NEET SS Nephrology (DM) Syllabus

Nephrology (DM) syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Nephrology (DM) in NEET SS, not a summary of it.

1. 1

   Glomerular Diseases

   3 topics

   • Nephrotic Syndrome
     • Minimal change disease and FSGS
     • Membranous nephropathy and PLA2R antibody
   • Nephritic Syndrome and RPGN
     • IgA nephropathy
     • ANCA-associated and anti-GBM disease
   • Lupus and Secondary Glomerulonephritis
     • ISN/RPS lupus nephritis classes
     • Diabetic kidney disease
2. 2

   Acute Kidney Injury and Critical Care Nephrology

   3 topics

   • AKI Definition and Etiology
     • KDIGO staging
     • Prerenal, intrinsic and postrenal causes
   • Acute Tubular Necrosis and Interstitial Nephritis
     • Ischemic and nephrotoxic ATN
   • Renal Replacement Therapy in AKI
     • Modalities and timing of dialysis
3. 3

   Chronic Kidney Disease and Dialysis

   3 topics

   • CKD Staging and Progression
     • eGFR and albuminuria categories
     • Mineral bone disorder (CKD-MBD)
     • Anemia management
   • Hemodialysis
     • Vascular access and adequacy (Kt/V)
     • Intradialytic complications
   • Peritoneal Dialysis
     • PD-related peritonitis
4. 4

   Fluid, Electrolyte and Acid-Base Disorders

   3 topics

   • Sodium and Water Balance
     • Hyponatremia and hypernatremia
     • SIADH and diabetes insipidus
   • Potassium, Calcium and Magnesium Disorders
     • Hyperkalemia and hypokalemia management
   • Acid-Base Disorders
     • Metabolic acidosis and anion gap
     • Renal tubular acidosis
5. 5

   Kidney Transplantation and Hereditary/Tubular Disorders

   3 topics

   • Renal Transplant Immunology
     • Immunosuppression protocols
     • Acute and chronic rejection
   • Transplant Infections and Complications
     • BK virus and CMV
   • Inherited and Cystic Kidney Diseases
     • ADPKD and Alport syndrome
     • Inherited tubulopathies (Bartter, Gitelman)

Nephrology (DM) flashcards for NEET SS

24 of 50 cards from the Nephrology (DM) deck — real questions with worked answers.

1. Define nephrotic syndrome by its diagnostic threshold of proteinuria and associated tetrad.

   Proteinuria >3.5 g/1.73m2/day, plus hypoalbuminemia (<3 g/dL), edema, and hyperlipidemia. Lipiduria (oval fat bodies, fatty casts) is commonly seen.

2. What is the most common cause of nephrotic syndrome in adults, and its classic histology?

   Focal segmental glomerulosclerosis (FSGS) is now the leading cause; light microscopy shows focal (some glomeruli) and segmental (part of tuft) sclerosis, with foot process effacement on EM.

3. Which nephrotic disease is associated with anti-PLA2R antibodies, and what is its EM finding?

   Membranous nephropathy. Anti-PLA2R antibodies are positive in ~70% of primary cases. EM shows subepithelial immune deposits with 'spikes' on silver stain; granular IgG/C3 on IF.

4. In nephrotic syndrome, what causes the hypercoagulable state and which vein thrombosis is classically linked to membranous nephropathy?

   Urinary loss of antithrombin III (and other anticoagulants) plus increased fibrinogen causes hypercoagulability. Renal vein thrombosis is classically associated with membranous nephropathy.

5. Differentiate the histology and steroid response of minimal change disease vs FSGS.

   MCD: normal LM, no IF deposits, diffuse foot process effacement on EM; highly steroid-responsive (esp. in children). FSGS: focal segmental sclerosis on LM; often steroid-resistant with higher progression to ESRD.

6. Define nephritic syndrome and list its core features.

   Glomerular inflammation producing hematuria with dysmorphic RBCs/RBC casts, sub-nephrotic proteinuria, hypertension, oliguria, and azotemia (reduced GFR).

7. What defines rapidly progressive glomerulonephritis (RPGN) histologically and clinically?

   Clinically: rapid loss of renal function (days to weeks). Histologically: crescents (extracapillary proliferation) in >50% of glomeruli.

8. Classify the three immunofluorescence patterns of RPGN with an example of each.

   Type I: linear (anti-GBM disease/Goodpasture). Type II: granular (immune complex, e.g., post-strep GN, lupus, IgA). Type III: pauci-immune (ANCA-associated vasculitis, e.g., GPA, MPA).

9. What serologic and clinical features characterize anti-GBM (Goodpasture) disease?

   Anti-GBM antibodies against the alpha-3 chain of type IV collagen; linear IgG on IF; presents with RPGN plus pulmonary hemorrhage. Treated with plasmapheresis, steroids, cyclophosphamide.

10. Distinguish c-ANCA vs p-ANCA associations in pauci-immune vasculitis.

    c-ANCA (anti-PR3) — granulomatosis with polyangiitis (GPA). p-ANCA (anti-MPO) — microscopic polyangiitis (MPA) and eosinophilic GPA (Churg-Strauss).

11. Describe IgA nephropathy's classic presentation and IF finding.

    Episodic gross hematuria 1-2 days after an upper respiratory/mucosal infection (synpharyngitic), most common GN worldwide. IF shows mesangial IgA deposition.

12. What are the typical complement and timing features of post-streptococcal glomerulonephritis?

    Occurs 1-3 weeks after group A strep pharyngitis (or 3-6 weeks after skin infection); low C3 (normalizes in 6-8 weeks); subepithelial 'humps' on EM; granular IgG/C3 IF.

13. List the 6 ISN/RPS classes of lupus nephritis and identify the most common/severe.

    I minimal mesangial, II mesangial proliferative, III focal, IV diffuse (most common and most severe), V membranous, VI advanced sclerosing. Class IV needs aggressive immunosuppression.

14. What is the characteristic finding and significance of a 'full-house' immunofluorescence pattern?

    Deposition of IgG, IgA, IgM, C3, and C1q together — characteristic of lupus nephritis. 'Wire-loop' lesions (subendothelial deposits) are seen in proliferative classes.

15. Name a secondary glomerulonephritis caused by hepatitis C and its typical pattern.

    Hepatitis C causes membranoproliferative GN (MPGN), often with mixed cryoglobulinemia; presents with low C3/C4, hematuria, proteinuria, and a tram-track GBM appearance.

16. State the KDIGO definition of acute kidney injury (AKI).

    Increase in serum creatinine >=0.3 mg/dL within 48 h; OR >=1.5x baseline within 7 days; OR urine output <0.5 mL/kg/h for 6 hours.

17. List the three etiologic categories of AKI with one example each.

    Prerenal (hypovolemia, sepsis), intrinsic/renal (ATN, AIN, glomerulonephritis), and postrenal (obstruction, e.g., BPH, stones).

18. How do FENa and urine osmolality help distinguish prerenal AKI from ATN?

    Prerenal: FENa <1%, urine osm >500, BUN:Cr >20:1, bland sediment. ATN: FENa >2%, urine osm <350 (isosthenuric), BUN:Cr ~10-15:1, muddy brown casts.

19. Give the formula for fractional excretion of sodium (FENa).

    FENa = (Urine Na x Plasma Cr) / (Plasma Na x Urine Cr) x 100. Use FEUrea (<35% prerenal) if the patient is on diuretics.

20. What is the hallmark urinary finding and cause of ischemic/nephrotoxic acute tubular necrosis?

    Muddy brown granular casts and renal tubular epithelial cell casts. Caused by ischemia (prolonged prerenal) or nephrotoxins (aminoglycosides, contrast, myoglobin, cisplatin).

21. Describe the classic triad of acute interstitial nephritis (AIN) and its key urinary finding.

    Triad: fever, rash, eosinophilia (full triad in <10%). Urinary eosinophils and WBC casts; commonly drug-induced (NSAIDs, beta-lactams, PPIs, allopurinol). Treat by stopping the drug +/- steroids.

22. What distinguishes the three phases of recovery in ATN?

    Initiation (injury), maintenance (oliguria, peak azotemia, complications), and recovery/polyuric phase (tubular regeneration with diuresis and risk of hypokalemia/volume depletion).

23. List the urgent indications (AEIOU) for renal replacement therapy in AKI.

    A - Acidosis (refractory metabolic), E - Electrolytes (refractory hyperkalemia), I - Intoxications (dialyzable toxins), O - Overload (refractory volume), U - Uremia (pericarditis, encephalopathy, bleeding).

24. Which toxins are effectively removed by hemodialysis (mnemonic)?

    I-STUMBLE / 'BLAST-ML': Barbiturates, Lithium, Alcohols (methanol, ethylene glycol), Salicylates (Aspirin), Theophylline, Methanol, Lithium. Low molecular weight, low protein binding, low Vd, water-soluble.

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