Acid Base and Electrolytes
A 68-year-old woman with COPD presents with confusion.
ABG: pH 7.31, pCO₂ 60, HCO₃⁻ 30.
What is the acid–base disorder?
Chronic Respiratory Acidosis
pH 7.31, pCO₂ 60 (↑20 mmHg above 40), HCO₃⁻ 30.
Compensation rules: acute rise in pCO₂ → HCO₃ rises ≈1 mEq/L per 10 mmHg; chronic → ≈3–4 mEq/L per 10 mmHg. For a 20 mmHg rise, expected chronic HCO₃ increase ≈ 6–8 → 30–32, which matches measured HCO₃ (30). That pattern = chronic respiratory acidosis (chronic CO₂ retention as with long-standing COPD).
A CKD stage 5 patient (not on dialysis) has:
Ca: 10.1
Phos: 7.8
Ca × P product = 78
PTH = 110
Current meds: calcium carbonate for reflux.
What is the best next step?
Stop calcium carbonate
Ca × P > 55 is dangerous → vascular calcification risk.
Patient’s Ca × P = 78, caused by:
High phos
High calcium from calcium carbonate
Next step:
→ Stop calcium-based binders
→ Switch to non-calcium binder after Ca drops
Nephrotic range proteinuria
>3.5 gm/day (in a 24 h urine sample)
A 45-year-old man passes a stone. Stone analysis shows hexagonal crystals and urine pH is 7.0.
Which condition is most likely?
Cystinuria
Hexagonal stones = pathognomonic for cystine stones.
Key points:
Occur in young patients
Positive cyanide-nitroprusside test
Require urine alkalinization and high fluid intake
A 55-year-old woman presents with Na 122.
Serum Osm: 265
Urine Osm: 150
Urine Na: 22
She drinks 3–4 L of water/day but not excessively.
Exam: euvolemic.
TSH, cortisol normal.
What is the diagnosis?
Low solute intake (“beer potomania” physiology)
The patient’s urine Osm is low-ish (150) — kidneys can dilute urine, but the ability to excrete free water per day is limited by solute excretion. Free water clearance (max daily excretion) = (solute excreted / minimal urine Osm). If daily solute intake is very low (e.g., beer or very low-protein/low-salt diets), even moderate fluid intake can exceed maximal free water excretion and cause hyponatremia.
Primary polydipsia usually involves very large water intake (>6–10 L/day) and typically produces very low Uosm (<100).
A 74-year-old woman is hospitalized with pneumonia and has been receiving high-dose IV vancomycin. Over 48 hours, her creatinine increases from 1.0 → 2.3 mg/dL, and urine output falls to 350 mL/day.
Urinalysis: muddy brown granular casts, no protein, no RBCs.
Vitals stable; no hypotension episodes.
Most likely diagnosis?
Acute tubular necrosis
Muddy brown granular casts → hallmark of ATN
Rising creatinine + oliguria
Vancomycin can cause both ATN and AIN, but AIN usually shows WBCs, WBC casts, eosinophils, rash, fever, none of which are present
A 32-year-old man presents with shortness of breath, hematuria, and edema.
Labs:
Cr: 3.8 mg/dL (baseline 1.0)
BUN: 52
UA: RBCs, dysmorphic RBCs, RBC casts
Complement C3: normal
C4: normal
ANCA: positive p-ANCA (MPO+)
Anti-GBM: negative
Hepatitis B/C: negative
What is the most appropriate next step?
Pulse IV methylprednisolone
This is RPGN (rapidly progressive glomerulonephritis) with:
Renal failure
Hematuria + RBC casts
Normal complement
MPO-ANCA positive
Before biopsy, if RPGN is suspected → start steroids immediately.
Board rule:
Do NOT wait for biopsy in suspected RPGN. Start pulse steroids.
A 62-year-old man with a 40-pack-year smoking history presents with painless gross hematuria. UA shows >50 RBCs/hpf, no casts, and no proteinuria. Urine culture is negative. Serum creatinine is normal.
Which of the following is the most appropriate next step?
CT urogram and cystoscopy
Painless hematuria in an older smoker = urothelial carcinoma until proven otherwise.
Workup requires upper tract (CT urogram) + lower tract (cystoscopy) evaluation.
CT urogram → best test for renal pelvis & ureter malignancy.
Ultrasound misses small lesions.
PSA irrelevant (no lower urinary tract symptoms).
Cystoscopy alone is incomplete — must image kidneys & ureters as well.
A 67-year-old woman is admitted for pneumonia. Initial labs:
Na⁺ 118 mEq/L
Serum Osmolality: 254 mOsm/kg
Urine Osmolality: 540 mOsm/kg
Urine Na⁺: 52 mEq/L
Creatinine normal
She is diagnosed with SIADH due to pneumonia and treated with fluid restriction and two 15-mg doses of tolvaptan 24 hours apart by an outside facility before transfer.
On arrival to you (36 hours after the last tolvaptan dose), she appears clinically euvolemic.
Repeat labs:
Na⁺ 126 mEq/L
Serum Osm: 262 mOsm/kg
Urine Osm: 120 mOsm/kg
Urine output over the past 8 hours: 3.2 L
Urine Na⁺: 18 mEq/L
Patient reports feeling “very thirsty”.
Two hours later, she becomes light-headed. Labs show:
Na⁺ 133 mEq/L
What is the cause of this rapid rise in Na?
Spontaneous Aquaresis
Acceptable answers: Free water excretion due to ADH shutdown
Tolvaptan causes V2 receptor antagonism → complete shutdown of ADH effect, leading to profuse electrolyte-free water excretion (aquaresis).
After the drug wears off, SIADH may “return,” but during the window of waning effect (24–48 hours), patients can have:
Massive, dilute urine output
Rapid rises in serum sodium
Risk of osmotic demyelination syndrome (ODS)
This patient’s findings scream spontaneous aquaresis:
Urine output: 3.2 L in 8 hours
Urine osmolality dropped to 120 mOsm/kg → kidneys dumping free water
Sodium increased from 126 to 133 in only 2 hours
Tolvaptan effect can last >24 hours, explaining continued aquaresis
A 63-year-old man with CKD stage 4 (eGFR 19) is seen for abnormal labs.
Labs:
Ca: 8.5 mg/dL
Phos: 6.3 mg/dL
PTH: 680 pg/mL
Alk phos: 99 U/L
25-OH vitamin D: 13 ng/mL
1,25-OH vitamin D: low
Albumin: 3.8
He is not on phosphate binders or vitamin D therapy.
What is the next BEST step?
Start non-calcium phosphate binder (sevelamer)
This patient has classic CKD-MBD:
High phos → 6.3
Low-normal Ca (expected because ↓ 1,25-OH Vit D)
Very high PTH → 680
Low 25-OH vit D
The first therapeutic target is phosphorus control, because:
Hyperphosphatemia is the major driver of secondary hyperparathyroidism
Treating vitamin D deficiency or giving calcitriol before phos control can increase Ca × P product → vascular calcification
Cinacalcet:
Used for dialysis patients or when Ca is high-normal—this patient has low-normal Ca and is not on dialysis.
A 57-year-old man with known membranous nephropathy presents with sudden rise in Cr from 1.1 to 3.6.
Findings:
Edema increased
UA: heavy proteinuria but no hematuria, no casts
Albumin: 2.4
Renal US: no obstruction
D-dimer elevated
What is the MOST likely cause?
Renal vein thrombosis
Membranous nephropathy → highest risk of renal vein thrombosis
Clues:
Sudden AKI
Heavy proteinuria
Hypercoagulability
No hematuria
High D-dimer
Not the others:
AIN → pyuria, WBC casts, eosinophils.
Rapid progression → would see hematuria, RBC casts.
NSAIDs → nephrotic-range proteinuria only with minimal change, not membranous.
Cholesterol emboli → livedo, eosinophilia.
A 48-year-old man presents with severe left flank pain, nausea, and vomiting. CT shows a 6 mm stone in the proximal left ureter with mild hydronephrosis.
Labs:
Creatinine: 2.5 mg/dL (baseline 1.0)
Normal BP and vitals
No infection signs
Best next step?
Urgent ureteral stent or nephrostomy
obstructing stone + rising creatinine = urgent decompression.
Even without infection, obstruction plus AKI requires urologic intervention.
Trial of passage is acceptable if creatinine is normal and pain is controlled.
ESWL is not appropriate with AKI.
A 57-year-old man with COPD and chronic back pain is admitted for shortness of breath.
Home meds include: furosemide 40 mg daily, spironolactone 25 mg, oxycodone, and ibuprofen.
On exam:
BP 102/62
HR 92
Dry mucous membranes
JVP not visible
No edema
Bibasilar crackles
Appears mildly confused
Labs:
Na: 122 mEq/L
K: 5.4 mEq/L
Cl: 86 mEq/L
HCO₃: 21 mEq/L
BUN: 34 mg/dL
Cr: 1.1 mg/dL
Serum Osm: 264 mOsm/kg
Urine Osm: 520 mOsm/kg
Urine Na: 68 mEq/L
Urine K: 22 mEq/L
Urine Urea: 350 mg/dL (elevated)
Uric acid: 2.1 mg/dL (low)
What is the MOST likely cause of hyponatremia?
Loop diuretic–induced natriuresis with true volume depletion
Acceptable answers: Volume depletion, hypovolemia
Urine Sodium >40 mEq/L does NOT always mean SIADH (Unreliable in the setting of diuretics)
Low uric acid (2.1 mg/dL) is typical in SIADH, but also:
In patients with diuretic-induced volume depletion, fractional excretion of uric acid becomes HIGH
When the effective arterial blood volume is low, kidneys dump uric acid to preserve sodium
This makes uric acid physiologically non-specific in the presence of diuretics.
The most reliable index here is the clinical picture + BUN
A 71-year-old woman on hemodialysis has:
Ca: 9.7
Phos: 4.0
PTH: 420
Alk phos: 48
On sevelamer, cholecalciferol
What is the diagnosis?
Adynamic bone disease
In dialysis patients:
Low Alk Phos → LOW BONE TURNOVER
PTH above normal but not very high (300–600) can still be misleading
Due to "PTH resistance," PTH may appear elevated but bone turnover is actually suppressed.
Key Board Clue → Low Alk Phos = adynamic bone disease
A 32-year-old man presents with edema and hypertension.
Labs:
Cr: 1.9 (baseline 0.9)
UA: 2+ protein, 2+ blood
Microscopy: dysmorphic RBCs, occasional RBC casts
Protein/Cr ratio: 1.2 g/day
Complement levels: normal
Recent URI 3 days ago
What is the MOST likely diagnosis?
IgA nephropathy
Clues for nephritic:
RBC casts
Dysmorphic RBCs
Rising creatinine
Mild proteinuria (<3 g/day)
Classic finding:
Hematuria synchronously with URI (“synpharyngitic”)
PIGN occurs 2–3 weeks after infection, not 3 days.
Minimal change & membranous → nephrotic, not nephritic.
FSGS → nephrotic or subnephrotic proteinuria but not RBC casts.
A 43-year-old woman has multiple UTIs with Proteus mirabilis. UA shows alkalinized urine. CT shows a large staghorn calculus occupying the collecting system.
Her GFR is normal.
Best management?
Percutaneous nephrolithotomy (PCNL)
Struvite (infection) stones → staghorn calculi → PCNL is the treatment.
ESWL won’t clear large staghorn stones.
Antibiotics alone fail because bacteria are harbored inside the stone.
A 29-year-old woman with Sjögren syndrome presents with fatigue and proximal muscle weakness. Labs:
Serum:
Na 138
K 2.9
Cl 112
HCO₃⁻ 14
Cr 0.8
Glucose normal
Serum osmolality normal
ABG:
pH 7.28, PaCO₂ 28 mmHg
Urine studies (simultaneous sample):
Urine Na 45 mEq/L
Urine K 12 mEq/L
Urine Cl 10 mEq/L
Urine pH 6.0
Urine osmolality 380
Additional tests:
Urine NH₄⁺ (measured): <20 mEq/day (low)
What is the diagnosis?
Type 1 (Distal) RTA
Identify the primary acid–base disturbance
pH = 7.28 → acidemia
HCO₃⁻ = 14 → metabolic acidosis
PaCO₂ 28 → appropriate respiratory compensation
This is a normal anion gap metabolic acidosis (NAGMA) because:
AG = 138 – (112 + 14) = 12 → Normal.
Differentiate renal vs extrarenal causes
Use urine anion gap (uAG).
uAG = (Na + K) – Cl = (45 + 12) – 10 = 47
A positive uAG → kidney is NOT excreting NH₄⁺ → renal tubular problem.
Also measured urine NH₄⁺ is very low, confirming RTA.
Differentiate RTA types
Clue 1: Potassium level
K = 2.9 → hypokalemia
Which RTAs cause low K?
Type 1 (distal): low K
Type 2 (proximal): low K
Type 4 (hypoaldosteronism): HIGH K ❌
So Type 4 RTA is ruled out.
Clue 2: Urine pH
Urine pH 6.0 in setting of metabolic acidosis
Normal response: urine pH < 5.3
Failure to acidify urine (<5.3) → Type 1 RTA
But urine pH around 6.0 could be:
Type 1 (distal) RTA: always high pH
Type 2 (proximal) RTA: urine pH initially high, but eventually <5.5 once HCO₃ depleted
Here, HCO₃⁻ = 14 (significantly depleted), so proximal RTA should show acidic urine (<5.5).
However, the urine pH remains 6.0, which is too high, supporting Type 1 RTA.
A 71-year-old man with multiple myeloma, CKD3b, and pneumonia is admitted with:
BP: 98/60
UOP: 1.2 L/day
BUN: 118 mg/dL
Cr: 6.2 mg/dL (baseline 1.8)
K: 4.6
HCO₃: 17
pH: 7.32
Na: 138
Phos: 7.2
Mental status: mild confusion, but arousable
Osmolality: normal
No pericardial rub
CXR: resolving pneumonia
What is the best next step?
Start dexamethasone, treat light-chain cast nephropathy
This is MM cast nephropathy—a classic board trap:
AKI with disproportionately high BUN & Cr
Non-oliguric
High phosphate
Normal potassium
Mild acidosis, no refractory fluid overload, no uremic pericarditis
Mild uremic symptoms (confusion), but not severe enough to require dialysis
In multiple myeloma AKI, treat the cause (steroids + chemotherapy) BEFORE dialysis — unless a classic AEIOU indication exists.
Dialysis does NOT remove light chains effectively unless using high-cutoff membranes (rare in US).
A 44-year-old man has hemoptysis and AKI:
Labs:
Cr: 5.2
UA: hematuria with RBC casts
C3, C4: normal
ANCA: negative
Anti-GBM: pending
Chest CT: diffuse alveolar hemorrhage.
What is the next BEST step?
Start plasmapheresis + pulse steroids
Alveolar hemorrhage + RPGN + ANCA-negative → anti-GBM highly likely.
Board rule:
Do NOT delay treatment for anti-GBM disease if pulmonary hemorrhage is present.
Plasmapheresis removes circulating anti-GBM antibodies.
A 54-year-old kidney transplant recipient (6 months post-transplant) presents with increased creatinine from 1.1 to 2.0 mg/dL.
Ultrasound: hydronephrosis of the transplant kidney, no fluid collections.
UA: bland. Tacrolimus levels are therapeutic.
Best next step?
Surgical/urologic evaluation
In transplant kidneys:
Ureteral anastomotic strictures are common at 3–12 months.
Hydronephrosis + rising Cr = obstruction until proven otherwise.
Biopsy comes after obstruction is excluded.