PA27.3-4 | Acute & Chronic Renal Failure — Summary & Reflection

REFLECT

Consider the following clinical vignette:

A 45-year-old man with hypertension and type 2 diabetes for 12 years is seen in outpatients. His creatinine was 1.2 mg/dL three years ago, 1.9 mg/dL one year ago, and today is 2.8 mg/dL. Urine albumin-to-creatinine ratio is 420 mg/g. He has been on metformin, amlodipine, and atorvastatin but NO ACE inhibitor or ARB.

1. Calculate his approximate GFR category using the CKD-EPI equation (assume he is a 45-year-old; GFR ≈ 60–75 × [1.142 for male] × [0.993^age] correction — or use clinical estimation: GFR roughly inversely proportional to creatinine). Which KDIGO stage is he in?

1. What two pharmacological interventions have the strongest evidence to slow progression of CKD in this patient, and what is the pathophysiological mechanism by which each works?

1. He asks you: 'Doctor, will my kidneys get better?' What is the truthful but empathetic response, and what endpoints (urine protein, BP targets) should you aim for in follow-up?

1. At what GFR should you typically refer this patient to a nephrologist for transplant listing? What is the advantage of pre-emptive transplantation over starting dialysis first?

Discuss your reasoning with a partner or write it out before the next session.

KEY TAKEAWAYS

Core take-aways from this module:

AKI Framework:
- AKI = rapid ↑creatinine (≥0.3 mg/dL/48h) + oliguria. Classified as prerenal, intrinsic (ATN commonest), or postrenal.
- Prerenal: FENa <1%, urine Na <20, urine Osm >500 — tubules intact, reversible with fluid resuscitation.
- ATN: FENa >2%, urine Na >40, urine Osm ~300 — tubules necrotic; 4 phases: initiation → oliguric → diuretic (hypokalaemia risk) → late recovery.
- Complications: hyperkalaemia, metabolic acidosis, fluid overload, uraemia; AEIOU = dialysis indications.

CKD Framework:
- CKD = ≥3 months GFR/structural abnormality. Main causes: DM, HTN, glomerulonephritis, PKD, obstruction.
- G1–G5 staging. End-stage = bilateral small contracted granular kidneys, glomerulosclerosis, tubular atrophy, fibrosis.
- Progression driven by hyperfiltration and RAAS; ACEi/ARBs are the cornerstone of slowing progression.

Uraemia Complications (ACARD mnemonic):
- Anaemia (↓EPO), Cardiovascular (LVH, pericarditis), Acidosis + electrolytes, Renal osteodystrophy (↓VitD → ↑PTH → ↑PO₄ → ↓Ca), Death (if untreated) → RRT/transplant.

AKI vs CKD: Small kidneys + severe anaemia + ↑PTH = CKD. Normal/large kidneys + acute precipitant = AKI.