Case 04: The Tired Teacher

Session 2 · Classroom case · 13 questions

Andrew Bland, MD, FACP, FAAP · October 2026

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Session S2 · 2026-10-27 · in-session · 37 min Anchor: Chronic kidney disease — staging, cause, anemia and blood pressure · Integrates: Hypertension (measurement, home BP, targets, resistant HTN, agent choice, lifestyle), NSAIDs, metabolic acidosis of CKD, MBD screen, referral One-line hook: A new PA inherits hundreds of charts that say "hypertensive kidney disease," and most of those patients are tired, on three blood-pressure pills, and quietly taking ibuprofen. This case is how you take that chart apart in one visit: measure the pressure properly, stage the kidney, question the label, find the iron, and know what is yours and what is nephrology's.

Learning Objectives

Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12 · Q13

Warm-Up (individual commit before the case)

Answers for this section: Q1 · Q2 · Q3

Three readiness items. Cards up, individually, before any discussion. These check vocabulary the case needs; they do not grade reasoning.

Q1When eGFR lies

eGFR — the estimated glomerular filtration rate, the kidney's filtering rate calculated from creatinine, age and sex by the CKD-EPI 2021 equation — assumes the creatinine is sitting still. In which patient does the reported eGFR least reliably reflect true kidney function?

A.

A 58-year-old woman whose creatinine has been 1.6–1.7 mg/dL at every check for two years

B.

A 70-year-old man in the emergency department whose creatinine rose from 1.0 to 2.4 mg/dL over 48 hours

C.

A 45-year-old man with a BMI of 31 and a creatinine of 1.1 mg/dL that has not changed in five years

D.

A 62-year-old woman on lisinopril for five years with a creatinine of 1.2 mg/dL at every visit

· Link to this question

Correct answer: B

Learning point: The equation was built from people with stable kidney function. When creatinine is rising, the number in the blood lags days behind the fall in filtration, so the eGFR printed on the report is far too flattering. Write "eGFR not valid — creatinine is moving" and follow the creatinine trend instead. The other known limits are extremes of muscle mass (body-builders, amputees, frail elders), drugs that block creatinine secretion (trimethoprim, cimetidine), creatine supplements and pregnancy; cystatin C is the confirmatory test when the creatinine estimate is in doubt. Why not the others: A, C and D are all steady state — the equation is doing exactly what it was designed to do; obesity (C) and an ACE inhibitor (D) do not invalidate a stable eGFR. Course reading: Evidence for this case

Evidence and objective for Q1

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Q2The reading you can act on

Four office blood pressures, four techniques. Which one is a reading you can make a treatment decision on?

A.

156/92 mmHg, correctly sized cuff, taken as she sat down while she described her week

B.

150/90 mmHg, mean of two readings, standard adult cuff on a 35-cm arm, the arm hanging at her side

C.

148/88 mmHg, a single reading after five minutes' rest, legs crossed, feet off the floor

D.

144/86 mmHg, mean of two readings after five minutes' seated rest, large adult cuff, no talking

· Link to this question

Correct answer: D

Learning point: Use quiet seated rest, supported back and feet, the arm supported at heart level, and an appropriately sized validated cuff. Obtain repeated readings separated by 1–2 minutes and average them. D follows those requirements. Technique errors can materially distort pressure, but their effects vary and should not be added as fixed numerical corrections to a patient's result. Why not the others: A is no rest plus talking; B is a cuff too small for the arm plus an arm below the heart; C is one reading with legs crossed — a single reading is never enough even when the posture is right. Course reading: Evidence for this case

Evidence and objective for Q2

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Q3Trace protein, A2 albumin

A first-morning urine dipstick reads "trace" protein; the UACR on the same sample is 180 mg/g. Which statement is correct?

A.

Trust the dipstick — trace protein means the albuminuria is too small to matter

B.

Trust the ratio — the dipstick misses most albuminuria in the A2 range (30–300 mg/g)

C.

They disagree, so a 24-hour urine protein collection is needed to settle it

D.

Repeat the dipstick on a concentrated afternoon specimen before trusting the ratio

· Link to this question

Correct answer: B

Learning point: The dipstick reads protein by concentration, with a chemistry that responds mainly to albumin and poorly at low levels, so it turns reliably positive only around the A3 line (300 mg/g) — a trace-or-greater strip catches variable and insufficient to exclude A2 of A2 patients (36 % sensitivity), and a dilute urine reads lower still. The UACR measures albumin by immunoassay and divides by creatinine, so dilution does not fool it, and 30–300 mg/g is A2 whatever the strip says. That is why KDIGO (the international kidney guideline group) stages albuminuria by the ratio and treats the dipstick as a screen: a trace or negative strip in a patient at risk for CKD is a reason to send the ratio, not reassurance. One ratio is a data point, not a trend — confirm it on a repeat first-morning sample before acting on it. Why not the others: A reads reassurance into a test that was never designed to see A2; C substitutes a cumbersome total-protein collection for a spot ratio that already answers the question — the 24-hour urine is for the rare case where the ratio is unreliable (extremes of muscle mass, pregnancy, very heavy proteinuria); D treats the dipstick's concentration problem as a specimen problem — the ratio has already corrected for dilution. Course reading: Evidence for this case

Evidence and objective for Q3

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Part 1 — Presentation

Answers for this section: Q4 · Q5 · Q6

Ms. Carol Jensen, 58, teaches seventh-grade science. Chief complaint, in her words: "I'm tired all the time, and it's October."

History of present illness. Four months of fatigue that gets worse through the school day. By fifth period she sits between classes, which she never used to do. The two flights of stairs to her classroom leave her short of breath where last spring they did not. Her legs feel "jumpy" at night and she has trouble keeping them still. No chest pain, no orthopnea, no leg swelling beyond the ankle puffiness she has had since the amlodipine was started. No gross hematuria (visible blood in the urine), no dysuria, no flank pain. Stools "look normal" as far as she has noticed; no vomiting, no black stools she is aware of. Postmenopausal for five years. Appetite fine, weight stable. She came straight from fifth period, parked two blocks away, took the stairs, and was describing the science fair when the medical assistant put the cuff on.

Past medical history. Hypertension for 15 years, diagnosed at 43. "Hypertensive kidney disease" — a label added two years ago when a creatinine of 1.6 mg/dL turned up on a pre-operative panel for knee arthroscopy; the arthroscopy was cancelled and nobody followed up the kidney. Osteoarthritis of both knees. Hyperlipidemia. No diabetes (hemoglobin A1c 5.6 % last year). No kidney stones, no urinary infections, no gout.

Family history. Mother: hypertension, "kidney trouble" in her 80s, never on dialysis. Father: myocardial infarction at 70. Nobody on dialysis before old age, no polycystic kidneys, no deafness, no family hematuria.

Social history. Lives with her husband; two grown children. Never smoked. Two or three glasses of wine a week. Exercise: "not much — the knees." Diet: cafeteria lunches, frozen dinners, a diet cola most afternoons.

Medications as charted.

Drug Dose Route Frequency Indication
Lisinopril 40 mg PO once daily Hypertension; albuminuria
Amlodipine 10 mg PO once daily Hypertension
Hydrochlorothiazide 25 mg PO once daily Hypertension
Atorvastatin 20 mg PO once daily (evening) Hyperlipidemia
Over-the-counter / supplements — — — Intake form: "nothing regular"

Allergies: none known.

Vitals. BP 158/94 mmHg — right arm, seated on the exam table with feet dangling, standard adult cuff, taken within two minutes of arrival while she talked. Heart rate 88. Respiratory rate 14. Temp 36.8 °C. SpO₂ 98 % on room air. Weight 84 kg, height 165 cm, BMI 30.9 kg/m². Mid-arm circumference 35 cm.

Examination. Pale conjunctivae. No jugular venous distension. Lungs clear. Heart regular, no murmur, no S3. Abdomen soft, no bruit. Trace bilateral ankle edema. Knees: crepitus, no effusion, no warmth. Fundi: arteriolar narrowing, no hemorrhages or exudates. Neurologically intact. ECG: sinus rhythm 84, left ventricular hypertrophy by voltage.

What the chart already holds. One creatinine of 1.6 mg/dL (August 2024, eGFR 38 at age 56). One UACR of 150 mg/g (2024). No urinalysis with microscopy, ever. No kidney imaging, ever.

Before the questions, the vocabulary. Two numbers stage a kidney. The eGFR says how fast it filters. The UACR — the urine albumin-to-creatinine ratio, measured on a spot sample — says how much albumin is leaking through the filter; it is corrected to creatinine so dilution does not fool you. KDIGO puts the two on a grid: G1–G5 for filtration, A1–A3 for albumin, with a color for the combined risk. The grid, not the label on the chart, is where this visit starts.

Pause — commit before the reveal

Q4What do you do with 158/94?

Ms. Jensen is on three antihypertensives and her office reading is 158/94 mmHg. What is the right response to that number today?

A.

Add a fourth antihypertensive — three drugs above goal is resistant hypertension by definition

B.

Double the hydrochlorothiazide from 25 to 50 mg daily — the diuretic is the weak link in CKD

C.

Remeasure correctly, then start a 7-day home blood pressure protocol before changing any drug

D.

Replace amlodipine with metoprolol succinate 50 mg daily — she has left ventricular hypertrophy

· Link to this question

Correct answer: C

Learning point: Remeasure using correct technique before making a routine medication change, then compare a properly collected home BP average. The initial reading followed exertion, talking and unsupported posture with an undersized cuff. Those errors can bias the result but do not establish a predictable additive error. A later controlled reading of 144/88 remains above target and still requires follow-up and treatment review. Why not the others: A treats a technique error as drug failure and commits her to a fourth drug she may not need; B escalates a drug on a bad reading — and doubling hydrochlorothiazide buys little extra pressure for more hyponatremia and hypokalemia (the diuretic question in CKD is which thiazide, not how much; see Q11); D swaps a first-line class for a beta-blocker, which is not first-line for hypertension without a cardiac indication — LVH is a reason to control pressure, not to pick a beta-blocker. Course reading: Evidence for this case

Evidence and objective for Q4

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Q5Where is she on the heat map?

Creatinine 1.72 mg/dL today (eGFR 34 mL/min/1.73 m² by CKD-EPI 2021), 1.6 mg/dL two years ago (eGFR 38), UACR 180 mg/g. Her KDIGO category, and what the 2024 value adds:

A.

G3a A2 — high (orange) risk; chronicity cannot be assumed from one old value

B.

G3b A3 — very high (red) risk; she needs a nephrology appointment this week

C.

G3b A2 — very high (red) risk; the 2024 value proves chronicity and shows a slow slope

D.

G4 A2 — very high (red) risk; a creatinine of 1.72 in a woman reads as an eGFR under 30

· Link to this question

Correct answer: C

Learning point: eGFR34 is G3b and UACR180 is A2; the combination is in the very-high-risk red cell. The prior abnormality establishes chronicity. Monitoring frequency and referral depend on risk, trajectory and complications. A red cell does not by itself mandate referral within one month; her difficult BP, anemia, diagnostic uncertainty and later KFRE support referral. The decline from eGFR38 to34 over two years is approximately2mL/min/1.73m² per year. Why not the others: A misclassifies GFR; B misclassifies albuminuria; D misclassifies the calculated GFR. Albuminuria referral criteria depend on magnitude and accompanying findings; A3 alone is not a universal automatic referral rule at every value. Course reading: Evidence for this case

Evidence and objective for Q5

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Pause — commit before the reveal

Q6The label on the chart

Her chart says "hypertensive kidney disease." She has never had a urinalysis with microscopy or a kidney ultrasound. What is the first-line work-up for the cause of her CKD, and what finding would make you doubt the label?

A.

Urinalysis with microscopy, repeat UACR and renal ultrasound — keep the label only if all three stay bland

B.

Kidney biopsy — nephrosclerosis is a tissue diagnosis and nothing short of tissue proves it

C.

The glomerular serology panel now (ANA, ANCA, anti-GBM, C3/C4) — every new CKD gets it before anything else

D.

No further work-up — 15 years of hypertension with LVH on the ECG is proof enough

· Link to this question

Correct answer: A

Learning point: "Hypertensive nephrosclerosis" (long-standing high pressure scarring the small arteries and the glomeruli behind them) is a diagnosis of exclusion — it is listed as the second cause of kidney failure in the United States, yet the clinical criteria for it have about 13 % sensitivity and it is rarely confirmed by biopsy, so much of what carries the label is another kidney disease with hypertension riding along. What fits: a long hypertension history, target-organ damage elsewhere (her LVH), a bland urine (no blood, no cellular casts), low-grade albuminuria (A2, under about 1 g/day), a slow slope, and two symmetric, smooth kidneys. What un-fits: A3 albuminuria or more than 1 g/day of protein, hematuria or red-cell casts, white-cell casts, a decline over 5 mL/min per year, onset young, a family history of kidney disease, or systemic symptoms. The three first-line tests answer exactly those questions — microscopy for cells and casts, a repeat UACR because one value is not a trend, an ultrasound for size, symmetry, cysts and obstruction — and if they come back clean the honest wording is "CKD, presumed nephrosclerosis," held loosely. Why not the others: B is above student level and above her need — biopsy is for an active urine, heavy proteinuria or unexplained rapid decline, not a bland G3b; C sends serologies before you know whether the urine is active — the panel is for a nephritic sediment or nephrotic-range protein, and reflexive ordering generates false positives; D is the error that made the chart: a label by assumption. Course reading: Evidence for this case

Evidence and objective for Q6

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Part 2 — Data

Answers for this section: Q7 · Q8 · Q9

Labs drawn fasting the morning after the visit; the urinalysis is a first-morning specimen; the ultrasound was done the same week. Reference ranges are the lab's.

Chemistry

Test Result Reference range
Sodium 139 mEq/L 136–145
Potassium 4.6 mEq/L 3.5–5.0
Chloride 108 mEq/L 98–107
Bicarbonate (HCO₃) 19 mEq/L 22–28
Anion gap, Na − (Cl + HCO₃) 12 mEq/L 8–12
BUN 26 mg/dL 8–20
Creatinine 1.72 mg/dL 0.6–1.1
eGFR (CKD-EPI 2021) 34 mL/min/1.73 m² ≥60
BUN : creatinine 15 : 1 10–20 : 1
Glucose (fasting) 94 mg/dL 70–99
Hemoglobin A1c 5.6 % <5.7
Calcium 9.1 mg/dL 8.5–10.5
Phosphorus 4.6 mg/dL 2.5–4.5
Albumin 4.1 g/dL 3.5–5.0
Intact PTH (parathyroid hormone) 118 pg/mL 15–65
25-OH vitamin D 17 ng/mL 30–100 (<20 = deficiency)
LDL cholesterol 96 mg/dL <100

Prior, for the trend (August 2024): creatinine 1.6 mg/dL, eGFR 38, BUN 22 mg/dL, potassium 4.4 mEq/L, bicarbonate 22 mEq/L.

Hematology and iron

Test Result Reference range
White cells 6.8 ×10³/µL 4.0–11.0
Hemoglobin 9.6 g/dL 12.0–15.5 (women)
Hematocrit 29.8 % 36–46
MCV (mean corpuscular volume — red-cell size) 78 fL 80–100
MCH 25 pg 27–33
RDW (red-cell distribution width — how varied the sizes are) 16.9 % 11.5–14.5
Platelets 318 ×10³/µL 150–400
Reticulocyte count 0.9 % 0.5–2.5
Vitamin B12 412 pg/mL 200–900
Folate 11 ng/mL >4
Iron studies (ferritin, iron, TIBC, TSAT) pending —
Stool guaiac card (office) pending negative

Urinalysis (first-morning, clean catch)

Dipstick Result Microscopy Result
Color / clarity yellow, clear RBC 0–2 /hpf
Specific gravity 1.012 WBC 0–2 /hpf
pH 5.5 Casts occasional hyaline; no cellular casts
Protein trace Crystals none
Blood negative Epithelial cells few squamous
Glucose, ketones, bilirubin negative Bacteria none
Leukocyte esterase, nitrite negative

UACR: 180 mg/g (visit); repeat three weeks later, first-morning: 164 mg/g. Both A2.

Renal ultrasound: right kidney 10.2 cm, left 10.0 cm; cortical echogenicity mildly increased bilaterally, cortical thickness preserved; no hydronephrosis, no stones, no cysts or masses; bladder normal, post-void residual 20 mL.

Read it the way the kidney works. The filter: eGFR 34, stable-slow, bland urine, two smooth symmetric kidneys of normal length — the structural picture of a chronic, slow process with nothing active. Notice the dipstick: trace protein against a UACR of 180 mg/g — the strip misses A2 albuminuria (Q3), which is why the ratio, not the dipstick, stages her. The acid handling: a bicarbonate of 19 with a normal anion gap, because a kidney with a third of its nephrons left cannot excrete the day's acid load as ammonium. The hormone jobs: erythropoietin (the kidney's signal to the marrow to make red cells) and activation of vitamin D both fall with nephron mass, and phosphate retention pushes PTH up.

Pause — commit before the reveal

Q7Why is she tired?

Hemoglobin 9.6 g/dL, MCV 78 fL, RDW 16.9 %, reticulocytes 0.9 %, eGFR 34; the iron studies and the stool guaiac card are still pending. What is the right anemia plan today?

A.

Start an erythropoiesis-stimulating agent (ESA) now — an eGFR of 34 explains the anemia and she is symptomatic

B.

Transfuse one unit of red cells today for the fatigue and the dyspnea she now has on the stairs

C.

Order a serum erythropoietin level first, to confirm erythropoietin deficiency before treating it

D.

No ESA yet — assess iron status and causes of blood loss; microcytosis points to iron deficiency

· Link to this question

Correct answer: D

Learning point: Microcytosis and high RDW suggest iron deficiency, which can coexist with CKD-related erythropoietin deficiency. Check ferritin and TSAT and investigate blood loss and other reversible causes before an ESA. A negative stool blood test does not exclude gastrointestinal blood loss and should not gate indicated GI evaluation. ESA initiation in nondialysis CKD is individualized after reversible causes are addressed; KDIGO 2026 recommends an ESA-treated hemoglobin target below 11.5 g/dL. Why not the others: A gives a growth signal to a marrow that may have no bricks — iron-deficient erythropoiesis does not respond, and the ESA risk is taken for nothing; B is for hemodynamic instability or a hemoglobin under 7 (under 8 with cardiac disease), not for stable fatigue, and transfusion sensitizes a future transplant candidate; C adds nothing — erythropoietin levels are "inappropriately normal" in CKD, are not used for dosing, and would not change the iron decision. Course reading: Evidence for this case

Evidence and objective for Q7

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Q8The bicarbonate of 19

Sodium 139, chloride 108, bicarbonate 19 mEq/L, albumin 4.1 g/dL. How do you read this, and what is first-line?

A.

High-anion-gap metabolic acidosis — send a lactate, β-hydroxybutyrate and a toxic-alcohol screen

B.

Likely normal-anion-gap metabolic acidosis — confirm persistence and individualize dietary or alkali treatment

C.

Appropriate compensation for a chronic respiratory alkalosis — nothing to treat

D.

Severe metabolic acidosis — intravenous sodium bicarbonate in the emergency department

· Link to this question

Correct answer: B

Learning point: The gap is 139 − (108 + 19) = 12. CKD-related acid retention is plausible, but a chemistry bicarbonate alone cannot exclude respiratory alkalosis; repeat and obtain a blood gas if the clinical distinction remains uncertain. KDIGO 2024 Practice Points 3.10.1–2 advise considering treatment to prevent clinically important acidosis, giving bicarbonate below 18 mmol/L as an example. A stable value of 19 does not mandate sodium bicarbonate. Discuss dietary measures or a monitored alkali trial according to persistence, symptoms, potassium, blood pressure and volume. Do not promise that alkali will slow CKD progression. Why not the others: A ignores the normal gap. C is possible physiology but not established by these data. D is disproportionate for this stable patient; acute severity is assessed with the clinical state and pH, not bicarbonate alone. Course reading: Evidence for this case

Evidence and objective for Q8

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Q9Whose job is the PTH?

Calcium 9.1 mg/dL, phosphorus 4.6 mg/dL, intact PTH 118 pg/mL (reference 15–65), 25-OH vitamin D 17 ng/mL. Which plan belongs to primary care at G3b?

A.

Cholecalciferol 2,000 IU daily, dietary phosphorus counselling, recheck in three to six months

B.

Calcitriol 0.25 mcg daily — a PTH of 118 is secondary hyperparathyroidism and needs to be suppressed

C.

Sevelamer 800 mg with each meal — the phosphorus of 4.6 is above the reference range

D.

Start an oral bisphosphonate and order a DXA scan — kidney bones are weak bones

· Link to this question

Correct answer: A

Learning point: This is the early pattern of CKD mineral and bone disorder (CKD-MBD): fewer nephrons retain phosphate, PTH rises to push it out, and the kidney makes less active vitamin D, so calcium absorption falls and PTH rises further — at G3b the serum phosphorus is usually still near normal (hers is barely over the line) while the PTH is already up. What primary care owns: the nutritional deficiency (25-OH D under 20 is deficiency, 20–29 insufficiency; cholecalciferol using a local replacement regimen and follow-up level), the diet (phosphate additives in processed food and colas are the first target; a renal dietitian helps), and the recheck schedule for G3b — calcium and phosphorus every 6–12 months when stable, PTH at intervals set by the trend. What nephrology owns: there is no established PTH target in non-dialysis CKD, so a single PTH of 118 is not a calcitriol indication; active vitamin D is reserved for severe, progressive hyperparathyroidism after the modifiable factors are fixed, and calcimimetics (drugs that quiet the parathyroid, used on dialysis) are not a G3b drug. The distinguishing feature is the vitamin D level — treat the deficiency you can measure, and follow the PTH you cannot yet target. Why not the others: B treats a number without a target and risks hypercalcemia and over-suppression (bone that stops remodelling); C starts a binder for a phosphorus of 4.6 when diet comes first — "no binders yet if phosphorus is normal or near it" is the rule at G3b; D answers a question nobody asked — DXA does not tell you the kidney bone type, and antifracture drugs in CKD are a specialist decision. Course reading: Evidence for this case

Evidence and objective for Q9

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Part 3 — Course and Decisions

Answers for this section: Q10 · Q11 · Q12

Three weeks later, at the follow-up visit, the anemia results are the first thing you open.

Q10Evidence update

Concordance-style practice: an exercise in updating, not a graded test. There is no expert panel behind the key, only the explanation below. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."

If you were thinking "this is anemia of CKD — erythropoietin deficiency from an eGFR of 34 explains the hemoglobin of 9.6," and you then learn that her ferritin is 48 ng/mL (inside the lab's range of 15–150), her TSAT is 13 % and the stool guaiac card is positive, the hypothesis that CKD alone explains her anemia becomes:

A.

Much less likely

B.

Less likely

C.

Unchanged

D.

More likely

E.

Much more likely

· Link to this question

Correct answer: A

Learning point: Her TSAT of 13% together with ferritin 48 ng/mL supports systemic iron deficiency in non-dialysis CKD. TSAT below 20% alone does not distinguish depleted iron stores from iron-restricted erythropoiesis. The ferritin is the finding whose meaning is conditional: 48 sits inside the lab's range, but that range is for people without kidney disease — KDIGO 2026 starts iron in non-dialysis CKD at a ferritin under 100 with TSAT under 40 % — and ferritin rises with inflammation, so 48 if anything overstates her stores. A positive guaiac card in a postmenopausal woman is gastrointestinal blood loss until proven otherwise, though her iron deficiency would have earned the gastroenterology referral without it. So "CKD alone" is much less likely — but not excluded: at eGFR 34 her erythropoietin reserve is limited and will cap how far iron can take her. The honest reading is "iron deficiency from GI loss on top of CKD": oral iron and a gastroenterology referral now, any ESA left to nephrology once the iron is replete. Course reading: Evidence for this case

Evidence and objective for Q10

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Iron studies and stool card Result Reference range
Ferritin 48 ng/mL 15–150 (women)
Serum iron 36 µg/dL 50–170
TIBC (total iron-binding capacity) 277 µg/dL 250–450
Transferrin saturation (TSAT), iron ÷ TIBC 13 % 20–50
Stool guaiac card (office) positive negative

Then the other two results.

The medication-reconciliation call. The nurse asks the question the intake form did not: "What do you take for your knees?" Ibuprofen 600 mg, one tablet most school mornings, sometimes a second after dismissal, for about three years — "from the big bottle at home; it isn't a prescription, so I didn't write it down." That is a non-steroidal anti-inflammatory drug (NSAID) roughly five days a week in a woman with an eGFR of 34, on a full-dose ACE inhibitor and a diuretic.

The home blood pressure log. Morning and evening, two readings each, seven days; day 1 discarded; 24 readings averaged: 144/88 mmHg. Pharmacy refill history: all three antihypertensives filled on time for the last 12 months. The repeat UACR was 164 mg/g.

Put the three together. Her hypertension is real (home average well over 130/80, so not white-coat), she is adherent, all three drugs are at maximal dose, and she is above goal on three drugs including a diuretic — the definition of resistant hypertension, with the pseudoresistance list (technique, adherence, white-coat effect, sub-maximal dosing) now fully worked. And standing in the middle of it is a drug that does three things to a kidney at once. Prostaglandins keep the afferent arteriole (the inflow vessel to each glomerulus) open and help the kidney excrete sodium. Block them with an NSAID and filtration falls — a hemodynamic, reversible drop in GFR — the kidney holds sodium, which raises blood pressure and blunts the diuretic and the ACE inhibitor, and potassium excretion falls. With an ACE inhibitor (which relaxes the outflow vessel) and a diuretic (which lowers the volume coming in) on board, that is the "triple whammy." The same drug erodes the stomach lining, and a stomach that bleeds a little every day is how a postmenopausal woman loses iron without ever seeing a black stool.

Pause — commit before the reveal

Q11Still above target

Home average 144/88 mmHg on lisinopril 40 mg, amlodipine 10 mg and hydrochlorothiazide 25 mg, adherence confirmed, eGFR 34, potassium 4.6 — and ibuprofen 600 mg most days. What is the best next change?

A.

Add spironolactone 25 mg daily with a potassium check — PATHWAY-2 made it the fourth-line drug for resistant hypertension

B.

Add losartan 50 mg daily to the lisinopril 40 mg to block the renin-angiotensin system at two points

C.

Stop the ibuprofen, swap hydrochlorothiazide for chlorthalidone 12.5 mg, BMP in 1–2 weeks, repeat the home log

D.

Add clonidine 0.1 mg twice daily as a fourth drug and recheck the 7-day home average in a month

· Link to this question

Correct answer: C

Learning point: First remove oral ibuprofen and reassess the home pressure, adherence and diuretic regimen. Refill history supports adherence but does not prove it, and hydrochlorothiazide 25 mg is not its maximum possible dose. Chlorthalidone is an option that can remain effective at low GFR; use a low starting dose and recheck sodium, potassium and creatinine within 1–2 weeks. This is apparent treatment-resistant hypertension until reversible causes and technique are addressed. Why not the others: A may eventually be useful, but her eGFR 34 and K 4.6 increase hyperkalemia risk, and PATHWAY-2 excluded eGFR below 45; that trial boundary is not an absolute contraindication. Seek specialist advice before adding it here. B combines ACE inhibitor and ARB without clinical benefit and increases harm. D adds a drug before correcting the reversible contributor. Course reading: Evidence for this case

Evidence and objective for Q11

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Q12The number that counts, and the referral

Six weeks after the ibuprofen stopped and the chlorthalidone started, her repeat 7-day home average is 138/86 mmHg. Which statement is correct?

A.

She is at goal — home targets run about 10 mmHg looser than office targets, so 138/86 at home is acceptable

B.

She is above goal — the home target is also under 130/80; refer to nephrology now with the data packet

C.

She is above goal — add hydralazine 25 mg three times daily and refer only if that fails

D.

Stop the lisinopril — three drugs have failed, and the ACE inhibitor is the one that can hurt a kidney

· Link to this question

Correct answer: B

Learning point: The target for an adult with CKD is under 130/80 (2025 AHA/ACC and ADA; KDIGO 2021 goes further to a standardized-office systolic under 120 when tolerated, a number that presumes a measurement most clinics do not make), and the home threshold is the same 130/80 — there is no looser home target, so 138/86 is better and it is not goal. Referral is not a failure, it is the next step her chart already earned twice over: "uncontrolled hypertension despite three drugs" is an urgent referral on the staging handout's chart, and G3b with albuminuria is a referral within a month. By KDIGO 2024 she qualifies on the kidney-failure risk equation (5-year risk about 11 % at eGFR 34, UACR 180, age 58, female — well above the 3–5 % threshold); the local chart's G3b-with-albuminuria and uncontrolled-hypertension rows are the same decision stated more simply. Send the data that lets nephrology start where you finished — the creatinine trend (1.6 in 2024, 1.72 now), the two UACRs, the microscopy, the ultrasound, the home log, the iron studies, the bicarbonate, the PTH and vitamin D, and the medication list with the ibuprofen on it — and keep counselling while she waits. Why not the others: A is a myth — home and office thresholds are both 130/80 in the current guideline frame; C adds a fourth drug with three-times-daily dosing, reflex tachycardia and fluid retention before the specialist who will manage her for years has seen her, and it postpones a referral she already qualifies for; D removes the one drug that lowers her albuminuria and protects the glomerulus — an ACE inhibitor is held for acute illness, hyperkalemia or a creatinine rise over 30 %, not for "didn't reach goal." Course reading: Evidence for this case

Evidence and objective for Q12

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Self-study checkpoint — after class

Answers for this section: Q13

This additional question is completed after class and does not extend the timed run sheet.

Q13Cardiovascular prevention in CKD

A 62-year-old woman has stable CKD G3b, eGFR 34 mL/min/1.73 m², and LDL cholesterol 104 mg/dL. Her blood pressure is controlled, she does not have diabetes, and she receives neither dialysis nor a kidney transplant. She has no statin contraindication and currently takes no lipid-lowering medicine. Which additional prevention plan is best?

A.

Defer lipid therapy unless LDL cholesterol reaches 190 mg/dL

B.

Begin aspirin routinely because CKD alone establishes an indication for primary prevention

C.

Offer a statin-based regimen to reduce cardiovascular risk, alongside lifestyle measures

D.

Wait until dialysis begins before starting a statin

· Link to this question

Correct answer: C

Learning point: CKD increases cardiovascular risk. KDIGO 2024 Recommendation 3.15.1.1 recommends a statin or statin/ezetimibe for adults aged at least 50 with eGFR below 60 who are not receiving chronic dialysis or a transplant. Her modest LDL does not remove that indication. Choose the regimen with her after reviewing interactions, tolerance and preferences. Why not the others: A uses an LDL threshold that is not required for this CKD indication. B confuses primary prevention with secondary prevention; CKD alone does not justify routine aspirin. D delays a recommended preventive intervention and incorrectly uses dialysis initiation as its trigger. Evidence: KDIGO 2024 CKD guideline, 3.15.1.1 and 3.15.2.1.

Evidence and objective for Q13

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Resolution and Teaching Points

Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12 · Q13

The plan from the visit. Ibuprofen stopped; acetaminophen 650 mg PO every six hours as needed (maximum 3 g/day) and diclofenac 1 % gel to both knees four times daily; physical therapy for the knees. Hydrochlorothiazide 25 mg stopped, chlorthalidone 12.5 mg PO daily started, BMP in 10–14 days. Ferrous sulfate 325 mg PO daily on an empty stomach, with the warning about constipation and dark stools. Gastroenterology referral for colonoscopy and upper endoscopy. Sodium bicarbonate 650 mg PO twice daily after the repeat bicarbonate came back 19 again. Cholecalciferol 2,000 IU PO daily. Renal dietitian: DASH pattern (the fruit-vegetable-low-fat-dairy eating pattern), sodium under 2.3 g/day, phosphate additives, no potassium salt substitute. Nephrology referral placed, with the data packet. Repeat 7-day home log in six weeks.

Twelve weeks later. Hemoglobin 10.9 g/dL, MCV 82, ferritin 96, TSAT 21 % — rising about 0.5 g/dL a month, the low end of the 0.5–1 g/dL a month oral iron should give, acceptable while the bleed was being found and stopped. Endoscopy: erosive gastritis consistent with NSAID injury, no ulcer; colonoscopy: one small tubular adenoma, removed, no cancer. Creatinine 1.6 mg/dL (eGFR 37) — the hemodynamic part of the NSAID effect reversed; potassium 4.4; sodium 138 on chlorthalidone; bicarbonate 23. Home average 138/86. Still above goal, so the referral stands. Nephrology confirmed CKD G3b A2, "presumed nephrosclerosis with an NSAID contribution — a label held loosely," agreed no ESA was indicated while the hemoglobin was rising on iron, and started the next layer of kidney protection, which is the next case's business. Spironolactone stayed off the table at eGFR 37. She finished the semester standing up.

Clinical Pearl — A blood pressure taken wrong is a number, not a diagnosis No rest, talking, a small cuff and dangling feet add more than 10 mmHg between them. Remeasure properly, then let a 7-day home average (morning and evening duplicates, discard day 1) make the drug decision. Home readings exclude white-coat hypertension and predict outcomes better than the office.

Clinical Pearl — "Hypertensive kidney disease" is a label you earn by exclusion It fits when the hypertension is long, the urine is bland, the albuminuria is low-grade, the decline is slow and the kidneys are symmetric. A3, hematuria or cellular casts, a fall over 5 mL/min per year, young onset or a family history send you looking for another disease. The first-line work-up is three tests: urinalysis with microscopy, a repeat UACR, a renal ultrasound.

Clinical Pearl — In CKD anemia, iron first — and iron deficiency has a cause Ferritin under 100 with TSAT under 40 means iron in non-dialysis CKD (KDIGO 2026). Microcytosis suggests iron deficiency, which can coexist with erythropoietin deficiency. Iron deficiency after menopause is a gastroenterology referral; a stool blood test cannot confirm or exclude the cause and should not gate indicated GI evaluation. ESAs are nephrology's call, after iron, with the hemoglobin kept under 11.5 g/dL.

Clinical Pearl — The G3b complication labs have owners Primary care can investigate persistent low bicarbonate and nutritional vitamin D deficiency. KDIGO 2024 individualizes acidosis treatment, giving bicarbonate <18 as an example rather than a mandatory cutoff at 22. Monitor blood pressure, volume and potassium if alkali is used. Correct vitamin D deficiency using an appropriate local regimen; avoid a universal 30–100 target. Follow calcium, phosphate and PTH trends; active vitamin D and ESA decisions require individualized specialist review.

Clinical Pearl — Resistant hypertension is a work-up before it is a fourth drug Confirm out-of-office pressure, assess adherence and optimize tolerated therapy, then remove reversible contributors such as oral NSAIDs. Chlorthalidone may be useful with electrolyte monitoring. Spironolactone at eGFR 34 and K 4.6 requires extra caution and specialist advice; the PATHWAY-2 eligibility thresholds are not universal contraindications. Do not combine ACEi and ARB. Use clinical complexity and kidney-failure risk to guide referral.

Pitfall — Treating the stairwell Adding a fourth antihypertensive, or doubling the thiazide, to a 158/94 taken over a sleeve two minutes after a flight of stairs. The patient collects a drug and a side effect; the pressure that was never real "improves."

Pitfall — Calling it "anemia of CKD" and reaching for the ESA A hemoglobin of 9.6 at an eGFR of 34 looks like erythropoietin deficiency until you look at the MCV and the ferritin. Miss the iron deficiency and you miss the bleed behind it — and you give a thrombotic drug to a marrow that cannot use it.

Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12 · Q13

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: ckd-01, ckd-02, ckd-03, ckd-04, ckd-05, ckd-07, ckd-10, ckd-14, ckd-15, ckd-16, ckd-19, ckd-21, ckd-26, htn-cardiorenal-01, htn-cardiorenal-02, htn-cardiorenal-04, htn-cardiorenal-06, htn-cardiorenal-10, htn-cardiorenal-16, structural-20.