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Question and answer links
- W1: A 58-year-old man who has smoked a pack a day for 35 years reports two episodes of painless, bright-red urine with small · Answer
- W2: A 9-year-old boy (height 136 cm, the 50th percentile for his age) has had three days of a non-blanching purple rash over · Answer
- W3: A 72-year-old man is three days out from septic shock that needed vasopressors. His creatinine has climbed from 1.0 to 2 · Answer
- Q4: Cola-colored urine, dipstick 3+ blood and 2+ protein, BP 148/92, day two of pharyngitis, no dysuria, no flank pain. Whic · Answer
- Q5: Her urine turned dark on day two of the sore throat. Before any serology is back, which statement about timing is correc · Answer
- Q6: Nephritic sediment on day two of a viral pharyngitis, UPCR 1.2 g/g, creatinine 1.0 with no prior value, C3 118 and C4 26 · Answer
- Q7: Creatinine 2.4 mg/dL today; her only prior value is 1.0 three weeks ago. The lab prints eGFR 29. The sediment is active · Answer
- Q8: You have named RPGN. It is 12:30 on a Monday in an outpatient clinic. Which set of orders is right for this afternoon? · Answer
- Q9: If you were thinking IgA nephropathy, and you then learn that today's C3 is 42 mg/dL and C4 is 8 mg/dL — both low — this · Answer
- Q10: Admission potassium 5.6 mEq/L, bicarbonate 18, creatinine 2.4 and rising, ECG sinus rhythm with normal intervals and no · Answer
- Q11: BP 158/98, UPCR 3.1 g/g, potassium 5.6, creatinine rising, urine hCG negative this morning, on a combined oral contracep · Answer
- Q12: A 28-year-old develops hemoptysis, hypoxemia, bilateral alveolar opacities, red-cell casts and a creatinine rise from 1. · Answer
Session S3 · 2026-10-28 · in-session · 37 min Anchor: Hematuria and nephritic syndrome that becomes RPGN (IgA vs post-infectious; lupus; ANCA; anti-GBM) · Integrates: Glomerular vs urologic hematuria routing, AKI staging and the invalid eGFR, AEIOU and hyperkalemia with AKI, ACEi contraindications and the pregnancy test, pediatric BP and HSP (warm-up) One-line hook: Cola-colored urine on day two of a sore throat reads like textbook IgA nephropathy — until she comes back three weeks later and every result has to be read again. A new PA will see this exact sequence. The skill is knowing which visit is the emergency.
Author: Andrew Bland, MD, FACP, FAAP — Medical Associates Dept of Nephrology | UICOMP | UDPA | Butler COM. Fictional patient.
Learning Objectives
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
- Define microhematuria by microscopy (≥3 RBC/hpf on a properly collected specimen, never by dipstick alone) and route it: dysmorphic red cells, acanthocytes, RBC casts or proteinuria go to nephrology; isomorphic cells with urothelial-cancer risk factors go to urology.
- Separate synpharyngitic IgA nephropathy from post-infectious glomerulonephritis using timing and the C3/C4 pattern, and name the supportive care and referral pace for each.
- Recognize rapidly progressive glomerulonephritis (a creatinine moving over days to weeks plus an active sediment), stage the AKI with KDIGO 2012, explain why the printed eGFR is invalid, send the stat serology panel, and call nephrology the same day without waiting for a biopsy.
- Manage what rides along with glomerular AKI at student level: pair the potassium with the ECG, run the AEIOU check, control blood pressure with a pregnancy test before any ACEi or ARB, and stop the NSAID.
- State that biopsy and immunosuppression are nephrology's decisions and that uncontrolled blood pressure is treated before a biopsy (other contraindications and the lupus every-visit checks are discussed in the Resolution, not tested).
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2 · W3
Three readiness items. Cards up, no discussion yet; they check that the prerequisites are in the room.
W1The painless gross hematuria
A 58-year-old man who has smoked a pack a day for 35 years reports two episodes of painless, bright-red urine with small clots at the end of the stream. No fever, no flank pain. BP 132/80. Urinalysis: 3+ blood, protein negative. Microscopy on a fresh specimen: >100 RBC/hpf, all uniform discs (isomorphic), no casts. Creatinine 0.9 mg/dL. Where does he go?
Nephrology, same day — gross hematuria is rapidly progressive glomerulonephritis until proven otherwise
Urology — isomorphic cells, no protein, no casts; gross hematuria in a 35-pack-year smoker is AUA/SUFU high-risk
Repeat the urinalysis in six weeks — most gross hematuria in older male smokers is prostatic and settles on its own
Primary care — start an ACE inhibitor for the hematuria and recheck the urinalysis in three months
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Red cells that squeeze through an inflamed glomerulus come out deformed; his are uniform discs, with no protein, no casts, and clots at the end of the stream — a pattern favoring nonglomerular urinary-tract bleeding; an upper-tract source remains possible. The question is no longer "which glomerulonephritis" but "which part of the urinary tract is bleeding, and is it a cancer." The AUA/SUFU microhematuria guideline's high-risk category is age ≥60, more than 30 pack-years, more than 25 RBC/hpf, or any gross hematuria — he qualifies on the pack-years and the gross hematuria alone. High risk means cystoscopy for the bladder and CT urography for the upper tract. Why not the others: A — the glomerular pathway applied to isomorphic cells with no casts or protein; C — a red flag treated as benign, and unexplained hematuria is not resolved hematuria; D — a proteinuric-disease drug given for a symptom with no proteinuria. Course reading: Evidence for this case
W2The boy with the rash
A 9-year-old boy (height 136 cm, the 50th percentile for his age) has had three days of a non-blanching purple rash over his buttocks and legs, sore swollen knees and ankles, and colicky belly pain. Urinalysis in the office shows 2+ blood and 1+ protein. His BP, repeated twice by auscultation with the correct cuff, is 128/84. What is the right read of these findings?
Viral exanthem with reactive arthritis; the BP is normal because 128/84 sits below the adult 130/80 cutoff
Immune thrombocytopenia; check a platelet count and call hematology before anything else is done
IgA vasculitis (Henoch-Schönlein purpura) with hypertensive-range BP for age and height; work up the kidney, follow the BP
Post-streptococcal glomerulonephritis; the rash is scarlet fever, the belly pain is viral, and the BP is elevated-range only
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Palpable purpura, joint pain, abdominal pain and hematuria/proteinuria suggest IgA vasculitis with kidney involvement. In the AAP Table 4 row for a 9-year-old boy at the 50th height percentile (136.3 cm), the 95th percentile is 115/76 and the 95th percentile plus 12 mmHg is 127/88. His repeated 128/84 is therefore in the stage 2 range by systolic pressure. The AAP table reproduced by Connecticut Children's, Appendix G, page 2 supplies the numerical row. This is a BP category at this visit, not proof of chronic primary hypertension. Active kidney findings warrant prompt pediatric assessment and nephrology advice; severe symptoms or marked pressure elevation require emergency evaluation. Why not the others: A — an adult cutoff applied to a child, the one error this warm-up exists to catch; B — vasculitic purpura mistaken for thrombocytopenic purpura (purpura you can feel is vasculitis); D — the wrong rash (scarlet fever is diffuse sandpaper, not dependent purpura) and an understaged BP. Course reading: Evidence for this case
W3Match the cast to the patient
A 72-year-old man is three days out from septic shock that needed vasopressors. His creatinine has climbed from 1.0 to 2.6 mg/dL, urine specific gravity is 1.010, and he is making 20 mL/h of urine. Which sediment do you expect under the microscope?
Muddy brown granular casts with renal tubular epithelial cells
RBC casts with dysmorphic red cells and acanthocytes above 5%
WBC casts with sterile pyuria and no bacteria on the Gram stain
Oval fat bodies and fatty casts with 4+ protein on the dipstick
Show answer and explanation · Link to this question
Correct answer: A
Learning point: A cast is a cylinder molded inside a kidney tubule around a protein core (uromodulin, the Tamm-Horsfall protein), so whatever is trapped inside came from the kidney — never the bladder, prostate or vagina — and names the injured compartment. Ischemia after shock kills tubular cells; they slough into the lumen and degrade into coarse granular debris that looks like mud. Muddy brown casts with tubular cells, a urine the kidney can no longer concentrate (specific gravity near 1.010) and oliguria three days after vasopressors is acute tubular necrosis. Why not the others: B — glomerular bleeding: red cells in a cast passed through a glomerulus, so RBC casts mean glomerulonephritis, where today's case lives; C — white cells from the kidney itself, pyelonephritis or interstitial nephritis, not shock; D — the lipid of the nephrotic syndrome, unrelated to a post-sepsis creatinine rise. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q4 · Q5
Visit 1 — a Tuesday afternoon in student health, late October.
Lena is 19, a sophomore, and she is embarrassed to be here. Two days ago her throat started to hurt — scratchy, then raw, worse on swallowing. Low fever last night. This morning her urine was the color of cola. No pain with urination, no flank pain, no clots. She has never had blood in her urine before, never been told her blood pressure was high, and has never had blood work done ("I've never been sick enough"). She rows for the club team, drinks on weekends, does not smoke or vape, and has no family history of kidney disease, deafness or lupus. Her last period was two weeks ago and regular on her pill.
She took ibuprofen around the clock for the throat.
Vitals: BP 148/92 (repeated, seated, right arm, 146/90) · HR 84 · T 38.1 °C (100.6 °F) · RR 16 · SpO₂ 99% room air · weight 61 kg · height 165 cm.
Exam: Pharynx red without exudate, tender anterior cervical nodes. No rash. No joint swelling. No periorbital or ankle edema. Lungs clear. Heart regular, no murmur. Abdomen soft, no flank tenderness. Rapid strep antigen in the office: negative.
Office dipstick: blood 3+, protein 2+, leukocyte esterase negative, nitrite negative, glucose negative.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Ibuprofen | 400 mg | PO | every 6 h as needed (taking 3 doses/day × 2 days) | sore throat, fever |
| Norethindrone 1 mg / ethinyl estradiol 35 mcg | 1 tablet | PO | daily | contraception |
| Cetirizine | 10 mg | PO | daily as needed | seasonal allergies |
Three facts sit in that stem that a new PA has to hold at once: a febrile pharyngitis, a blood pressure of 148/92 in a 19-year-old rower, and a dipstick that says blood and protein. The first question is whether that dipstick is even hematuria.
Q4Is it blood, and where is it from?
Cola-colored urine, dipstick 3+ blood and 2+ protein, BP 148/92, day two of pharyngitis, no dysuria, no flank pain. Which single step tells you whether this is hematuria and whether it comes from the glomerulus?
Treat as a urinary tract infection with empiric cephalexin and recheck the dipstick once the course is finished
CT urography today — gross hematuria in an adult is imaged before anything else is ordered
Repeat the dipstick in one week; a positive heme pad during a febrile illness is often transient
Microscopy on a fresh specimen — RBC count, shape and casts — plus a urine protein-to-creatinine ratio
Show answer and explanation · Link to this question
Correct answer: D
Learning point: A dipstick heme pad turns positive for intact red cells, free hemoglobin from hemolysis and myoglobin from muscle breakdown alike; it cannot tell them apart and it cannot see shape. Hematuria is a microscope word — the AUA/SUFU guideline defines microhematuria as three or more red cells per high-power field on a properly collected specimen, confirmed before a positive pad triggers any evaluation. The same drop of urine then answers the second question: misshapen (dysmorphic) cells, ring forms with blebs (acanthocytes) or cells packed into a cast came through a glomerulus, and the UPCR puts a number on the protein pad. Why not the others: A — an infection invented with negative leukocyte esterase and nitrite and no dysuria; B — the urology pathway (W1) applied to a febrile teenager with 2+ protein; C — a week's wait on a BP of 148/92 when a microscope settles it today. Course reading: Evidence for this case
Pause — commit before the reveal
Q5The clock
Her urine turned dark on day two of the sore throat. Before any serology is back, which statement about timing is correct?
Gross hematuria 1–3 weeks after pharyngitis is the IgA nephropathy pattern; hematuria during the infection itself points to post-streptococcal GN
Gross hematuria within 1–3 days of the infection ("synpharyngitic") is the IgA pattern; post-streptococcal GN follows pharyngitis by 1–3 weeks
Hematuria on day two is post-streptococcal GN, because streptococcus triggers both diseases and the latency is the same for each
Timing does not separate the two diseases at the bedside; only a kidney biopsy read by a pathologist can tell them apart
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Two diseases, two clocks. In IgA nephropathy the abnormal IgA is already sitting in the mesangium, so a mucosal infection lights it up within a day or two — cola urine while the throat still hurts, peaking in young adults. Post-infectious GN has to wait for an antibody response, immune-complex formation and deposition: 1–3 weeks after a strep throat, 3–6 weeks after impetigo. A sore throat on Sunday and dark urine on Tuesday is the wrong tempo for post-streptococcal disease, and her negative rapid strep fits — most synpharyngitic flares follow a viral pharyngitis, not strep. Why not the others: A — the clocks reversed; C — "strep triggers it" read as "strep triggers it today," ignoring the latency; D — defeatist: timing and complement sort the probability at the bedside, and biopsy settles the histology. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q6 · Q7 · Q8
Visit 1 laboratory results (same afternoon).
| Test | Result | Reference range |
|---|---|---|
| Sodium | 139 mEq/L | 135–145 |
| Potassium | 4.2 mEq/L | 3.5–5.0 |
| Chloride | 104 mEq/L | 98–107 |
| Bicarbonate | 24 mEq/L | 22–28 |
| Anion gap (Na − [Cl + HCO₃]) | 11 mEq/L | 8–12 mEq/L |
| BUN | 14 mg/dL | 7–20 |
| Creatinine | 1.0 mg/dL | 0.5–1.0 (female) |
| BUN:creatinine | 14:1 | 10–20:1 |
| eGFR (CKD-EPI 2021, printed by the lab) | 83 mL/min/1.73 m² | >90 — valid only if creatinine is stable; no prior value exists, so a repeat at 48–72 h is ordered |
| Glucose | 92 mg/dL | 70–99 |
| Calcium | 9.3 mg/dL | 8.5–10.5 |
| Albumin | 3.9 g/dL | 3.5–5.0 |
| Hemoglobin | 12.8 g/dL | 12.0–16.0 |
| WBC | 9.8 ×10³/µL | 4.0–11.0 |
| Platelets | 265 ×10³/µL | 150–400 |
| C3 | 118 mg/dL | 90–180 |
| C4 | 26 mg/dL | 16–47 |
| ASO titer | 120 IU/mL | <200 (drawn day 2 — too early to rise; a baseline for a repeat) |
| Throat culture | pending (later: no group A strep) | — |
Urinalysis with microscopy (fresh clean-catch, read within 30 minutes).
| Parameter | Result | Reference |
|---|---|---|
| Color / clarity | brown ("cola"), slightly hazy | yellow, clear |
| Specific gravity | 1.018 | 1.005–1.030 |
| pH | 6.0 | 4.5–8.0 |
| Blood | 3+ | negative |
| Protein | 2+ | negative |
| Leukocyte esterase / nitrite | negative / negative | negative |
| Glucose / ketones | negative | negative |
| RBC | 40/hpf; >50% dysmorphic; acanthocytes about 12% of red cells | 0–2/hpf; acanthocytes <5% |
| RBC casts | 2–3 per low-power field | none |
| WBC | 0–2/hpf | 0–5/hpf |
| Squamous epithelial cells | none | few — "many" means a contaminated specimen |
| Bacteria | none | none |
| Urine protein-to-creatinine ratio (UPCR) | 1.2 g/g | <0.15 g/g |
Read it the way the chapter teaches: are the red cells deformed, and are there casts? Both. Acanthocytes at 12% are above the 5% threshold that Köhler found 98% specific for glomerular bleeding, and red cell casts prove the cells were inside the nephron. Protein 1.2 g/g — real, but under the nephrotic 3.5 g/g line. Blood pressure up. Creatinine 1.0 — at the upper limit for a woman, and the lab's own eGFR of 83 is below its >90 reference. In a 19-year-old that may be a rower's muscle mass or a 30% loss of filtration; with no prior value, nobody can say which. That uncertainty is one more reason the call happens today.
That is the nephritic pattern: hematuria with casts, sub-nephrotic proteinuria, hypertension, and a kidney that may or may not be losing function. The nephrotic pattern is the other animal — more than 3.5 g of protein a day, albumin under 3, edema, high cholesterol, and a sediment that is bland except for fat. She is nephritic.
And the complements are normal.
Q6What the normal complements buy you, and what you do this afternoon
Nephritic sediment on day two of a viral pharyngitis, UPCR 1.2 g/g, creatinine 1.0 with no prior value, C3 118 and C4 26 (both normal), rapid strep negative. Which pairing of working diagnosis and plan is correct for today?
IgA nephropathy — call nephrology today, stop the ibuprofen, treat the BP, send ANA, ANCA and anti-GBM, repeat creatinine and UPCR at 48–72 h
Post-streptococcal GN — penicillin V for 10 days, acetaminophen in place of the ibuprofen, and recheck the urinalysis and creatinine in three weeks
Lupus nephritis — start prednisone 1 mg/kg today and refer to rheumatology; the serology can follow once the steroid has started
Urologic bleeding — CT urography and cystoscopy first, with nephrology contact only if the imaging is unrevealing
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Complement is the first sort in a nephritic sediment: both low → classical pathway (lupus, cryoglobulinemia — antibodies that clump in the cold, usually from hepatitis C — endocarditis, MPGN); low C3 with normal C4 → alternative pathway (post-infectious GN, C3 glomerulopathy); both normal → IgA nephropathy, ANCA vasculitis and anti-GBM disease, which do not consume complement. Normal complement plus synpharyngitic timing in a 19-year-old makes IgA the working diagnosis. Complement sorts the probability; it does not replace the panel — ANA goes with every nephritic sediment, ANCA and anti-GBM with any that could be RPGN. The plan follows the sediment, not the creatinine: RBC casts with proteinuria earn a phone call today, not a referral form, and the NSAID stops. Why not the others: B — fights the clock and the complement (day two is too early for PSGN, which runs a low C3), and antibiotics treat a strep infection, not a GN; C — immunosuppression started from student health before the serology, a decision that is nephrology's; D — W1's pathway applied to dysmorphic cells, casts and protein. Course reading: Evidence for this case
What actually happened. Nephrology took the call, agreed with the IgA working diagnosis, and asked that the ANA, ANCA and anti-GBM go on the same slip as the 72-hour creatinine and UPCR — one draw, one trip to the lab — with a clinic visit in two weeks. Nephrology deferred an antihypertensive to the 72-hour visit, to re-measure off the NSAID — a visit that never happened. Lena's throat got better in four days. The urine cleared to its usual color. The lab slip for the 72-hour draw, serology and all, went in her backpack. Midterms came. The clinic referral went by fax and no one owned the follow-up.
Visit 2 — three weeks later, the same clinic, a Monday morning.
She comes back because she cannot get out of bed. Two weeks of fatigue that sleep does not fix. Wrists, knuckles and knees ache and feel stiff for an hour every morning. A rash across both cheeks and the bridge of her nose came up after a weekend outside and has not faded; it skips the folds beside her nose. Low fevers in the evenings. She has been taking naproxen for the joints for eight days. Her urine is dark again and she thinks she is making less of it. Her weight is 63 kg — up 2 kg. No cough, no hemoptysis, no shortness of breath, no chest pain. No sinus pain, no nosebleeds. No new medications besides the naproxen.
Vitals: BP 158/98 (repeat 156/96) · HR 88 · T 37.9 °C · RR 18 · SpO₂ 98% room air.
Exam: Malar rash sparing the nasolabial folds. One shallow painless ulcer on the hard palate. Mild synovitis at both wrists and the second and third MCP joints; knees without effusion. Trace bilateral ankle edema. Lungs clear, no crackles. Heart regular, no rub, no murmur. No JVD. Alert, oriented, no asterixis (the flapping hand tremor of uremia). Abdomen soft.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Naproxen (OTC) | 220 mg | PO | twice daily × 8 days | joint pain |
| Norethindrone 1 mg / ethinyl estradiol 35 mcg | 1 tablet | PO | daily | contraception |
| Cetirizine | 10 mg | PO | daily as needed | seasonal allergies |
| Ibuprofen | — | — | stopped at visit 1 | — |
Visit 2 laboratory results (drawn 10:15, resulted by noon).
| Test | Result | Reference range | Visit 1 (3 weeks ago) |
|---|---|---|---|
| Sodium | 137 mEq/L | 135–145 | 139 |
| Potassium | 5.6 mEq/L | 3.5–5.0 | 4.2 |
| Chloride | 107 mEq/L | 98–107 | 104 |
| Bicarbonate | 18 mEq/L | 22–28 | 24 |
| Anion gap | 12 mEq/L (albumin-corrected 14) | 8–12 mEq/L | 11 |
| BUN | 44 mg/dL | 7–20 | 14 |
| Creatinine | 2.4 mg/dL | 0.5–1.0 | 1.0 |
| BUN:creatinine | 18:1 | 10–20:1 | 14:1 |
| eGFR (printed) | 29 mL/min/1.73 m² | not valid — creatinine is moving | 83 |
| Glucose | 94 mg/dL | 70–99 | 92 |
| Calcium | 8.6 mg/dL (albumin-corrected 9.2) | 8.5–10.5 | 9.3 |
| Phosphorus | 4.9 mg/dL | 2.5–4.5 | — |
| Magnesium | 2.0 mg/dL | 1.7–2.2 | — |
| Albumin | 3.2 g/dL | 3.5–5.0 | 3.9 |
| Hemoglobin | 10.4 g/dL | 12.0–16.0 | 12.8 |
| WBC | 3.4 ×10³/µL (lymphocytes 0.7) | 4.0–11.0 | 9.8 |
| Platelets | 142 ×10³/µL | 150–400 | 265 |
| ESR | 68 mm/h | <20 | — |
| Urine hCG | negative | negative | — |
| ECG | sinus rhythm 88, PR 150 ms, QRS 86 ms, QTc 410 ms, no peaked T waves | — | — |
Urinalysis with microscopy (fresh clean-catch, read within 30 minutes) — visit 2 beside visit 1.
| Parameter | Result (visit 2) | Reference | Visit 1 (3 weeks ago) |
|---|---|---|---|
| Color / clarity | dark brown, hazy | yellow, clear | brown ("cola"), slightly hazy |
| Specific gravity | 1.012 | 1.005–1.030 | 1.018 |
| pH | 6.0 | 4.5–8.0 | 6.0 |
| Blood | 3+ | negative | 3+ |
| Protein | 3+ | negative | 2+ |
| Leukocyte esterase / nitrite | trace / negative | negative | negative / negative |
| RBC | 60/hpf; mostly dysmorphic; acanthocytes about 15% | 0–2/hpf; acanthocytes <5% | 40/hpf; >50% dysmorphic; acanthocytes about 12% |
| RBC casts | 4–6 per low-power field | none | 2–3 per low-power field |
| WBC | 8/hpf, no bacteria | 0–5/hpf | 0–2/hpf |
| Granular casts | occasional | none | none |
| Squamous epithelial cells | none | few | none |
| Urine protein-to-creatinine ratio (UPCR) | 3.1 g/g | <0.15 g/g | 1.2 g/g |
The arithmetic first, because the room will reach for the eGFR. Anion gap 137 − (107 + 18) = 12; her albumin is 3.2, so add 2.5 × 0.8 = 2 → corrected gap 14. A mild acidosis of falling filtration — retained acid plus bicarbonate the kidney is no longer regenerating. BUN:creatinine 18, not the >20 of a dry patient; she is not dry. White count down, hemoglobin down, platelets down — three cell lines moving the wrong way in three weeks. And a creatinine that has gone from 1.0 to 2.4.
Pause — commit before the reveal
Q7Name what this is
Creatinine 2.4 mg/dL today; her only prior value is 1.0 three weeks ago. The lab prints eGFR 29. The sediment is active (dysmorphic RBCs, acanthocytes, RBC casts) and UPCR has risen to 3.1 g/g. She has fatigue, arthralgia and a malar rash. Which statement is correct?
CKD stage G4 (eGFR 15–29) — refer routinely, repeat the creatinine in three months, and begin CKD education
KDIGO stage 1 AKI at most — a creatinine rise spread over three weeks cannot be staged any higher than that
At least stage 2 AKI by creatinine ratio (7-day window presumed); the printed eGFR is not valid; treat as RPGN until proven otherwise
Not AKI — an eGFR of 29 in an otherwise healthy 19-year-old is a laboratory error, and the sample should be redrawn before any action is taken
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The creatinine ratio is 2.4, which fits stage 2 if the increase is known or reasonably presumed to have occurred within seven days. Her acute illness and active nephritic sediment make acute worsening concerning, but the three-week-old baseline alone cannot establish that interval. Document presumed AKI, obtain the intervening trend urgently and treat possible rapidly progressive GN without waiting for perfect staging. A changing creatinine also makes the printed steady-state eGFR unreliable. Why not the others: A — a non-steady-state eGFR read as a chronic stage, the commonest error with this number, and "routine" would cost her the kidneys; B — misreads the window, not the table: KDIGO writes the ratio criterion for a rise within 7 days, so with a three-week gap the baseline is presumed, and the ≥0.3 mg/dL-in-48-hours criterion is met by 06:00 the next morning (2.4 → 2.9) — either way she is staged and treated as AKI, and the tempo argues for more urgency, not less; D — a coherent story (three low cell lines, active sediment, rising protein, rash) called lab error; redraw if you like, but act now. Course reading: Evidence for this case
Q8This afternoon's orders
You have named RPGN. It is 12:30 on a Monday in an outpatient clinic. Which set of orders is right for this afternoon?
ANA, anti-dsDNA and C3/C4 drawn today; nephrology clinic in two weeks with the results in hand for the visit
Cystoscopy and CT urography this week, with a routine urology referral for painless gross hematuria
Arrange the kidney biopsy first, and send the serologies only after the tissue result so the two can be interpreted together
ANCA (PR3/MPO), anti-GBM, ANA/anti-dsDNA, C3/C4, blood cultures, chest film and renal ultrasound today; call nephrology now
Show answer and explanation · Link to this question
Correct answer: D
Learning point: RPGN has three immune causes and one stat panel finds all three: ANCA (PR3 and MPO) for the pauci-immune vasculitides — pauci-immune means few or no antibody deposits on biopsy, which is why the ANCA pattern needs a blood test to find — anti-GBM antibody for anti-GBM disease, and ANA with anti-dsDNA and both complements for lupus. Blood cultures ride along in anyone febrile, because endocarditis causes a low-complement GN that will fool you; the chest film looks for pulmonary hemorrhage; the ultrasound confirms two normal-sized, unobstructed kidneys before anyone considers a needle. All of it leaves the clinic within the hour, and "RPGN" said aloud to a nephrologist buys a same-day evaluation. Do not wait for the biopsy to send the serology, and do not wait for the serology to make the call. Why not the others: A — a lupus-only panel that misses ANCA and anti-GBM (the two with pulmonary hemorrhage) and waits two weeks on a disease measured in days; B — the bladder imaged in a patient with casts, wrong compartment; C — the order inverted: biopsy is nephrology's call, often within 48 hours of admission, and the serology must be drawn before treatment changes it. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q9 · Q10 · Q11
Nephrology saw her at 15:40 the same day and admitted her to a monitored medical bed. Urine output on the ward 35 mL/h (about 0.55 mL/kg/h at 63 kg). The chest film was clear with a normal heart size. Renal ultrasound: right kidney 11.8 cm, left 12.1 cm, mildly echogenic cortex, no hydronephrosis, post-void residual 25 mL. Repeat chemistry and ECG ordered for 16:00 and 06:00.
The panel came back over the next 36 hours, the complements first. Three weeks ago both were normal and the room — correctly, on the evidence it had — called this IgA nephropathy.
Q9Evidence update
If you were thinking IgA nephropathy, and you then learn that today's C3 is 42 mg/dL and C4 is 8 mg/dL — both low — 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
Learning point: IgA nephropathy does not consume serum complement — it sits in the normal-complement column with ANCA vasculitis and anti-GBM disease, which is why her normal C3 and C4 three weeks ago supported it. Both C3 and C4 low is the classical-pathway fingerprint of circulating immune complexes — lupus nephritis first, then cryoglobulinemia (check hepatitis C), endocarditis (hence the cultures) and MPGN — so the hypothesis moves a long way: "much less likely," not "excluded," because serology is a probability and nephrology still has to see tissue. The circumstance that gives the finding its meaning is that it is both complements; C3 42 with a normal C4 would be the alternative pathway (post-infectious GN, C3 glomerulopathy) and a different move — read the C4 before you move. None of the alternatives fits a 19-year-old woman with a malar rash, oral ulcer, arthritis and three low cell lines, and the panel below confirms it: this is lupus nephritis presenting as RPGN, and the first complements were not wrong, they were early. Course reading: Evidence for this case
The rest of the panel:
| Test | Result | Reference range |
|---|---|---|
| C3 | 42 mg/dL | 90–180 |
| C4 | 8 mg/dL | 16–47 |
| ANA | 1:1280, homogeneous | <1:80 |
| Anti-dsDNA | 318 IU/mL | <30 |
| MPO-ANCA | <0.2 (negative) | negative |
| PR3-ANCA | <0.2 (negative) | negative |
| Anti-GBM antibody | negative | negative |
| Hepatitis B surface antigen / hepatitis C antibody / HIV | negative / negative / negative | negative |
| Blood cultures × 2 | no growth at 48 h | no growth |
| ASO (3 weeks after the throat) | 110 IU/mL | <200 — a titer that did not rise argues against strep |
| Anti-DNase B | normal | normal |
| Creatinine, day 2 (06:00) | 2.9 mg/dL | 0.5–1.0 — now 2.9× her known value |
| Potassium, day 2 | 5.4 mEq/L | 3.5–5.0 |
| Bicarbonate, day 2 | 19 mEq/L | 22–28 |
Now both complements are low, the ANA strongly positive, the anti-dsDNA ten times the upper limit. The sore throat did not come back. Something else did.
The diagnosis has changed. Her potassium has not waited for it.
Q10The AEIOU check
Admission potassium 5.6 mEq/L, bicarbonate 18, creatinine 2.4 and rising, ECG sinus rhythm with normal intervals and no peaked T waves, lungs clear, no edema beyond trace ankle, alert with no asterixis, urine output 35 mL/h. Which plan is correct tonight?
IV calcium gluconate 1 g now — any potassium above 5.5 with acute kidney injury needs membrane stabilization before anything else
Stop the naproxen, no dietary or IV potassium, repeat potassium and ECG in 2–4 h, tell nephrology; no AEIOU indication tonight
Call for emergency dialysis tonight — a potassium above 5.5 in acute kidney injury is the "E" of AEIOU
Sodium bicarbonate 50 mEq IV now to correct the acidosis and bring the potassium down along with it
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Her potassium 5.6 with worsening AKI needs close reassessment, removal of contributors and nephrology involvement. A normal ECG does not exclude hyperkalemic arrhythmic risk, and specific ECG patterns cannot be assigned reliable potassium ranges. Give IV calcium for toxic hyperkalemic ECG changes; severe potassium elevation needs urgent potassium-lowering treatment even without ECG changes. Empiric calcium when an ECG or monitoring is unavailable is a protocol-dependent emergency decision, not a universal potassium-only rule. Calcium does not remove potassium. Stop naproxen and avoid potassium supplementation; repeat potassium and ECG in 2–4 hours, sooner for deterioration. There is no current refractory electrolyte/acid-base disorder, pulmonary edema, relevant dialyzable toxin or uremic complication establishing an immediate dialysis indication. Continue reassessing the whole clinical picture. Why not the others: A treats any potassium above 5.5 as an automatic calcium indication, which is incorrect. C makes mild hyperkalemia alone a dialysis indication; severity, trajectory, response to medical treatment and other emergencies determine urgency. D uses bicarbonate as an isolated rescue treatment without a supporting indication in this stable vignette. Course reading: Evidence for this case
Pause — commit before the reveal
Q11Blood pressure, proteinuria, and what the student does not start
BP 158/98, UPCR 3.1 g/g, potassium 5.6, creatinine rising, urine hCG negative this morning, on a combined oral contraceptive. Nephrology plans a biopsy within 48 hours. Which plan is correct tonight?
Lisinopril 10 mg tonight — proteinuria of 3 g/g is the indication and the ACE inhibitor is first-line for it
Hold all blood pressure treatment until the biopsy result defines the disease and its treatment
Amlodipine 5 mg tonight after the negative hCG; defer the ACEi/ARB while potassium is 5.6 and creatinine is moving
Prednisone and mycophenolate from the admitting team tonight so the biopsy is not delayed by untreated inflammation
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Treat the hypertension while arranging urgent nephrology evaluation and biopsy. Amlodipine is a reasonable temporary choice while K is 5.6 and kidney function is deteriorating. Biopsy blood-pressure thresholds are center-specific; uncontrolled hypertension increases bleeding risk and requires management. Defer initiation of ACEi/ARB until potassium, kidney trajectory and reproductive precautions have been reviewed. The pregnancy test is already negative. Immunosuppression is the specialist team's decision; in some rapidly progressive syndromes, treatment should not wait for biopsy results. Why not the others: A starts a RAAS blocker during hyperkalemia and worsening AKI; the pregnancy test is not missing. B leaves significant hypertension untreated. D begins a disease-specific regimen without the specialist diagnostic decision. Referral must be urgent, not delayed while primary care selects immunosuppression. Course reading: Evidence for this case
Counterfactual — discuss, no cards. Had Lena arrived at visit 2 coughing up blood, what changes? Hemoptysis plus a glomerular AKI is the pulmonary-renal syndrome, and it narrows the differential to two serologies that must be drawn together: ANCA and anti-GBM. c-ANCA with PR3 points to granulomatosis with polyangiitis (sinuses, lungs, kidneys); p-ANCA with MPO points to microscopic polyangiitis (lungs and kidneys, no upper airway). Anti-GBM disease — Goodpasture syndrome when the lungs are involved — is the glomerulonephritis where nephrology starts plasma exchange on the serology, before the biopsy, because the antibody is the disease and the lungs can bleed fatally. The student's job does not change: send both antibodies with the rest of the panel, get the chest film, and say "pulmonary-renal syndrome" on the phone. Nothing about plasma exchange, its dose or its duration is a student decision. Her chest film was clear and both antibodies were negative — but the panel was sent as if they might not be. → Vasculitis and Complement-Mediated GN student handout — III. Anti-GBM Disease · Course reading: Vasculitis and Complement handout — Anti-GBM Disease (Goodpasture Syndrome)
Self-study checkpoint — after class
Answers for this section: Q12
This additional question is completed after class and does not extend the timed run sheet.
Q12The pulmonary–renal emergency
A 28-year-old develops hemoptysis, hypoxemia, bilateral alveolar opacities, red-cell casts and a creatinine rise from 1.0 to 3.4 mg/dL over five days. Anti-GBM antibodies are strongly positive; ANCA is negative. Which working diagnosis and immediate response are most appropriate?
IgA nephropathy; repeat creatinine in one week before referral
Anti-GBM disease with pulmonary–renal involvement; arrange immediate hospital nephrology and critical-care assessment for treatment while urgent diagnostic confirmation proceeds
ANCA-associated vasculitis established by the lung–kidney pattern; ignore the anti-GBM result
Post-infectious glomerulonephritis; wait for kidney biopsy before escalating care
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Pulmonary hemorrhage with rapidly progressive glomerulonephritis is an emergency. The strongly positive anti-GBM result identifies the leading diagnosis; the lung–kidney pattern alone cannot distinguish anti-GBM disease from ANCA-associated vasculitis. KDIGO advises urgent serology and biopsy, and treatment without delay when anti-GBM disease is suspected. Specialist-directed plasma exchange and immunosuppression may begin before final confirmation; the student's task is recognition and immediate escalation. Why not the others: A and D delay care for organ-threatening disease. C treats a syndrome as a specific diagnosis while disregarding the more discriminating antibody result. Negative ANCA does not exclude every vasculitis, but it does not outweigh the positive anti-GBM evidence here. Evidence: KDIGO anti-GBM key takeaways, Figure 1 and diagnosis/treatment recommendations.
Resolution and Teaching Points
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
Naproxen was stopped on admission, a potassium-restricted diet was ordered, and amlodipine 5 mg was started that evening after the negative hCG. Day 2: BP 136/84 on amlodipine, platelets 142, INR 1.0, no anticoagulants, two 12-cm kidneys — nephrology biopsied her that afternoon. Creatinine peaked at 3.1 on day 3 — 3.1× her known value, stage 3 at the peak, exactly the restaging Q7 promised — and started down. The biopsy showed a proliferative lupus nephritis; nephrology and rheumatology started glucocorticoids, a second immunosuppressant (mycophenolate) and hydroxychloroquine — the class names are the student's to know, the doses are not. Potassium was 4.6 at discharge on day 5 with a creatinine of 2.6 and falling. The combined pill was stopped on admission — estrogen is avoided in active nephritis, uncontrolled hypertension and nephrotic-range proteinuria — and contraception was reviewed with rheumatology and gynecology before discharge; she left on a progestin-only method, with a levonorgestrel IUD arranged.
Week 6 in nephrology clinic: creatinine 1.6, potassium 4.4, urine hCG negative again, contraception confirmed (IUD placed) — lisinopril started. Month 3: creatinine 1.2, UPCR 0.9 g/g, C3 88, C4 15, anti-dsDNA 96 and falling, BP 124/78. She is back on the water with the rowing team. Every visit, for the rest of her life with this disease, gets the same three things: a urinalysis, a UPCR and a creatinine — because lupus nephritis declares itself in the urine before it declares itself anywhere else.
The sore throat never came back. It was a viral pharyngitis that unmasked a disease already underway, and a creatinine of 1.0 — the upper limit, with no baseline to judge it against — beside casts on day two was the first chance to catch it. The second chance was a 72-hour lab slip that no one owned.
Clinical Pearl — Hematuria is a microscope word Three or more red cells per high-power field on a properly collected specimen. The dipstick cannot distinguish red cells from hemoglobin or myoglobin, and it cannot see shape or casts. Acanthocytes at or above 5% are 98% specific for glomerular bleeding; red cell casts prove the cells were inside the nephron. Their absence excludes nothing — sensitivity runs 20–52%.
Clinical Pearl — Two diseases, two clocks Cola urine within 1–3 days of a sore throat is synpharyngitic IgA nephropathy. Post-infectious GN follows pharyngitis by 1–3 weeks and impetigo by 3–6 weeks, runs a low C3 with a normal C4; the C3 normalizes within 6–8 weeks in most patients, and a C3 still low at 12 weeks is no longer post-infectious GN until proven otherwise.
Clinical Pearl — Read the complement pattern before the names Both low → classical pathway: lupus, cryoglobulinemia, endocarditis, MPGN. Low C3 and normal C4 → alternative pathway: post-infectious GN, C3 glomerulopathy. Both normal → IgA nephropathy, ANCA vasculitis, anti-GBM disease. Read the C4 before you move the hypothesis.
Clinical Pearl — RPGN is a tempo, and the eGFR cannot keep up A creatinine rising over days to weeks with an active sediment is RPGN until proven otherwise. Stage it by the creatinine ratio (KDIGO 2012), write "eGFR not valid — creatinine is moving," send ANCA (PR3/MPO), anti-GBM, ANA/anti-dsDNA, C3/C4, blood cultures, a chest film and a renal ultrasound, and call nephrology today. Do not wait for the biopsy to send the serology; do not wait for the serology to make the call.
Clinical Pearl — Before any ACEi or ARB Before ACEi/ARB initiation, assess pregnancy potential and counsel about fetal risk, review potassium and kidney function, and plan laboratory follow-up. In this case pregnancy testing is already negative, but K 5.6 and worsening AKI justify deferral. A potassium number is a context-dependent prescribing decision, not a stand-alone universal rule.
Pitfall — The referral form that was supposed to be a phone call Red cell casts or acanthocytes with proteinuria sit in the same-day row of the referral table even when the creatinine is 1.0, because day two does not tell you where day five will be. A fax is not a handoff. Someone owns the 72-hour labs — serology included — and it is the clinician who ordered them.
Pitfall — Treating the number instead of the patient "eGFR 29" on a moving creatinine is not CKD G4. Potassium 5.6 with a normal ECG is not an indication for calcium, and it is not the "E" of AEIOU — that is refractory hyperkalemia or hyperkalemia with ECG changes. Both reflexes come from reading a printout instead of the trend and the tracing.
Concept Links
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
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-01, aki-02, aki-22, aki-24, glom-02, glom-03, glom-06, glom-07, glom-12, glom-13, glom-14, glom-15, glom-16, glom-17, glom-23, htn-cardiorenal-08, htn-cardiorenal-17.