System 04 · ~8% of exam
Renal & GU
AKI by pre/intra/post-renal. CKD staging and its complications. Electrolytes by mechanism. Acid-base by systematic approach. Hematuria by glomerular vs non-glomerular.
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Chief complaints
BUILD THE DIFFERENTIAL
Vignettes enter through one of these doors. Each complaint lays out the full differential, marks the can't-miss diagnoses, and tells you the next right action for each.
CHIEF COMPLAINT · HIGH-YIELD
Acute kidney injury
Pre-renal, intra-renal, post-renal. Fractional excretion of sodium and urine microscopy separate them.
Approach
AKI = rise in Cr ≥ 0.3 in 48 hr or ≥ 1.5× baseline. Pre-renal: volume depletion, HF, cirrhosis, sepsis (FeNa < 1%). Intra-renal: ATN, AIN, glomerulonephritis (FeNa > 2%). Post-renal: obstruction (bladder scan, renal US).
The differential
| Diagnosis | Key features / clues | Next step |
|---|---|---|
| Pre-renal azotemia | Volume depletion (vomiting, diarrhea, diuretics), HF, cirrhosis. BUN/Cr > 20. FeNa < 1%. | IV fluids · treat underlying cause |
| Acute tubular necrosis | Ischemic (prolonged pre-renal) or toxic (contrast, aminoglycosides, cisplatin, rhabdo). Muddy brown casts. FeNa > 2%. | Supportive · remove offending agent · dialysis if AEIOU indication |
| Acute interstitial nephritis | Drug reaction (NSAIDs, PPIs, penicillins, sulfas). Rash, fever, eosinophilia (classic triad), WBC casts, urine eosinophils. | Stop offending drug · steroids if severe |
| Rhabdomyolysis | Crush injury, prolonged immobilization, statins, seizure. CK > 5× upper limit. Tea-colored urine, dipstick positive for blood but no RBCs. | Aggressive IV fluids · urine alkalinization (controversial) · watch K |
| Post-renal obstruction | Older male with BPH, stones, malignancy. Oliguria or anuria. | Bladder scan · renal US · relieve obstruction (Foley, nephrostomy, etc.) |
| Contrast-induced nephropathy | Rise in Cr 24–72 hr after contrast. Risk: CKD, DM, volume depletion. | IV fluids pre-procedure (normal saline or isotonic bicarb) · minimize contrast |
| Rapidly progressive glomerulonephritis | Hematuria, red cell casts, rising Cr over days to weeks, hypertension. | Renal biopsy · treatment depends on cause (anti-GBM, ANCA, immune complex) |
⚑ = can't-miss diagnosis · rule out first
Classic vignette
Exam-style stem
A 72-year-old man 3 days after coronary angiography has a rise in Cr from 1.1 to 2.4. BP 128/72. Urine output adequate. UA: hyaline casts.
Most likely diagnosis?
Answer › Contrast-induced nephropathy. Peaks at 3–5 days. Supportive care, hold nephrotoxins, ensure volume status. Usually resolves within 1–2 weeks.
Pearls
Pearl
AEIOU indications for dialysis: severe Acidosis, Electrolyte abnormalities (K > 6.5 refractory), Ingestion (toxic alcohol, lithium, salicylates), Overload (refractory), Uremia (pericarditis, encephalopathy, bleeding).
Pearl
Urine microscopy is the cheapest, most high-yield test in AKI. Muddy brown casts (ATN), WBC casts (pyelo or AIN), RBC casts (GN), eosinophils (AIN), hyaline casts (pre-renal).
Pearl
If AKI doesn't improve with fluids and there's no obstruction, the kidney is the problem. Urine microscopy and consider biopsy.
CHIEF COMPLAINT
Hematuria
Glomerular (RBC casts, dysmorphic RBCs, proteinuria) vs non-glomerular (normal RBCs, no casts).
Approach
Glomerular: GN, IgA nephropathy, Alport, thin basement membrane. Non-glomerular: stones, infection, malignancy, trauma, BPH. Painless hematuria in an older patient is bladder cancer until proven otherwise. Cystoscopy.
The differential
| Diagnosis | Key features / clues | Next step |
|---|---|---|
| Bladder/urothelial cancer | Painless hematuria, older smoker, occupational exposure (aniline dyes). | CT urogram · cystoscopy |
| Renal cell carcinoma | Flank pain + hematuria + mass (classic but late triad). Paraneoplastic syndromes. | CT abdomen with contrast · nephrectomy |
| Nephrolithiasis | Severe colicky flank pain radiating to groin, hematuria. | Non-contrast CT abdomen · analgesia · medical expulsive therapy (alpha blocker) |
| IgA nephropathy | Gross hematuria within days of URI. Young patient. | Renal biopsy if persistent · ACEi for proteinuria |
| UTI / pyelonephritis | Dysuria, frequency, urgency, suprapubic pain. Pyelo: flank pain, fever. | UA · urine culture · antibiotics |
| Post-strep glomerulonephritis | Child, 2–4 wk after strep throat or impetigo. Hematuria, HTN, edema, low C3. | Supportive · usually self-limited |
⚑ = can't-miss diagnosis · rule out first
Pearls
Pearl
A dipstick positive for blood with no RBCs on microscopy is myoglobin (rhabdo) or hemoglobin (hemolysis). Check CK and haptoglobin.
Pearl
Painless gross hematuria in any adult over 35 needs cystoscopy. Do not accept 'probably a UTI' as the answer.
Pearl
Red urine is not always blood. Pigments from beets, rifampin, phenazopyridine. Dipstick differentiates.
CHIEF COMPLAINT · HIGH-YIELD
Hyperkalemia
The ECG changes are the emergency, not the number. Stabilize the membrane first.
Approach
Causes: pseudo (hemolysis from the draw), renal failure, ACEi/ARB/spironolactone, cell lysis (rhabdo, tumor lysis), adrenal insufficiency, acidosis. ECG: peaked T waves → PR prolongation → QRS widening → sine wave → VF.
The differential
| Diagnosis | Key features / clues | Next step |
|---|---|---|
| Life-threatening hyperkalemia (K > 6.5 or ECG changes) | Peaked T waves, widened QRS, sine wave. Renal failure, meds, cell lysis. | Calcium gluconate (stabilize membrane) → insulin + glucose, albuterol, bicarb if acidotic (shift) → furosemide, kayexalate, patiromer, dialysis (remove) |
| Renal failure | Elevated Cr, oliguria. | Treat K, dialysis if AEIOU |
| Medication-induced | ACEi, ARB, spironolactone, NSAIDs, trimethoprim. | Discontinue offending agent |
| Adrenal insufficiency | Hyperkalemia + hyponatremia + hypotension + hypoglycemia. Weight loss, fatigue, hyperpigmentation. | Random cortisol, cosyntropin stim · hydrocortisone |
| Tumor lysis syndrome | Chemotherapy for hematologic malignancy. Hyperuricemia, hyperphosphatemia, hypocalcemia, hyperkalemia, AKI. | Aggressive hydration, rasburicase or allopurinol |
| Pseudohyperkalemia | Hemolyzed sample, severe leukocytosis or thrombocytosis. | Repeat specimen properly collected |
⚑ = can't-miss diagnosis · rule out first
Classic vignette
Exam-style stem
A 70-year-old man with CKD and HF on lisinopril and spironolactone has K 6.8. ECG: peaked T waves, QRS 140 ms.
Next step?
Answer › IV calcium gluconate first to stabilize the cardiac membrane (onset in minutes, effect 30–60 min). Then insulin + glucose and albuterol to shift. Then loop diuretic, kayexalate/patiromer, or dialysis to remove. Stop ACEi and spironolactone.
Pearls
Pearl
The sequence matters: STABILIZE (calcium), SHIFT (insulin, albuterol, bicarb), REMOVE (diuretic, kayexalate/patiromer, dialysis).
Pearl
Calcium gluconate does not lower potassium. It protects the myocardium while you work on the K.
Pearl
Hyperkalemia + hyponatremia + hypotension in a chronically ill patient is primary adrenal insufficiency until proven otherwise.
CHIEF COMPLAINT · HIGH-YIELD
Hyponatremia
Volume status separates the differential. Correct slowly to avoid osmotic demyelination.
Approach
Step 1: measure serum osmolality. Hypertonic (hyperglycemia, mannitol). Isotonic (pseudo, hyperlipidemia, paraproteinemia). Hypotonic: volume status. Hypovolemic: vomiting, diuretics, third-spacing. Euvolemic: SIADH, hypothyroid, adrenal insufficiency, primary polydipsia. Hypervolemic: HF, cirrhosis, nephrotic.
The differential
| Diagnosis | Key features / clues | Next step |
|---|---|---|
| SIADH | Euvolemic hyponatremia, low serum osm, inappropriately concentrated urine (uosm > 100, uNa > 40). Causes: CNS disease, lung disease, malignancy (SCLC), drugs. | Fluid restriction · treat cause · salt tabs · tolvaptan if refractory |
| Hypovolemic hyponatremia | Volume depletion signs, uNa < 20 (except diuretics). | Isotonic saline |
| Hypervolemic hyponatremia | Edema, HF/cirrhosis/nephrotic. | Salt and water restriction · treat underlying · consider tolvaptan |
| Hyperglycemic pseudohyponatremia | Glucose high. Corrected Na = measured Na + 1.6 × (glucose − 100)/100. | Treat hyperglycemia |
| Beer potomania / low solute intake | Low protein/solute intake, high fluid intake. Low urine osm. | Nutrition · solute |
| Symptomatic severe hyponatremia (Na < 120 with seizures/coma) | Altered mental status, seizures. | 3% hypertonic saline (150 mL bolus) · raise Na by 4–6 mEq/L then stop · correct < 8 mEq/L in 24 hours |
⚑ = can't-miss diagnosis · rule out first
Pearls
Pearl
Correct Na by no more than 8 mEq/L in 24 hours. Faster correction → osmotic demyelination (central pontine myelinolysis).
Pearl
SIADH is a diagnosis of exclusion. Rule out hypothyroidism and adrenal insufficiency first, they mimic SIADH and missing them is harmful.
Pearl
Hypertonic saline is for neurologically symptomatic severe hyponatremia. Give a small bolus, reassess, stop at 4–6 mEq/L rise.
✦
Disease deep dives
DEFINITIVE DX
Once you've identified the likely diagnosis from the chief complaint, these pages give you the presentation, workup, management, and exam pearls in depth.
Chronic Kidney Disease
Stages, complications (anemia, CKD-MBD, acidosis, HTN, CV risk), and when to refer for dialysis/transplant.
Nephritic Syndrome
Hematuria (dysmorphic RBCs, RBC casts), HTN, edema, mild proteinuria, oliguria. The differential is by mechanism.
Nephrotic Syndrome
Proteinuria > 3.5 g/d, hypoalbuminemia, edema, hyperlipidemia. Primary vs secondary.
DISEASE DEEP DIVE
Chronic Kidney Disease
Stages, complications (anemia, CKD-MBD, acidosis, HTN, CV risk), and when to refer for dialysis/transplant.
Presentation
Asymptomatic early. Late: fatigue, pruritus, nausea, anorexia, edema, pericardial friction rub, asterixis.
Workup
- eGFR staging. G1 ≥ 90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29, G5 < 15 or dialysis.
- Albuminuria. A1 < 30, A2 30–300, A3 > 300 mg/g. Both eGFR and albuminuria determine prognosis.
- Complications. CBC (anemia), Ca/Phos/PTH/vit D (CKD-MBD), bicarbonate (metabolic acidosis), lipids, glucose, BP.
Management
- Slow progression. BP < 130/80 with ACEi or ARB (especially if proteinuria). SGLT2 inhibitor in diabetic and non-diabetic CKD. Finerenone in diabetic CKD. Low-protein diet in later stages.
- Anemia. Iron repletion first (IV if dialysis). ESA (erythropoietin) when Hb < 10 with target Hb 10–11.
- CKD-MBD. Phosphate binders (calcium acetate, sevelamer), active vitamin D (calcitriol), calcimimetics (cinacalcet). Avoid aluminum.
- Acidosis. Sodium bicarbonate when bicarb < 22.
- Renal replacement. Start dialysis when symptomatic uremia, fluid overload, refractory hyperkalemia, refractory acidosis, or eGFR < 10.
- Transplant. Best long-term outcome. Refer early (eGFR < 20).
Pearls
Pearl
Every CKD patient gets an ACEi or ARB for renoprotection (unless contraindicated). SGLT2 inhibitors now standard in diabetic and non-diabetic CKD.
Pearl
Do not withhold contrast for eGFR > 30 based on CIN fear alone. Risk-benefit, with hydration.
Pearl
Pre-dialysis patients need an AV fistula placed 3–6 months before anticipated dialysis for maturation.
Classic vignette
Exam-style stem
A 62-year-old man with DM has Cr 2.4, eGFR 28, urine ACR 450. BP 148/88.
Answer › CKD stage G4 A3. ACEi (renoprotective, slows progression), SGLT2 inhibitor (empagliflozin or dapagliflozin), optimize glycemic control, statin, BP target < 130/80. Refer to nephrology for transplant evaluation.
DISEASE DEEP DIVE
Nephritic Syndrome
Hematuria (dysmorphic RBCs, RBC casts), HTN, edema, mild proteinuria, oliguria. The differential is by mechanism.
Presentation
Cola-colored urine, peripheral edema, hypertension. Elevated Cr.
Workup
- UA + sediment. RBC casts, dysmorphic RBCs. Proteinuria usually < 3.5 g/d.
- Serologies. ANCA, anti-GBM, ASO, anti-DNase B, ANA, dsDNA, complement (C3, C4), cryoglobulins, hep B/C/HIV.
- Renal biopsy. Often needed for definitive diagnosis.
Management
- Post-strep GN. Supportive. Self-limited in most children.
- IgA nephropathy. ACEi for proteinuria. Steroids for rapid progression.
- Anti-GBM (Goodpasture). Plasmapheresis + steroids + cyclophosphamide.
- ANCA-associated vasculitis (GPA, MPA). Steroids + rituximab or cyclophosphamide. Plasmapheresis in severe disease.
- Lupus nephritis. Steroids + mycophenolate or cyclophosphamide.
Pearls
Pearl
Low C3 differential: post-strep GN, MPGN, lupus nephritis, cryoglobulinemic GN. Normal C3: IgA, anti-GBM, ANCA-associated.
Pearl
IgA is the most common GN worldwide. Presents with synpharyngitic hematuria (within days of URI, not 2 weeks like post-strep).
Pearl
Pulmonary-renal syndrome: hemoptysis + nephritic → anti-GBM (Goodpasture) or ANCA-associated vasculitis (GPA).
Classic vignette
Exam-style stem
A 20-year-old man with hemoptysis and hematuria. Cr 3.2. Anti-GBM positive. Renal biopsy: crescentic GN with linear IgG.
Answer › Goodpasture syndrome (anti-GBM disease). Plasmapheresis + high-dose steroids + cyclophosphamide.
DISEASE DEEP DIVE
Nephrotic Syndrome
Proteinuria > 3.5 g/d, hypoalbuminemia, edema, hyperlipidemia. Primary vs secondary.
Presentation
Periorbital and peripheral edema, frothy urine, fatigue. Severe: anasarca, pleural effusions, ascites.
Workup
- Urine protein. Spot urine protein/Cr ratio or 24-hour protein.
- Serologies. ANA, hep B/C, HIV, SPEP/UPEP (amyloid, myeloma), complement.
- Renal biopsy. In adults usually needed to determine subtype.
Management
- Minimal change disease. Common in children. Steroids highly effective.
- FSGS. Common in Black patients, HIV, obesity, heroin. Steroids + cyclosporine.
- Membranous. Most common primary nephrotic in adults. Associated with solid tumors, hep B, lupus, gold, penicillamine. Anti-PLA2R. Steroids + cyclophosphamide or rituximab.
- Diabetic nephropathy. Most common cause of nephrotic-range proteinuria overall. ACEi/ARB, SGLT2 inhibitor, glycemic and BP control.
- Amyloid. Biopsy with Congo red, apple-green birefringence. Treat underlying (myeloma, inflammation).
- Supportive. ACEi/ARB (reduce proteinuria), statin, salt restriction, diuretics, anticoagulation if severe (renal vein thrombosis risk).
Pearls
Pearl
Hypercoagulability in nephrotic syndrome, especially membranous, because of urinary loss of antithrombin III. Consider prophylactic anticoagulation if severe.
Pearl
Minimal change disease is triggered by NSAIDs, Hodgkin lymphoma. Steroid-responsive in a day or two.
Pearl
FSGS in a Black patient with HIV is HIV-associated nephropathy. Collapsing variant.