Acute Kidney Injury & CKD for NEET PG — Complete Guide 2026

Version 1.0 — Published February 2026

Acute kidney injury (AKI) and chronic kidney disease (CKD) are disorders of renal function with distinct definitions but overlapping management principles — and together they represent one of the highest-weighted nephrology topics in NEET PG. The student who masters KDIGO criteria, urinary indices, and dialysis indications has covered the foundation for 3–4 marks across papers. Pair this guide with daily MCQ practice on the Medicine subject hub and cross-reference the high-yield medicine topics overview for how nephrology intersects with the rest of internal medicine.

Definition of AKI — KDIGO criteria

Acute kidney injury is an abrupt decline in kidney function defined by either a rise in serum creatinine or a drop in urine output over hours to days.

KDIGO 2012 criteria (any one):

• Rise in serum creatinine by >=0.3 mg/dL within 48 hours
• Rise in serum creatinine to >=1.5 times baseline within the prior 7 days
• Urine output <0.5 mL/kg/hr for at least 6 hours

KDIGO AKI staging:

NEET PG trap: Serum creatinine is insensitive in early AKI — GFR can fall by 50% before creatinine rises detectably. Novel biomarkers (NGAL, KIM-1, IL-18) detect AKI earlier but are not yet standard of care.

Pre-renal vs renal vs post-renal classification remains the clinically useful framework for diagnosis and initial management.

Pre-renal AKI

Pre-renal AKI is reduced kidney perfusion with intact tubular function, and it is the most common cause of community-acquired AKI (70% of cases).

Causes:

• True hypovolemia: Hemorrhage, GI losses (vomiting, diarrhea), burns, diuretics
• Effective hypovolemia: Heart failure, cirrhosis, sepsis (early), nephrotic syndrome
• Renal vasoconstriction: NSAIDs (afferent), ACE inhibitors/ARBs (efferent), radiocontrast, hepatorenal syndrome
• Large vessel occlusion: Renal artery stenosis, thromboembolism

Why ACE inhibitors cause pre-renal AKI: In bilateral renal artery stenosis (or single kidney with RAS), angiotensin II-mediated efferent vasoconstriction maintains GFR. Blocking this with ACEi drops GFR precipitously. A >30% creatinine rise within 7 days of starting ACEi flags RAS.

Why NSAIDs cause pre-renal AKI: Prostaglandins maintain afferent arteriole vasodilation in low-perfusion states. NSAIDs block COX-1/COX-2, removing this safety net. Risk is highest in elderly, dehydrated, CKD, and cirrhotic patients.

Management: Restore volume (isotonic crystalloid), discontinue offending drugs, treat underlying cause. Reversible if addressed early.

Intrinsic AKI

Intrinsic AKI is direct injury to kidney parenchyma — tubules, interstitium, glomeruli, or vessels — and is further classified by anatomic site.

Acute tubular necrosis (ATN)

ATN is the most common cause of intrinsic AKI (45%), caused by ischemia or nephrotoxins that damage tubular epithelial cells.

Ischemic ATN: Prolonged pre-renal insult (shock, hypotension) that progresses beyond functional decline to tubular cell death.

Nephrotoxic ATN:

• Exogenous: Aminoglycosides (accumulate in PCT), amphotericin B, cisplatin, iodinated contrast
• Endogenous: Myoglobin (rhabdomyolysis — crush injury, seizure, statin), hemoglobin (intravascular hemolysis), uric acid (tumor lysis syndrome), myeloma light chains

Urinary finding: Muddy brown granular casts (pathognomonic) + renal tubular epithelial cell casts.

Three phases:

1. Initiation (hours to days): injury occurs
2. Maintenance (1–2 weeks): oliguria, rising creatinine
3. Recovery (days to weeks): polyuric phase with electrolyte losses

Acute glomerulonephritis

Glomerulonephritis is inflammation of glomeruli presenting with hematuria, proteinuria, hypertension, and AKI (nephritic syndrome).

Urinary finding: Red blood cell casts + dysmorphic RBCs + sub-nephrotic-range proteinuria.

NEET PG classifications:

• Low complement (C3): Post-streptococcal GN, membranoproliferative GN (MPGN), lupus nephritis, cryoglobulinemia, infective endocarditis
• Normal complement: IgA nephropathy (Berger disease — most common GN worldwide), ANCA-associated vasculitis, anti-GBM disease (Goodpasture)
• Rapidly progressive GN (crescentic): Anti-GBM (type I), immune-complex (type II), pauci-immune/ANCA (type III)

Acute interstitial nephritis (AIN)

AIN is allergic/inflammatory infiltration of the interstitium, caused by drugs in 70% of cases.

Classic trio: Fever + rash + eosinophilia (only 10% have all three).

Drugs:

• Antibiotics: Beta-lactams (methicillin, penicillin), cephalosporins, rifampin, sulfas, ciprofloxacin
• NSAIDs: Any class
• PPIs: Omeprazole, pantoprazole
• Diuretics: Thiazides, furosemide

Urinary finding: WBC casts, eosinophiluria (Hansel stain), sterile pyuria.

Treatment: Discontinue offending drug. Steroids if no response in 7 days.

Post-renal AKI

Post-renal AKI is obstruction of urine flow anywhere from the renal pelvis to the urethra. Bilateral obstruction (or unilateral in a single kidney) is required for AKI.

Causes:

• Bladder outlet: BPH (most common cause in elderly men), prostate cancer, urethral stricture
• Bilateral ureteral: Retroperitoneal fibrosis, pelvic malignancy (cervical, prostatic), stones (bilateral or solitary kidney)
• Intratubular: Uric acid crystals (tumor lysis), acyclovir crystals, sulfa crystals, myeloma casts

Diagnosis: Renal ultrasound showing hydronephrosis (sensitivity 90%). Absent hydronephrosis does not rule out obstruction in early or retroperitoneal fibrosis cases.

Management: Relieve obstruction — Foley catheter for BPH, percutaneous nephrostomy or ureteral stent for ureteral obstruction.

Urinary indices — differentiating AKI causes

Urinary indices are laboratory parameters used to differentiate pre-renal from intrinsic AKI, especially ATN — and they are a high-yield NEET PG calculation.

Fractional excretion of sodium (FeNa) formula:

FeNa = (Urine Na x Plasma Cr) / (Plasma Na x Urine Cr) x 100

Exceptions (pre-renal with FeNa >1%): Diuretic use, CKD baseline, adrenal insufficiency. Use FeUrea instead.

Exceptions (ATN with FeNa <1%): Contrast nephropathy, rhabdomyolysis, early sepsis-induced AKI, hepatorenal syndrome. These are "ATN mimics" with pre-renal indices.

CKD staging

Chronic kidney disease is structural or functional kidney abnormality present for >=3 months, staged by eGFR and albuminuria.

eGFR staging (KDIGO 2012):

Albuminuria staging:

• A1: <30 mg/g (normal to mildly increased)
• A2: 30–300 mg/g (moderately increased — previously microalbuminuria)
• A3: >300 mg/g (severely increased — previously macroalbuminuria)

eGFR formulas:

• CKD-EPI 2021 (race-free, preferred) — most accurate
• MDRD (older, uses creatinine + age + sex + race)
• Cockcroft-Gault (uses creatinine + age + weight + sex) — for drug dosing

Top causes of CKD in India:

1. Diabetic nephropathy (35–40%)
2. Hypertensive nephrosclerosis (20–25%)
3. Chronic glomerulonephritis (10–15%)
4. Chronic interstitial nephritis / obstructive uropathy (10–15%)
5. Polycystic kidney disease (5%)

Dialysis indications — AEIOU

Emergency dialysis is indicated when uremia or its complications become life-threatening, independent of absolute creatinine value.

AEIOU mnemonic:

• A — Acidosis (metabolic, pH <7.1, refractory to bicarbonate)
• E — Electrolyte disturbance (refractory hyperkalemia >6.5 mEq/L with ECG changes, severe hypercalcemia, hyponatremia)
• I — Ingestions (dialyzable toxins — mnemonic SLIME: Salicylates, Lithium, Isopropanol, Methanol/ethylene glycol, metformin-induced lactic acidosis)
• O — Overload (pulmonary edema refractory to diuretics)
• U — Uremia (pericarditis, encephalopathy, uremic bleeding — symptomatic uremia, not just high BUN)

Non-emergent initiation in CKD: Plan at eGFR <=15–10 mL/min/1.73 m² OR onset of uremic symptoms (nausea, anorexia, fatigue, pruritus). IDEAL trial showed no mortality benefit of early (eGFR 10–14) versus late (eGFR 5–7) start.

Drugs that are dialyzable (SMALL MDMA): Small size (<500 Da), low protein binding, low volume of distribution. Examples: lithium, methanol, ethylene glycol, salicylates, phenobarbital, atenolol.

Drugs NOT dialyzable: Digoxin (high Vd), tricyclic antidepressants (high protein binding), benzodiazepines, phenytoin.

Renal replacement therapy modalities

RRT is the replacement of kidney function by artificial means, with four principal modalities each suited to specific clinical contexts.

Vascular access:

• Arteriovenous fistula (AVF): First choice, lowest infection risk, best patency. Radiocephalic (snuffbox) > brachiocephalic > brachiobasilic. Requires 6–8 weeks to mature.
• AV graft: PTFE interposition. Matures in 2 weeks but higher infection and thrombosis rates.
• Central venous catheter: Last choice. Highest infection rate (Staphylococcus aureus bacteremia). Tunneled preferred over non-tunneled for long-term use.

Transplant outcomes: 1-year graft survival >95%, 10-year survival 60–70% for living donor, 50–60% for deceased donor. HLA matching at DR locus has highest impact.

Mineral bone disease in CKD (CKD-MBD)

CKD-mineral and bone disorder is a systemic syndrome of biochemical, bone, and vascular abnormalities in CKD — testable on the pharmacology and pathology papers.

Biochemical abnormalities:

1. Phosphate retention — reduced renal excretion when eGFR <30
2. Decreased calcitriol (1,25-OH-vitamin D) — impaired renal 1-alpha-hydroxylation
3. Hypocalcemia — reduced gut absorption (low calcitriol) + phosphate binding
4. Secondary hyperparathyroidism — PTH rises to maintain calcium
5. Increased FGF-23 — phosphaturic hormone, rises earliest (marker of early MBD)

Bone abnormalities:

• Osteitis fibrosa cystica — high-turnover bone disease from hyperparathyroidism (most common pattern)
• Adynamic bone disease — low-turnover, over-suppressed PTH (often from excess calcium or calcitriol)
• Osteomalacia — aluminum toxicity (historical) or severe vitamin D deficiency

Vascular calcification: Accelerated by high calcium-phosphate product. Predicts cardiovascular mortality.

Management:

1. Dietary phosphate restriction — 800–1000 mg/day
2. Phosphate binders:
   • Calcium-based (calcium carbonate, calcium acetate) — first-line; limit to avoid hypercalcemia
   • Non-calcium (sevelamer, lanthanum) — preferred if hypercalcemia or vascular calcification
   • Iron-based (ferric citrate, sucroferric oxyhydroxide) — newer
3. Active vitamin D (calcitriol, paricalcitol) — suppresses PTH
4. Calcimimetics (cinacalcet, etelcalcetide) — activate Ca-sensing receptor, suppress PTH without raising calcium
5. Parathyroidectomy — for refractory severe tertiary hyperparathyroidism

Anemia of CKD

Anemia of CKD is normocytic normochromic anemia resulting primarily from deficient erythropoietin production by failing kidneys.

Pathophysiology (multifactorial):

1. Erythropoietin deficiency — primary cause; EPO is produced by peritubular fibroblasts
2. Iron deficiency — absolute (GI bleeding from uremic platelet dysfunction, phlebotomy losses) or functional (inflammation-mediated iron sequestration via hepcidin)
3. Uremic inhibitors of erythropoiesis
4. Shortened RBC lifespan (90 vs 120 days)
5. Folate deficiency (dialysis loss)

Evaluation:

• Serum ferritin, transferrin saturation (TSAT)
• Reticulocyte count
• B12, folate
• Rule out GI bleeding

Treatment:

1. Iron repletion first — target ferritin >=200 ng/mL and TSAT >=20% (IV iron preferred in HD patients). Give before ESAs.
2. Erythropoiesis-stimulating agents (ESAs) — epoetin-alfa, darbepoetin-alfa. Target Hb 10–11.5 g/dL. DO NOT exceed Hb 13 (increased cardiovascular risk — TREAT, CHOIR, CREATE trials).
3. HIF-PH inhibitors (roxadustat, daprodustat) — oral, stabilize HIF, increase endogenous EPO production. Newer class, increasingly tested.
4. Blood transfusion — symptomatic severe anemia; avoid if possible (sensitizes future transplant recipients).

Sources and references

1. KDIGO Clinical Practice Guideline for Acute Kidney Injury (Kidney International Supplements, 2012) — the definitive global reference for AKI definition, staging, and management.
2. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease (Kidney International Supplements, 2013).
3. Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo et al., 2022) — Chapters on Acute Kidney Injury and Chronic Kidney Disease.
4. Brenner and Rector's The Kidney, 11th Edition (Yu et al., 2019) — comprehensive reference for nephrology pathophysiology.
5. UKPDS and IDEAL trials — landmark evidence for CKD progression and dialysis initiation timing.
6. API Textbook of Medicine, 11th Edition (Munjal et al., 2019) — Indian-context epidemiology and CKD management.

Frequently asked questions

How many AKI/CKD questions appear in NEET PG?

Renal disease contributes 3-4 direct questions per NEET PG paper across medicine, pharmacology, and pathology. KDIGO AKI staging, dialysis indications (AEIOU), and FeNa interpretation are the three most frequently tested subtopics based on 2019-2025 pattern analysis.

What are the KDIGO criteria for AKI?

AKI is defined by any of: rise in serum creatinine by 0.3 mg/dL within 48 hours, rise to 1.5 times baseline within 7 days, or urine output less than 0.5 mL/kg/hr for 6 hours. Staging uses both creatinine (Stage 1 to 3) and urine output criteria, with Stage 3 defined by creatinine 3 times baseline or greater than 4.0 mg/dL or initiation of RRT.

How do I differentiate pre-renal AKI from intrinsic AKI (ATN)?

Pre-renal AKI has FeNa less than 1 percent, urine osmolality greater than 500 mOsm/kg, urine sodium less than 20, BUN to creatinine ratio greater than 20 to 1, and bland urine sediment. Intrinsic AKI (ATN) has FeNa greater than 2 percent, urine osmolality less than 350, urine sodium greater than 40, BUN to creatinine ratio under 15 to 1, and muddy brown granular casts.

What are the AEIOU indications for dialysis?

AEIOU is the mnemonic for emergency dialysis indications: Acidosis (pH less than 7.1 refractory), Electrolytes (refractory hyperkalemia greater than 6.5 with ECG changes), Ingestions (salicylates, lithium, methanol, ethylene glycol, metformin), Overload (volume overload causing pulmonary edema unresponsive to diuretics), Uremia (encephalopathy, pericarditis, bleeding diathesis). Presence of any one is sufficient for urgent RRT.

At what eGFR should dialysis be planned in CKD?

In CKD Stage 5 (eGFR less than 15 mL/min/1.73 m2), dialysis planning should begin. Absolute indication is eGFR less than 6 OR uremic symptoms. The IDEAL trial showed no benefit of starting dialysis early (eGFR 10-14) versus late (eGFR 5-7) — most patients are initiated based on symptoms rather than eGFR alone.

What is the earliest sign of diabetic nephropathy?

Glomerular hyperfiltration with increased eGFR is the earliest functional change. The earliest clinically detectable sign is microalbuminuria (urine albumin 30-300 mg/day or albumin-creatinine ratio 30-300 mg/g). Without intervention, microalbuminuria progresses to overt proteinuria and declining GFR over 5-10 years. ACE inhibitors or ARBs slow this progression.

Why does CKD cause anemia?

CKD causes normocytic normochromic anemia primarily due to reduced erythropoietin production by peritubular fibroblasts of the kidney. Secondary contributors are iron deficiency, uremic suppression of bone marrow, shortened RBC lifespan, and chronic inflammation. Treatment includes iron (target ferritin over 200 ng/mL, TSAT over 20 percent) before erythropoiesis-stimulating agents (target Hb 10-11.5 g/dL).

What is CKD-MBD (mineral bone disease)?

CKD-MBD is the triad of (1) biochemical abnormalities (low calcium, high phosphate, high PTH, low calcitriol, high FGF-23), (2) bone abnormalities (osteitis fibrosa cystica, adynamic bone disease, osteomalacia), and (3) vascular/soft-tissue calcification. Treatment: phosphate binders (sevelamer, lanthanum), active vitamin D (calcitriol), calcimimetics (cinacalcet) for secondary hyperparathyroidism.

Which drugs should be avoided in AKI?

Avoid NSAIDs (decrease afferent arteriole vasodilation), ACE inhibitors and ARBs (decrease efferent vasoconstriction) in pre-renal states, aminoglycosides and amphotericin B (direct ATN), iodinated contrast (contrast-induced nephropathy), and metformin (lactic acidosis risk when eGFR less than 30). Review every drug for renal dose adjustment in AKI and CKD.

What is hepatorenal syndrome?

Hepatorenal syndrome (HRS) is functional AKI in advanced cirrhosis with ascites, characterized by intense renal vasoconstriction in the setting of splanchnic vasodilation. Type 1 HRS is rapidly progressive (creatinine doubling to over 2.5 mg/dL in under 2 weeks); Type 2 is slower. Treatment: terlipressin + albumin; definitive therapy is liver transplantation.

Ready to test your nephrology knowledge? Convert this guide into exam marks with active MCQ recall — cross-link to the common mistakes in medicine guide for traps and use the AI tutor to drill FeNa calculations and cast identification on demand.

Start practicing nephrology MCQs free →

Explore our pricing plans for unlimited practice across all 19 subjects, AI-powered doubt resolution, and personalized study plans.

---

Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: February 2026

This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.