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.
Save and export your first responses
First choices and optional confidence stay in this browser and are not sent to the website. Opening an explanation first is recorded. Revisiting an unchanged case preserves the first response; revised cases receive a new version. Website visit analytics are separate. On a shared device, export and clear the history when finished.
Sections in this case
Question and answer links
- W1: A 44-year-old man with no prior stones presents with 3 hours of sudden left flank pain radiating to the groin, vomiting, · Answer
- W2: Four patients have a potassium result back. Which one gets IV calcium gluconate in the next five minutes? · Answer
- W3: An 81-year-old man with known benign prostatic hyperplasia (BPH — an enlarged prostate narrowing the bladder outlet) has · Answer
- Q4: A 58-year-old man with a solitary right kidney, 14 hours of right flank colic, no urine for 12 hours, creatinine 5.1 mg/ · Answer
- Q5: Same patient, 09:55. K⁺ 7.0 mEq/L on the point-of-care cartridge (free-flowing sample; formal chemistry pending), QRS 15 · Answer
- Q6: A 7-mm proximal ureteral stone in a 44-year-old with two kidneys usually leaves the creatinine near normal. Why did this · Answer
- Q7: At 10:45, with the ECG settled, he is still writhing (pain 10/10), and the nurse asks for an analgesic order; the colic · Answer
- Q8: If you were thinking "an obstructed solitary kidney requiring urgent drainage, but without a superimposed infection," an · Answer
- Q9: 11:45. Infected obstruction of a solitary kidney with sepsis physiology (T 38.6 °C, pulse 118, BP 102/58, lactate 3.1 mm · Answer
- Q10: Four hours after decompression of a solitary obstructed kidney: urine output 350 mL/h × 4 h, hemodynamically stable, no · Answer
- Q11: At the 2-week post-discharge visit: creatinine 1.2 mg/dL, K⁺ 4.3, BP 148/88, stone analysis calcium oxalate monohydrate, · Answer
Session S4 · 2026-10-29 · in-session · 37 min Anchor: Acute kidney injury — obstructive nephropathy presenting with hyperkalemia (an obstructing ureteral stone in a solitary kidney) · Integrates: nephrolithiasis (colic recognition, non-contrast CT, infected obstruction, stone type and prevention), hyperkalemia emergency sequence, bladder scan first and BPH retention as the other post-renal pattern, post-obstructive diuresis, antibiotic dosing to the creatinine trend One-line hook: A man with one working kidney, flank pain and almost no urine — and a potassium that sets the pace for everything else you do.
Learning Objectives
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11
- Recognize renal colic, choose the first imaging test (non-contrast CT for most adults; ultrasound first in pregnancy, children and many recurrent stone formers), and choose analgesia that spares the kidney (no NSAIDs in AKI or with a solitary kidney).
- Explain why obstruction of the only functioning kidney can sharply reduce total filtration, why unilateral obstruction can still accompany AKI when other disease is present, and why an empty bladder does not exclude upper-tract obstruction.
- Sequence the hyperkalemia emergency — calcium for the wide QRS, insulin with dextrose and albuterol to shift, then removal — and explain why a loop diuretic needs urine flow, why a binder (which removes potassium through the gut at any urine output) is too slow to be the emergency step, and why relieving the obstruction, or dialysis, is the removal therapy here.
- Identify infected obstruction (fever, pyuria, sepsis physiology) and sequence the response: cultures, an antibiotic without delay (appropriate initial dosing, then pharmacy-guided reassessment during changing renal function), and decompression — how soon, and by which route.
- Anticipate and manage post-obstructive diuresis, and write the stone-prevention plan for a calcium oxalate former with a solitary kidney, including who gets a 24-hour urine.
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2 · W3
W1First imaging for colic
A 44-year-old man with no prior stones presents with 3 hours of sudden left flank pain radiating to the groin, vomiting, and microscopic hematuria. He is afebrile and his creatinine is 1.0 mg/dL. Which imaging test do you order first?
Plain abdominal radiograph of the kidneys, ureters and bladder (KUB)
Non-contrast CT of the abdomen and pelvis (stone protocol)
CT urogram with IV contrast, including delayed excretory images
Intravenous pyelogram (IVP) with timed post-contrast films
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Non-contrast CT is highly accurate for an adult with suspected ureteral colic: it shows stone size and position, obstruction and alternative diagnoses. Ultrasound may precede CT and is preferred initially when radiation matters most, including pregnancy and children. Anuria, fever or a solitary kidney makes imaging urgent. Why not the others: A — KUB misses radiolucent and some small stones and does not assess obstruction well. C — IV contrast is usually unnecessary for the initial stone study, although a different suspected diagnosis may require it. D — CT has largely replaced IVP. Course reading: Evidence for this case
W2Who gets calcium
Four patients have a potassium result back. Which one gets IV calcium gluconate in the next five minutes?
K⁺ 5.6 mEq/L, normal ECG, on lisinopril
K⁺ 6.2 mEq/L, normal ECG, sample flagged "hemolyzed," repeat draw pending
K⁺ 6.0 mEq/L, sinus tachycardia at 110/min, narrow QRS, normal T waves
K⁺ 7.0 mEq/L, PR 220 ms, flattened P waves, QRS 150 ms
Show answer and explanation · Link to this question
Correct answer: D
Learning point: A potassium of 7.0 with PR prolongation and a widened QRS is a cardiac emergency. IV calcium stabilizes the myocardium without lowering potassium; reassess the ECG and repeat per the local resuscitation protocol if toxic changes persist. ECG changes do not progress in a reliable sequence, and a normal ECG would not make severe hyperkalemia safe. Why not the others: A — K⁺ 5.6 with a normal ECG needs a cause and a medication review, not calcium. B — a hemolyzed sample is a pseudohyperkalemia candidate: repeat it now, and treat if it is real or the ECG changes. C — sinus tachycardia from pain or volume loss is not a potassium effect; the QRS and T waves are normal. Course reading: Evidence for this case
W3The other post-renal pattern
An 81-year-old man with known benign prostatic hyperplasia (BPH — an enlarged prostate narrowing the bladder outlet) has passed no urine for 18 hours, has lower abdominal fullness, and a creatinine of 3.4 mg/dL (baseline 1.2). What is the first test, and what follows if it is abnormal?
Bladder scan for retained urine; if the volume is large, place a Foley catheter and recheck the BMP
Renal ultrasound first; if both kidneys show hydronephrosis, call urology for bilateral ureteral stents
Urine sodium and creatinine for a FENa to separate prerenal azotemia from acute tubular necrosis
Non-contrast CT of the abdomen and pelvis to look for an obstructing stone or a pelvic mass
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Anuria (under 100 mL of urine a day) plus a rising creatinine in an older man with BPH is lower-tract obstruction until proven otherwise, and the fastest test is a bedside bladder scan (interpret the volume with the inability to void and the clinical setting). A bladder holding several hundred milliliters is acute retention: the Foley is both diagnosis and treatment, followed by a repeat BMP, a watch for post-obstructive diuresis, and an α-blocker (tamsulosin 0.4 mg daily) with urology follow-up. A blocked bladder outlet backs urine up into both kidneys at once, which is why it raises the creatinine. Why not the others: B — renal ultrasound is the next step if the bladder is empty, and stents treat ureteral, not bladder-outlet, obstruction. C — urine indices cannot reliably exclude obstruction. D — CT is the stone test and adds radiation and delay to a question a bladder scan answers in a minute. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q4 · Q5
09:30, emergency department, Thursday. Mr. Halvorsen is a 58-year-old farm-equipment mechanic brought in by his wife. For three days he has had a dull ache in his right flank and has been passing less urine than usual; he put both down to long days in a hot shop. At 19:30 last night, pain started in his right flank "like a knife" and within an hour was wrapping around to his right groin and testicle, coming in waves. He vomited four times overnight and could not keep water down. He took ibuprofen 400 mg three times (22:00, 01:00, 04:00) with no relief. His last urination was a small one around 21:00; he has not passed urine since — about 12 hours — and he tells you, "I'd go if I could. Nothing's there." He has never had a kidney stone.
Past history. Left nephrectomy at age 22 after a motorcycle crash, 36 years ago — he has one kidney. Hypertension, well controlled. Hyperlipidemia. His last clinic visit 3 months ago recorded a creatinine of 1.1 mg/dL and an eGFR of 78 mL/min/1.73 m². No diabetes. No prior urologic procedures.
Social. Married, two adult children. Drinks "a pot of coffee and maybe one glass of water" on a workday in a hot shop. Thirty pack-years, quit 5 years ago. Two beers on weekends. Works alone; no sick days this year.
Vitals (triage 09:32): T 37.9 °C oral · pulse 112 regular · BP 108/64 · respirations 22 · SpO₂ 96 percent on room air · weight 92 kg, height 180 cm.
Exam. Restless, cannot lie still, pale and sweaty. Dry mucous membranes. Lungs clear. Heart tachycardic, no murmur, no JVD. Abdomen soft, no peritoneal signs, no palpable bladder, no suprapubic dullness. Marked right costovertebral angle (CVA) tenderness. A healed midline laparotomy scar from the crash surgery. No edema. Neurologically intact.
Medications on arrival:
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Lisinopril | 20 mg | PO | daily | Hypertension |
| Atorvastatin | 20 mg | PO | nightly | Hyperlipidemia |
| Ibuprofen (over the counter) | 400 mg | PO | q3h × 3 doses overnight (22:00, 01:00, 04:00) | Flank pain, self-treated |
First results (09:45–09:50). The ECG at 09:45: sinus rhythm 112/min, PR 220 ms, low-amplitude P waves, QRS 150 ms, tall peaked T waves in V2–V4. The point-of-care cartridge at 09:47, run on a free-flowing venous sample, reads potassium 7.0 mEq/L, total CO₂ 17 mEq/L, BUN 48 mg/dL and creatinine 5.1 mg/dL; the formal chemistry drawn at 09:40 is still running.
The bedside bladder scan at 09:50 reads 0 mL. Five minutes later it reads 0 mL again.
Your attending, who has been up all night, says: "Empty bladder — so he's not obstructed. Probably prerenal from all the vomiting plus the ibuprofen. Let's run two liters and send a FENa."
Pause — commit before the reveal
Q4The empty bladder
A 58-year-old man with a solitary right kidney, 14 hours of right flank colic, no urine for 12 hours, creatinine 5.1 mg/dL (baseline 1.1), and a bladder scan of 0 mL. What does the empty bladder mean, and what is the next step?
He is not obstructed, because the bladder is empty; treat prerenal AKI with 2 L of isotonic crystalloid and send a FENa
He has ATN from ibuprofen and vomiting; send urine microscopy for muddy brown casts and hold imaging until he is resuscitated
Nothing is reaching the bladder: the block is above it, in his only ureter; renal ultrasound now and urology called
Place a Foley catheter to relieve the obstruction, then recheck the creatinine and potassium in 2 hours
Show answer and explanation · Link to this question
Correct answer: C
Learning point: A bladder scan answers one question — is urine pooling in the bladder? — and 0 mL says no; it says nothing about the ureter above. In a man with one kidney, one ureter, flank colic and no urine, an empty bladder is exactly what complete obstruction above the bladder looks like: nothing is getting past the stone. Renal ultrasound shows hydronephrosis (a dilated collecting system) at the bedside in minutes, with no radiation or contrast, and urology needs to hear about an obstructed solitary kidney now, while the potassium is treated in parallel. Why not the others: A — profound volume depletion can cause anuria, but it cannot safely explain away colic in a solitary kidney; assess volume and image urgently rather than giving an automatic large bolus. B — intrinsic injury remains possible, but imaging must not be deferred. D — a Foley can confirm an empty bladder but cannot bypass a ureteral stone. Course reading: Evidence for this case
Pause — commit before the reveal
Q5The potassium
Same patient, 09:55. K⁺ 7.0 mEq/L on the point-of-care cartridge (free-flowing sample; formal chemistry pending), QRS 150 ms with flattened P waves, total CO₂ 17 mEq/L, anuric for 12 hours, on lisinopril, vomiting. Which plan is correct for the next 15 minutes?
IV calcium now and again if the QRS stays wide; insulin–dextrose and albuterol to shift; a binder as a bridge; urology and nephrology called now
Furosemide 80 mg IV with sodium zirconium cyclosilicate 10 g PO to remove potassium, then recheck the level in 4 hours before giving anything else
Hold treatment until the formal laboratory potassium excludes pseudohyperkalemia, then give insulin with dextrose and a binder if it is confirmed
Sodium bicarbonate 100 mEq IV as the single agent, since his acidosis is what is driving potassium out of the cells, then recheck in 1 hour
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Three jobs run in parallel: stabilize, shift, remove. Calcium protects the heart for 30–60 minutes, and insulin with dextrose plus high-dose albuterol pushes potassium into cells for a few hours, but none of them removes any. A loop diuretic needs urine flow he does not have; a binder does remove potassium through the gut whatever the urine output, but over hours — too slowly to be the emergency step. Removal here means relieving the obstruction, or dialysis if decompression is delayed or the potassium rebounds, so urology and nephrology are called now, not after the CT. Why not the others: B — furosemide does nothing without urine flow, and leaving a 150-ms QRS without calcium for 4 hours is the dangerous omission. C — the potassium result plus toxic ECG changes is convincing enough to treat; a convincing emergency is treated while the repeat runs, never after it. D — bicarbonate is not a reliable stand-alone potassium treatment and is never the only agent for a wide QRS. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q6 · Q7
What happened between 09:55 and 11:00. Calcium gluconate 1 g IV (10 mL of the 10% solution over 2–3 minutes) was given at 09:56 and again at 10:04 when the QRS was still 140 ms; by 10:12 the QRS was 108 ms and P waves had returned. Regular insulin 10 units IV with 25 g dextrose (glucose checked before insulin, every 30 minutes for the first 2 hours, then hourly through 6 hours; longer if hypoglycemia occurs), nebulized albuterol 20 mg, ondansetron 4 mg IV and then sodium zirconium cyclosilicate 10 g PO followed — stabilize, shift, then remove . Lisinopril and ibuprofen were stopped. Urology and nephrology were called at 10:00. A straight catheter at 10:02 returned 30 mL of cloudy urine, which went for urinalysis and culture. The formal chemistry (drawn 09:40, hemolysis index negative) came back at 10:00 and confirmed the potassium at 7.1 mEq/L.
Serum chemistry (drawn 09:40):
| Test | Result | Reference range |
|---|---|---|
| Sodium | 136 mEq/L | 136–145 |
| Potassium | 7.1 mEq/L (point-of-care 7.0; hemolysis index negative) | 3.5–5.0 |
| Chloride | 101 mEq/L | 98–107 |
| Bicarbonate | 17 mEq/L | 22–29 |
| Anion gap | 18 = 136 − (101 + 17) | 8–12 |
| BUN | 48 mg/dL | 7–20 |
| Creatinine | 5.1 mg/dL (baseline 1.1 three months ago) | 0.7–1.3 |
| BUN:creatinine | about 9:1 | a ratio alone cannot assign the mechanism |
| eGFR (CKD-EPI 2021, as printed by the lab) | 12 mL/min/1.73 m² — not valid: creatinine is moving | ≥60 |
| Glucose | 142 mg/dL | 70–99 |
| Calcium | 8.9 mg/dL | 8.5–10.5 |
| Phosphorus | 5.2 mg/dL | 2.5–4.5 |
| Magnesium | 2.0 mg/dL | 1.7–2.3 |
| Albumin | 3.9 g/dL | 3.5–5.0 |
Arterial blood gas (10:05): pH 7.32 · pCO₂ 34 mmHg · HCO₃⁻ 17 mEq/L. Winter's formula: expected pCO₂ = 1.5 × 17 + 8 = 33.5 ± 2 (31.5–35.5), so breathing has compensated appropriately. Delta-delta = (18 − 10) / (24 − 17) = 8/7, about 1.1: the gap accounts for the whole fall in bicarbonate, so this is a single anion-gap metabolic acidosis — acids (phosphate, sulfate) that a non-filtering kidney cannot excrete, plus anything not yet measured. No lactate was sent with the first draw.
CBC (09:40): WBC 16.2 × 10⁹/L (4.0–11.0), neutrophils 88 percent · Hgb 14.2 g/dL (13.5–17.5) · platelets 240 × 10⁹/L (150–400).
Urinalysis and culture from the 30-mL straight-catheter specimen: sent at 10:02 as a combined urinalysis with microscopy; not yet resulted.
Bedside renal ultrasound (10:05): solitary right kidney 12.4 cm with moderate (grade 2) hydronephrosis and a dilated proximal ureter; cortex of normal thickness; no stone seen within the kidney; surgically absent left kidney; bladder empty.
Non-contrast CT abdomen and pelvis, stone protocol (10:40): a 7-mm calculus in the right proximal ureter at the level of L3, with the ureter and kidney dilated above it (hydroureteronephrosis), haziness in the fat around the kidney (perinephric stranding) and a little fluid beside it; no other stones; left nephrectomy; empty bladder; no free air; normal-caliber aorta.
So: KDIGO stage 3 AKI — creatinine 4.6 × baseline, and anuria for more than 12 hours — from an obstructing 7-mm proximal ureteral stone in a solitary kidney.
Q6Why 5.1 and not 1.1
A 7-mm proximal ureteral stone in a 44-year-old with two kidneys usually leaves the creatinine near normal. Why did this man's creatinine go from 1.1 to 5.1 mg/dL over three days?
Proximal stones cause more back-pressure injury than distal stones, so his creatinine rose faster than usual
With one kidney, blocking its only ureter stops nearly all filtration — the same physiology as bilateral obstruction
Ibuprofen on top of lisinopril and vomiting caused acute tubular necrosis; the stone is incidental to the kidney injury
Vomiting and a hot workplace caused volume depletion and prerenal AKI, which his high BUN of 48 mg/dL confirms
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Creatinine reflects total filtration. With two functioning kidneys, the unobstructed kidney often preserves enough filtration that an isolated ureteral stone causes little creatinine change. That protection is absent when the only functioning kidney is obstructed: total filtration falls and potassium and acid accumulate. Unilateral obstruction can still accompany AKI when the other kidney is impaired or additional injury is present. Why not the others: A — stone position changes the odds of passage (distal stones pass more readily), not how much filtration is lost. C — the NSAID and ACE inhibitor contribute, which is why they were stopped, but ATN does not dilate the collecting system or explain the anuria. D — the BUN is high because nothing is excreted; a ratio of about 9:1 does not even suggest prerenal, and no BUN:creatinine ratio settles the mechanism. Course reading: Evidence for this case
Pause — commit before the reveal
Q7Pain control
At 10:45, with the ECG settled, he is still writhing (pain 10/10), and the nurse asks for an analgesic order; the colic order set offers ketorolac. Creatinine 5.1 mg/dL, K⁺ now 6.1 mEq/L, total CO₂ 17, lisinopril and ibuprofen already held. Which analgesic plan is correct?
Ketorolac 30 mg IV — the first-line drug for renal colic — with tamsulosin 0.4 mg daily to help the stone pass
Acetaminophen 1,000 mg PO alone, since every other analgesic is nephrotoxic or unsafe in a man with one kidney
Ketorolac 15 mg IV, half the usual dose to allow for his kidney function, with ondansetron 4 mg IV
Hydromorphone 0.5–1 mg IV titrated to pain, scheduled ondansetron, IV acetaminophen as an adjunct; no NSAID
Show answer and explanation · Link to this question
Correct answer: D
Learning point: NSAIDs are first-line for colic when both kidneys are healthy, but they block the prostaglandins that hold the afferent arteriole — the vessel feeding the glomerulus — open, and an underperfused, injured kidney may depend on that support. With stage 3 AKI, a potassium of 6.1 and three doses of ibuprofen already given, no NSAID dose is safe. An IV opioid titrated to effect, with acetaminophen as an adjunct, controls the pain without touching kidney perfusion, and a scheduled antiemetic keeps his oral medicines down. Why not the others: A — ketorolac is the reflex answer and the wrong one, and tamsulosin (medical expulsive therapy) is for a 5–10 mm distal stone that can safely be watched, not a proximal stone blocking a solitary kidney. B — acetaminophen alone will not control colic, and oral drugs are unreliable in a vomiting man. C — there is no safe NSAID dose in AKI; "renally reduced ketorolac" is still an NSAID. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q8 · Q9 · Q10 · Q11
11:30. The potassium is 6.1 at 10:45 and 5.6 at 11:30; the QRS is 100 ms. The day team's plan from the 11:00 huddle, with urology's resident on the phone, reads: "Obstructing 7-mm stone, solitary kidney, AKI — needs a stent; OR is full today, booked first case 07:30 tomorrow. Continue hyperkalemia protocol, NPO, BMP q4h."
Then three results land within fifteen minutes. A rectal temperature at 11:30, ordered because he has started to shiver: 38.6 °C. The lactate, added when the fever was documented: 3.1 mmol/L (0.5–2.0). Blood pressure 102/58, heart rate 118. And the urinalysis from the 10:02 straight-catheter specimen:
| Test | Result | Reference |
|---|---|---|
| Color / clarity | amber, cloudy | yellow, clear |
| Specific gravity / pH | 1.012 / 6.0 | 1.005–1.030 / 4.5–8.0 |
| Protein / glucose / ketones | trace / negative / negative | negative |
| Blood | 2+ | negative |
| Leukocyte esterase / nitrite | 2+ / positive | negative / negative |
| WBC / RBC (microscopy) | 40/hpf / 10–20/hpf | 0–5/hpf / 0–2/hpf |
| Bacteria / casts / crystals | many / none / a few calcium oxalate | none / none / none |
Q8Evidence update
Concordance-style practice: there is no expert panel behind this key, the teaching explanation. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."
If you were thinking "an obstructed solitary kidney requiring urgent drainage, but without a superimposed infection," and you then learn he has a rectal temperature of 38.6 °C with rigors, a catheter urinalysis with 40 WBC/hpf, many bacteria and a positive nitrite, and a lactate of 3.1 mmol/L, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · 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: Two circumstances decide what this finding means: the kidney is obstructed, and the 37.9 °C triage reading was oral, in a man breathing 22 times a minute, five and a half hours after ibuprofen — an antipyretic. A stone alone can put white cells in the urine, but not bacteria, a positive nitrite and rigors; fever with that urine behind a blockage is infected obstruction, and a lactate of 3.1 with a falling blood pressure is sepsis physiology. Superimposed infection is now strongly supported. Anuria in the only kidney already required urgent drainage; these findings add sepsis resuscitation and antibiotics, not the first reason to act urgently. Why not the others: B — "less likely" undersells three independent signs of infection: rigors with a rectal fever, bacteria with a positive nitrite, and a raised lactate. C — "unchanged" treats the fever as noise, when the oral triage reading had hidden it. D and E — nothing here supports an uninfected obstruction. Course reading: Evidence for this case
Pause — commit before the reveal
Q9The next two hours
11:45. Infected obstruction of a solitary kidney with sepsis physiology (T 38.6 °C, pulse 118, BP 102/58, lactate 3.1 mmol/L), K⁺ 5.6 and falling on the protocol, creatinine 5.1 mg/dL. What is the right plan for the next two hours?
Blood and urine cultures, IV broad-spectrum antibiotics and fluid now; keep the 07:30 stent, since the antibiotics will control the infection overnight
Ureteroscopy with laser lithotripsy this evening to remove the stone and relieve the obstruction in one procedure, then IV antibiotics
Blood cultures, then an IV broad-spectrum antibiotic within the hour, measured fluid boluses, and decompression now by stent or nephrostomy
Shock-wave lithotripsy this evening to break up the stone so the fragments pass, with cultures and IV antibiotics given alongside it
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Infection behind an obstructed collecting system requires urgent drainage together with antibiotics and sepsis care. A stent or nephrostomy can provide source control; choose the feasible prompt route with the procedural team. Obtain cultures without materially delaying antibiotics. Use an appropriate initial antibiotic dose, then pharmacy-guided maintenance adjusted to the evolving kidney function, organism and infusion protocol; brisk urine output alone does not establish drug clearance. Why not the others: A — antibiotics alone against an undrained, infected system is the classic fatal delay. B — instrumenting an infected, obstructed system to remove the stone risks spreading the infection; drain first, treat the stone once the infection has cleared. D — lithotripsy does not drain the kidney and can push infection into the blood; it is a later, elective option. Course reading: Evidence for this case
What happened. Blood cultures × 2 were drawn at 11:50; piperacillin-tazobactam 4.5 g IV was given at 12:05; 1 L of lactated Ringer's ran over 30 minutes and a further 500 mL at 12:40, with the blood pressure rising to 118/70. Interventional radiology placed a right percutaneous nephrostomy under ultrasound guidance at 13:10; 180 mL of frankly purulent urine drained immediately and was sent for culture. Urine output over the next hour: 350 mL. The potassium at 14:00 was 4.9 mEq/L; at 20:00, 4.2.
Antibiotics dosed to the creatinine trend (hospital days 0–5):
| Day | Creatinine (mg/dL) | Urine output | Drug | Dose | Route | Frequency | Rationale |
|---|---|---|---|---|---|---|---|
| 0 (12:05) | 5.1, anuric, not yet drained | 0 | Piperacillin-tazobactam | 4.5 g | IV | once | Initial sepsis dose selected with pharmacy; maintenance must be reviewed separately |
| 0 (18:00) | 4.6 at 17:00 and falling; draining since 13:10 | 350 mL/h | Piperacillin-tazobactam | Individualized | IV | Per local AKI protocol | Pharmacy reassesses clearance and infection severity; urine volume is not a clearance measurement |
| 1 | 3.9, falling | 300 mL/h | Piperacillin-tazobactam | Reassessed daily | IV | Per local AKI protocol | A falling creatinine makes steady-state equations unreliable; do not infer full dosing from diuresis |
| 2 | 2.4, falling fast | 180 mL/h | Ceftriaxone (narrowed) | 1 g | IV | q24h | Cultures: E. coli susceptible to ceftriaxone and ciprofloxacin, resistant to TMP-SMX; usual ceftriaxone doses generally need no adjustment for isolated renal impairment; review severe combined renal and hepatic dysfunction |
| 4 | 1.6 | 110 mL/h | Ceftriaxone | 1 g | IV | q24h | Afebrile 48 h, tolerating oral intake |
| 5 (discharge) | 1.3 | normal | Ciprofloxacin | 500 mg | PO | q12h, to complete 14 days total | Creatinine near baseline (Cockcroft–Gault about 80 mL/min): no adjustment; the label specifies 250–500 mg q12h at a stable CrCl of 30–50 mL/min |
Clinical Pearl — Dose the antibiotic to the trend, not to the number printed yesterday Do not estimate antibiotic clearance from urine volume alone. Severe infection needs prompt adequate initial treatment, while maintenance doses require pharmacy review as kidney function changes. The piperacillin–tazobactam label uses creatinine-clearance bands, but ordinary clearance equations assume a steady creatinine. Avoid nitrofurantoin for kidney infection regardless of eGFR; TMP-SMX was unsuitable here because of hyperkalemia risk and resistance.
Day 0, 17:00 — four hours after the nephrostomy. Urine output 350 mL/h for four hours running. BP 126/76, pulse 86, no orthostatic drop, mucous membranes moist. Repeat BMP: Na 134, K 4.6, HCO₃⁻ 19, creatinine 4.6. Net fluid balance since arrival about +0.2 L. The night PA asks whether to "match the output with normal saline so he doesn't dry out" or "give furosemide so we don't overload him."
Q10Post-obstructive diuresis
Four hours after decompression of a solitary obstructed kidney: urine output 350 mL/h × 4 h, hemodynamically stable, no orthostasis, creatinine falling (5.1 → 4.6), Na 134, K 4.6. What is the right management?
Match each hour's urine output 1:1 with IV normal saline so that he cannot become volume depleted during the night
Oral fluids and individualized partial IV replacement if needed; frequent volume and electrolyte checks
Furosemide 40 mg IV now to head off fluid overload, since he has received 1.5 L of crystalloid since he arrived at 09:30
Restrict fluids to 1 L/day, because his sodium has fallen from 136 to 134 mEq/L and is likely to keep falling
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Sustained urine output above 200 mL/h after decompression raises concern for post-obstructive diuresis. Follow intake, output, weight, blood pressure and electrolytes. Allow oral intake when safe and replace a tailored portion of losses intravenously if needed; select fluid composition from volume status and the sodium trend. Avoid automatically matching every milliliter, but do not permit hypovolemia. Sodium, potassium, magnesium and phosphorus need frequent checks, initially every 6–12 hours or more often if unstable. Why not the others: A — automatic 1:1 replacement may prolong diuresis or overload him; replacement must follow the examination and losses. C — a loop adds avoidable electrolyte losses. D — a sodium of 134 does not by itself justify fluid restriction in a patient losing large volumes; reassess water and salt balance. Course reading: Evidence for this case
Days 1–5. Output peaked at 400 mL/h overnight and was under 150 mL/h by hour 36. Day 2: Na 133, K 3.3 (potassium chloride 40 mEq PO given twice), Mg 1.6 (magnesium sulfate 2 g IV once), phosphorus 2.3, creatinine 2.4. Afebrile from the morning of day 2. Blood cultures: E. coli in both bottles; nephrostomy urine grew the same organism. Creatinine 1.6 on day 4, 1.3 on day 5; home on day 5 with the nephrostomy draining to a leg bag (the stone still blocks the ureter), oral ciprofloxacin, oxycodone for 3 days, and no lisinopril yet. Ten days later, afebrile and off antibiotics, urology performed ureteroscopy with laser lithotripsy and removed the nephrostomy. The fragments went to the lab: calcium oxalate monohydrate.
Q11Preventing the next one
At the 2-week post-discharge visit: creatinine 1.2 mg/dL, K⁺ 4.3, BP 148/88, stone analysis calcium oxalate monohydrate, first stone ever, solitary kidney. Which prevention plan is correct?
Restrict dietary calcium to under 400 mg/day and avoid dairy, since the stone is made of calcium; repeat imaging in a year
Start hydrochlorothiazide 25 mg daily today for prevention; no urine studies are needed after a first calcium oxalate stone
Fluids to at least 2.5 L/day of urine, sodium under 2.3 g/day, normal dietary calcium; no 24-hour urine after a first stone
Fluids to at least 2.5 L/day of urine, sodium under 2.3 g/day, normal dietary calcium, and two 24-hour urines once recovered
Show answer and explanation · Link to this question
Correct answer: D
Learning point: Calcium oxalate points to low urine volume (his coffee-and-one-glass-of-water workday in a hot shop), high sodium, excess animal protein and sometimes low citrate or high oxalate, so every former gets fluids, less sodium, moderate protein and normal calcium (1,000–1,200 mg/day with meals). The 24-hour urine is for recurrent formers and high-risk first-time formers, and a man whose next stone could again block his only kidney is high-risk. Collect twice on his usual diet, several weeks after the episode and the procedure, and let the results choose the drug: a thiazide for hypercalciuria, potassium citrate for hypocitraturia. Why not the others: A — restricting calcium leaves more oxalate free to be absorbed and excreted, so it promotes stones. B — a thiazide treats documented hypercalciuria, so it waits for the urine results. C — the diet is right, but "no 24-hour urine after a first stone" does not apply to a high-risk former. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11
At the 2-week visit his blood pressure was 148/88 off lisinopril; the creatinine was 1.2 and the potassium 4.3, so lisinopril was restarted at 10 mg daily with a BMP ten days later (creatinine 1.3, potassium 4.6 — a rise under 30%, inside the ≤30% that the KDIGO 2024 CKD guideline says to accept) and a sick-day rule written on the after-visit summary: hold lisinopril during a dehydrating illness with poor intake under a written restart plan, and avoid self-prescribed NSAIDs; ask the kidney team before using them. His two 24-hour urines at six weeks: volume 1.4 L, calcium 320 mg/day, oxalate 32 mg/day, citrate 350 mg/day, sodium 3,800 mg/day — a low-volume, high-sodium, mildly hypercalciuric pattern. He left with a 2.5-L water bottle for the shop and a sodium target; the thiazide waits for the repeat collection. At three months his creatinine was 1.1 — his old baseline. The problem list now reads "AKI stage 3, obstructive, 10/2026, resolved; solitary kidney; calcium oxalate nephrolithiasis," and a renal ultrasound is booked at 6 months — ultrasound, not another CT, for a man with one kidney who will be imaged for decades to come.
The counterfactual the room should hear: had interventional radiology been unavailable until 06:00 and the potassium rebounded to 6.8 with a 140-ms QRS at 15:00 despite calcium, insulin, albuterol and a binder, the answer would have been hemodialysis through a temporary catheter that afternoon. Refractory hyperkalemia with ECG changes is the E in AEIOU, and in an obstructed, anuric kidney there is no other fast route out — the binder works, but over hours. The temporizing drugs exist to cover the interval until either the drain or the dialysis catheter is in.
Clinical Pearl — The bladder is downstream A bladder scan answers "is the bladder retaining urine?" and nothing more. In an anuric patient a reading of 0 mL does not mean "not obstructed"; in a man with one kidney and flank pain it means nothing is getting past the stone. Bladder scan first for any anuric AKI (a full bladder is the BPH pattern — Foley, recheck), then renal ultrasound, then non-contrast CT.
Clinical Pearl — One kidney and one stone equals two blocked ureters Creatinine tracks total filtration. A unilateral stone in a two-kidney patient leaves the creatinine alone; the same stone in a solitary kidney, or stones in both ureters, means anuric AKI with hyperkalemia and acidosis. Obstruction plus any one of these — a solitary kidney, both sides blocked, AKI, or fever — is a drainage emergency.
Clinical Pearl — Stabilize, shift, then find the exit Calcium protects the heart for 30–60 minutes; insulin and albuterol hide potassium inside cells for a few hours. None of them removes any. In an obstructed, anuric kidney there is no urinary exit: furosemide has nothing to act on, and a binder removes potassium through the gut but too slowly for an emergency. The removal therapy is decompression — and dialysis if decompression is delayed or the potassium stays up with ECG changes. Make both phone calls in the first fifteen minutes.
Clinical Pearl — Fever turns a stone into an emergency Fever, pyuria and sepsis physiology behind an obstructing stone equal infected obstruction. Cultures, then antibiotics within the hour (appropriate initial dosing, then pharmacy-guided reassessment during changing renal function), and decompression the same day by stent or nephrostomy. Antibiotics alone do not reach pus under pressure; medical expulsive therapy asks for time the patient does not have.
Clinical Pearl — After the drain, expect the flood Sustained output above 200 mL/h after decompression warrants a post-obstructive diuresis plan: intake/output, weight, volume examination and frequent electrolytes. Use oral intake and tailored partial IV replacement; choose the fluid from the sodium and volume trends. Neither automatic fluid restriction nor automatic liter-for-liter replacement is safe.
Pitfall — Ketorolac for the colic The reflex stone analgesic is an NSAID. In an AKI — especially one already primed by three doses of ibuprofen and an ACE inhibitor — there is no safe NSAID dose. IV opioid plus a scheduled antiemetic, acetaminophen as an adjunct, and write "no NSAIDs" on the discharge summary of anyone with one kidney.
Concept Links
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11
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: aki-03, aki-07, aki-13, aki-17, aki-18, aki-22, aki-25, lytes-12, lytes-13, structural-01, structural-02, structural-03, structural-05, structural-06, structural-07, structural-08, structural-14, structural-20.