Case 20: The Stone Former with Low Potassium

Session 1 · Required self-study · 6 questions

Andrew Bland, MD, FACP, FAAP · October 2026

Commit to an answer before revealing the explanation. Use the section menu to navigate; each question and answer has its own link. Five-option evidence updates ask for the most defensible direction of change; discuss a justified adjacent response.

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Session S1 · 2026-10-22 · supplementary · 20 min Anchor: Fluids, electrolytes and acid-base — non-gap acidosis, the urine anion gap and the RTA table, built around one patient · Integrates: nephrolithiasis (calcium phosphate stones, nephrocalcinosis, prevention and the 24-h urine), hypokalemia replacement, an autoimmune clue (Sjögren) One-line hook: Her third kidney stone brings her in; the chemistry panel and a remark she makes on the way out decide whether she leaves with a strainer or a diagnosis.

Fictional patient. Every name, date and number in this case is invented for teaching. Self-study: about 20 minutes. Commit to an answer before you open each folded callout.

Learning Objectives

Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6

By the end of this case the student can:

  1. Choose the first imaging test for suspected renal colic (the pregnancy test and the ultrasound exceptions: discussed, not tested).
  2. Read a non-gap metabolic acidosis from the BMP and blood gas, and use the urine anion gap with a paired urine pH to separate the gut from the kidney.
  3. Place a patient in the RTA table (types 1, 2 and 4) from potassium, urine pH, urine anion gap and stones, and name the adult cause to test for in type 1.
  4. Choose the alkali for distal RTA, explain the order of potassium and alkali, and give first-line stone prevention.
  5. Decide who gets a 24-hour urine, and when (discussed, not tested).

Warm-Up (individual commit before the case)

Answers for this section: W1 · W2

Two readiness items.

W1The first picture

A 41-year-old man has sudden, severe left flank pain radiating to the groin. He cannot lie still, has no fever, and his urine shows blood. Which test best confirms a stone?

A.

A CT of the abdomen and pelvis with IV contrast, to show the kidneys and ureters together

B.

A plain abdominal X-ray (KUB), because most stones contain calcium and show on film

C.

A low-dose non-contrast CT of the abdomen and pelvis (CT KUB, the stone protocol)

D.

A urinalysis alone, because blood in the urine with flank pain confirms the stone

· Link to this question

Correct answer: C

Learning point: Non-contrast CT is the first-line test: it detects most stone types — including the uric acid stones a plain film misses — gives size and location, shows hydronephrosis, and finds the alternatives such as an aortic aneurysm. No contrast is needed, and a low-dose stone protocol limits the radiation. Ultrasound is the choice in pregnancy, so a woman of reproductive age has a pregnancy test first. Why not the others: A — IV contrast is usually unnecessary for the initial stone study, although another suspected diagnosis may require it. B — KUB misses radiolucent and some small stones and does not adequately assess obstruction. D — blood may be absent with stones or present for other reasons; it cannot replace imaging when indicated. Course reading: Evidence for this case

Evidence and objective for W1

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W2Reading the urine anion gap

A 50-year-old man has had five days of watery diarrhea: sodium 136, chloride 112, bicarbonate 16 (anion gap 8). A spot urine shows sodium 30, potassium 25 and chloride 85 mEq/L. What does the urine anion gap tell you?

A.

+30 — the kidney is failing to excrete acid, so look for a renal tubular acidosis

B.

−30 — the kidney is excreting ammonium chloride; the base was lost from the gut

C.

−30 — the kidney is failing to excrete acid, which proves a distal tubular acidosis

D.

It cannot be read here, because the urine anion gap only works in a gap acidosis

· Link to this question

Correct answer: B

Learning point: The urine anion gap is (30 + 25) − 85 = −30. In this non-gap acidosis, a negative gap is consistent with increased ammonium excretion, often as ammonium chloride, and supports an appropriate renal response to diarrhea. It is an indirect index: unusual urinary anions, low distal sodium delivery and bicarbonaturia can make it misleading. A negative gap does not exclude proximal RTA; direct urine ammonium is preferable when available and the distinction remains uncertain. Why not the others: A — the calculated sign is negative. C — preserved ammonium excretion argues against a distal acid-excretion defect but does not exclude every RTA subtype. D — the urine anion gap can inform a non-gap acidosis when its limitations are respected. Course reading: Evidence for this case

Evidence and objective for W2

Back to W2 · All answers in this case

Part 1 — Presentation

Answers for this section: Q3 · Q4

Setting: Emergency department, 14:20 on a Saturday.

Patient: Ms. Maya Delgado, 32, a dental hygienist, 58 kg, with three hours of colicky left flank pain radiating to the left labia, and nausea. No fever, no dysuria.

Stone history: This is her third stone. At 27 she passed one; at 30 one needed ureteroscopy. Both were analyzed: calcium phosphate (apatite). She was told to drink more water; no blood or urine work-up followed.

Other history (it comes out at the end): Two weeks of loose stools, two or three a day, since a stomach bug went through her house. Months of leg cramps and fatigue. Her eyes feel "gritty, like sand"; her mouth is dry — she keeps a water bottle to swallow crackers — and her own dentist found three new cavities along the gumline this year.

Medications: levonorgestrel IUD; ibuprofen as needed. No diuretics, laxatives, supplements or acetazolamide. Family history: no stones, no kidney disease.

Vitals: T 36.9 °C · heart rate 102 · BP 132/80 · RR 18 · SpO₂ 99% on room air.

Exam: Writhing, unable to find a comfortable position; left costovertebral-angle tenderness; abdomen soft. Dry oral mucosa with sticky saliva; mild, nontender swelling of both parotid glands. No rash; joints normal.

ED course: Urine pregnancy test negative. Low-dose non-contrast CT: a 4-mm stone at the left ureterovesical junction with mild left hydronephrosis; bilateral medullary nephrocalcinosis; two 3-mm non-obstructing stones in the right kidney. Ketorolac 30 mg IV and ondansetron 4 mg IV control the pain. ECG: sinus rhythm 98/min, U waves in V2–V3, QTc 450 ms.

Test (triage, 14:40, before any IV fluid) Result Reference range
Sodium 139 mEq/L 135–145
Potassium 3.0 mEq/L 3.5–5.0
Chloride 114 mEq/L 98–107
Bicarbonate 17 mEq/L 22–28
BUN 12 mg/dL 7–20
Creatinine 0.8 mg/dL (0.8 a year ago; eGFR 100 mL/min/1.73 m², CKD-EPI 2021) 0.6–1.1
Glucose 92 mg/dL 70–99
Calcium 9.4 mg/dL 8.5–10.5
Albumin 4.3 g/dL 3.5–5.0
Phosphorus 3.0 mg/dL 2.5–4.5
Magnesium 2.0 mg/dL 1.7–2.2
Arterial blood gas pH 7.33 · pCO₂ 33 mmHg · HCO₃ 17 mEq/L pH 7.35–7.45 · pCO₂ 35–45 · HCO₃ 22–26
Urinalysis (triage sample) pH 6.5, specific gravity 1.012, blood 3+, protein negative, leukocyte esterase and nitrite negative; 20–50 RBC/hpf, 0–2 WBC/hpf, no bacteria, no casts pH 4.5–8.0

The ED resident's plan: "Two weeks of diarrhea — that explains the low bicarbonate and the low potassium. Replete potassium, strainer, home."

Q3Name the disorder, then the test

Sodium 139, chloride 114, bicarbonate 17, potassium 3.0; arterial pH 7.33 with a pCO₂ of 33. What is the acid–base disorder, and what should be added to her triage urine?

A.

Anion-gap acidosis from starvation ketosis — add serum β-hydroxybutyrate and a lactate

B.

Primary respiratory alkalosis from pain, with renal compensation — no further tests needed

C.

Non-gap acidosis from the diarrhea — send stool studies and replace the potassium only

D.

Non-gap acidosis with expected compensation — add urine sodium, potassium and chloride

· Link to this question

Correct answer: D

Learning point: A pH of 7.33 with a bicarbonate of 17 is a metabolic acidosis. The anion gap is 139 − (114 + 17) = 8 (normal 8–12), so it is non-gap (hyperchloremic), and Winter's formula, 1.5 × 17 + 8 = 33.5 ± 2, matches her pCO₂ of 33 — one disorder, properly compensated. A non-gap acidosis has two homes, the gut and the kidney, and the urine anion gap, from electrolytes added to the triage urine collected before any IV fluid, helps distinguish them, while direct urine ammonium and the full clinical context can resolve uncertainty. Why not the others: A — the gap is normal and nothing is filling it; B — the pH is acidemic, and a primary respiratory alkalosis raises it; C — it names the diagnosis before testing it, and stool studies cannot show whether the kidney is responding. Course reading: Evidence for this case

Evidence and objective for Q3

Back to Q3 · All answers in this case

16:10 — the add-on urine electrolytes return: urine sodium 52, potassium 38, chloride 68 mEq/L. Urine anion gap = (52 + 38) − 68 = +22 mEq/L.

Q4Evidence update

Concordance-style practice: a judgment about how a finding should move your thinking, not a graded test. There is no expert panel behind the key, the teaching explanation. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."

If you were thinking diarrhea-related non-gap acidosis, and you then learn that her urine anion gap is +22 mEq/L (on the triage urine, pH 6.5, taken while her blood pH was 7.33), this hypothesis becomes:

A.

Much less likely

B.

Less likely

C.

Unchanged

D.

More likely

E.

Much more likely

· Link to this question

Correct answer: A

Formative evidence update: The letter is a teaching anchor. Accept a justified adjacent response; this is not an expert-panel-validated score. Learning point: The positive urine anion gap during systemic acidosis suggests an inadequate ammonium response, weakening diarrhea as the main explanation. The alkaline urine, recurrent calcium phosphate stones and nephrocalcinosis make a distal acidification disorder more coherent. The gap is a proxy, not a measured ammonium concentration; review confounders and use direct ammonium or specialist testing if findings are discordant. Diarrhea may still contribute. What else could it mean, and what would move you: the diarrhea may be adding a little, but two weeks of loose stools do not explain three calcium phosphate stones in five years, nephrocalcinosis or months of cramps. A negative gap on a repeat sample would have kept the gut in play. Course reading: Evidence for this case

Evidence and objective for Q4

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Part 2 — Data

Answers for this section: Q5

Nephrology clinic, three weeks later. The stone passed on day 2; analysis: calcium phosphate (apatite) 90%, calcium oxalate 10%. The loose stools stopped two weeks ago. Her 24-hour urine was collected last week on her usual diet; the 24-hour creatinine of 870 mg (15 mg/kg) is plausible for her body size, but collection duration, missed voids and repeat consistency still determine adequacy.

Test Result Reference range
Sodium 140 mEq/L 135–145
Potassium 3.1 mEq/L 3.5–5.0
Chloride 113 mEq/L 98–107
Bicarbonate 18 mEq/L 22–28
Anion gap 9 mEq/L 8–12
Creatinine 0.8 mg/dL 0.6–1.1
Calcium 9.3 mg/dL 8.5–10.5
Intact PTH 38 pg/mL 15–65
Urine pH (first morning) 6.6 4.5–8.0
24-hour urine volume 1.4 L/day goal at least 2.5
24-hour urine calcium 290 mg/day high above 250 (women)
24-hour urine citrate 90 mg/day low below 320
24-hour urine pH 6.8 interpret by stone type

Q5Which RTA, and what next?

Off diarrhea for two weeks: bicarbonate 18, potassium 3.1, urine pH 6.6, urine anion gap +22 at the first visit, calcium phosphate stones with nephrocalcinosis, normal calcium and PTH, dry eyes and mouth. Which RTA, and what do you send next?

A.

Type 2 (proximal) — send serum protein electrophoresis and free light chains for myeloma

B.

Type 1 (distal) — send ANA, anti-Ro/SSA, anti-La/SSB and rheumatoid factor for Sjögren

C.

Type 4 (hyperkalemic) — send renin and aldosterone and review her potassium-sparing drugs

D.

Primary hyperparathyroidism — order a sestamibi scan to find the parathyroid adenoma

· Link to this question

Correct answer: B

Learning point: A low potassium, a urine pH above 5.5 during acidemia, a positive urine anion gap, and calcium phosphate stones with nephrocalcinosis add up to type 1 (distal) RTA: the collecting duct cannot pump acid into the urine, so it cannot acidify, it wastes potassium, and its alkaline, citrate-poor, calcium-rich urine grows calcium phosphate. Sjögren syndrome is an important acquired cause in an adult with sicca symptoms; her dry eyes, dry mouth, gumline cavities and parotid swelling are the clue, so the screen is ANA, anti-Ro/SSA, anti-La/SSB and rheumatoid factor. Why not the others: A — type 2 can acidify once bicarbonate has fallen below its reduced threshold; stones are much less characteristic; C — type 4 runs a high potassium; D — a calcium of 9.3 with a PTH of 38 has already answered the hyperparathyroidism question every calcium phosphate stone raises. Course reading: Evidence for this case

Evidence and objective for Q5

Back to Q5 · All answers in this case

Results: ANA 1:640, speckled; anti-Ro/SSA and anti-La/SSB positive; rheumatoid factor positive. Rheumatology confirms primary Sjögren syndrome with eye and salivary-flow testing.

The RTA table. Fill in your own three rows before reading this one. The loading tests and fractional bicarbonate excretion on the full RTA page are fellowship work.

Type What fails, where Urine pH during acidemia Serum K Urine anion gap Stones Adult causes to know Treatment
1 — distal Acid secretion by the collecting duct Above 5.5 — cannot acidify Low Positive Calcium phosphate stones, nephrocalcinosis Sjögren (leading adult cause), lupus, amphotericin B, lithium Potassium citrate
2 — proximal Bicarbonate reclaim by the proximal tubule Can fall below 5.5 once bicarbonate is low Low Variable; often negative once bicarbonate is depleted and distal acidification is intact Uncommon Myeloma with Fanconi syndrome, tenofovir, acetazolamide Large alkali doses ± thiazide; treat the cause
4 — hyperkalemic Aldosterone low or resisted Usually below 5.5 High Usually positive Rare Diabetes, ACE inhibitors/ARBs, NSAIDs, trimethoprim, spironolactone Review contributing drugs; individualized potassium treatment; selected patients may receive a diuretic or specialist-directed fludrocortisone

Part 3 — Course and Decisions

Answers for this section: Q6

Same visit. She wants to know what will stop the stones and the cramps.

Q6The treatment plan

Distal RTA from Sjögren syndrome, 58 kg: potassium 3.1, bicarbonate 18; 24-hour urine volume 1.4 L, calcium 290 mg/day, citrate 90 mg/day, pH 6.8. Which plan is best?

A.

Sodium bicarbonate 650 mg three times daily now; add potassium chloride later if potassium stays low

B.

Hydrochlorothiazide 25 mg for the urine calcium, and a low-calcium diet to starve the stones

C.

Potassium citrate 20 mEq three times a day; fluids for 2.5 L of urine; low salt; normal calcium

D.

Fluids alone for three months, then decide on alkali if a fourth stone shows that it is needed

· Link to this question

Correct answer: C

Learning point: Potassium citrate replaces the potassium the tubule wastes, becomes bicarbonate, and raises urine citrate, a stone inhibitor — and it delivers the potassium with the alkali, which matters because raising the blood pH drives potassium into cells. The stone lecture calls citrate double-edged in calcium phosphate disease since alkali raises urine pH, but in distal RTA the urine is already alkaline from the defect and correcting the acidosis lowers urine calcium — so the RTA sources prefer it, with urine pH rechecked. Fluids, low salt and normal calcium complete the plan. Why not the others: A — alkali first and potassium later is the dangerous order, and the sodium load raises urine calcium; B — a thiazide deepens the potassium loss, and cutting dietary calcium raises oxalate absorption; D — the acidosis, the hypokalemia and the nephrocalcinosis are already here. Course reading: Evidence for this case

Evidence and objective for Q6

Back to Q6 · All answers in this case

Resolution and Teaching Points

Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6

She started potassium citrate 20 mEq three times a day (60 mEq/day, about 1 mEq/kg), with an early BMP within a week for potassium and renal safety, then a BMP at 2 weeks: potassium 3.7, bicarbonate 21. At 6 weeks the cramps were gone, potassium 3.9, bicarbonate 23. The repeat 24-hour urine showed volume 2.6 L, citrate 340 mg/day, calcium 210 mg/day and pH 7.0: citrate up, calcium down now that the acidosis no longer draws on bone. The urine pH and calcium phosphate supersaturation stay on the follow-up list, because higher urine pH can favor calcium phosphate while improved citrate and lower calcium can offset that effect; the net supersaturation should be measured — the stone lecture calls citrate "double-edged" in calcium phosphate disease. Rheumatology manages the Sjögren syndrome; her dentist added fluoride. A renal ultrasound at one year — chosen over CT for a young, recurrent stone former — showed unchanged nephrocalcinosis and no new stones.

Clinical Pearl — An outpatient non-gap acidosis has two homes The gut (diarrhea, fistulas) or the kidney (RTA, early CKD, acetazolamide); in hospital, a large saline load is a third. The urine anion gap decides between gut and kidney: negative means the kidney is excreting ammonium and the problem is elsewhere; positive means the kidney is the problem.

Clinical Pearl — A urine pH means something only next to a blood pH Above 5.5 during acidemia, with a positive urine anion gap, means the collecting duct cannot acidify — type 1. The same urine pH with a normal blood pH means nothing.

Clinical Pearl — Calcium phosphate stones send you looking Every calcium phosphate stone former is screened for primary hyperparathyroidism and distal RTA. In a woman with distal RTA, ask about dry eyes and a dry mouth — Sjögren is the leading adult cause; lithium is on the same list.

Clinical Pearl — Potassium with or before the alkali Correct potassium before or together with alkali. The potassium response to a pH change is variable and cannot be predicted by a fixed conversion rule. Potassium citrate supplies potassium and base and improves hypocitraturia; monitor potassium, renal function, urine citrate and calcium phosphate supersaturation.

Clinical Pearl — Who gets a 24-hour urine Recurrent or high-risk stone formers — young, calcium phosphate stones, nephrocalcinosis, a systemic disease — collected weeks after the episode on the usual diet (the stone lecture asks for two collections), checked for completeness by the 24-hour creatinine, and repeated on treatment.

Pitfall — "Two weeks of diarrhea explains it" The diarrhea was real and the story was tidy. Three calcium phosphate stones, nephrocalcinosis and months of cramps were not explained by it, and a positive urine anion gap during acidemia put the kidney in charge.

Pitfall — Reading the urine anion gap backwards Two linked student references print the sign backwards for distal RTA — the RTA handout's Type 1 test table and the nephrolithiasis handout's calcium phosphate work-up. Negative is the gut ("neGUTive"); positive is the kidney. The acid-base handout, the metabolic acidosis lecture and the RTA lecture page have it right.

Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6

Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.

Concepts: lytes-11, lytes-23, lytes-24, structural-01, structural-03.