100+ Free ABP Pediatric Nephrology Practice Questions

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Question 1

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A 4-year-old with gastroenteritis has serum Na 122 mEq/L, urine osmolality 100 mOsm/kg, and urine Na 10 mEq/L. Which is the most likely mechanism?

Hypovolemic hyponatremia with appropriate renal water/salt conservation

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Cerebral salt wasting

Nephrogenic diabetes insipidus

to track

2026 Statistics

Key Facts: ABP Pediatric Nephrology Exam

~150

Total MCQ Items

Single-best-answer, 4-5 options

~4 hr

Exam Time

Half-day CBT at Pearson VUE

180

Passing Score

1-300 scale; criterion-referenced

$2,992

2026 Regular Fee

Includes $750 processing fee

3 yr

Required Fellowship

ACGME-accredited pediatric nephrology

Spring

2026 Administration

Listed as 2026 spring subspecialty exam

The ABP Pediatric Nephrology certifying exam is a half-day (~4-hour) CBT of approximately 150 single-best-answer MCQs delivered at Pearson VUE. Scored on a 1-300 scale with 180 passing (criterion-referenced, modified Angoff). The 2026 fee is $2,992 regular ($750 processing), $3,337 late. Content domains include fluid/electrolyte/acid-base (~15%), glomerular disorders (~15%), AKI (~10%), CKD/dialysis/transplant (~15%), hypertension (~8%), CAKUT/cystic (~10%), fetal/neonatal, UTI, stones, hematuria/proteinuria, HUS/TMA, tubular disorders, and core diagnostics. Pediatric Nephrology is scheduled as a 2026 spring subspecialty exam.

Sample ABP Pediatric Nephrology Practice Questions

Try these sample questions to test your ABP Pediatric Nephrology exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 4-year-old with gastroenteritis has serum Na 122 mEq/L, urine osmolality 100 mOsm/kg, and urine Na 10 mEq/L. Which is the most likely mechanism?

A.Hypovolemic hyponatremia with appropriate renal water/salt conservation

B.Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

C.Cerebral salt wasting

D.Nephrogenic diabetes insipidus

Explanation: Hypovolemic hyponatremia from GI losses is characterized by dilute urine (in early volume loss ADH has not yet maximally concentrated) or concentrated urine with low urine Na (<20 mEq/L) reflecting renal Na conservation via aldosterone. SIADH has concentrated urine (Uosm >100) with urine Na >20-40 mEq/L and euvolemia. Cerebral salt wasting has volume depletion with high urine Na. Nephrogenic DI causes hypernatremia.

2A 3-month-old presents with polyuria, polydipsia, dehydration, and serum Na 160 mEq/L. Despite DDAVP administration, urine osmolality remains 100 mOsm/kg. Which diagnosis is most likely?

A.SIADH

B.Central diabetes insipidus

C.Primary polydipsia

D.Nephrogenic diabetes insipidus

Explanation: Nephrogenic DI (AVPR2 X-linked or AQP2 autosomal) fails to concentrate urine despite DDAVP because the kidney cannot respond to ADH. Central DI responds to DDAVP (urine concentrates). Primary polydipsia has low baseline Na and appropriate response to water deprivation. SIADH causes hyponatremia, not hypernatremia. In infants, suspect congenital NDI — treat with thiazide + low-solute diet + amiloride or indomethacin.

3A 10-year-old presents with hypokalemic hyperchloremic non-anion-gap metabolic acidosis, urine pH 6.5, nephrocalcinosis, and short stature. Which diagnosis?

A.Diarrheal bicarbonate loss

B.Proximal (type 2) renal tubular acidosis

C.Type 4 renal tubular acidosis

D.Distal (type 1) renal tubular acidosis

Explanation: Distal RTA (type 1) is caused by impaired H+ secretion in the α-intercalated cell (SLC4A1/AE1, ATP6V1B1, ATP6V0A4). Hallmarks: inability to acidify urine below pH 5.5 despite systemic acidosis, hypokalemia, hypercalciuria, and nephrocalcinosis/stones (calcium phosphate). ATP6V1B1 is associated with sensorineural deafness. Treatment: oral alkali (bicarbonate or citrate) to correct acidosis, prevent stones, and restore growth.

4Which finding best distinguishes Gitelman syndrome from Bartter syndrome?

A.Hypercalciuria and normal Mg in Gitelman

B.Hypocalciuria and hypomagnesemia in Gitelman

C.Hypertension in Gitelman

D.Metabolic acidosis in Gitelman

Explanation: Gitelman syndrome (SLC12A3 — NCC transporter in distal convoluted tubule) mimics thiazide action: hypokalemic metabolic alkalosis, HYPOcalciuria, and hypomagnesemia. Bartter syndrome (SLC12A1, KCNJ1, CLCNKB, BSND, CASR — NKCC2 / ROMK / ClC-Kb in thick ascending limb) mimics loop diuretic action: hypokalemic alkalosis with HYPERcalciuria, often nephrocalcinosis, and presentation in infancy with polyhydramnios. Both are normotensive.

5A 5-year-old boy develops steroid-sensitive nephrotic syndrome. Which histologic finding is most likely on biopsy?

A.Mesangial proliferation with IgA deposits

B.Segmental sclerosis on LM with foot process effacement

C.Diffuse GBM thickening with subepithelial deposits

D.Normal light microscopy with foot process effacement on EM (minimal change disease)

Explanation: Minimal change disease (MCD) is the most common cause of childhood nephrotic syndrome and is steroid-responsive in >90%. LM is normal; IF is negative; EM shows diffuse podocyte foot process effacement. FSGS shows segmental sclerosis and scars. Membranous nephropathy (PLA2R) causes subepithelial spikes. IgA nephropathy presents with hematuria and mesangial IgA.

6A 14-year-old with steroid-resistant nephrotic syndrome has an NPHS2 mutation. Which diagnosis is most likely?

A.IgA nephropathy

B.Minimal change disease

C.Membranous nephropathy

D.Focal segmental glomerulosclerosis (FSGS)

Explanation: NPHS2 encodes podocin, a slit diaphragm protein. Biallelic NPHS2 mutations cause steroid-resistant nephrotic syndrome with FSGS histology. NPHS1 (nephrin) causes congenital nephrotic syndrome of Finnish type. Other podocin/slit diaphragm and podocyte cytoskeleton genes (ACTN4, INF2, TRPC6, WT1, LAMB2, APOL1) also cause hereditary FSGS. Genetic FSGS typically does not respond to immunosuppression and has high recurrence risk on transplant only with nongenetic FSGS.

7A 7-year-old boy develops gross hematuria, edema, hypertension, and low C3 two weeks after a skin infection. Which diagnosis is most likely?

A.Minimal change disease

B.IgA nephropathy

C.Alport syndrome

D.Post-streptococcal glomerulonephritis

Explanation: Post-streptococcal glomerulonephritis (PSGN) follows group A strep infection (2-3 weeks after pharyngitis; 3-6 weeks after impetigo). Hallmarks: acute nephritic syndrome (hematuria, edema, hypertension) with depressed C3 (normalizing by 8-12 weeks) and normal C4, positive anti-DNase B (more sensitive for skin infection than ASO). Biopsy shows subepithelial humps on EM. IgA presents with synpharyngitic hematuria; C3 is usually normal. Alport has familial hematuria and hearing loss.

8Which C3 and C4 pattern is most consistent with membranoproliferative glomerulonephritis (MPGN) / C3 glomerulopathy?

A.Persistently low C3 with normal C4

B.Low C3 and low C4

C.Normal C3 and low C4

D.Elevated C3 and elevated C4

Explanation: C3 glomerulopathy (C3GN and dense deposit disease) is driven by dysregulation of the alternative complement pathway (C3 nephritic factor, CFH, CFI, CFB, C3 mutations). C3 is persistently low with normal C4 (alternative pathway only). Lupus nephritis (classical pathway activation) shows low C3 AND low C4. PSGN shows low C3 that normalizes by 8-12 weeks — persistent depression beyond 12 weeks suggests C3 glomerulopathy.

9A 13-year-old girl with SLE has lupus nephritis biopsy showing endocapillary proliferation in >50% of glomeruli with subendothelial deposits ('wire loops'). Which ISN/RPS class?

A.Class V (membranous)

B.Class II (mesangial proliferative)

C.Class IV (diffuse lupus nephritis)

D.Class VI (advanced sclerosing)

Explanation: ISN/RPS 2018 Class IV (diffuse lupus nephritis) involves ≥50% of glomeruli with endocapillary or extracapillary proliferation; wire-loop lesions reflect subendothelial immune deposits. Class IV is the most severe proliferative lesion and requires induction with high-dose steroids + MMF (or IV cyclophosphamide NIH/Euro-Lupus regimen). Class II is mesangial. Class V is membranous with subepithelial deposits. Class VI is >90% globally sclerotic.

10A 16-year-old boy has recurrent gross hematuria following upper respiratory infections. Biopsy shows mesangial IgA deposition. Which diagnosis?

A.Post-streptococcal glomerulonephritis

B.IgA nephropathy

C.Alport syndrome

D.C3 glomerulopathy

Explanation: IgA nephropathy (Berger disease) is the most common primary glomerulonephritis worldwide. Classic presentation is synpharyngitic hematuria (gross hematuria within 1-3 days of URI, in contrast to PSGN which occurs 1-3 weeks after). IF shows mesangial IgA deposits (with C3, sometimes IgG). Oxford MEST-C score guides prognosis. Treat with RAAS blockade; steroids/immunosuppression for progressive disease per KDIGO.

About the ABP Pediatric Nephrology Exam

The ABP Pediatric Nephrology subspecialty certifying exam validates expert-level knowledge of fluid/electrolyte/acid-base balance, glomerular disorders (minimal change, FSGS, IgA nephropathy, PSGN, lupus nephritis, HUS/TMA), AKI, CKD/ESRD, CAKUT, ARPKD/ADPKD and ciliopathies, tubular disorders (Bartter, Gitelman, distal/proximal/type 4 RTA), UTI/VUR, urolithiasis, pediatric hypertension, dialysis (HD, PD, CRRT), and kidney transplantation. Half-day computer-based exam of ~150 MCQs in ~4 hours. Requires ABP General Pediatrics certification plus a 3-year ACGME-accredited pediatric nephrology fellowship.

Questions

150 scored questions

Time Limit

~4 hours (half-day CBT)

Passing Score

Scaled score of 180 on a 1-300 scale (criterion-referenced, modified Angoff)

Exam Fee

$2,992 regular ($750 processing fee); $3,337 with late fee (American Board of Pediatrics (ABP) / Pearson VUE)

ABP Pediatric Nephrology Exam Content Outline

~15%

Fluid, Electrolyte, Acid-Base

Na/K/Ca/Mg/P disorders, SIADH, cerebral salt wasting, DI, RTA types 1/2/4, Bartter/Gitelman, anion-gap vs non-gap acidosis, mixed disorders, fractional excretion calculations.

~15%

Glomerular Disorders

MCD (steroid-sensitive NS), FSGS (primary/secondary, APOL1, NPHS1/2), membranous (PLA2R), IgA, PSGN, MPGN/C3GN, lupus nephritis (ISN/RPS classes I-VI), HSP, ANCA, anti-GBM, Alport (COL4A5).

~15%

CKD, ESRD, Dialysis, Transplantation

CKD staging, GFR estimation (bedside Schwartz, CKiD U25), CKD-MBD, anemia of CKD, HD vs PD, transplant immunology, induction (basiliximab, thymoglobulin), maintenance (tac/MMF/steroids), Banff rejection, BK, CMV, PTLD, recurrence.

~10%

Acute Kidney Injury (AKI)

KDIGO staging, prerenal/intrinsic/postrenal, ATN, AIN, tumor lysis, rhabdomyolysis, contrast-associated AKI, hepatorenal, CRRT modalities, indications for RRT.

~10%

Cystic and Structural Disorders (CAKUT)

ARPKD (PKHD1, congenital hepatic fibrosis), ADPKD (PKD1/2), nephronophthisis and ciliopathies, MCDK, PUV, duplex collecting systems, UPJ obstruction, VUR grading.

~8%

Hypertension

AAP 2017 BP tables, primary vs secondary HTN, renovascular (FMD, Takayasu), monogenic HTN (Liddle, GRA, AME), pheochromocytoma, ABPM, hypertensive emergency, ACEi/ARB/CCB/diuretic pharmacology.

~6%

Tubular Disorders

Fanconi (cystinosis CTNS, Dent, Lowe), distal RTA (SLC4A1, ATP6 subunits), proximal RTA (SLC4A4), type 4 RTA, Bartter types 1-5, Gitelman (SLC12A3), Liddle, PHA1/2.

~6%

Urinary Tract Infection and Micturition

AAP UTI guideline (2-24 mo febrile UTI), VCUG/DMSA indications, VUR grading I-V, RIVUR prophylaxis, neurogenic bladder, dysfunctional voiding, enuresis.

~6%

Hematuria and Proteinuria Evaluation

Isolated microscopic hematuria, gross hematuria differential, orthostatic proteinuria, first-morning Upr/Ucr, nephrotic-range threshold, biopsy indications.

~5%

Fetal and Neonatal Nephrology

Antenatal hydronephrosis (SFU, UTD), oligohydramnios/Potter, neonatal AKI, renal vein thrombosis, congenital nephrotic syndrome (NPHS1 Finnish), GFR maturation.

~5%

Urolithiasis

Calcium oxalate (idiopathic hypercalciuria, Dent, primary hyperoxaluria AGXT), uric acid, cystine (SLC3A1/SLC7A9), struvite, 24-hour urine, ultrasound-first imaging.

~4%

HUS and Thrombotic Microangiopathy

STEC-HUS (O157:H7), atypical HUS (CFH, CFI, MCP, CFB, C3; eculizumab), DGKE, TTP (ADAMTS13), cobalamin C, pneumococcal HUS (T-antigen).

~5%

Core Diagnostics and Renal Masses

Urine microscopy (RBC casts, WBC casts, crystals), GFR measurement (inulin, iohexol), renal US/DMSA/MAG3, biopsy technique, nephrogenic rests, Wilms overview.

How to Pass the ABP Pediatric Nephrology Exam

What You Need to Know

Passing score: Scaled score of 180 on a 1-300 scale (criterion-referenced, modified Angoff)
Exam length: 150 questions
Time limit: ~4 hours (half-day CBT)
Exam fee: $2,992 regular ($750 processing fee); $3,337 with late fee

Keys to Passing

Complete 500+ practice questions
Score 80%+ consistently before scheduling
Focus on highest-weighted sections
Use our AI tutor for tough concepts

ABP Pediatric Nephrology Study Tips from Top Performers

1Distal RTA (type 1) clue: hypokalemic hyperchloremic non-gap acidosis + alkaline urine (pH > 5.5) + hypercalciuria + nephrocalcinosis + calcium-phosphate stones. Causes: SLC4A1 (dominant + Southeast Asian ovalocytosis), ATP6V1B1 (recessive + sensorineural deafness), ATP6V0A4. Treat with alkali (bicarbonate or citrate).

2Bartter vs Gitelman rule: both cause hypokalemic metabolic alkalosis without hypertension. Bartter (loop-like, SLC12A1/KCNJ1/CLCNKB/BSND) presents in infancy with polyhydramnios, hypercalciuria, and nephrocalcinosis. Gitelman (DCT-like, SLC12A3) presents later with hypomagnesemia and HYPOcalciuria. Remember: 'Gitelman = low Mg, low Ca in urine.'

3Atypical HUS key fact: complement dysregulation (CFH, CFI, MCP/CD46, CFB, C3, THBD) — eculizumab (anti-C5) is life-saving and ideally started within 24-48 hours. Distinguish from STEC-HUS (E. coli O157:H7, Shiga toxin, bloody diarrhea prodrome; supportive care; plasma exchange NOT routinely indicated) and TTP (ADAMTS13 <10%).

4Alport syndrome: X-linked (COL4A5, ~80%) > AR (COL4A3/A4, ~15%) > AD. Boys present earlier and more severely. Triad = progressive sensorineural hearing loss + anterior lenticonus + microscopic hematuria/nephritis. EM: lamellated 'basket-weave' GBM. Note: anti-GBM disease may develop after kidney transplant (against the foreign Goodpasture antigen).

5Bedside Schwartz GFR in children: eGFR = 0.413 × (height in cm / serum creatinine in mg/dL). Use for ages 1-17 with stable kidney function. The CKiD U25 equation (age, height, sex, creatinine and/or cystatin C) now extends through young adulthood and is preferred in many pediatric nephrology clinics.

Frequently Asked Questions

What is the ABP Pediatric Nephrology subspecialty certification?

The ABP Pediatric Nephrology subspecialty certification is awarded by the American Board of Pediatrics to pediatricians who demonstrate expert-level knowledge in the diagnosis and management of kidney and urinary tract disease in children. It qualifies diplomates to lead pediatric nephrology services, dialysis programs, and kidney transplant care at children's hospitals.

Who is eligible to take the ABP Pediatric Nephrology exam?

Candidates must hold primary ABP General Pediatrics certification in good standing and have completed 3 years of full-time training in an ACGME-accredited pediatric nephrology fellowship. A valid unrestricted medical license is required. The fellowship includes clinical nephrology, dialysis, transplantation, and scholarly/research activity meeting the ABP scholarly requirement.

What is the format of the ABP Pediatric Nephrology exam?

It is a half-day (~4-hour) computer-based exam administered at Pearson VUE Professional Testing Centers, consisting of approximately 150 single-best-answer multiple-choice questions. Questions have four or five answer options with exactly one correct answer. The exam includes vignette-style items with labs, imaging, biopsy images, and pharmacology.

How much does the 2026 ABP Pediatric Nephrology exam cost?

The 2026 regular registration fee is $2,992, which includes a $750 nonrefundable processing fee. Late registration is $3,337 (includes a $345 late fee). Pediatric Nephrology is scheduled as a 2026 Spring Subspecialty Exam.

How is the exam scored?

The exam is scored on a 1-300 scale with 180 designated as the passing mark. ABP uses a criterion-referenced scoring model: a panel of practicing, board-certified pediatric nephrologists determines the passing standard using the modified Angoff method. Results are reported as scaled scores, not percentile ranks.

What are the highest-yield topics?

Fluid/electrolyte/acid-base and glomerular disease together cover roughly 30% of the exam. Master RTA types 1/2/4, Bartter vs Gitelman, Fanconi syndrome and cystinosis, nephrotic (MCD/FSGS/membranous) vs nephritic (IgA, PSGN, MPGN, lupus), lupus nephritis ISN/RPS classes, Alport (COL4A5), and the complement pathway in atypical HUS (eculizumab). Also master CKD-MBD, transplant immunology (Banff rejection, BK, CMV), and the AAP 2017 pediatric BP tables.

How should I study for this exam?

Use a 6-12 month structured plan during your final fellowship year. Start with fluid/electrolyte/acid-base and tubular disorders (highest volume, daily practice). Then master glomerular disease, HUS/TMA, and lupus nephritis. Next, CKD/ESRD, CKD-MBD, dialysis, and transplantation. Finally, CAKUT, UTI/VUR, stones, hypertension, and fetal/neonatal topics. Take 2-3 timed full-length mock exams. Integrate the ASPN Board Review Course, Avner-Harmon-Niaudet Pediatric Nephrology textbook, KDIGO guidelines, and AAP/AAP+ESPN guidelines.

What are my continuing certification requirements after passing?

After initial certification, diplomates maintain certification via the ABP's Maintenance of Certification Assessment for Pediatricians (MOCA-Peds) — a longitudinal assessment with quarterly questions over a 5-year cycle. Diplomates must also complete Part 2 (self-assessment CME) and Part 4 (improvement in medical practice) activities and maintain an unrestricted license.