AKI, CKD, electrolyte disorders, and glomerulonephritis
This is an original, question-bank-style learning set designed for general internal medicine residents. It uses concise vignettes, a single-best-answer format, focused diagnostic clues, and explanations of the distractors. It is inspired by the high-yield structure of postgraduate clinical question banks but does not reproduce proprietary Amboss content.
Educational disclaimer: These fictional cases support postgraduate learning only. They do not replace local emergency protocols, specialist review, current prescribing information, or individualized clinical judgment. Emergency electrolyte disorders and rapidly progressive glomerulonephritis require supervised, protocol-based care.
Case 1 — Sepsis-associated AKI
A 72-year-old man is admitted with fever, hypotension, confusion, and right lower-lobe pneumonia. His baseline serum creatinine is 0.9 mg/dL; it is now 2.4 mg/dL. He has received no iodinated contrast. Urinalysis shows 1+ protein and no dysmorphic erythrocytes. Urine microscopy shows renal tubular epithelial cells and muddy brown granular casts. He remains hypotensive after initial assessment.
Which is the most appropriate interpretation and immediate priority?
| Option | Answer |
|---|---|
| A | The urine findings establish prerenal azotemia; aggressive loop diuresis should be started to restore urine output. |
| B | The findings support acute tubular injury in the setting of sepsis; restore and reassess perfusion, give timely infection-directed therapy and source control, review nephrotoxins, and monitor complications. |
| C | A kidney biopsy is required before treating the sepsis because granular casts are nonspecific. |
| D | The creatinine rise is too modest to be clinically meaningful unless dialysis is immediately required. |
Correct answer: B. Muddy brown granular casts and tubular epithelial cells in a patient with shock support acute tubular injury. The immediate priorities are resuscitation tailored to perfusion and congestion, prompt antimicrobial/source-control decisions, medication review, and surveillance for electrolyte, acid–base, and volume complications. Urine output is an important monitoring signal but should not be pursued with diuretics solely to “treat” AKI. [1]
Why the other options are less appropriate: A mistakes tubular-injury sediment for a low-perfusion-only state; a loop diuretic may be used for clinically important congestion but does not reverse tubular injury. C delays treatment of a time-sensitive cause of AKI; biopsy is reserved for selected unresolved cases where it will change management. D is unsafe because even a moderate creatinine rise can represent clinically important AKI and requires prompt evaluation.
Clinical pearl: In AKI, identify the cause while simultaneously treating reversible threats; do not wait for a perfect etiologic label before correcting shock, infection, obstruction, or exposure to nephrotoxins.
Case 2 — Postrenal AKI from urinary retention
A 78-year-old man with progressive nocturia, hesitancy, and weak stream presents with suprapubic discomfort and nausea. He has passed only a few drops of urine over 18 hours. Serum creatinine has risen from 1.1 to 3.0 mg/dL over 4 days. Examination shows a palpable, tender bladder. Bedside bladder scan estimates 950 mL of retained urine.
What is the best next step?
| Option | Answer |
|---|---|
| A | Start high-dose IV furosemide to establish a brisk diuresis before imaging. |
| B | Begin an ACE inhibitor to reduce intraglomerular pressure while awaiting outpatient urology review. |
| C | Perform prompt bladder decompression, monitor urine output and hemodynamics, and evaluate the cause and upper-tract involvement. |
| D | Defer intervention until a 24-hour urine collection confirms intrinsic AKI. |
Correct answer: C. This is strongly suggestive of postrenal AKI from acute urinary retention. Prompt bladder decompression is both diagnostic and therapeutic. After decompression, monitor closely for post-obstructive diuresis, volume depletion, electrolyte disturbances, and recovery of kidney function; establish the obstructive cause and assess for hydronephrosis or persistent upper-tract obstruction as indicated. [1]
Why the other options are less appropriate: A does not relieve the obstruction and may worsen hypovolemia after decompression. B is not an acute treatment for obstruction and may further lower filtration pressure in an unstable AKI context. D unnecessarily delays relief of a reversible kidney threat.
Clinical pearl: A bladder scan and focused examination can rapidly identify a reversible cause of AKI. In suspected complete obstruction, decompression takes priority over elaborate urine indices.
Case 3 — Drug-induced acute interstitial nephritis
A 43-year-old woman receives amoxicillin–clavulanate for sinusitis. Ten days later, she develops malaise, a pruritic maculopapular rash, low-grade fever, and an increase in serum creatinine from 0.7 to 1.8 mg/dL. Urinalysis shows pyuria and mild proteinuria; there are no red-cell casts. Blood eosinophils are mildly elevated. She is euvolemic and has no evidence of obstruction.
Which action is most appropriate now?
| Option | Answer |
|---|---|
| A | Stop the likely offending drug, document the suspected reaction, assess for other causes of AKI, and arrange follow-up of kidney recovery; seek nephrology input if recovery is incomplete or diagnosis is uncertain. |
| B | Continue the antibiotic because pyuria proves persistent bacterial infection. |
| C | Start empiric high-dose immunosuppression before reviewing the drug timeline or excluding infection. |
| D | Diagnose acute tubular injury solely because creatinine has risen. |
Correct answer: A. The temporal association with a beta-lactam, rash, fever, eosinophilia, sterile pyuria, and AKI makes drug-induced acute interstitial nephritis (AIN) a leading diagnosis. The first action is withdrawal of the suspected medication, careful review of all exposures, and longitudinal assessment of renal recovery. The clinical pattern is supportive but not perfectly specific; persistent AKI or diagnostic uncertainty may warrant nephrology assessment and, in selected cases, biopsy. [1]
Why the other options are less appropriate: B confuses inflammatory urinary findings with ongoing urinary infection. C may expose the patient to harm before the diagnosis and infectious context have been clarified; immunosuppression decisions are specialist-led and individualized. D ignores a highly informative exposure-and-hypersensitivity pattern.
Clinical pearl: Urine eosinophils are neither sensitive nor specific enough to confirm AIN. Medication chronology and the broader clinical picture matter more.
Case 4 — Albuminuric diabetic CKD
A 59-year-old man with type 2 diabetes and hypertension has an eGFR of 42 mL/min/1.73 m² and urine albumin–creatinine ratio of 780 mg/g, confirmed on repeat testing. He is taking maximally tolerated losartan. His blood pressure is 126/74 mmHg, potassium is 4.6 mmol/L, and he has no symptomatic volume depletion, active ketoacidosis, or recurrent severe genital infection.
Which additional measure is most appropriate to discuss and initiate if no contraindication emerges?
| Option | Answer |
|---|---|
| A | Combine an ACE inhibitor with losartan to maximize renin–angiotensin system blockade. |
| B | Stop losartan because albuminuria remains present despite treatment. |
| C | Start maintenance dialysis because the patient has CKD G3b with severe albuminuria. |
| D | Add an SGLT2 inhibitor while continuing risk-based CKD care and monitoring kidney function, volume status, and tolerability. |
Correct answer: D. In albuminuric CKD, care is layered rather than limited to one medication. An SGLT2 inhibitor should be considered in eligible patients in addition to optimized renin–angiotensin system inhibition, blood-pressure management, cardiovascular-risk reduction, and medication stewardship. A small early eGFR dip can occur and should be interpreted in clinical context rather than prompting automatic discontinuation. [2]
Why the other options are less appropriate: A increases adverse-event risk and is not routine kidney-protective therapy. B removes a key albuminuria- and blood-pressure-lowering therapy without a stated contraindication. C confuses CKD risk stratification with indications for kidney replacement therapy; dialysis is based on symptoms, complications, and overall clinical context, not eGFR or albuminuria alone at this stage.
Clinical pearl: “Persistent albuminuria” should trigger optimization and layering of evidence-based care, not abandonment of treatments that are tolerated and beneficial.
Case 5 — Metabolic acidosis in advanced CKD
A 67-year-old woman with CKD G4 due to hypertensive nephrosclerosis reports stable exertional fatigue but no vomiting, diarrhea, confusion, dyspnea, edema, or chest pain. Her eGFR is 23 mL/min/1.73 m², serum bicarbonate is 17 mmol/L on repeat testing, potassium is 4.9 mmol/L, and blood pressure is controlled. She has no evidence of diabetic ketoacidosis, lactic acidosis, or an acute decline in GFR.
Which approach is most appropriate?
| Option | Answer |
|---|---|
| A | Ignore the bicarbonate value because metabolic acidosis is expected in CKD and has no management implications. |
| B | Confirm the chronic acid–base context and contributors, then use a monitored treatment plan to avoid persistent clinically important acidosis while following blood pressure, volume status, potassium, and kidney trajectory. |
| C | Treat the bicarbonate value as an automatic indication for urgent dialysis despite clinical stability. |
| D | Prescribe a fixed alkali dose indefinitely without repeat bicarbonate or volume assessment. |
Correct answer: B. Persistent bicarbonate of 17 mmol/L in advanced CKD warrants a structured assessment and a monitored plan to prevent ongoing clinically important metabolic acidosis. The plan must account for cause, diet, blood pressure, sodium/volume tolerance, potassium, and serial bicarbonate values. Treatment goals should avoid both persistent acidemia and overshooting into alkalemia; this is not a simple “one value, one permanent dose” problem. [2]
Why the other options are less appropriate: A misses a modifiable CKD complication. C overcalls urgency; dialysis is not triggered by a bicarbonate value alone in a stable patient without refractory or life-threatening complications. D ignores the sodium load and monitoring needs of alkali therapy.
Clinical pearl: In CKD, treat the patient and trajectory—not a bicarbonate number in isolation. Verify that acidosis is chronic and not a clue to a new acute process.
Case 6 — Severe symptomatic hypotonic hyponatremia
A 63-year-old woman taking hydrochlorothiazide develops nausea, headache, confusion, and a generalized tonic–clonic seizure. Serum sodium is 112 mmol/L, serum osmolality is low, and glucose is normal. She is receiving airway support and is in a monitored emergency setting.
Which is the most appropriate immediate strategy?
| Option | Answer |
|---|---|
| A | Correct the sodium concentration to the normal range within several hours. |
| B | Restrict fluids alone and recheck sodium the following morning. |
| C | Give desmopressin alone as the initial treatment for the seizure. |
| D | Give protocol-based intermittent 3% hypertonic saline for severe symptoms, with frequent sodium and urine-output monitoring; aim initially for symptom improvement and a modest rise rather than rapid normalization. |
Correct answer: D. Seizure represents severe symptomatic hypotonic hyponatremia, requiring urgent monitored therapy. Contemporary guidance favors rapid intermittent 3% hypertonic saline for severe symptoms, with close reassessment. The immediate objective is relief of cerebral edema symptoms and an initial modest increase—commonly about 4–6 mmol/L—not normalization. Subsequent correction must be risk-adjusted, with readiness to halt or relower sodium if overcorrection occurs. [3]
Why the other options are less appropriate: B is unsafe in a patient with seizures. C can have a role in preventing or managing overcorrection under protocol but does not replace initial hypertonic-saline rescue for severe symptoms. A risks osmotic demyelination, especially when chronicity is unknown or risk factors are present.
Clinical pearl: In dangerous hyponatremia, distinguish the early symptom-relief goal from the maximum safe correction limit. The latter is a ceiling, not a target.
Case 7 — Hyperkalemia with ECG changes
A 70-year-old man with CKD G4 takes lisinopril and spironolactone. He presents with weakness. Serum potassium is 7.1 mmol/L on a nonhemolyzed sample. ECG shows broad QRS complexes and absent P waves. He is hemodynamically stable and has continuous cardiac monitoring.
What is the most appropriate treatment sequence?
| Option | Answer |
|---|---|
| A | Administer IV calcium promptly for myocardial stabilization, then begin protocol-based potassium redistribution and organize definitive potassium removal with repeat potassium, ECG, and glucose monitoring. |
| B | Give a loop diuretic alone, regardless of urine output or intravascular volume. |
| C | Begin an oral potassium binder and wait for the potassium to fall before addressing the ECG. |
| D | Stop potassium-containing drugs and recheck the potassium in 24 hours without acute treatment. |
Correct answer: A. Hyperkalemia with conduction abnormalities is an immediate cardiac emergency. The first principle is myocardial stabilization with IV calcium, followed by therapies that transiently shift potassium intracellularly and measures that remove potassium from the body. Insulin–glucose requires serial glucose monitoring, and dialysis is the most reliable potassium-removal therapy when severe hyperkalemia is refractory or kidney failure prevents adequate elimination. [4]
Why the other options are less appropriate: C is too slow and does not stabilize the myocardium. B is not reliably effective in an oliguric or volume-depleted patient. D ignores ECG toxicity and could permit fatal arrhythmia.
Clinical pearl: Think in three steps: stabilize the heart, shift potassium, remove potassium. An oral binder is never the first response to an ECG-toxic emergency.
Case 8 — Hypercalcemia, volume depletion, and AKI
A 66-year-old woman with weight loss, constipation, polyuria, and confusion has an albumin-adjusted calcium of 3.7 mmol/L (14.8 mg/dL), creatinine of 2.0 mg/dL from a baseline of 0.8 mg/dL, and dry mucous membranes. ECG shows a shortened QT interval. She has no clinical pulmonary edema.
Which is the best initial management plan?
| Option | Answer |
|---|---|
| A | Give a loop diuretic immediately to lower calcium, without replacing intravascular volume. |
| B | Start a thiazide diuretic to increase urinary calcium excretion. |
| C | Begin monitored isotonic-saline rehydration, obtain directed testing including PTH and malignancy evaluation, and add cause- and severity-specific calcium-lowering therapy with renal-aware specialist input. |
| D | Delay treatment until a parathyroid hormone assay identifies the cause. |
Correct answer: C. Severe hypercalcemia with neurocognitive symptoms, volume depletion, ECG changes, and AKI requires urgent, supervised treatment. Volume restoration with isotonic saline is an initial priority when the patient is depleted, while fluid balance is monitored carefully in kidney impairment. The cause must be clarified (including PTH-based categorization). For severe hypercalcemia of malignancy, antiresorptive therapy and short-course calcitonin may be used according to severity, kidney function, and specialist guidance. [5]
Why the other options are less appropriate: A may worsen hypovolemia; loop diuretics are not routine calcium-lowering therapy and are reserved for fluid overload after rehydration. B worsens hypercalcemia. D inappropriately delays stabilization for a dangerous biochemical and clinical syndrome.
Clinical pearl: Treat the physiology while investigating the cause. In hypercalcemia-associated AKI, polyuria and volume depletion frequently amplify the fall in GFR.
Case 9 — Infection-related nephritic syndrome
A 24-year-old man develops periorbital edema, cola-colored urine, and hypertension 2 weeks after untreated impetigo. Serum creatinine is 1.5 mg/dL, urinalysis shows dysmorphic erythrocytes and red-cell casts, urine protein–creatinine ratio is 1.2 g/g, and complement C3 is low. He has no hemoptysis, purpura, or systemic lupus features.
Which statement best reflects the likely diagnosis and initial management?
| Option | Answer |
|---|---|
| A | This is most consistent with minimal change disease, and high-dose glucocorticoids should be started immediately. |
| B | The pattern is consistent with infection-related glomerulonephritis; assess for and treat active infection, manage blood pressure and fluid complications, monitor kidney function and complement recovery, and seek nephrology input if the course is atypical. |
| C | The low C3 level proves ANCA-associated vasculitis, so immunosuppression should precede any infection assessment. |
| D | Red-cell casts exclude a glomerular process because bleeding must arise below the glomerulus. |
Correct answer: B. The latent period after impetigo, nephritic urine sediment, edema/hypertension, and low C3 support infection-related glomerulonephritis. Initial management emphasizes identification and treatment of active infection if present, supportive care for blood pressure and volume, and surveillance of kidney function and complement trajectory. Atypical, progressive, or nonresolving presentations merit nephrology evaluation and may require biopsy to distinguish alternative complement- or immune-mediated disease. [6]
Why the other options are less appropriate: A describes a nephrotic, not nephritic, pattern and proposes treatment that may be harmful in an infection-related context. C overinterprets low complement; ANCA vasculitis is typically not diagnosed by low C3 alone. D is false: red-cell casts strongly point to glomerular inflammation.
Clinical pearl: In a nephritic syndrome, combine the timing of infection, sediment, complement pattern, and kidney trajectory. None of these clues should be interpreted in isolation.
Case 10 — Pulmonary–renal syndrome
A 48-year-old man presents with 5 days of hemoptysis, dyspnea, fatigue, and dark urine. Oxygen saturation is 90% on room air. Hemoglobin has fallen from 13.5 to 9.6 g/dL, creatinine has risen from 0.9 to 3.6 mg/dL, and urinalysis shows protein, dysmorphic erythrocytes, and red-cell casts. Chest imaging shows bilateral alveolar opacities. There is no evidence of heart failure.
Which is the most appropriate next step?
| Option | Answer |
|---|---|
| A | Treat as uncomplicated community-acquired pneumonia and defer kidney evaluation until the pulmonary infiltrates resolve. |
| B | Start an ACE inhibitor and arrange routine outpatient urinalysis in 2 weeks. |
| C | Treat this as a nephrologic emergency: obtain urgent nephrology and pulmonary/critical-care input; send ANCA, anti-GBM, complement, and other directed studies; pursue kidney biopsy when feasible; and, after urgent assessment for competing infection and other mimics, begin institution-specific specialist-led treatment promptly when clinical suspicion is high; biopsy should not delay life-preserving care. |
| D | Reassure the patient that hemoptysis and hematuria are unrelated because they occur in different organ systems. |
Correct answer: C. Hemoptysis/alveolar hemorrhage plus rapidly progressive glomerulonephritis is a pulmonary–renal syndrome until proven otherwise. ANCA-associated vasculitis and anti-GBM disease are critical considerations. Time-sensitive multidisciplinary assessment, serology, kidney biopsy when feasible, and specialist-directed therapy are required; treatment decisions must balance the risk of irreversible renal/pulmonary injury against infection and other mimics. [6] [7]
Why the other options are less appropriate: A dangerously fragments a unified syndrome. B delays urgent evaluation and does not address the active glomerular and pulmonary process. D misses a classic multi-organ vasculitic or anti-GBM presentation.
Clinical pearl: In suspected pulmonary–renal syndrome, do not wait for a complete diagnostic panel before escalating care. Diagnostic sampling and life-saving treatment often proceed in parallel.
Resident takeaway table
| Problem pattern | First cognitive move | Immediate safety priority |
|---|---|---|
| AKI with shock or infection | Classify the hemodynamic and intrinsic injury context; review sediment and exposures | Perfusion, infection/source control, nephrotoxin stewardship, and complication monitoring |
| AKI with retention | Look for a reversible obstructive lesion | Prompt decompression and monitoring for post-obstructive diuresis |
| Albuminuric CKD | Layer risk-reducing therapies rather than selecting one “renal drug” | Monitor eGFR, albuminuria, blood pressure, volume status, potassium, and tolerability |
| Severe hyponatremia | Assess symptom severity and chronicity/risk of overcorrection | Monitored hypertonic-saline rescue for severe symptoms; avoid rapid normalization |
| Hyperkalemia with ECG toxicity | Stabilize, shift, remove | IV calcium first, then protocol-based redistribution and definitive elimination |
| Nephritic or pulmonary–renal syndrome | Recognize active glomerular inflammation from sediment and trajectory | Control volume/BP and urgently involve nephrology for rapidly progressive disease |
References
[2] [inline_viewer url="https://kdigo.org/wp-content/uploads/2024/03/KDIGO-2024-CKD-Guideline.pdf"]
[3] Spasovski G. Hyponatraemia-treatment standard 2024. Nephrology Dialysis Transplantation.
[6] [inline_viewer url="https://kdigo.org/wp-content/uploads/2017/02/KDIGO-2021-Glomerular-Diseases-Guideline_English_LN-2024-Update.pdf"]
[7] KDIGO. 2024 Clinical Practice Guideline for the Management of ANCA-Associated Vasculitis.
Intermediate Self-Assessment
Complete the 10-question Intermediate self-assessment below. Detailed explanations are provided after submission.