American Board of Internal Medicine Certification (ABIM Board Certification) Nephrology & Electrolyte Disorders Syllabus

Nephrology & Electrolyte Disorders syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Nephrology & Electrolyte Disorders in American Board of Internal Medicine Certification (ABIM Board Certification), not a summary of it.

1. 1

   Acute Kidney Injury

   4 topics

   • Prerenal, intrinsic, and postrenal AKI
     • Urinalysis and microscopy interpretation
     • FENa and diagnostic indices
   • Acute tubular necrosis and acute interstitial nephritis
   • Contrast-associated and drug-induced nephropathy
   • Indications for renal replacement therapy
2. 2

   Chronic Kidney Disease

   4 topics

   • CKD staging and progression management
   • Mineral and bone disorder
   • Anemia of CKD
   • Dialysis and transplant evaluation
3. 3

   Glomerular & Tubulointerstitial Disease

   4 topics

   • Nephrotic syndrome
     • Minimal change, FSGS, membranous nephropathy
   • Nephritic syndrome and glomerulonephritis
   • Diabetic and hypertensive kidney disease
   • Polycystic and hereditary kidney disease
4. 4

   Fluid, Electrolyte & Acid-Base Disorders

   4 topics

   • Sodium and water disorders
     • Hyponatremia diagnostic algorithm
     • Hypernatremia and diabetes insipidus
   • Potassium disorders
   • Calcium, phosphate, and magnesium disorders
   • Metabolic acidosis and alkalosis
     • Anion gap and osmolar gap analysis

Nephrology & Electrolyte Disorders flashcards for American Board of Internal Medicine Certification (ABIM Board Certification)

23 of 55 cards from the Nephrology & Electrolyte Disorders deck — real questions with worked answers.

1. How is acute kidney injury (AKI) defined by KDIGO criteria?

   Any of: rise in serum creatinine >=0.3 mg/dL within 48 hours; rise in creatinine to >=1.5x baseline within 7 days; or urine output <0.5 mL/kg/h for 6 hours.

2. In prerenal AKI, what are the expected values for FENa, urine sodium, urine osmolality, and BUN:creatinine ratio?

   FENa <1%, urine Na <20 mEq/L, urine osmolality >500 mOsm/kg (concentrated), and BUN:creatinine ratio >20:1.

3. What is the formula for the fractional excretion of sodium (FENa)?

   FENa = (urine Na x plasma creatinine) / (plasma Na x urine creatinine) x 100.

4. Why is FEurea preferred over FENa for distinguishing prerenal AKI from ATN in a patient on diuretics?

   Diuretics force renal sodium excretion, falsely raising FENa above 1%. Urea handling is less affected, so FEurea <35% still indicates a prerenal state.

5. What urine microscopy finding is the hallmark of acute tubular necrosis (ATN)?

   Muddy-brown (pigmented) granular casts and renal tubular epithelial cell casts.

6. What is the classic clinical triad of acute interstitial nephritis (AIN), and its characteristic urinary finding?

   Triad: fever, rash, and eosinophilia (all three present only in a minority). Urinalysis classically shows sterile pyuria with white-cell casts; urine eosinophils have poor sensitivity/specificity.

7. Name the major drug classes that cause acute interstitial nephritis.

   Antibiotics (beta-lactams, sulfonamides, rifampin, fluoroquinolones), NSAIDs, proton pump inhibitors, diuretics, and allopurinol.

8. What are the most common causes of postrenal AKI, and what test confirms it?

   Bilateral ureteral obstruction (or unilateral in a solitary kidney), bladder outlet obstruction (BPH, prostate cancer), and neurogenic bladder. Renal ultrasound showing hydronephrosis confirms it.

9. What are the key risk factors for contrast-associated nephropathy (CA-AKI)?

   Pre-existing CKD (eGFR <30 highest risk), diabetic nephropathy, volume depletion, heart failure, high contrast volume, and concurrent nephrotoxins.

10. What is the timing and creatinine pattern of contrast-associated nephropathy?

    Creatinine rises within 24-48 hours after contrast, peaks at 3-5 days, and typically returns to baseline by 7-10 days. Prevention is mainly isotonic IV fluid (volume expansion).

11. Which crystal-related drugs cause crystalline nephropathy, and how is it prevented?

    Acyclovir, sulfonamides, methotrexate, indinavir, and high-dose vitamin C (oxalate). Prevention: aggressive hydration; urine alkalinization for methotrexate.

12. What classic urine/serum osmolar pattern distinguishes ATN from prerenal azotemia?

    ATN: urine osm ~300 (isosthenuric, ~serum), urine Na >40, FENa >2%. Prerenal: urine osm >500, urine Na <20, FENa <1%.

13. What are the urgent (emergent) indications for renal replacement therapy (the AEIOU mnemonic)?

    Acidosis (refractory metabolic), Electrolytes (refractory hyperkalemia), Intoxications (dialyzable toxins), Overload (refractory volume overload/pulmonary edema), and Uremia (pericarditis, encephalopathy, bleeding).

14. Which intoxications are classically treated with hemodialysis (the I-STUMBLE / dialyzable toxins)?

    Salicylates, Lithium, Toxic alcohols (methanol, ethylene glycol), Metformin (lactic acidosis), Theophylline, and Valproate/barbiturates. Generally low-molecular-weight, water-soluble, low protein binding, small volume of distribution.

15. How is chronic kidney disease (CKD) defined?

    Abnormalities of kidney structure or function present for >=3 months: either GFR <60 mL/min/1.73m2, or markers of damage (albuminuria, urine sediment, electrolyte/structural/histologic abnormalities).

16. What are the GFR (G) stages of CKD?

    G1: >=90 (with damage); G2: 60-89; G3a: 45-59; G3b: 30-44; G4: 15-29; G5: <15 (kidney failure).

17. What are the albuminuria (A) categories of CKD by urine albumin-to-creatinine ratio (ACR)?

    A1: <30 mg/g (normal/mildly increased); A2: 30-300 mg/g (moderately increased, 'microalbuminuria'); A3: >300 mg/g (severely increased, 'macroalbuminuria').

18. Which interventions slow CKD progression in proteinuric and diabetic kidney disease?

    ACE inhibitor or ARB (reduce proteinuria), SGLT2 inhibitors, blood pressure control (<130/80), glycemic control, and finerenone (in diabetic CKD). Avoid combining ACEi with ARB.

19. What is the pathophysiology of CKD-mineral and bone disorder (CKD-MBD)?

    Declining GFR -> phosphate retention and reduced 1,25-(OH)2 vitamin D -> hypocalcemia and elevated FGF-23 -> secondary hyperparathyroidism. Net pattern: high phosphate, low calcium, low calcitriol, high PTH.

20. What is the renal bone disease of high-turnover secondary hyperparathyroidism, and what is adynamic bone disease?

    High-turnover: osteitis fibrosa cystica (from high PTH). Adynamic bone disease: low bone turnover from over-suppressed PTH (often from excess calcium/vitamin D/calcimimetics), increasing fracture and vascular calcification risk.

21. Name the treatment classes for secondary hyperparathyroidism in CKD.

    Dietary phosphate restriction, phosphate binders (non-calcium: sevelamer, lanthanum; calcium-based), active vitamin D analogs (calcitriol, paricalcitol), and calcimimetics (cinacalcet, etelcalcetide).

22. What causes anemia of CKD and what are its characteristics?

    Primarily reduced erythropoietin production by failing kidneys (plus iron deficiency, uremic RBC survival reduction). It is normocytic, normochromic with low reticulocyte count.

23. What iron and hemoglobin targets guide ESA therapy in CKD anemia?

    Replete iron first (target transferrin saturation >30% and ferritin >500 may indicate adequate stores; treat if TSAT <30% and ferritin <500). Start ESA when Hb <10 g/dL; do not target normal Hb (>11.5 increases stroke/CV/thrombosis risk).

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