Master AKI and CKD for NEET PG 2027: KDIGO criteria, pre-renal vs intrinsic vs post-renal, urinary indices (FeNa), CKD staging, dialysis indications (AEIOU), mineral bone disease, and anemia of CKD.
NEETPGAI EditorialPublished 7 Jan 2026Updated 29 Sept 202615 min read
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
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Comparison of the authorities that shape NEET PG, INI-CET, FMGE, and Indian medical education: NMC (regulator), NBEMS (exam conductor), MCC (AIQ counseling), DGHS (health services), AIIMS (INI-CET), plus state councils and FMG pathway — clarifies who does what.
Intrinsic AKI — ATN (ischemic or nephrotoxic, most common), glomerulonephritis, interstitial nephritis. Muddy brown casts in ATN; RBC casts in GN; WBC casts + eosinophils in AIN
Post-renal AKI — BPH, stones, tumors, retroperitoneal fibrosis. Rule out with ultrasound (hydronephrosis)
Urinary indices — FeNa = (UNa x PCr)/(PNa x UCr) x 100. FeNa <1% pre-renal; >2% ATN. FeUrea if on diuretics (<35% pre-renal)
CKD-MBD — Low Ca, high PO4, high PTH (secondary hyperparathyroidism), high FGF-23, low calcitriol. Treat: phosphate binders, active vitamin D, cinacalcet
Anemia of CKD — Normocytic normochromic, low EPO. Treat: iron first (ferritin >200, TSAT >20%), then ESA (target Hb 10–11.5 g/dL, not >13)
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:
Stage
Serum creatinine
Urine output
Stage 1
1.5–1.9x baseline OR >=0.3 mg/dL rise
<0.5 mL/kg/hr for 6–12 hr
Stage 2
2.0–2.9x baseline
<0.5 mL/kg/hr for >=12 hr
Stage 3
3.0x baseline OR >=4.0 mg/dL OR initiation of RRT
<0.3 mL/kg/hr for >=24 hr OR anuria >=12 hr
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
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.
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
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.
Index
Pre-renal AKI
Intrinsic AKI (ATN)
FeNa
<1%
>2%
FeUrea (if on diuretics)
<35%
>50%
Urine osmolality
>500 mOsm/kg
<350 mOsm/kg
Urine sodium
<20 mEq/L
>40 mEq/L
BUN:creatinine ratio
>20:1
<15:1
Urine specific gravity
>1.020
<1.010 (isosthenuria)
Urinary sediment
Bland; hyaline casts
Muddy brown granular casts
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.
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.
Modality
Mechanism
Best for
Limitations
Intermittent hemodialysis (IHD)
Diffusion across semipermeable membrane, 4-hour sessions 3x/week
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:
Phosphate retention — reduced renal excretion when eGFR <30
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):
Erythropoietin deficiency — primary cause; EPO is produced by peritubular fibroblasts
Iron deficiency — absolute (GI bleeding from uremic platelet dysfunction, phlebotomy losses) or functional (inflammation-mediated iron sequestration via hepcidin)
Uremic inhibitors of erythropoiesis
Shortened RBC lifespan (90 vs 120 days)
Folate deficiency (dialysis loss)
Evaluation:
Serum ferritin, transferrin saturation (TSAT)
Reticulocyte count
B12, folate
Rule out GI bleeding
Treatment:
Iron repletion first — target ferritin >=200 ng/mL and TSAT >=20% (IV iron preferred in HD patients). Give before ESAs.
Blood transfusion — symptomatic severe anemia; avoid if possible (sensitizes future transplant recipients).
Sources and references
KDIGO Clinical Practice Guideline for Acute Kidney Injury (Kidney International Supplements, 2012) — the definitive global reference for AKI definition, staging, and management.
KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease (Kidney International Supplements, 2013).
Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo et al., 2022) — Chapters on Acute Kidney Injury and Chronic Kidney Disease.
Brenner and Rector's The Kidney, 11th Edition (Yu et al., 2019) — comprehensive reference for nephrology pathophysiology.
UKPDS and IDEAL trials — landmark evidence for CKD progression and dialysis initiation timing.
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.
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
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.
