • Rapidly rising creatinine or urea • Signs of uremia (pericarditis, vomiting, drowsiness)

Answer 33

• Fluid restriction: Based on insensible loss and urine output • Salt restriction: To control edema and hypertension • Diuretics: For fluid overload (e.g., furosemide) • Antihypertensives: Calcium channel blockers, beta-blockers • Monitor renal function, electrolytes, and BP closely

Answer 34

• First-line: Nifedipine, amlodipine (calcium channel blockers) • Beta-blockers: Labetalol in emergencies • ACE inhibitors/ARBs: Useful in proteinuric patients but avoid in acute renal failure • Hydralazine: As adjunct • IV options: Nicardipine or sodium nitroprusside in hypertensive emergencies

Answer 35

• Crescentic or rapidly progressive GN on biopsy • Lupus nephritis (Class III–V) • Severe IgA nephropathy with nephrotic-range proteinuria • ANCA-associated vasculitis Therapy may include corticosteroids, cyclophosphamide, or rituximab. Treatment decisions are biopsy-guided.

Answer 36

RPGN is a clinical syndrome characterized by rapid loss of renal function (rise in serum creatinine over days to weeks) with crescent formation in ≥50% glomeruli on biopsy. Causes include: • ANCA-associated vasculitis • Lupus nephritis • Anti-GBM disease • Severe IgA nephropathy It requires urgent biopsy and immunosuppressive therapy.

Answer 37

HSP, now known as IgA vasculitis, is the most common systemic small-vessel vasculitis in children. It is immune complex-mediated, primarily involving IgA. It affects skin, joints, GI tract, and kidneys. The renal component is termed HSP nephritis, pathologically similar to IgA nephropathy.

Answer 38

The classic tetrad includes: 1. Palpable purpura: Non-blanching rash, mainly on lower limbs and buttocks 2. Arthritis/arthralgia: Large joints (knees, ankles) 3. Abdominal pain: Colicky, may be associated with GI bleeding 4. Renal involvement: Hematuria, proteinuria, hypertension

Answer 39

HSP nephritis involves IgA-dominant immune complex deposition in the glomerular mesangium, triggering complement activation (mostly via the alternative and lectin pathways), mesangial proliferation, and glomerular injury. Pathologically, it mimics IgA nephropathy. Severity varies from asymptomatic hematuria to crescentic GN.

Answer 40

HSP primarily affects children aged 3 to 15 years, with a peak incidence between 4–6 years. Boys are slightly more commonly affected. It often follows an upper respiratory tract infection and occurs more frequently in winter and spring.

Answer 41

The most common renal manifestation is microscopic hematuria, often with or without proteinuria. Gross hematuria and nephrotic-range proteinuria may also occur. Renal involvement typically appears within 1–8 weeks of the rash but can be delayed.

Answer 42

• Hematuria: Microscopic or gross • Proteinuria: Can range from minimal to nephrotic range • Hypertension • Edema (if nephrotic) • Elevated serum creatinine in progressive disease These signs warrant regular monitoring post-HSP diagnosis.

Answer 43

Diagnosis is clinical, based on characteristic rash and systemic symptoms. Renal involvement is confirmed by urinalysis and protein quantification. Renal biopsy is reserved for atypical or severe presentations (e.g., nephrotic syndrome, rising creatinine, crescentic disease).

Answer 44

Urinalysis helps detect early renal involvement and includes: • Microscopic hematuria • Proteinuria (qualitative and quantitative) • RBC casts if glomerular involvement Monitoring should continue for at least 6–12 months, even if initial urinalysis is normal.

Answer 45

• Urinalysis: RBCs, protein, casts • Urine protein/creatinine ratio • Serum creatinine, urea, electrolytes • Serum albumin (if proteinuria present) • Blood pressure monitoring • Serologic tests to exclude other causes (ANA, C3, ASO if needed)

Answer 46

Indications include: • Nephrotic-range proteinuria • Persistent proteinuria >4–6 weeks • Rising serum creatinine or declining GFR • Presence of RBC casts or severe hematuria with impaired function Biopsy helps classify histologic severity and guide immunosuppressive therapy.

Answer 47

Renal biopsy in HSP nephritis typically shows: • Mesangial proliferation on light microscopy • IgA deposition in the mesangium on immunofluorescence • May show crescents in severe cases Histological findings mirror those of IgA nephropathy, and severity is graded by the percentage of crescents or degree of sclerosis.

Answer 48

Severity is based on clinical and histologic findings: • Mild: Isolated microscopic hematuria • Moderate: Hematuria with non-nephrotic proteinuria • Severe: Nephrotic-range proteinuria, impaired GFR, or crescentic glomerulonephritis This classification guides the need for biopsy and immunosuppressive therapy.

Answer 49

• Supportive care: Adequate hydration, pain relief (acetaminophen) • Monitor blood pressure and urine findings regularly • No corticosteroids are typically required • Regular follow-up for at least 6–12 months to detect delayed worsening Prognosis is excellent in these cases

Answer 50

• Corticosteroids: Prednisolone 1–2 mg/kg/day initially • Add immunosuppressive agents (cyclophosphamide, MMF) for crescents or nephrotic syndrome • ACE inhibitors or ARBs: If persistent proteinuria • Close monitoring of renal function and proteinuria • Hospitalization may be required for severe presentations

Answer 51

Corticosteroids (e.g., prednisone) are the mainstay of therapy in moderate-to-severe disease. They help: • Reduce proteinuria • Control inflammation • Prevent progression to chronic kidney disease They are generally not needed in mild disease with isolated hematuria.

Answer 52

Indicated when there is: • Steroid-resistant proteinuria • Crescentic glomerulonephritis on biopsy • Rapidly progressive glomerulonephritis Common agents include cyclophosphamide, azathioprine, mycophenolate mofetil (MMF). Often used in combination with corticosteroids.

Answer 53

Overall prognosis is excellent: • ~85–90% of children recover completely • Mild hematuria may persist but resolves in most • Risk of chronic kidney disease is <5% • Prognosis worsens with nephrotic-range proteinuria, hypertension, or crescents on biopsy

Answer 54

Poor prognostic indicators include: • Nephrotic syndrome at onset • Sustained proteinuria >1 g/day • Hypertension • Decline in GFR or elevated creatinine • Histology showing crescents in >50% of glomeruli These patients need close monitoring and often immunosuppression.

Answer 55

• Initial phase: Every 1–2 weeks for 1–2 months • Then monthly for 6–12 months • Test includes urinalysis (hematuria, proteinuria) and urine protein/creatinine ratio • Monitor BP and serum creatinine as needed Follow-up may extend beyond 12 months if abnormalities persist.

Answer 56

• At least 6–12 months, even if initial urine tests are normal • Extended monitoring if there is persistent proteinuria or impaired renal function • Monitoring includes urinalysis, proteinuria quantification, BP, and renal function Goal is early identification of progressive renal disease

Answer 57

HUS is a form of thrombotic microangiopathy (TMA) characterized by the triad of: 1. Microangiopathic hemolytic anemia (MAHA) 2. Thrombocytopenia 3. Acute kidney injury (AKI) It is the most common cause of AKI in children and involves endothelial injury and microvascular thrombosis.

Answer 58

The clinical triad includes: • Anemia: Due to intravascular hemolysis with schistocytes • Thrombocytopenia: Platelet consumption due to thrombi • Renal impairment: Hematuria, proteinuria, rising creatinine Other features: pallor, lethargy, edema, oliguria, seizures (if CNS involved)

Answer 59

Typical HUS (also called D+ HUS) occurs after a prodrome of bloody diarrhea, often from shiga toxin-producing E. coli (STEC). It affects children <5 years. The shiga toxin causes endothelial injury, especially in renal vessels, leading to microangiopathy.

Answer 60

The most common cause is Escherichia coli O157:H7, a shiga toxin-producing strain. Other enterohemorrhagic E. coli (EHEC) strains and Shigella dysenteriae type 1 can also cause HUS. Infection is typically foodborne or waterborne.

Answer 61

Atypical HUS is non-diarrhea associated and results from dysregulation of the complement alternative pathway, often due to genetic mutations in complement regulatory proteins (e.g., factor H, I, MCP). It has a worse prognosis and high risk of recurrence and progression to ESRD.

Answer 62

• Bloody diarrhea (in >90% of cases) • Pallor, fatigue (due to anemia) • Purpura or bruising (due to thrombocytopenia) • Oliguria, edema, hypertension • May develop seizures, coma (neurologic complications) • Symptoms appear 5–10 days after diarrhea onset

Answer 63

aHUS may be spontaneous or triggered by infections, drugs (e.g., calcineurin inhibitors), malignancy, pregnancy, or transplantation. It involves excessive activation of complement causing endothelial injury and thrombosis.

Answer 64

• CBC: Anemia, thrombocytopenia • Peripheral smear: Schistocytes (fragmented RBCs) • Elevated LDH, low haptoglobin, reticulocytosis • Negative Coombs test • Increased creatinine, BUN • Stool culture for STEC • Coagulation profile is usually normal (helps distinguish from DIC)

Answer 65

The direct Coombs test is negative in HUS. This helps distinguish it from autoimmune hemolytic anemia, where the test would be positive due to antibody-coated RBCs. Negative Coombs supports a microangiopathic process.

Answer 66

• Hematuria: Microscopic or gross • Proteinuria: May be mild or nephrotic-range • May see RBC casts and low urine output (oliguria) • Urinalysis reflects glomerular involvement due to endothelial injury and microthrombi in renal vasculature

Answer 67

Renal involvement varies from mild AKI to anuric renal failure requiring dialysis. GFR is reduced due to glomerular capillary thrombosis and endothelial damage. Labs show elevated serum creatinine, urea, electrolyte disturbances (e.g., hyperkalemia, acidosis). Recovery may take weeks; some develop permanent renal impairment.

Answer 68

• Renal ultrasound is the initial imaging: - Kidneys may appear enlarged and hyperechogenic - Loss of corticomedullary differentiation in severe cases • Doppler US may show reduced perfusion • Imaging primarily helps exclude other causes of AKI (e.g., obstruction).

Answer 69

• Supportive care is the cornerstone: - Careful fluid management: avoid overload - Electrolyte correction (esp. hyperkalemia, acidosis) - Blood transfusions for anemia (avoid platelet transfusion unless bleeding) - Control hypertension • Monitor urine output, BP, and renal function closely.

Answer 70

No. In STEC-HUS (typical HUS), antibiotics are not recommended because they may increase shiga toxin release and worsen endothelial injury. Antimotility agents are also avoided. Antibiotics may be used only in documented infections unrelated to STEC.

Answer 71

• Severe uremia (encephalopathy, pericarditis) • Volume overload unresponsive to diuretics • Refractory hyperkalemia or acidosis • Anuria or oliguria (<0.5 mL/kg/hr) • Usually temporary; peritoneal dialysis or hemodialysis may be used.

Answer 72

Plasma exchange (plasmapheresis) helps remove autoantibodies and replace deficient complement regulatory proteins in aHUS. Indicated in: • aHUS with no access to eculizumab • Refractory or relapsing cases • Hemolysis with worsening renal function

Answer 73

Eculizumab is a monoclonal antibody against complement protein C5. It prevents formation of the membrane attack complex (MAC), reducing complement-mediated endothelial injury. It is the first-line treatment for genetic or relapsing aHUS, significantly improving outcomes and renal survival.

Answer 74

• Renal: CKD, hypertension, proteinuria, ESRD • Neurologic: Seizures, stroke, coma • Hematologic: Recurrent hemolysis, persistent anemia • Cardiac: Heart failure (due to fluid overload or uremia) Long-term follow-up is essential.

Answer 75

Prognosis in typical HUS is generally good: • ~85% of children recover completely • 5–10% develop long-term renal complications (HTN, CKD) • Mortality is low (~3–5%) in well-managed settings Prompt supportive care improves outcomes significantly.

Answer 76

Poor outcomes are associated with: • Severe AKI with prolonged anuria (>7 days) • Neurological complications (seizures, coma) • High WBC count or CRP at presentation • Young age (<1 year) • Delayed presentation or treatment • Underlying complement mutations in aHUS

Answer 77

AKI is a sudden decline in kidney function, leading to impaired fluid, electrolyte, and waste product excretion. It results in azotemia, oliguria or anuria, and metabolic disturbances. AKI can be reversible and may progress through prerenal, intrinsic, and postrenal phases.

Answer 78

AKI is classified into: 1. Prerenal: Due to hypoperfusion (e.g., dehydration, heart failure) 2. Intrinsic: Direct damage to nephrons (e.g., ATN, GN) 3. Postrenal: Obstruction of urinary outflow (e.g., PUV, stones) This helps guide diagnosis and management.

Answer 79

• Dehydration (diarrhea, vomiting, poor intake) • Sepsis with hypotension • Hemorrhage • Congestive heart failure • Nephrotic syndrome with intravascular volume depletion These reduce renal perfusion without intrinsic nephron damage.

Answer 80

• Acute tubular necrosis (ATN): Ischemic or nephrotoxic • Glomerulonephritis: PSGN, lupus nephritis, HSP nephritis • Interstitial nephritis: Drug-induced (NSAIDs, antibiotics) • HUS • Vasculitis: ANCA-associated GN

Answer 81

• Posterior urethral valves (PUV): Common in male infants • Neurogenic bladder • Ureteric obstruction: Stones, strictures, tumors • Extrinsic compression: Pelvic masses Diagnosis often requires renal/bladder ultrasound.

Answer 82

AKI is defined by any of the following: • Increase in serum creatinine by ≥0.3 mg/dL within 48 hours • Increase to ≥1.5× baseline within 7 days • Urine output <0.5 mL/kg/hr for ≥6 hours Used for staging and severity assessment.

Answer 83

• Oliguria (<0.5 mL/kg/hr) or anuria • Generalized edema • Hypertension • Tachypnea (metabolic acidosis) • Fatigue, lethargy, nausea • In severe cases: seizures or coma (uremic encephalopathy)

Answer 84

• Elevated serum creatinine and BUN • Hyperkalemia, hyperphosphatemia • Metabolic acidosis with low bicarbonate • Hyponatremia (dilutional) • May also see anemia and thrombocytopenia in severe AKI

Answer 85

• Stage 1: <0.5 mL/kg/hr for 6–12 hours • Stage 2: <0.5 mL/kg/hr for >12 hours • Stage 3: <0.3 mL/kg/hr for ≥24 hours or anuria for ≥12 hours Used alongside creatinine to define KDIGO staging.

Answer 86

FENa helps differentiate prerenal vs. intrinsic AKI: • FENa <1% suggests prerenal AKI (intact tubular reabsorption) • FENa >2% suggests intrinsic AKI (ATN) Limitations: FENa may be unreliable in neonates or with diuretic use.

Answer 87

• Renal ultrasound is the first-line tool: - Assesses kidney size, echogenicity, and structure - Detects hydronephrosis, obstruction, or congenital anomalies • Bladder scan to assess post-void residual in suspected obstruction • Doppler may be used for renal perfusion if vascular AKI is suspected

Answer 88

• Identify and treat the underlying cause (e.g., dehydration, infection) • Discontinue nephrotoxic drugs • Manage fluid and electrolyte imbalances • Monitor urine output, BP, and renal function • Early recognition prevents progression to severe renal dysfunction

Answer 89

• Indicated in hypovolemic (prerenal) AKI due to: - Dehydration - Diarrhea/vomiting - Sepsis-induced hypotension • Give isotonic saline bolus (20 mL/kg over 20–30 min) and reassess • Avoid overhydration, especially in oliguric or intrinsic AKI

Answer 90

• Fluid restriction to insensible loss + urine output • Diuretics: IV furosemide (1–2 mg/kg), possibly continuous infusion • Monitor for pulmonary edema, hypertension • If refractory, consider dialysis (e.g., peritoneal, hemodialysis)

Answer 91

• Refractory hyperkalemia • Severe metabolic acidosis (pH <7.1) • Fluid overload causing respiratory or cardiac compromise • Uremic symptoms: encephalopathy, pericarditis • Persistent oliguria/anuria with rising creatinine

Answer 92

• Electrolyte disturbances: hyperkalemia, hyponatremia, hypocalcemia • Fluid overload: pulmonary edema • Metabolic acidosis • Hypertension • Uremia: anorexia, nausea, encephalopathy • Infections and long-term risk of CKD

Answer 93

• NSAIDs: Reduce renal perfusion via prostaglandin inhibition • Aminoglycosides: Nephrotoxic (e.g., gentamicin) • ACE inhibitors/ARBs: Worsen GFR in volume-depleted or bilateral renal artery stenosis • Radiocontrast agents: Risk of contrast-induced nephropathy Adjust all medications based on renal function

Answer 94

• Neonates have immature renal function: lower GFR, limited ability to concentrate urine • Urine output may be normal despite impaired function • Higher risk of prerenal AKI due to dehydration, birth asphyxia • Drug dosing and fluid management require extreme caution

Answer 95

• Maintain adequate hydration, especially during illness or surgery • Avoid nephrotoxic medications when possible • Close monitoring of renal function if on potentially harmful drugs • Use contrast precautions (hydration, N-acetylcysteine) before imaging

Answer 96

• Prognosis depends on etiology and promptness of treatment • Most recover fully if AKI is recognized and treated early • Long-term risks: hypertension, proteinuria, CKD • Children with severe or repeated AKI episodes require long-term follow-up

Answer 97

CKD is defined as kidney damage or reduced kidney function (GFR <60 mL/min/1.73 m²) lasting ≥3 months, regardless of cause. It includes structural abnormalities (e.g., small kidneys, proteinuria) or persistently reduced GFR. CKD is progressive and may lead to ESRD.

Answer 98

CKD stages are based on estimated GFR (eGFR): • Stage 1: GFR ≥90 with signs of kidney damage (e.g., proteinuria) • Stage 2: GFR 60–89 • Stage 3a: GFR 45–59 • Stage 3b: GFR 30–44 • Stage 4: GFR 15–29 • Stage 5: GFR <15 or dialysis-dependent (ESRD)

Answer 99

• Congenital anomalies of the kidney and urinary tract (CAKUT): e.g., renal dysplasia, obstructive uropathy • Glomerular diseases: FSGS, HUS, Alport syndrome • Hereditary nephropathies: e.g., polycystic kidney disease • Reflux nephropathy • Chronic pyelonephritis

Answer 100

CAKUT includes: • Renal hypoplasia/dysplasia • Posterior urethral valves • Vesicoureteral reflux (VUR) • Ureteropelvic junction obstruction These anomalies often present with recurrent UTIs, hydronephrosis, or poor growth and are the leading cause of pediatric CKD.

Answer 101

• Growth retardation due to metabolic acidosis, poor nutrition • Polyuria, polydipsia (due to concentrating defect) • Anemia (due to low erythropoietin) • Hypertension • Bone pain or deformities (renal osteodystrophy) • Fatigue, pallor in advanced stages

Answer 102

• Nocturia or polyuria due to impaired urinary concentrating ability • Growth failure or delayed puberty • Mild anemia or poor appetite • Mild hypertension • These may be subtle and easily missed in early CKD stages

Answer 103

• Anemia (normocytic, normochromic) • Hyperphosphatemia, hypocalcemia • Secondary hyperparathyroidism • Metabolic acidosis (low bicarbonate) • Elevated serum creatinine and BUN • Low GFR estimation

Answer 104

GFR estimation is essential for: • Staging CKD • Monitoring disease progression • Adjusting medication doses • Determining timing of dialysis or transplant referral eGFR is calculated using serum creatinine, height, and age-adjusted formulas.

Answer 105

The Schwartz formula is most widely used: GFR (mL/min/1.73 m²) = (k × height in cm) / serum creatinine Where k is a constant based on age and sex: • 0.45 for term infants • 0.55 for children • 0.70 for adolescent males

Answer 106

ESRD refers to irreversible kidney failure with GFR <15 mL/min/1.73 m², requiring renal replacement therapy (RRT): dialysis or kidney transplantation. It represents stage 5 CKD and is associated with profound metabolic disturbances and multi-system complications.

Answer 107

Strict blood pressure control is critical to slow CKD progression and prevent cardiovascular complications. Goal BP is typically below the 90th percentile for age/height. Antihypertensives also reduce proteinuria and glomerular hyperfiltration.

Answer 108

ACE inhibitors (e.g., enalapril) or ARBs (e.g., losartan) are preferred due to their ability to reduce both blood pressure and proteinuria, preserving renal function. Monitor for hyperkalemia and rising creatinine after initiation.

Answer 109

Anemia is managed with: • Iron supplementation (oral or IV) • Erythropoiesis-stimulating agents (ESAs) if Hb <10 g/dL • Monitor ferritin and transferrin saturation (TSAT) • Target Hb: 11–12 g/dL Rule out other causes (e.g., blood loss, inflammation)

Answer 110

• Chronic metabolic acidosis • Poor appetite and malnutrition • Anemia • Secondary hyperparathyroidism • Uremic toxins • Resistance to growth hormone Early and aggressive nutritional and hormonal interventions improve growth outcomes.

Answer 111

• Dietary phosphate restriction • Phosphate binders (e.g., calcium carbonate) • Vitamin D analogs (calcitriol) for secondary hyperparathyroidism • Monitor serum calcium, phosphorus, PTH • Avoid hypercalcemia and adynamic bone disease

Answer 112

• Ensure adequate caloric intake for growth • Protein intake tailored to GFR and dialysis status • Sodium restriction for hypertension/edema • Phosphorus and potassium restriction if hyperphosphatemia/hyperkalemia • Involve a pediatric renal dietitian early

Answer 113

• GFR <10–15 mL/min/1.73 m² with symptoms • Severe uremia (anorexia, nausea, encephalopathy) • Fluid overload not responsive to diuretics • Refractory hyperkalemia or acidosis • Growth failure, severe anemia despite medical therapy

Answer 114

• Peritoneal dialysis (PD): Preferred in infants and young children; allows home treatment • Hemodialysis (HD): For older children; requires vascular access Choice depends on age, availability, family preference, and comorbidities

Answer 115

Referral is indicated for: • CKD stage 3 or higher (GFR <60) • Persistent proteinuria or hematuria • Uncontrolled hypertension • Growth failure or anemia • Congenital anomalies of the kidney/urinary tract • Need for dialysis or transplant planning

Answer 116

With early detection and comprehensive care, many children with CKD can reach adulthood with stable renal function. However, risks include: • Progression to ESRD • Growth failure • Cardiovascular disease Multidisciplinary follow-up is essential for improved outcomes.

Answer 117

CAKUT stands for Congenital Anomalies of the Kidney and Urinary Tract. It includes a spectrum of structural malformations that arise during fetal kidney and urinary tract development and represent the most common cause of pediatric CKD and ESRD worldwide.

Answer 118

Examples of CAKUT include: • Renal agenesis (unilateral or bilateral) • Renal hypoplasia • Renal dysplasia • Multicystic dysplastic kidney (MCDK) • Hydronephrosis • Posterior urethral valves (PUV) • Ureteropelvic junction obstruction (UPJO) • Vesicoureteral reflux (VUR)

Answer 119

• Family history of renal anomalies • Genetic syndromes (e.g., VACTERL, Branchio-Oto-Renal, HNF1B) • Maternal diabetes or drug exposure • Oligohydramnios • Consanguinity Many cases are sporadic; 10–20% have a recognized genetic basis.

Answer 120

Kidney development starts around week 5 of gestation, progressing from the pronephros → mesonephros → metanephros (permanent kidney). Ureteric bud and metanephric mesenchyme interaction is critical. Nephrogenesis continues until 32–36 weeks gestation.

Answer 121

Renal agenesis is the congenital absence of one or both kidneys: • Unilateral: Often asymptomatic, detected incidentally • Bilateral: Incompatible with life, causes Potter sequence (oligohydramnios, pulmonary hypoplasia, limb deformities)

Answer 122

Renal hypoplasia is a reduced number of nephrons in a normally structured kidney, leading to small kidney size. It may cause hypertension, proteinuria, and eventual CKD. Often detected by renal ultrasound showing small kidneys with preserved architecture.

Answer 123

Renal dysplasia refers to abnormal kidney development, with disorganized architecture, undifferentiated tissues, and nonfunctioning nephrons. It may be associated with urinary tract obstruction. Ultrasound may show echogenic kidneys with cysts.

Answer 124

MCDK is a nonfunctional kidney replaced by multiple noncommunicating cysts. It is usually unilateral and detected antenatally. The contralateral kidney may have anomalies. Over time, the affected kidney involutes. Risk of hypertension and Wilms tumor is low.

Answer 125

Hydronephrosis is the dilation of the renal pelvis and calyces due to obstruction of urinary flow. It may be physiologic in utero or due to pathologic causes like UPJO or PUV. Diagnosed by antenatal or postnatal ultrasound. Requires grading and follow-up.

Answer 126

• Ureteropelvic junction obstruction (UPJO) • Vesicoureteral reflux (VUR) • Posterior urethral valves (PUV) • Ureterocele • Duplication anomalies • Physiologic (transient) in up to 50% of cases Management depends on etiology and severity.

Answer 127

PUV is a congenital obstructive membrane in the posterior urethra in males. It causes bladder outlet obstruction, leading to hydronephrosis, urinary retention, and renal damage. PUV is the most common cause of lower urinary tract obstruction in male infants and a major cause of pediatric ESRD.

Answer 128

Prenatal ultrasound may show: • Bilateral hydronephrosis • Thick-walled bladder • Dilated posterior urethra ('keyhole sign') • Oligohydramnios (if severe obstruction) These suggest lower urinary tract obstruction and warrant early postnatal evaluation.

Answer 129

VUR is the retrograde flow of urine from bladder into ureters ± kidneys. It may occur as part of CAKUT, especially in dysplastic or hypoplastic kidneys. VUR predisposes to recurrent UTIs, renal scarring, and long-term risk of hypertension and CKD.

Answer 130

Severity is based on anterior-posterior renal pelvic diameter (APRPD): • Mild: 4–6 mm in 2nd trimester, 7–9 mm in 3rd • Moderate: 7–10 mm (2nd), 9–15 mm (3rd) • Severe: >10 mm (2nd), >15 mm (3rd) This guides postnatal follow-up and imaging.

Answer 131

• Renal-bladder ultrasound (RBUS): Initial screening • Voiding cystourethrogram (VCUG): If hydronephrosis or abnormal RBUS • DMSA scan: For renal scarring and differential function • MAG3 scan: For drainage and obstruction assessment

Answer 132

VCUG evaluates the lower urinary tract, especially for: • Vesicoureteral reflux (VUR) • Posterior urethral valves (PUV) • Bladder outlet obstruction Contrast is introduced via catheter and imaged during voiding.

Answer 133

DMSA is a renal cortical scan used to detect: • Cortical defects (scarring from pyelonephritis) • Differential renal function • Renal dysplasia It is the gold standard for identifying renal scarring and long-term damage from VUR.

Answer 134

Indications include: • High-grade obstruction (e.g., PUV, UPJO) • Significant loss of differential renal function • Recurrent febrile UTIs with high-grade VUR • Bladder dysfunction not responding to conservative therapy

Answer 135

Severe CAKUT increases risk for: • Chronic kidney disease (CKD) • Hypertension • Recurrent UTIs and renal scarring • Need for dialysis or transplant Early monitoring and intervention are crucial to prevent progression.

Answer 136

Early diagnosis allows: • Timely urologic intervention (e.g., PUV ablation) • Monitoring and prevention of UTI and scarring • Optimization of growth and nutrition • Reduction in CKD progression risk • Better long-term renal survival

Answer 137

A UTI is an infection of the urinary system involving the urethra, bladder, ureters, or kidneys. It may be classified as lower UTI (cystitis) or upper UTI (pyelonephritis). UTIs are common in children and may lead to renal scarring if untreated.

Answer 138

• Escherichia coli: Most common (80–90%) • Klebsiella, Proteus, Enterococcus, and Pseudomonas (especially in abnormal anatomy or catheter use) Neonates may also have group B Streptococcus or Staphylococcus saprophyticus.

Answer 139

• Female gender (shorter urethra) • Uncircumcised males • Vesicoureteral reflux (VUR) • Urinary tract obstruction (e.g., PUV) • Bladder-bowel dysfunction • Neurogenic bladder, poor hygiene, constipation

Answer 140

• Fever without source • Irritability, poor feeding, vomiting • Failure to thrive • Jaundice (especially in neonates) Presentation is often nonspecific, so urine testing is essential in febrile infants.

Answer 141

• Dysuria, urinary urgency, frequency • Suprapubic or abdominal pain • Fever (suggests upper UTI) • New-onset incontinence or foul-smelling urine Hematuria or vomiting may be present in pyelonephritis.

Answer 142

Pyelonephritis is a bacterial infection of the kidney parenchyma and renal pelvis. It presents with fever, flank pain, vomiting, and systemic symptoms. It can cause renal scarring and hypertension if not promptly treated.

Answer 143

Diagnosis requires: • Positive urinalysis (pyuria, nitrites/leukocyte esterase) • Confirmed urine culture: >50,000 CFU/mL from catheter or >100,000 CFU/mL from clean catch Symptoms guide interpretation in older children.

Answer 144

• Clean-catch midstream: Preferred in toilet-trained children • Catheterization: Preferred in young children for sterile sample • Suprapubic aspiration: Gold standard in neonates • Urine bag: Risk of contamination—used only for screening

Answer 145

• Leukocyte esterase: Suggests WBCs • Nitrites: Produced by gram-negative bacteria (e.g., E. coli) • Pyuria: >5–10 WBCs/hpf • Bacteriuria, positive Gram stain Positive findings support diagnosis but need culture confirmation

Answer 146

A urine culture is the gold standard: • ≥100,000 CFU/mL from clean catch • ≥50,000 CFU/mL from catheter specimen • Any growth from suprapubic aspiration Essential for guiding antibiotic therapy and evaluating for CAKUT if recurrent

Answer 147

Urine culture is indicated in: • All febrile infants <24 months with suspected UTI • Recurrent UTIs • Atypical presentation (e.g., poor response to antibiotics) • Abnormal urinalysis Culture confirms infection and guides antibiotic therapy.

Answer 148

A renal and bladder ultrasound (RBUS) is recommended after the first febrile UTI in children <2 years. It detects: • Hydronephrosis • Anomalies (e.g., CAKUT) • Bladder wall abnormalities RBUS is noninvasive and helps guide further evaluation.

Answer 149

RBUS is used to assess: • Renal size, echogenicity • Hydronephrosis or scarring • Bladder wall thickness or incomplete emptying It is indicated after first febrile UTI in young children or if recurrent UTIs or abnormal voiding symptoms are present.

Answer 150

VCUG is indicated: • After two or more febrile UTIs • Abnormal RBUS (e.g., hydronephrosis, scarring) • Atypical or recurrent UTIs • Suspected VUR or posterior urethral valves (PUV) VCUG detects reflux and bladder outlet obstruction.

Answer 151

First-line oral antibiotics: • Third-generation cephalosporins (e.g., cefixime, cefdinir) • Alternatives: amoxicillin-clavulanate, TMP-SMX (if low resistance) Empirical IV therapy (e.g., ceftriaxone) may be used in toxic or hospitalized cases. Adjust based on culture.

Answer 152

• 7–10 days for febrile UTI (pyelonephritis) • 3–5 days for afebrile cystitis in older children • IV to oral step-down when improved clinically Follow-up culture is usually not needed if child improves, unless atypical features present.

Answer 153

• Age <2 months • Toxic appearance, poor feeding • Vomiting, inability to take oral antibiotics • Urosepsis or pyelonephritis with dehydration • Known urological abnormalities or social concerns Hospitalization allows IV antibiotics and monitoring.

Answer 154

• Renal scarring • Hypertension • Chronic kidney disease (CKD) • Proteinuria • Recurrent febrile UTIs Early diagnosis and proper antibiotic treatment reduce long-term complications.

Answer 155

VUR is the retrograde flow of urine from the bladder into the ureters and kidneys. It predisposes to recurrent UTIs, renal scarring, and hypertension. Classified from grade I (mild) to grade V (severe dilation). Managed based on grade and clinical history.

Answer 156

• Ensure complete bladder emptying • Treat constipation • Encourage regular voiding (every 2–3 hrs) • Antibiotic prophylaxis in select VUR cases • Teach proper perineal hygiene • Address bladder-bowel dysfunction if present

Answer 157

• Primary VUR: Due to congenital incompetence of the ureterovesical junction (UVJ) without obstruction. • Secondary VUR: Caused by increased bladder pressure due to obstruction (e.g., PUV, neurogenic bladder).

Answer 158

Primary VUR arises from abnormal insertion of the ureter into the bladder wall, leading to short intramural length and failure of the valve-like mechanism. It may be familial and associated with renal dysplasia or hypoplasia.

Answer 159

Secondary VUR results from high intravesical pressure due to: • Bladder outlet obstruction (e.g., PUV) • Neurogenic bladder • Detrusor overactivity This pressure forces urine backward into the ureters and kidneys.

Answer 160

VUR is graded I to V based on VCUG: • Grade I: Reflux into ureter only • Grade II: Into renal pelvis without dilation • Grade III: Mild dilation of ureter and pelvis • Grade IV: Moderate dilation and tortuosity • Grade V: Gross dilation with loss of papillary impressions

Answer 161

Voiding cystourethrogram (VCUG) is the gold standard to diagnose and grade VUR. It uses contrast instilled via a catheter, followed by imaging during filling and voiding. It visualizes reflux, posterior urethral valves, and bladder abnormalities.

Answer 162

Untreated VUR may lead to: • Recurrent pyelonephritis • Renal scarring • Hypertension • Proteinuria • Chronic kidney disease (CKD) Risk is highest in high-grade or bilateral VUR

Answer 163

VUR allows retrograde passage of infected urine from the bladder to the kidney. This facilitates bacterial ascent and increases risk for pyelonephritis and renal damage, especially in children with bladder-bowel dysfunction or poor voiding habits.

Answer 164

Renal scarring is permanent damage to the renal cortex due to inflammation or infection. It is commonly caused by febrile UTIs in children with high-grade VUR. Scarring is best detected by DMSA scan and may lead to CKD.

Answer 165

• High-grade VUR (Grade III–V) • Recurrent febrile UTIs • Delayed diagnosis or treatment of UTI • Bladder-bowel dysfunction • Age <1 year at first UTI • Bilateral reflux

Answer 166

• Low-grade VUR (I–III) often resolves spontaneously with age • High-grade VUR (IV–V) less likely to resolve and may cause renal damage • Close monitoring, prophylaxis, and possibly surgery are required depending on grade and complications

Answer 167

VUR is often detected during evaluation of a febrile UTI, especially in infants or young children. Voiding cystourethrogram (VCUG) is the definitive test. Indirect signs may appear on renal ultrasound (e.g., hydronephrosis), prompting further testing.

Answer 168

VCUG is indicated: • After recurrent febrile UTIs • After first febrile UTI with abnormal renal ultrasound • In infants with high-risk features (e.g., poor urine stream, hydronephrosis) It confirms reflux and grades severity.

Answer 169

DMSA scan is used to evaluate: • Renal scarring from past infections • Differential renal function • Underlying renal dysplasia It is the gold standard for detecting cortical damage and is done 4–6 months after UTI.

Answer 170

• Most cases resolve spontaneously (especially <5 years) • Watchful waiting with close follow-up • Ensure good hygiene and bladder-bowel management • Consider prophylactic antibiotics in <2 years or recurrent UTIs

Answer 171

• Requires long-term follow-up • Daily antibiotic prophylaxis to prevent UTI • DMSA scan for baseline scarring • Surgery considered if breakthrough infections or persistent high-grade reflux after age 5

Answer 172

• Low-dose daily antibiotics (e.g., TMP-SMX, nitrofurantoin) • Used in: - Children <2 years with VUR and history of febrile UTI - High-grade VUR - Recurrent UTIs • Goal: Prevent UTIs until spontaneous resolution or surgery

Answer 173

Surgery is indicated when: • Recurrent febrile UTIs despite prophylaxis • Noncompliance with medical therapy • Persistent high-grade VUR beyond age 5 • Significant renal damage or scarring on DMSA

Answer 174

• Ureteral reimplantation: Creates a longer submucosal tunnel to prevent reflux; high success rate • Endoscopic injection (e.g., Deflux): Minimally invasive; lower success than reimplantation Choice depends on VUR grade and patient factors

Answer 175

• Excellent in low-grade VUR with full resolution • High-grade VUR has increased risk of renal scarring and CKD • Early detection, good UTI control, and bladder-bowel management improve outcomes • Some require long-term nephrology follow-up

Answer 176

• Clinical monitoring: UTI symptoms, growth, blood pressure • Urinalysis and cultures periodically • Annual renal ultrasound to monitor growth and scarring • DMSA scan if recurrent infections • Reassess VCUG if breakthrough UTI occurs

Answer 177

Renal tubular disorders are a group of inherited or acquired conditions where the renal tubules fail to properly reabsorb or secrete substances, leading to electrolyte imbalances, acidosis, or growth disturbances. They include RTA, Bartter syndrome, Gitelman syndrome, and others.

Answer 178

• Fanconi syndrome (global proximal tubular dysfunction) • Isolated proximal RTA • Associated with cystinosis, Wilson disease, galactosemia • May be inherited or drug-induced (e.g., ifosfamide, acetazolamide)

Answer 179

• Primary distal RTA (autosomal dominant/recessive) • Sjögren syndrome, autoimmune diseases • Hypercalciuria, nephrocalcinosis • Drugs: amphotericin B, lithium

Answer 180

In proximal RTA, there's defective reabsorption of bicarbonate in the proximal tubule. Initially, bicarbonate is lost in urine, leading to metabolic acidosis. As serum bicarbonate decreases, filtered load drops, and urinary bicarbonate loss lessens.

Answer 181

In distal RTA, the distal nephron fails to secrete hydrogen ions, preventing urine acidification. This results in alkaline urine (pH >5.5) despite systemic metabolic acidosis, leading to hypokalemia, nephrocalcinosis, and bone demineralization.

Answer 182

• Failure to thrive and poor growth • Polyuria, polydipsia • Vomiting, dehydration • Muscle weakness • Rickets or osteomalacia • Nephrocalcinosis in distal RTA

Answer 183

• Normal anion gap metabolic acidosis • Hyperchloremia • Hypokalemia (especially distal RTA) • Low serum bicarbonate • Urine pH >5.5 in distal RTA • Positive urine anion gap

Answer 184

Diagnosis involves: • ABG: Shows non-anion gap metabolic acidosis • Urine pH and electrolytes • Urine anion gap and ammonium excretion • Rule out chronic diarrhea and other causes of acidosis • Genetic testing for inherited forms

Answer 185

• Requires large doses of oral bicarbonate (10–20 mEq/kg/day) • Often combined with potassium citrate • May need thiazide diuretics to reduce bicarbonate loss • Treat underlying cause if identifiable (e.g., cystinosis)

Answer 186

• Requires alkali therapy (1–3 mEq/kg/day bicarbonate) • Potassium citrate to correct hypokalemia and acidosis • Thiazides if hypercalciuria present • Monitor for growth improvement, nephrocalcinosis, and bone health

Answer 187

Fanconi syndrome is a generalized proximal tubular dysfunction, leading to impaired reabsorption of glucose, amino acids, phosphate, bicarbonate, and uric acid. It results in polyuria, hypophosphatemic rickets, metabolic acidosis, and growth failure. Causes include inherited disorders (e.g., cystinosis, Wilson disease) and acquired ones (e.g., ifosfamide toxicity).

Answer 188

• Glucosuria with normal serum glucose • Aminoaciduria • Phosphaturia → hypophosphatemic rickets • Bicarbonaturia → metabolic acidosis • Polyuria, dehydration • Growth retardation and osteomalacia

Answer 189

Bartter syndrome is a rare inherited tubulopathy due to a defect in the thick ascending limb of the loop of Henle, leading to impaired sodium, potassium, and chloride reabsorption. This results in hypokalemia, metabolic alkalosis, and high renin/aldosterone with normal BP.

Answer 190

• Polyuria, polydipsia • Failure to thrive, growth retardation • Muscle weakness, dehydration • Vomiting and salt craving • Onset in infancy or early childhood

Answer 191

• Hypokalemia • Metabolic alkalosis • Hypercalciuria, may lead to nephrocalcinosis • Normal to low magnesium • Elevated renin and aldosterone, but no hypertension

Answer 192

Gitelman syndrome is an autosomal recessive defect in the distal convoluted tubule, specifically in the thiazide-sensitive Na-Cl co-transporter, leading to hypokalemia, metabolic alkalosis, hypocalciuria, and hypomagnesemia.

Answer 193

• Gitelman presents later (school-age to adolescence) • Hypocalciuria and hypomagnesemia in Gitelman (vs hypercalciuria in Bartter) • Less severe symptoms • Gitelman resembles chronic thiazide diuretic use, Bartter resembles loop diuretic use

Answer 194

• Muscle cramps, fatigue • Salt craving, tetany, paresthesias • Growth delay if onset is early • May be asymptomatic and diagnosed incidentally

Answer 195

• Salt supplementation • Potassium and magnesium replacement • NSAIDs (e.g., indomethacin) to reduce prostaglandin-mediated salt loss • Aldosterone antagonists (e.g., spironolactone) may be used • Monitor growth, electrolytes, and renal function

Answer 196

• Growth failure • Nephrocalcinosis and CKD (especially Bartter) • Persistent electrolyte abnormalities • Decreased bone mineralization • Requires lifelong follow-up and therapy

Answer 197

Hypertension is defined as systolic and/or diastolic blood pressure ≥95th percentile for age, sex, and height measured on 3 separate occasions. For adolescents ≥13 years, it aligns with adult criteria: ≥130/80 mmHg.

Answer 198

Classification (children 1–13 years): • Elevated BP: 90th to <95th percentile • Stage 1 HTN: 95th to <95th + 12 mmHg • Stage 2 HTN: ≥95th + 12 mmHg or ≥140/90 (whichever lower) Adolescents ≥13 years use adult thresholds.

Answer 199

• Obesity and metabolic syndrome • Family history of hypertension • High salt intake • Sedentary lifestyle • Often asymptomatic; more common in adolescents Diagnosis of exclusion after ruling out secondary causes

Answer 200

Secondary hypertension is common in younger children and includes: • Renal parenchymal disease • Renovascular disease • Coarctation of the aorta • Endocrine disorders (e.g., hyperthyroidism, pheochromocytoma) • Medications

Answer 201

• Glomerulonephritis (e.g., post-streptococcal GN, IgA nephropathy) • Polycystic kidney disease (ADPKD) • Reflux nephropathy • Hemolytic uremic syndrome (HUS) • Chronic kidney disease (CKD)

Answer 202

• Coarctation of the aorta: Classic cause; BP discrepancy between upper and lower limbs • Patent ductus arteriosus (with CHF) • Aortic stenosis or insufficiency Cardiac etiology should be considered with murmur or unequal pulses.

Answer 203

• Congenital adrenal hyperplasia (CAH) • Pheochromocytoma and paraganglioma • Hyperaldosteronism • Cushing syndrome • Thyroid dysfunction (hyperthyroidism > hypothyroidism) These usually have additional systemic signs.

Answer 204

• Use correct cuff size (width ≥40% of arm circumference, bladder 80–100% of arm length) • Child should be seated, calm, no caffeine/exercise in prior 30 min • Right arm preferred for consistency • Take 3 readings, average the last two

Answer 205

• Onset age <6 years • Stage 2 hypertension • Poor response to treatment • Signs of systemic illness • Abnormal physical findings (e.g., café-au-lait spots, bruit, edema) • Family history of renal or endocrine disease

Answer 206

• Headache • Visual disturbances • Vomiting • Seizures • Nosebleeds • Irritability or altered mental status These may indicate hypertensive urgency or emergency, especially in young children

Answer 207

• Urinalysis: Assess for hematuria or proteinuria • Serum electrolytes, BUN, creatinine: Evaluate renal function • Lipid profile, fasting glucose: Especially if obese • Renal ultrasound: Screen for CAKUT • Echocardiogram: Assess for left ventricular hypertrophy

Answer 208

• Plasma renin and aldosterone levels • Thyroid function tests (TSH, free T4) • Catecholamines/metanephrines (urine or plasma) for pheochromocytoma • Cortisol levels or dexamethasone suppression test for Cushing • Doppler renal ultrasound or MRA for renovascular disease

Answer 209

• Lifestyle modification is first-line for all stages: – Weight reduction – DASH diet (low sodium, high fruits/vegetables) – Regular aerobic exercise (30–60 min/day) – Limit screen time and sugar-sweetened beverages

Answer 210

• ACE inhibitors (e.g., enalapril) or ARBs are first-line in children, especially with: – Proteinuria – CKD – Diabetes • Alternatives: calcium channel blockers (e.g., amlodipine), thiazide diuretics Start low and titrate gradually

Answer 211

• ACE inhibitors/ARBs • Calcium channel blockers • Beta-blockers (less commonly) • Diuretics (thiazides or loop diuretics) Choice depends on underlying etiology, comorbidities, and age

Answer 212

• Dry cough (due to bradykinin buildup) • Hyperkalemia • Acute kidney injury, especially with renal artery stenosis • Angioedema (rare but serious) Monitor renal function and potassium after initiation

Answer 213

Indications for pharmacologic therapy: • Stage 2 hypertension regardless of symptoms • Stage 1 hypertension that persists despite 6 months of lifestyle changes • Symptomatic hypertension • Evidence of end-organ damage • CKD, diabetes, or high-risk conditions

Answer 214

Hypertensive emergency is defined as severe BP elevation with acute target organ damage, including: • Encephalopathy • Seizures • Heart failure • Retinopathy • AKI Immediate hospitalization and IV therapy are required

Answer 215

• ICU admission • Use IV antihypertensives: – Nicardipine, labetalol, or sodium nitroprusside • Avoid rapid BP drop: reduce no more than 25% in first 8 hours, then gradually normalize • Continuous monitoring of BP and organ function

Answer 216

• Early detection and management reduce risk of complications • Untreated hypertension can lead to: – Left ventricular hypertrophy – CKD progression – Cardiovascular disease in adulthood • Requires long-term follow-up with focus on lifestyle and adherence

Answer 217

Renal stones are crystalline mineral deposits formed in the kidneys or urinary tract due to supersaturation of urine with stone-forming substances like calcium, oxalate, uric acid, and cystine. Pediatric nephrolithiasis may be associated with metabolic or structural anomalies.

Answer 218

• Calcium oxalate (most common, ~60–70%) • Calcium phosphate • Uric acid • Struvite (magnesium ammonium phosphate; infection-related) • Cystine (in cystinuria) Stones may be mixed in composition.

Answer 219

Hypercalciuria is excessive urinary calcium excretion, a major risk factor for calcium stone formation. It may be idiopathic or secondary to systemic disorders and promotes stone formation by increasing calcium crystallization in urine.

Answer 220

• Dehydration / low urine volume • Hypercalciuria • Hyperoxaluria • Hypocitraturia • Hyperuricosuria • Cystinuria • Urinary tract infections (struvite stones) • Family history of nephrolithiasis

Answer 221

• Idiopathic hypercalciuria (most common) • Hyperparathyroidism • Vitamin D intoxication • Immobilization • Renal tubular acidosis (especially distal) • Sarcoidosis • Glucocorticoid therapy

Answer 222

• Flank or abdominal pain, colicky in nature • Hematuria (microscopic or gross) • Dysuria, urinary frequency, urgency • Vomiting, irritability in infants • May be asymptomatic and found incidentally

Answer 223

• Urinary calcium/creatinine ratio >0.2 mg/mg in a random urine sample (in children >6 months) • Alternatively, 24-hour urinary calcium >4 mg/kg/day Values must be interpreted in age-appropriate context and dietary calcium intake considered.

Answer 224

• Urinalysis: hematuria, crystals • Urine culture: rule out UTI • Serum calcium, phosphorus, magnesium, uric acid, creatinine • Spot urine calcium/creatinine ratio • Family and dietary history

Answer 225

Renal and bladder ultrasound (RBUS) is the first-line imaging for children. It avoids radiation, can detect hydronephrosis, echogenic foci, and bladder anomalies. However, it may miss small or ureteral stones.

Answer 226

Non-contrast helical CT (NCCT) is the gold standard for stone detection. It can detect very small stones, define location, size, and density, and identify obstruction. Due to radiation, it is reserved for inconclusive ultrasound or complex cases.

Answer 227

• 24-hour urine study (if age-appropriate): calcium, oxalate, citrate, uric acid, cystine, volume • Spot urine calcium/creatinine ratio • Serum tests: calcium, phosphorus, magnesium, uric acid, PTH, bicarbonate • Genetic/metabolic workup if recurrent or family history present

Answer 228

• High sodium intake: promotes calciuria • High animal protein: increases uric acid, lowers urine pH and citrate • Low fluid intake: concentrated urine • Excessive oxalate-rich foods (e.g., spinach, nuts) • Low calcium diet paradoxically increases oxalate absorption

Answer 229

• Increase fluid intake: aim for >1.5 L/m²/day • Limit sodium: <2 mEq/kg/day • Moderate calcium intake (not restricted unless hypercalcemia) • Reduce animal protein and oxalate-rich foods • Encourage fruits and vegetables (increase citrate)

Answer 230

• Thiazide diuretics (e.g., hydrochlorothiazide): reduce urinary calcium excretion • Potassium citrate: alkali therapy that also inhibits stone formation • Monitor electrolytes, especially potassium and bicarbonate

Answer 231

Hypocitraturia is low urinary citrate, a natural inhibitor of stone formation. Citrate binds calcium, reducing supersaturation and crystal growth. It is common in metabolic acidosis, RTA, high-protein diets. Treat with potassium citrate.

Answer 232

Struvite stones (magnesium ammonium phosphate) are associated with urease-producing bacteria like Proteus, Klebsiella, Pseudomonas. They occur in chronic UTIs and can form staghorn calculi. Require antimicrobial and surgical management.

Answer 233

Cystinuria is an autosomal recessive disorder causing impaired reabsorption of cystine and dibasic amino acids (COLA: cystine, ornithine, lysine, arginine). Cystine is poorly soluble, forming hexagonal crystals and recurrent stones.

Answer 234

• Obstructing stones with infection • Failure of medical therapy • Large stone burden or staghorn calculi • Non-passage after conservative management • Anatomic anomalies requiring correction

Answer 235

• Extracorporeal shock wave lithotripsy (ESWL): non-invasive; best for stones <1.5 cm • Ureteroscopy with laser lithotripsy • Percutaneous nephrolithotomy (PCNL): for large or complex stones • Open surgery is rare

Answer 236

• Good with early diagnosis and metabolic evaluation • High recurrence if risk factors not addressed • Long-term prevention with hydration, diet, and medications • Regular monitoring for recurrence and renal function is key

Answer 237

Cystic kidney diseases involve abnormal development or dilation of renal tubules, leading to formation of fluid-filled cysts. These can be hereditary (e.g., ARPKD, ADPKD) or acquired (e.g., multicystic dysplastic kidney, acquired cystic kidney disease in CKD). They cause progressive renal dysfunction, hypertension, and may involve extrarenal organs.

Answer 238

• Autosomal recessive polycystic kidney disease (ARPKD) • Autosomal dominant polycystic kidney disease (ADPKD) • Multicystic dysplastic kidney (MCDK) • Nephronophthisis • Acquired cystic kidney disease (in dialysis patients)

Answer 239

ARPKD is a rare genetic disorder caused by mutations in the PKHD1 gene. It leads to fusiform dilatation of collecting ducts, causing bilaterally enlarged echogenic kidneys, impaired renal function, and hepatic fibrosis. Presentation varies from severe neonatal to late childhood.

Answer 240

ARPKD is caused by mutations in the PKHD1 gene on chromosome 6p12, which encodes fibrocystin/polyductin, a protein involved in renal and biliary duct development.

Answer 241

• Oligohydramnios leading to Potter sequence (flattened facies, pulmonary hypoplasia) • Enlarged, firm kidneys on palpation • Respiratory distress at birth • Hypertension, renal failure, poor urine output

Answer 242

• Bilateral kidney enlargement • Loss of corticomedullary differentiation • Hyperechogenicity on ultrasound • Progressive renal dysfunction and early end-stage renal disease in severe cases

Answer 243

• Congenital hepatic fibrosis: the hallmark • Portal hypertension: splenomegaly, varices • Hepatic cysts (in older children) • Risk of cholangitis, growth failure, and hepatosplenomegaly

Answer 244

• Bilateral enlarged echogenic kidneys • Poor corticomedullary differentiation • No discrete cysts seen—reflects microscopic cysts • May show compressed bladder and oligohydramnios in utero

Answer 245

• High neonatal mortality if severe pulmonary hypoplasia • Survivors often develop early renal failure, hepatic fibrosis, and portal hypertension • Requires multidisciplinary care including nephrology, hepatology, and possibly liver/kidney transplantation

Answer 246

ADPKD is a progressive hereditary cystic disorder caused by mutations in PKD1 or PKD2 genes. Although classically adult-onset, cysts can be seen in childhood, especially with family history. It presents with flank pain, hematuria, hypertension, and progressive renal failure.

Answer 247

ADPKD is usually asymptomatic in childhood, but early-onset cases may present with hypertension, hematuria, or renal cysts detected incidentally or via family screening. Routine ultrasound may detect cysts even in early life, especially in PKD1 mutations.

Answer 248

ADPKD is caused by mutations in: • PKD1 (chromosome 16p13) – ~85% of cases; earlier and more severe • PKD2 (chromosome 4q21) – ~15% of cases; later onset and milder Both genes encode polycystin proteins involved in tubular integrity and signaling.

Answer 249

• Hypertension • Hematuria (microscopic or gross) • Flank pain or palpable kidneys • Proteinuria (usually subnephrotic) • Early-onset CKD in severe mutations • Rare: liver cysts, intracranial aneurysm family history

Answer 250

• Renal ultrasound: multiple bilateral renal cysts – ≥2 cysts in one kidney or one cyst in each kidney (in children with family history) • MRI or CT for confirmation • Genetic testing if imaging inconclusive or for family planning

Answer 251

• Hypertension (most common in children) • Progressive CKD • Hematuria, urinary tract infections • Cyst rupture or hemorrhage • Liver cysts, especially in older age • Intracranial aneurysms in some families

Answer 252

A positive family history supports early diagnosis, especially with known mutation. In autosomal dominant inheritance, a parent usually has ADPKD. Screening of at-risk children is controversial but may be done in hypertensive or symptomatic individuals.

Answer 253

MCDK is a non-functional kidney replaced by multiple non-communicating cysts with no normal renal parenchyma. It is a congenital malformation, usually unilateral, due to abnormal metanephric-mesenchymal interaction during renal development.

Answer 254

• Often detected antenatally on prenatal ultrasound as unilateral multicystic mass • May present postnatally as abdominal mass • Rarely, associated with hypertension, UTI, or bilateral disease (fatal)

Answer 255

• Conservative: serial ultrasounds to monitor contralateral kidney growth and MCDK involution • Blood pressure monitoring • Avoid nephrectomy unless complications (e.g., hypertension, mass effect) • Ensure contralateral kidney function is normal

Answer 256

• Annual blood pressure checks • Renal ultrasound to monitor compensatory hypertrophy of the normal kidney • Urinalysis for proteinuria • Renal function tests periodically Risk of CKD in cases with contralateral anomalies or solitary kidney syndrome

Answer 257

• End-stage renal disease (ESRD) due to: – Congenital anomalies of kidney and urinary tract (CAKUT) – Glomerulonephritis – Nephronophthisis, cystic kidney diseases • Growth failure, poor quality of life, or dialysis-related complications despite medical management

Answer 258

• Living related donor (parent/sibling): best outcomes • Living unrelated donor • Deceased donor (cadaveric): longer wait times, higher early risk Kidneys are matched based on HLA typing, blood group compatibility, and crossmatch testing.

Answer 259

• Blood group compatibility • Negative crossmatch (no donor-specific antibodies) • HLA matching (better outcomes with more matched alleles) • Complete infectious disease screening • Evaluation for urological anomalies, bladder function, and psychosocial readiness

Answer 260

Triple therapy includes: • Calcineurin inhibitors (CNIs): tacrolimus or cyclosporine • Antimetabolites: mycophenolate mofetil (MMF) or azathioprine • Corticosteroids: prednisone Induction agents: basiliximab, anti-thymocyte globulin (ATG)

Answer 261

Acute rejection is a cell-mediated or antibody-mediated immune attack on the graft. It typically occurs within weeks to months post-transplant. It leads to rising creatinine, graft tenderness, and urine output decline.

Answer 262

• Rising serum creatinine or oliguria • Graft biopsy: gold standard • Histological findings: interstitial inflammation, tubulitis, vascular rejection • Doppler ultrasound may aid but is not diagnostic

Answer 263

• Inadequate immunosuppression • Recurrent acute rejections • Drug toxicity (e.g., CNI nephrotoxicity) • Hypertension, hyperlipidemia • BK virus nephropathy • Poor adherence to treatment

Answer 264

• Acute and chronic rejection • Infections (CMV, EBV, BK virus, fungal, TB) • Post-transplant lymphoproliferative disorder (PTLD) • Drug toxicities (CNI-induced nephrotoxicity, diabetes, bone loss) • Hypertension, dyslipidemia, growth delay

Answer 265

• Vascular thrombosis (renal artery or vein) is the most common cause of early graft loss, especially in young children • Other causes: hyperacute rejection, technical complications during surgery

Answer 266

• Prophylactic antibiotics: TMP-SMX for Pneumocystis jirovecii, bacterial UTI • Antiviral prophylaxis: valganciclovir for CMV, if high-risk • Vaccination before transplant (no live vaccines post-transplant) • Regular monitoring and infection screening post-operatively

Answer 267

• Complete all routine immunizations per schedule • Live vaccines (e.g., MMR, varicella, BCG) should be given ≥4 weeks before transplant • Pneumococcal (PCV13 + PPSV23), Hepatitis B, Influenza, Meningococcal recommended • No live vaccines post-transplant due to immunosuppression

Answer 268

Relapse is the reappearance of nephrotic-range proteinuria after a prior remission. It is a common feature of minimal change disease, especially in frequently relapsing or steroid-dependent cases. Relapse may be triggered by infection, stress, or noncompliance.

Answer 269

• Respiratory infections (most common) • Gastrointestinal illness • Allergens, stress, vaccinations • Steroid tapering • Poor medication adherence • Relapse risk highest in children <6 years or with FRNS

Answer 270

Defined as proteinuria ≥3+ on urine dipstick for 3 consecutive days or urine protein:creatinine ratio >2 mg/mg after remission. May also be accompanied by edema and hypoalbuminemia. Requires prompt initiation of therapy.

Answer 271

• Start high-dose oral prednisolone (2 mg/kg/day) until remission (proteinuria <1+ for 3 days) • Then taper to alternate-day dosing and gradually reduce over weeks • Supportive care: salt restriction, fluid balance, infection control

Answer 272

SDNS is defined as 2 relapses during steroid tapering or within 14 days of stopping steroids. These children often require long-term steroid therapy and are at risk of complications from corticosteroid toxicity.

Answer 273

FRNS is defined as ≥2 relapses in the first 6 months or ≥4 relapses in any 12-month period. FRNS may progress to steroid dependence or require steroid-sparing immunosuppressants for control.

Answer 274

Indicated in: • Steroid dependence • Frequent relapses • Steroid toxicity (e.g., obesity, hypertension, growth delay) • Poor adherence or quality of life concerns Goal: reduce cumulative steroid exposure while maintaining remission

Answer 275

• Cyclophosphamide (cytotoxic, finite duration) • Calcineurin inhibitors (CNI): tacrolimus, cyclosporine • Mycophenolate mofetil (MMF) • Rituximab (anti-CD20 monoclonal antibody) Choice depends on side-effect profile and relapse pattern

Answer 276

• Primary nephrotic syndrome (e.g., minimal change) rarely recurs post-transplant • FSGS has high recurrence rate (~30–50%), may cause graft loss • Recurrence managed with plasma exchange, rituximab • Overall graft survival is excellent with adherence and early intervention

Answer 277

Enuresis is involuntary voiding of urine during sleep, most commonly at night (nocturnal enuresis), in children ≥5 years of age. It must occur ≥2 times per week for ≥3 months, or cause significant distress or impairment, in the absence of congenital or acquired urologic anomalies.

Answer 278

Enuresis is classified based on: • Timing: – Primary: child has never achieved 6+ months of dryness – Secondary: recurrence after a dry period ≥6 months • Symptoms: – Monosymptomatic: no daytime symptoms – Non-monosymptomatic: with urgency, frequency, or incontinence

Answer 279

Primary enuresis refers to persistent bedwetting without prior sustained dryness. It is usually due to delayed maturation of bladder control, nocturnal polyuria, or deep sleep arousal deficit. Most common form in younger children.

Answer 280

Secondary enuresis is defined as resumption of bedwetting after at least 6 months of nighttime dryness. It often has a psychological, medical, or urological trigger (e.g., UTI, stress, diabetes, abuse).

Answer 281

Monosymptomatic enuresis is bedwetting without any lower urinary tract symptoms such as urgency or daytime incontinence. It typically reflects a developmental delay in nighttime bladder control, not a structural problem.

Answer 282

Non-monosymptomatic enuresis includes bedwetting with daytime urinary symptoms, such as frequency, urgency, or incontinence. It is more likely to have an underlying urological or behavioral disorder (e.g., constipation, overactive bladder).

Answer 283

Enuresis is considered pathological after age 5 years, based on expected milestones for nighttime bladder control. Occasional bedwetting before age 5 is developmentally normal. Diagnosis requires persistence, frequency, and social/emotional impact.

Answer 284

• Stressful life events (e.g., divorce, school change) • Urinary tract infections • Diabetes mellitus or insipidus • Constipation • Emotional disturbances or trauma • Sleep disorders

Answer 285

• Family history of enuresis (strong genetic component) • Male gender • Delayed developmental milestones • Small functional bladder capacity • Sleep arousal difficulties • High nocturnal urine production

Answer 286

Enuresis is highly familial: • If one parent had enuresis, risk is ~45% • If both parents, risk rises to ~75% This reflects polygenic inheritance affecting bladder function, ADH secretion, or sleep arousal.

Answer 287

It involves a mismatch between nocturnal urine production, bladder capacity, and arousal. Children produce more urine at night (due to low ADH), have small functional bladder capacity, and fail to awaken in response to bladder fullness.

Answer 288

• Detailed history: onset, frequency, dry periods, family history • Voiding diary: document fluid intake, voiding times, bedwetting episodes • Urinalysis: check for glucose, protein, signs of infection • Physical exam: focus on spine, abdomen, and perineum

Answer 289

• Daytime symptoms (urgency, frequency, incontinence) • Recurrent UTI history • Constipation or stool incontinence • Abnormal physical findings (e.g., spinal anomalies) • Treatment failure after behavioral and medical therapy

Answer 290

A voiding diary tracks voiding frequency, volumes, fluid intake, and wetting patterns. It helps assess functional bladder capacity, identify polyuria, or detect behavioral patterns. Essential for tailored treatment planning.

Answer 291

• Behavioral modification: – Limit fluids 2 hours before bed – Encourage scheduled voiding – Positive reinforcement • Alarm therapy • Treat constipation if present • Family support and reassurance

Answer 292

Alarm therapy uses a moisture-sensitive alarm that awakens the child at the start of wetting. Over time, it conditions the child to wake or hold urine, improving bladder awareness. Most effective long-term intervention, especially with family support.

Answer 293

Desmopressin (DDAVP), a synthetic analog of ADH, reduces nocturnal urine production. Used for children >6 years with monosymptomatic nocturnal enuresis, particularly when behavioral therapy fails or for short-term control (e.g., sleepovers).

Answer 294

• Hyponatremia (risk increases with excessive fluid intake) • Headache • Nausea, abdominal pain To prevent hyponatremia, restrict fluids 1 hour before and 8 hours after administration.

Answer 295

Used in non-monosymptomatic enuresis with signs of bladder overactivity (e.g., urgency, frequency). Common drugs include oxybutynin and solifenacin. Often combined with desmopressin if bladder instability is present.

Answer 296

• Most children achieve spontaneous resolution (~15% annually) • Good response to alarm therapy and desmopressin • Prognosis is excellent with family support, proper evaluation, and adherence • Some may have persistent symptoms into adolescence if untreated

Nephrology Flashcards

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