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PA27.3-4 | Acute & Chronic Renal Failure — SDL Guide (Part 2)

Phases of ATN

Phases of Acute Tubular Necrosis

ATN progresses through four stereotyped phases. Recognising which phase a patient is in guides clinical management.

Phase 1 — Initiation (hours to 1–2 days): The injurious event (ischaemia or toxin) begins. GFR starts to fall but may not yet be clinically apparent. Prompt correction of ischaemia here can prevent full ATN.

Phase 2 — Maintenance/Oliguric phase (typically 10–14 days): GFR severely reduced. Oliguria (<400 mL/day) or even anuria. BUN and creatinine rise steadily. This is the phase of greatest metabolic derangement: hyperkalaemia, metabolic acidosis, fluid overload, uraemia. Management is supportive ± dialysis. Renal biopsy (if done) shows peak tubular necrosis.

Phase 3 — Early recovery/Diuretic phase: Tubular epithelium regenerates (tubular cells have high regenerative capacity). GFR begins to recover. A polyuric phase may follow — urine output rises steeply (2–3 L/day). The regenerating tubules are functionally immature: cannot yet concentrate urine or reabsorb electrolytes → hypokalaemia and hyponatraemia can occur paradoxically. Monitor electrolytes closely.

Phase 4 — Late recovery: Complete tubular repair. GFR returns to near-baseline over weeks to months. Some patients with severe or repeated ATN develop residual CKD.

Four Phases of Acute Tubular Necrosis

Complications of AKI

Complications of Acute Kidney Injury

The oliguric phase of AKI generates life-threatening metabolic derangements that require urgent recognition:

1. Hyperkalaemia — ↓GFR + acidosis (H⁺/K⁺ exchange pushes K⁺ out of cells). Serum K⁺ >6.5 mmol/L → cardiac arrhythmia risk (peaked T waves → widened QRS → VF). Indication for emergency dialysis.

2. Metabolic acidosis — kidneys cannot excrete H⁺ or regenerate HCO₃⁻. High anion-gap metabolic acidosis (phosphates, sulphates accumulate). Worsens hyperkalaemia and myocardial function.

3. Fluid overload — oliguria + continued fluid intake → pulmonary oedema, hypertension, hyponatraemia (dilutional).

4. Uraemic syndrome — accumulation of urea and other nitrogenous waste products: nausea, vomiting, encephalopathy, asterixis, pericarditis (serofibrinous; 'bread-and-butter' appearance), bleeding tendency (platelet dysfunction), pruritus.

5. Anaemia — shortened red-cell survival + ↓EPO production (early in AKI, prominent in CKD).

6. Hyperphosphataemia and hypocalcaemia — impaired phosphate excretion → ↑PO₄³⁻ → complexes Ca²⁺ → ↓iCa²⁺ → tetany risk.

Remember the acronym AEIOU for dialysis indications in AKI: Acidosis (pH <7.1), Electrolytes (refractory hyperkalaemia), Intoxication (dialysable toxins), Overload (pulmonary oedema refractory to diuretics), Uraemia (encephalopathy/pericarditis/bleeding).

Chronic Kidney Disease — Definition, Causes, and Staging

Chronic Kidney Disease: Definition, Causes, and GFR Staging

Chronic kidney disease (CKD) is defined by KDIGO as: abnormalities of kidney structure or function (or both) present for ≥3 months with implications for health. This 3-month threshold distinguishes CKD from AKI.

Five major causes (MBBS examination staples):
1. Diabetic nephropathy — global #1 cause (~35–40% in developed nations; ~30% in India). Kimmelstiel-Wilson nodules, diffuse glomerulosclerosis.
2. Hypertensive nephrosclerosis — arteriolar and arterial disease → ischaemic glomerulosclerosis.
3. Chronic glomerulonephritis — post-streptococcal GN, IgA nephropathy, FSGS, membranous nephropathy (late).
4. Polycystic kidney disease (PKD) — autosomal dominant (ADPKD, PKD1/PKD2 mutations); bilateral cysts replace parenchyma.
5. Obstructive uropathy — posterior urethral valves (children), BPH, recurrent stones → chronic back-pressure damage.

KDIGO GFR staging:

Stage	GFR (mL/min/1.73 m²)	Description
G1	≥90	Normal/high GFR with kidney damage markers
G2	60–89	Mildly decreased
G3a	45–59	Mild-moderately decreased
G3b	30–44	Moderate-severely decreased
G4	15–29	Severely decreased
G5	<15	Kidney failure (renal replacement therapy)

Albuminuria category (A1/A2/A3) is overlaid on the GFR stage to risk-stratify — a G3a patient with heavy proteinuria (A3) progresses faster than one without.