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A 58-year-old man with diabetes presents with Cr 4.2 mg/dL (baseline unknown). Ultrasound shows bilateral small kidneys (8 cm). Which finding most suggests this is chronic rather than acute?
AKI — Acute Kidney Injury
- Hours to days
- Cr rises ≥0.3 mg/dL in 48h or ≥1.5x baseline in 7 days
- Often reversible
- Kidneys: normal or large on US
- No anemia (usually)
- No bone disease
- Can progress to CKD if severe/prolonged
CKD — Chronic Kidney Disease
- Months to years
- GFR <60 mL/min for ≥3 months
- Usually irreversible
- Kidneys: small and scarred on US
- Anemia (low EPO)
- Renal osteodystrophy (low vitamin D, high PTH)
- Can have AKI on top of CKD ("acute on chronic")
The three types of AKI map to where the blood flow is blocked or damaged:
Problem: Not enough blood getting TO the kidney. The kidney itself is fine.
- Causes: Dehydration, hemorrhage, heart failure, sepsis, NSAIDsNSAIDs constrict the afferent arteriole, reducing renal blood flow. This is prerenal injury because the kidney parenchyma is undamaged — it's just not getting enough flow., ACE inhibitorsACEi/ARBs dilate the efferent arteriole, dropping filtration pressure. Again, the kidney itself is fine — it's the hemodynamics that change.
- Labs: BUN:Cr >20:1, FENa <1%, concentrated urine (high specific gravity), bland sediment
- Key insight: The kidney is trying to hold on to everything because it thinks the body is dry. So sodium is low in urine (FENa <1%), urine is concentrated, BUN is reabsorbed disproportionately.
Problem: The kidney itself is damaged. Tubules, glomeruli, or interstitium.
- ATN (Acute Tubular Necrosis): Most common intrinsic AKI. Ischemic (from prolonged prerenal) or nephrotoxic (aminoglycosidesGentamicin, tobramycin — accumulate in proximal tubular cells and cause direct toxicity. Classic board answer for drug-induced ATN., contrast dye, myoglobin)
- AIN (Acute Interstitial Nephritis): Drug hypersensitivity reaction. Triad: fever, rash, eosinophilia. Think penicillins, sulfonamides, NSAIDs, PPIs
- Glomerulonephritis: RPGN, lupus nephritis, anti-GBM — see nephrotic vs nephritic page
Labs: BUN:Cr <20:1, FENa >2% (in ATN), muddy brown casts (ATN), WBC casts + eosinophils (AIN), RBC casts (GN)
Problem: Urine can't get OUT. Obstruction downstream of the kidney.
- Causes: BPH (most common in older men), kidney stones (bilateral or solitary kidney), cancer (cervical, bladder, prostate), neurogenic bladder
- Diagnosis: Ultrasound shows hydronephrosis (dilated collecting system)
- Treatment: Relieve the obstruction. Foley catheter for BPH, stent or nephrostomy for stones/cancer
| Feature | AKI | CKD |
|---|---|---|
| Timeline | Hours to days | Months to years |
| Kidney size (US) | Normal or large | Small (<9 cm bilateral) |
| Anemia | Usually absent | Present (low EPO) |
| Bone disease | Absent | Renal osteodystrophy |
| Broad waxy casts | No | Yes |
| Reversibility | Often reversible | Usually irreversible |
| Hyperkalemia | Yes | Yes (late stage) |
| Metabolic acidosis | Yes | Yes |
| Edema/fluid overload | Yes | Yes |
| PTH | Normal | Elevated (secondary hyperPTH) |
| Phosphate | Can be elevated | Chronically elevated |
| Calcium | Variable | Low (can't activate vitamin D) |
This comparison shows up on almost every exam. The kidney's response tells you if the tubules still work.
| Lab | Prerenal | ATN (Intrinsic) |
|---|---|---|
| BUN:Cr | >20:1 | <20:1 |
| FENa | <1% | >2% |
| Urine Na | <20 mEq/L | >40 mEq/L |
| Urine osmolality | >500 mOsm/kg | <350 mOsm/kg |
| Specific gravity | >1.020 | <1.010 |
| Urine sediment | Bland / hyaline casts | Muddy brown granular casts |
| Response to fluids | Cr improves | Cr does NOT improve |
Step through this when you see rising creatinine on boards:
Step 1: Is there obstruction?
Get a renal ultrasound. Look for hydronephrosis.
US shows bilateral hydronephrosis. What type of AKI?
Step 2: Check volume status
Dry mucous membranes? Tachycardia? Orthostatic hypotension? Give a fluid challenge.
Cr improves with IV fluids. What type?
Step 3: Check FENa and sediment
FENa <1% with bland sediment = prerenal (still not responding to fluids? Check cardiac output). FENa >2% = intrinsic. Look at casts.
Muddy brown casts + FENa 4%. Diagnosis?
Step 4: Identify the intrinsic cause
Sediment tells you everything:
- Muddy brown casts = ATN
- WBC casts + eosinophils = AIN (drug reaction)
- RBC casts = Glomerulonephritis
- Bland sediment with intrinsic labs = consider vascular (TTP, HUS, renal vein thrombosis)
Patient started amoxicillin 2 weeks ago. Now has fever, rash, eosinophilia, and WBC casts. Diagnosis?
Boards expects you to know what happens at each stage:
| Stage | GFR (mL/min) | What's Happening | Action |
|---|---|---|---|
| 1 | ≥90 | Kidney damage, normal GFR | Manage risk factors, ACEi/ARB if proteinuria |
| 2 | 60-89 | Mild decrease | Estimate progression rate |
| 3a | 45-59 | Mild-moderate | Monitor complications, adjust drug doses |
| 3b | 30-44 | Moderate-severe | Refer to nephrology |
| 4 | 15-29 | Severe. Bone disease, anemia, acidosis | Prepare for RRT, AV fistula |
| 5 | <15 | Kidney failure | Dialysis or transplant |
Everything connects. Low GFR starts a chain reaction:
- Anemia: Kidneys can't make EPOErythropoietin is made by peritubular cells in the kidney cortex. As nephrons die, EPO production drops. Treat with synthetic EPO (epoetin alfa) when Hgb <10. Always check iron stores first — EPO won't work without iron. → normocytic anemia → treat with EPO + iron
- Bone disease: Can't activate vitamin D (1α-hydroxylase is in the kidney) → low calcium → high PTH → renal osteodystrophy
- Hyperkalemia: Can't excrete K+ → arrhythmia risk → restrict dietary K+, kayexalate, dialysis
- Metabolic acidosis: Can't excrete H+ or regenerate HCO3 → non-anion-gap (early) or anion-gap (late)
- Fluid overload: Can't excrete water → edema, HTN, pulmonary edema
- Uremic symptoms: GFR <15 → nausea, pericarditis, encephalopathy, asterixisFlapping tremor of the hands when wrists are extended. Seen in uremia, hepatic encephalopathy, and CO2 narcosis. In the kidney context, it means toxins are building up — time for dialysis.
A = Acidosis (refractory)
E = Electrolytes (hyperK refractory to medical treatment)
I = Ingestion (toxic alcohols, lithium, salicylates)
O = Overload (fluid, refractory to diuretics)
U = Uremia (pericarditis, encephalopathy, bleeding)
Drag each feature to the correct category:
Work through a patient with new Cr elevation:
Patient presents with Cr 3.8 (was 1.0 last month). What's your FIRST step?
Good. US shows NO hydronephrosis, normal-sized kidneys. Now what?
You've ruled out postrenal obstruction and the kidneys aren't small (not chronic). This is AKI.
Not quite.
Always rule out obstruction first with ultrasound. Postrenal AKI is the easiest to fix and the most dangerous to miss. FENa comes AFTER you rule out obstruction.
Way too aggressive.
Biopsy is reserved for when non-invasive workup doesn't give you the answer. Start with ultrasound to rule out obstruction.
Patient is tachycardic, dry mucous membranes. You give 2L NS. Cr drops to 2.1 in 24h.
Cr is responding to fluids. What's your diagnosis?
Not quite.
ATN does NOT respond to fluids — the tubules are dead. If Cr improves with IV fluids, the kidney was underperfused but structurally intact. That's prerenal.
No. Way too early.
Dialysis is for refractory hyperK, acidosis, fluid overload, or uremic symptoms (AEIOU). You haven't even figured out what's causing the AKI yet. Assess volume status first — most AKI is prerenal and fixes with fluids.
Correct. Prerenal AKI from dehydration.
Key takeaways:
1. Always US first to rule out obstruction
2. Fluid challenge before labs — if it responds, you have your answer
3. FENa <1% confirms prerenal, but clinical response to fluids is the real test
4. If fluids DON'T work → check FENa and sediment → intrinsic AKI workup
Boards gives you a vignette. You tell them what's happening:
Scenario 1 of 6
72M with BPH presents with Cr 5.1 (baseline 0.9). US shows bilateral hydronephrosis. No prior renal disease.
Scenario 2 of 6
45F with SLE presents with Cr 2.8, bilateral small kidneys (8.5 cm), Hgb 9.2, PTH 180 (elevated). No recent medication changes.
Scenario 3 of 6
68M with CHF (EF 20%) presents with Cr 3.2 (baseline 1.1). BUN:Cr 28:1. FENa 0.4%. Urine concentrated. Bland sediment.
Scenario 4 of 6
55M post-cardiac surgery. Cr was 1.0 pre-op, now 4.5 on day 3. FENa 3.8%. Urine sediment shows muddy brown granular casts.
Scenario 5 of 6
30F started TMP-SMX 10 days ago for UTI. Now has fever, maculopapular rash, Cr 2.4 (baseline 0.8). CBC shows eosinophilia. Urine: WBC casts, eosinophiluria.
Scenario 6 of 6
62M marathon runner found unconscious. Cr 6.8. CPK 45,000. Urine is dark brown. Urine dipstick: positive for blood. Microscopy: NO RBCs.