Chronic Kidney Disease
A Step 2 CK high-yield lesson on chronic kidney disease covering hyperfiltration pathophysiology, KDIGO CGA staging, complications (anemia, CKD-MBD, acidosis, uremia), and guideline management, with board vignettes and next-best-step decisions on RAAS blockade, SGLT2 inhibitors, finerenone, and dialysis indications.
Definition & Pathophysiology
Chronic kidney disease (CKD) is defined by KDIGO as abnormal kidney structure or function present for ≥3 months: either GFR <60 mL/min/1.73 m², or markers of damage (albuminuria ≥30 mg/g, abnormal sediment, electrolyte/histologic/structural abnormalities, or a kidney transplant).
The final common pathway is nephron loss. As nephrons drop out, survivors compensate by hyperfiltration: efferent arteriolar constriction by angiotensin II raises intraglomerular pressure. This adaptation is initially protective but ultimately drives glomerulosclerosis, proteinuria, and further nephron loss — a self-perpetuating cycle. This is exactly why RAAS blockade (dilating the efferent arteriole, lowering intraglomerular pressure) slows progression.
Leading causes on boards: diabetes mellitus (#1), hypertension (#2), glomerulonephritis, and ADPKD. Diabetes and HTN together account for roughly two-thirds of ESRD.
- Diagnose/stage with eGFR (creatinine ± cystatin C) plus urine albumin-to-creatinine ratio (ACR) — stage by BOTH (CGA: Cause, GFR, Albuminuria).
- G1–G2 (GFR ≥60) counts as CKD only if a damage marker (e.g., albuminuria) is present.
- Chronicity clues: bilateral small, echogenic kidneys on ultrasound, normocytic anemia, CKD-MBD, broad waxy casts, and a stably elevated baseline creatinine.
- Normal/large kidneys despite CKD: diabetic nephropathy, ADPKD, HIV-associated nephropathy, amyloidosis, obstruction — an enlarged kidney does not exclude chronicity.
- Biopsy is usually avoided once kidneys are small/scarred (bleeding risk, and it won't change management).
- Always confirm chronic vs. acute — compare to prior labs before labeling.
KDIGO Staging (GFR + Albuminuria)
| GFR category | eGFR (mL/min/1.73 m²) | Term |
|---|---|---|
| G1 | ≥90 | Normal/high\* |
| G2 | 60–89 | Mildly decreased\* |
| G3a | 45–59 | Mildly–moderately decreased |
| G3b | 30–44 | Moderately–severely decreased |
| G4 | 15–29 | Severely decreased |
| G5 | <15 | Kidney failure (ESRD) |
AKI vs. CKD — Distinguishing Features
| Feature | AKI | CKD |
|---|---|---|
| Baseline Cr | Acute rise from normal | Chronically elevated |
| Kidney size (US) | Normal/enlarged | Small, echogenic (usually) |
| Anemia | Absent (unless other cause) | Present (normocytic, ↓EPO) |
| CKD-MBD (↑PO₄, ↓Ca, ↑PTH) | Absent | Present |
| Urine output | Often oliguric | Variable, often preserved |
| Reversibility | Often reversible | Irreversible |
- Anemia: normocytic, normochromic from ↓erythropoietin (± iron deficiency). Replete iron first, then start an ESA; do not target Hgb >11.5 g/dL (stroke/thrombosis risk).
- CKD-MBD: ↓renal 1-α-hydroxylase → ↓calcitriol plus phosphate retention → ↓Ca²⁺ → secondary hyperparathyroidism → renal osteodystrophy. FGF-23 rises earliest (before overt ↑PO₄ or ↑PTH).
- Metabolic acidosis: normal-AG early → high-AG later; treat with oral sodium bicarbonate (goal HCO₃⁻ ≥22).
- Hyperkalemia and volume overload/HTN.
- Uremia: pericarditis, encephalopathy/asterixis, platelet dysfunction → bleeding (treat bleeding with DDAVP), nausea, pruritus.
CKD-MBD: Secondary vs. Tertiary Hyperparathyroidism
| Lab | Secondary (CKD) | Tertiary |
|---|---|---|
| Calcium | Low–normal | High |
| Phosphate | High | High |
| PTH | High | Very high |
| Calcitriol (1,25-D) | Low | Low |
| Glands | Reactive to ↓Ca/↓vitD/↑PO₄ | Autonomous after chronic 2° |
Vignette: A 58-year-old man with 12-year T2DM has BP 148/88. Labs: eGFR 52, urine ACR 320 mg/g, K⁺ 4.4; he takes metformin.
Dx: Diabetic kidney disease — CKD G3a, A3.
Next best steps (progression-slowing quartet):
- Start an ACE inhibitor or ARB (albuminuria + HTN); recheck Cr/K⁺ in 1–2 weeks — a ≤30% creatinine rise that then stabilizes is acceptable.
- Add an SGLT2 inhibitor (e.g., dapagliflozin) — slows CKD progression in diabetic and nondiabetic CKD.
- Add finerenone (nonsteroidal MRA) for residual albuminuria in T2DM.
- BP <130/80 (KDIGO suggests SBP <120 by standardized measurement); statin; glycemic control.
Do NOT combine ACEi + ARB (↑hyperkalemia/AKI, no added benefit).
Vignette: A 63-year-old woman with CKD G5 (eGFR 9) has pleuritic chest pain worse when supine. Exam: pericardial friction rub and elevated JVP; the ECG lacks the diffuse ST-elevation/PR-depression of typical viral pericarditis (a classic uremic clue), and troponin is normal.
Dx: Uremic pericarditis.
Next best step: Urgent hemodialysis — uremic pericarditis is an absolute indication for dialysis (typically run heparin-free to avoid hemorrhagic effusion; NSAIDs/steroids are not first-line here). Watch for tamponade.
Other absolute indications: refractory hyperkalemia, refractory metabolic acidosis, diuretic-resistant volume overload/pulmonary edema, uremic encephalopathy, and select intoxications. Note: the trigger is a complication, not a fixed eGFR number.
AEIOU — the classic trigger to "pull the trigger" on dialysis:
- A — Acidosis (severe, refractory metabolic acidosis)
- E — Electrolytes (refractory hyperkalemia)
- I — Intoxications (methanol, ethylene glycol, salicylates, lithium)
- O — Overload (fluid/pulmonary edema, diuretic-resistant)
- U — Uremia (pericarditis, encephalopathy, bleeding)
A true board classic — reach for it whenever a CKD/ESRD vignette lists one of these findings.
- Slow progression: RAAS blockade (ACEi/ARB) if albuminuria/diabetes; SGLT2 inhibitor; BP <130/80; glycemic control; avoid nephrotoxins (NSAIDs, iodinated contrast, aminoglycosides).
- Treat complications: phosphate binders + vitamin D/cinacalcet (CKD-MBD); oral bicarbonate (acidosis); iron + ESA (anemia — start ESA when Hgb <10, cap ~11.5); K⁺ binders/diet (hyperkalemia).
- CVD risk: statin (cardiovascular disease is the leading cause of death in CKD); vaccinate (hepatitis B, pneumococcal, influenza).
- Prepare for RRT at G4–G5: education, early AV fistula before hemodialysis, transplant evaluation.
- Refer to nephrology for eGFR <30, rapidly declining GFR, or A3 albuminuria.
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