NEET SS Nephrology (DM) Syllabus

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.

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).

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).

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.

Does continuous (CRRT) vs intermittent hemodialysis improve survival in AKI, and when is CRRT preferred?

No proven mortality difference. CRRT is preferred in hemodynamically unstable patients (e.g., shock, pressors) because of gentler, continuous fluid/solute removal.

Give the staging of CKD by GFR (G1-G5).

G1 >=90 (with damage), G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15 (kidney failure). All require markers of kidney damage if GFR >=60.

How is albuminuria categorized in CKD (A1-A3)?

A1 <30 mg/g (normal-mild), A2 30-300 mg/g (moderate), A3 >300 mg/g (severe). Combined with GFR (G) staging in the KDIGO heat map for risk prognosis.

What are the key drivers of CKD progression and the cornerstone interventions to slow it?

Drivers: hypertension, proteinuria, diabetes, glomerular hyperfiltration. Interventions: RAAS blockade (ACEi/ARB), SGLT2 inhibitors, BP and glycemic control, and dietary sodium/protein moderation.

Describe the pathophysiology of CKD-mineral bone disorder (CKD-MBD).

Decreased phosphate excretion and reduced 1,25-(OH)2 vitamin D cause hyperphosphatemia, hypocalcemia, elevated FGF-23 and PTH (secondary hyperparathyroidism), leading to renal osteodystrophy.

What is the principle of solute clearance in hemodialysis and how does it differ from convection?

Diffusion: solutes move across a semipermeable membrane down a concentration gradient (efficient for small molecules). Convection (ultrafiltration/hemofiltration): solvent drag clears larger 'middle' molecules via a pressure gradient.

What is the preferred long-term hemodialysis vascular access and why?

Native arteriovenous (AV) fistula — lowest rates of infection and thrombosis and best long-term patency. Order of preference: fistula > graft > tunneled catheter (highest infection risk).

Define dialysis adequacy targets using Kt/V and URR.

Single-pool Kt/V >=1.2 per session (target ~1.4) and urea reduction ratio (URR) >=65% for thrice-weekly hemodialysis.

What is dialysis disequilibrium syndrome and how is it prevented?

Cerebral edema from rapid urea removal causing an osmotic gradient (water shifts into brain); presents with headache, nausea, seizures. Prevented by slow, shorter initial dialysis sessions in new/severely uremic patients.

Explain the mechanism of fluid and solute removal in peritoneal dialysis.

The peritoneal membrane acts as the dialyzer; solutes diffuse into dialysate, and water is removed by an osmotic gradient created by dextrose (or icodextrin) in the dialysate.

What is the most common serious complication of peritoneal dialysis and its diagnostic criteria?

PD peritonitis. Diagnosis requires 2 of 3: cloudy effluent with WBC >100/uL (>=50% neutrophils), abdominal pain, and positive dialysate culture. Most often gram-positive (Staph). Treat with intraperitoneal antibiotics.

Compare hemodialysis and peritoneal dialysis on hemodynamic stability and patient autonomy.

PD: continuous/gentle (better hemodynamic stability), home-based with greater autonomy, no anticoagulation needed. HD: intermittent (more rapid shifts/hypotension), usually center-based, requires vascular access and anticoagulation.

What is the role of the peritoneal equilibration test (PET) in PD?

PET classifies transport status (high, high-average, low-average, low) by measuring dialysate-to-plasma creatinine ratio over a dwell. High transporters absorb glucose fast (poor ultrafiltration) and suit short, frequent dwells (APD).

Give the formula and correction for serum sodium in hyperglycemia.

Corrected Na = measured Na + 1.6 (or 2.4) x [(glucose - 100)/100]. Hyperglycemia draws water into the extracellular space, causing dilutional (translocational) hyponatremia.

Outline the diagnostic approach to hyponatremia by volume status.

First check serum osmolality (true hypotonic hyponatremia), then volume: Hypovolemic (UNa <20 GI/skin loss, >20 renal loss), Euvolemic (SIADH, hypothyroid, adrenal insufficiency), Hypervolemic (CHF, cirrhosis, nephrotic - low UNa).

What is the maximum safe correction rate for chronic hyponatremia and the risk of overcorrection?

Correct <8-10 mEq/L per 24 h (some say 6-8). Overly rapid correction causes osmotic demyelination syndrome (central pontine myelinolysis).

List ECG changes of hyperkalemia in order of progression and the first-line membrane-stabilizing treatment.

Peaked T waves -> prolonged PR -> widened QRS -> loss of P waves -> sine wave -> arrest. First give IV calcium gluconate (stabilizes myocardium); then insulin+glucose, beta-agonists shift K+; loop diuretics/K-binders/dialysis remove it.

Differentiate the urinary potassium response in renal vs extrarenal hypokalemia.

Urine K+ <20 mEq/day (or low TTKG) suggests extrarenal loss (GI/diarrhea). Urine K+ >20 indicates renal wasting (diuretics, hyperaldosteronism, Bartter/Gitelman, RTA).

How do calcium and magnesium disorders interrelate, and what is a classic feature of hypocalcemia?

Hypomagnesemia impairs PTH secretion/action causing refractory hypocalcemia (must correct Mg first). Hypocalcemia features: tetany, Chvostek and Trousseau signs, prolonged QT, perioral paresthesia.

State the Winter's formula and what it assesses.

Expected PaCO2 = 1.5 x [HCO3-] + 8 (+/- 2). It checks for appropriate respiratory compensation in metabolic acidosis; a measured PaCO2 above range means concurrent respiratory acidosis, below means respiratory alkalosis.

How do you calculate and interpret the anion gap, and what does an elevated gap with normal delta ratio indicate?

AG = Na - (Cl + HCO3); normal 8-12. High AG acidosis causes (GOLD MARK): glycols, oxoproline, L/D-lactate, methanol, ASA, renal failure, ketoacidosis. Delta ratio ~1-2 = pure HAGMA; <1 suggests concurrent NAGMA; >2 suggests metabolic alkalosis.

Differentiate type 1 (distal), type 2 (proximal), and type 4 renal tubular acidosis by urine pH and potassium.

Type 1 (distal): cannot acidify urine, urine pH >5.5, hypokalemia, nephrolithiasis. Type 2 (proximal): impaired HCO3 reabsorption, urine pH variable (<5.5 when serum HCO3 low), hypokalemia, Fanconi. Type 4: hypoaldosteronism, hyperkalemia, urine pH <5.5.

Which HLA loci are most important in renal transplant matching, and which is most immunogenic?

HLA-A, -B (class I) and HLA-DR (class II) are matched (6-antigen system). HLA-DR mismatch has the greatest impact on graft survival; minimizing mismatches improves outcomes.

Compare hyperacute, acute, and chronic renal allograft rejection by timing and mechanism.

Hyperacute: minutes-hours, preformed anti-donor antibodies (complement-mediated thrombosis) - now rare with crossmatching. Acute: days-months, T-cell (cellular) or antibody-mediated (donor-specific antibodies). Chronic: months-years, interstitial fibrosis/tubular atrophy and transplant glomerulopathy.

What is the timeline of post-transplant infections (0-1 month, 1-6 months, >6 months)?

0-1 month: nosocomial/surgical, donor-derived, reactivation. 1-6 months: opportunistic (CMV, BK virus, PCP, fungal) when immunosuppression peaks. >6 months: community-acquired infections, late CMV/BK, malignancy (PTLD).

Describe BK virus nephropathy and CMV disease in transplant recipients and their key management step.

BK polyomavirus nephropathy: rising creatinine, decoy cells in urine, 'owl-eye' tubular inclusions; managed by reducing immunosuppression. CMV: fever, leukopenia, organ involvement; managed with ganciclovir/valganciclovir and reduced immunosuppression. Note: PTLD is linked to EBV.