4.4 Acute Kidney Injury (AKI), Chronic Kidney Disease (CKD), & Nephrology
Key Takeaways
KDIGO criteria define AKI by a serum creatinine increase ≥ 26.5 µmol/L in 48h, a creatinine increase ≥ 1.5x baseline within 7 days, or urine output < 0.5 mL/kg/h for 6 hours.
Prerenal AKI features FENa < 1% (FeUrea < 35% on diuretics), urine Na < 20 mmol/L, and hyaline casts; Intrinsic ATN features FENa > 2%, urine Na > 40 mmol/L, and muddy brown granular casts.
Nephrotic syndrome presents with heavy proteinuria (> 3.5 g/day or UACR > 220 mg/mmol), hypoalbuminemia (< 30 g/L), edema, and hyperlipidemia; Nephritic syndrome presents with dysmorphic RBCs, RBC casts, hypertension, oliguria, and mild-moderate proteinuria.
CKD management focuses on delaying progression using ACE inhibitors or ARBs for proteinuria (UACR > 3.0 mg/mmol) and SGLT2 inhibitors (empagliflozin, dapagliflozin) for eGFR ≥ 20 mL/min/1.73m² regardless of diabetes status.
Urgent hemodialysis indications follow the AEIOU mnemonic: Acidosis (pH < 7.10), Electrolytes (refractory K+ > 6.5 mmol/L), Intoxications (SLIME), Overload (refractory pulmonary edema), Uremia (encephalopathy, pericarditis, bleeding).
4.4 Acute Kidney Injury (AKI), Chronic Kidney Disease (CKD), & Nephrology
KDIGO Staging & Etiology Differentiation of AKI
According to KDIGO (Kidney Disease: Improving Global Outcomes) guidelines, Acute Kidney Injury (AKI) is defined by meeting any of the following:
- Increase in serum creatinine by ≥ 26.5 µmol/L within 48 hours.
- Increase in serum creatinine to ≥ 1.5 times baseline within 7 days.
- Urine volume < 0.5 mL/kg/h for 6 consecutive hours.
KDIGO AKI Staging Grid
| Stage | Serum Creatinine Threshold | Urine Output Threshold |
|---|---|---|
| Stage 1 | 1.5 – 1.9x baseline OR increase ≥ 26.5 µmol/L | < 0.5 mL/kg/h for 6 – 12 hours |
| Stage 2 | 2.0 – 2.9x baseline | < 0.5 mL/kg/h for ≥ 12 hours |
| Stage 3 | 3.0x baseline OR creatinine ≥ 353.6 µmol/L OR initiation of RRT | < 0.3 mL/kg/h for ≥ 24 hours OR Anuria for ≥ 12 hours |
Etiological Classification & Diagnostic Indices
| Feature | Prerenal AKI | Intrinsic AKI (ATN) | Intrinsic AKI (AIN) | Postrenal AKI |
|---|---|---|---|---|
| Primary Cause | Hypovolemia, HF, Sepsis, ACEi/ARB + NSAIDs | Ischemia, Contrast, Aminoglycosides, Rhabdomyolysis | Drug hypersensitivity (PPIs, NSAIDs, Penicillins) | BPH, Prostate Cancer, Bilateral Calculi, Neurogenic Bladder |
| BUN:Cr Ratio | > 80:1 (mmol:mmol) | < 40:1 | < 40:1 | Variable |
| FENa (%) | < 1% (FeUrea < 35%) | > 2% | > 1% | Variable |
| Urine Sodium | < 20 mmol/L | > 40 mmol/L | > 20 mmol/L | Variable |
| Urine Osmolality | > 500 mOsm/kg | < 350 mOsm/kg | Variable | < 350 mOsm/kg |
| Urinalysis / Casts | Hyaline casts | Muddy brown granular casts | WBC casts, Eosinophiluria | Normal / RBCs / Pyuria |
| Renal Ultrasound | Normal | Normal | Normal / Enlarged | Hydronephrosis / Hydroureter |
Formula for Fractional Excretion of Sodium (FENa): FENa (%) = [(Urine Na x Serum Cr) / (Serum Na x Urine Cr)] x 100. In patients taking loop diuretics, FeUrea (< 35%) is more accurate than FENa.
Glomerular Diseases: Nephrotic vs Nephritic Syndromes
Nephrotic vs Nephritic Syndrome Comparison
| Diagnostic Parameter | Nephrotic Syndrome | Nephritic Syndrome |
|---|---|---|
| Primary Pathology | Podocyte damage -> breakdown of filtration barrier | Glomerular inflammation -> cell proliferation & capillary damage |
| Clinical Triad | Anasarca, Heavy Proteinuria, Hypoalbuminemia | Hematuria, Oliguria, Hypertension |
| Proteinuria Level | > 3.5 g/24h (UACR > 220 mg/mmol) | Mild to Moderate (< 3.5 g/24h) |
| Serum Albumin | Hypoalbuminemia (< 30 g/L) | Normal or mildly decreased |
| Urine Sediment | Oval fat bodies, fatty casts, "Maltese cross" | Dysmorphic RBCs, RBC Casts |
| Major Complications | Hypercoagulability (loss of antithrombin III -> RVT/DVT), Hyperlipidemia | AKI, Hypertensive Emergency, Fluid Overload |
Key Glomerular Etiologies
- Minimal Change Disease: Most common cause of nephrotic syndrome in children. Normal glomeruli on light microscopy; podocyte effacement on electron microscopy. Highly responsive to corticosteroids (prednisone).
- Membranous Nephropathy: Most common primary nephrotic syndrome in Caucasian adults. Associated with anti-PLA2R antibodies, HBV, solid tumors, and NSAIDs. Thickened basement membrane with "spike and dome" pattern on silver stain.
- Diabetic Nephropathy: Nodular glomerulosclerosis (Kimmelstiel-Wilson nodules), mesangial expansion, and progressive albuminuria.
- Post-Streptococcal GN (PSGN): Nephritic syndrome presenting 1–3 WEEKS AFTER group A beta-hemolytic streptococcal pharyngitis or impetigo. Characterized by LOW serum C3 complement and lumpy-bumpy subepithelial deposits.
- IgA Nephropathy (Berger Disease): Most common primary GN worldwide. Young adult presenting 1–2 DAYS AFTER an upper respiratory infection (synpharyngitic hematuria). Characterized by NORMAL serum C3 complement and mesangial IgA deposition.
- ANCA Vasculitis (GPA / Wegener): PR3-ANCA / c-ANCA positive. Triad of upper respiratory sinus lesions, lower respiratory pulmonary nodules/hemoptysis, and pauci-immune crescentic GN.
- Anti-GBM (Goodpasture) Disease: Autoantibodies against alpha-3 chain of type IV collagen causing pulmonary hemorrhage PLUS Rapidly Progressive GN. Linear IgG deposition along glomerular basement membrane.
Chronic Kidney Disease (CKD) Staging & Progression Delay
CKD is defined by kidney damage or eGFR < 60 mL/min/1.73m² present for > 3 months.
KDIGO Staging Matrix
- eGFR Categories: G1 (≥ 90), G2 (60–89), G3a (45–59), G3b (30–44), G4 (15–29), G5 (< 15 or Dialysis).
- Albuminuria Categories: A1 (UACR < 3.0 mg/mmol - Normal/Mild), A2 (UACR 3.0–30.0 mg/mmol - Moderate), A3 (UACR > 30.0 mg/mmol - Severe).
Evidence-Based Interventions to Slow CKD Progression
- RAAS Blockade (ACEi or ARB): Titrated to maximum tolerated dose in all patients with CKD and hypertension or albuminuria (UACR > 3.0 mg/mmol). Reduces intraglomerular pressure by dilating efferent arterioles. Expect up to a 30% rise in serum creatinine upon initiation; do NOT discontinue unless creatinine rises > 30% or refractory hyperkalemia develops.
- SGLT2 Inhibitors (Empagliflozin, Dapagliflozin): Indicated for all CKD patients with eGFR ≥ 20 mL/min/1.73m² and UACR > 3.0 mg/mmol, regardless of diabetes status. Reduces hyperfiltration, slows eGFR decline, and reduces ESKD/death.
- Blood Pressure Control: Target BP < 120/80 mmHg per KDIGO 2021 guidelines using standardized measurement.
- Lifestyle Modifications: Dietary sodium restriction (< 2.0 g/day), protein intake 0.8 g/kg/day, avoidance of nephrotoxins (NSAIDs, IV contrast).
Indications for Urgent Hemodialysis (AEIOU Mnemonic)
| Letter | Emergency Indication | Clinical Diagnostic Threshold |
|---|---|---|
| A | Acidosis | Severe refractory metabolic acidosis with pH < 7.10 despite medical management |
| E | Electrolytes | Severe refractory hyperkalemia with K+ > 6.5 mmol/L or ECG changes persistent despite therapy |
| I | Intoxications | Poisoning with dialyzable toxins (SLIME: Salicylates, Lithium, Isopropanol, Methanol, Ethylene glycol) |
| O | Overload | Refractory volume overload / Acute pulmonary edema non-responsive to high-dose IV loop diuretics |
| U | Uremia | Symptomatic uremia: Uremic Pericarditis, uremic encephalopathy/asterixis, uremic bleeding |
Important
MCCQE1 High-Yield Distinction: IgA Nephropathy vs Post-Streptococcal GN • IgA Nephropathy (Berger Disease): Recurrent gross hematuria occurring CONCURRENTLY (1–2 days after) an upper respiratory tract infection. Serum C3 complement levels are NORMAL. • Post-Streptococcal GN: Hematuria occurring 1–3 WEEKS AFTER a streptococcal pharyngeal or skin infection. Serum C3 complement levels are LOW (hypocomplementemia).
A 68-year-old male with a history of hypertension and osteoarthritis presents with weakness and oliguria 4 days after undergoing a contrast-enhanced CT angiogram. Current medications include Ramipril and Naproxen. Labs show BUN 32 mmol/L and Creatinine 340 µmol/L (baseline 90 µmol/L). Urinalysis demonstrates urine Na 58 mmol/L, FENa 2.6%, and dark muddy brown granular casts on microscopy. What is the primary diagnosis?
Acute Tubular Necrosis (ATN) secondary to contrast toxicity
Prerenal Azotemia secondary to NSAID therapy
Acute Interstitial Nephritis (AIN) secondary to Naproxen
Postrenal obstruction secondary to BPH
A 19-year-old university student presents with dark, tea-colored urine that began yesterday alongside a sore throat and fever. Blood pressure is 138/86 mmHg. Physical exam reveals mild pharyngeal erythema but no edema. Labs: Creatinine 115 µmol/L, Serum C3 complement level 1.1 g/L (Normal 0.9–1.8 g/L), and Serum C4 level normal. Urinalysis reveals 3+ blood, dysmorphic RBCs, and 1+ protein. What is the most likely diagnosis?
Post-Streptococcal Glomerulonephritis
IgA Nephropathy (Berger Disease)
Minimal Change Disease
Anti-GBM / Goodpasture Disease
A 62-year-old female with ESKD missing hemodialysis for 5 days presents to the ED confused and dyspneic. Vitals: BP 178/104 mmHg, HR 110/min, RR 26/min, SpO2 86% on room air. Physical exam demonstrates bilateral lung crackles, elevated JVP, and a pericardial friction rub. Labs show K+ 6.8 mmol/L with peaked T waves on ECG, arterial pH 7.08, and BUN 42 mmol/L. In addition to medical hyperkalemia management, what emergency intervention is indicated?
Urgent Emergency Hemodialysis
Continuous Ambulatory Peritoneal Dialysis over 48 hours
High-dose oral Furosemide 120 mg IV bolus
Empiric broad-spectrum IV antibiotics for pericarditis
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