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Case Level: Advanced

This original five-case addendum uses the same concise, high-yield question-bank format as the resident-level nephrology set. It is designed for senior residents, nephrology trainees, and clinicians rotating through dialysis and transplant services. It is inspired by the educational structure of clinical question banks but does not reproduce proprietary Amboss content.

Educational disclaimer: These fictional cases support postgraduate education only. They do not replace dialysis-unit policies, local antimicrobial protocols, transplant-center instructions, current prescribing information, or individualized specialist clinical judgment. Dialysis access loss, suspected bloodstream infection, peritoneal-dialysis peritonitis, and acute allograft dysfunction require urgent specialist coordination.

Case 11 — Abrupt loss of arteriovenous fistula thrill

A 58-year-old man receives maintenance hemodialysis through a left brachiocephalic arteriovenous fistula. Before today’s session, he notices that the usual palpable thrill has disappeared. The dialysis nurse cannot obtain an adequate blood flow. He has no fever, hand pain, or bleeding. Examination shows a firm fistula with no thrill or bruit. His potassium is 5.4 mmol/L, he is euvolemic, and he has no urgent dialysis indication.

Which is the most appropriate next step?

Option Answer
A Schedule elective outpatient surveillance imaging several weeks later because he has no volume overload.
B Treat this as likely access thrombosis: urgently contact the dialysis/access team for diagnostic confirmation and access-salvage planning; use a temporary catheter only if dialysis cannot safely wait or the access cannot be restored.
C Cannulate repeatedly at different sites until a blood flow sufficient for dialysis is achieved.
D Begin systemic anticoagulation without imaging or access-specialist assessment.

Correct answer: B. Abrupt loss of a previously present thrill and bruit with failure to deliver dialysis strongly suggests thrombosis of the AV fistula, often on a background of clinically significant stenosis. This is an access-preservation problem: prompt involvement of the dialysis vascular-access team for imaging and endovascular or surgical management offers the best chance of restoring the fistula. Whether and when a temporary catheter is needed depends on urgency of dialysis, anticipated time to salvage, and the patient’s broader access plan. [1]

Why the other options are less appropriate: A delays a potentially salvageable access. C risks infiltration, hematoma, and loss of remaining cannulation sites. D is not a substitute for defining and correcting the access lesion, and empiric anticoagulation can increase bleeding risk without restoring access patency.

Clinical pearl: A functioning fistula is a limited long-term resource. In a stable patient, the question is not simply “How can I dialyze today?” but also “How can I preserve the patient’s future access options?”

Case 12 — Fever during dialysis through a tunnelled catheter

A 71-year-old woman with limited vascular-access options has a right internal-jugular tunnelled hemodialysis catheter. Forty minutes into dialysis, she develops rigors, temperature 39.2°C, and blood pressure 102/64 mmHg. The exit site is mildly erythematous but there is no obvious purulent drainage. She is alert and has no focal back pain, new murmur, or pulmonary symptoms. Her pre-dialysis white-cell count is 15,000/µL.

Which management approach is most appropriate?

Option Answer
A Give acetaminophen and continue the session; blood cultures are unnecessary unless the fever persists for 48 hours.
B Remove the catheter immediately in every case before obtaining cultures or assessing hemodynamic stability.
C Presume this is a dialyzer reaction and restart dialysis with the same catheter at the next scheduled session.
D Activate a suspected catheter-related bloodstream infection pathway: assess for sepsis, obtain appropriate cultures before antibiotics when feasible, begin local empiric antimicrobial therapy promptly, and make catheter-salvage, exchange, or removal decisions with dialysis/infectious-disease input based on organism, tunnel involvement, bacteremia persistence, and metastatic infection.

Correct answer: D. Rigors during dialysis in a patient with a tunnelled catheter are highly concerning for catheter-related bloodstream infection (CRBSI). Management proceeds in parallel: stabilize the patient and evaluate for sepsis; collect cultures from the catheter/dialysis circuit and peripheral blood according to local procedure when feasible; start empiric therapy promptly; and plan catheter management based on the organism, clinical response, exit-site/tunnel infection, persistent bacteremia, and evidence of endocarditis or other metastatic infection. [1]

Why the other options are less appropriate: A risks delayed treatment of sepsis. B may sacrifice a scarce access site before cultures, stability, organism, and source-control needs have been assessed; some situations, however, will mandate removal. C ignores a high-risk device-associated infection syndrome.

Clinical pearl: In a catheter-dependent patient, access preservation is important—but it must never outweigh stabilization and source control when severe infection, persistent bacteremia, tunnel infection, or metastatic complications are present.

Case 13 — Cloudy peritoneal-dialysis effluent

A 46-year-old man on automated peritoneal dialysis reports diffuse abdominal pain and cloudy drainage fluid since this morning. He is afebrile, blood pressure is stable, and the exit site appears clean. His PD effluent has 620 leukocytes/µL with 84% neutrophils after an adequate dwell. The nephrology service is available by phone, but microbiology results will not return for at least 24 hours.

Which is the best immediate management step?

Option Answer
A Treat this as PD-associated peritonitis: send PD effluent for cell count/differential and culture using the local protocol, then begin prompt empiric intraperitoneal antimicrobial coverage that addresses gram-positive and gram-negative organisms and adjust treatment once culture data and clinical response are available.
B Wait for culture results before starting treatment because the patient is hemodynamically stable.
C Switch permanently to hemodialysis immediately; PD peritonitis always requires catheter removal.
D Give an oral antibiotic selected for uncomplicated diverticulitis and continue PD without effluent reassessment.

Correct answer: A. Cloudy effluent plus abdominal pain and neutrophilic effluent meets the working diagnosis of PD-associated peritonitis. Sampling should be obtained promptly, but empiric treatment should not be delayed while culture results are pending. ISPD guidance supports empiric intraperitoneal coverage chosen for local pathogen susceptibility patterns and later narrowed to the cultured organism. Refractory, relapsing, fungal, or catheter-associated infection may require catheter removal and modality planning; it is not automatic for every first episode. [2]

Why the other options are less appropriate: B delays treatment and can increase peritoneal injury and technique failure. C overgeneralizes; catheter removal is reserved for defined or clinically failing scenarios. D does not provide a guideline-concordant PD-peritonitis strategy and fails to direct therapy to the peritoneal cavity.

Clinical pearl: For PD peritonitis, the urgent action is culture first if it does not delay therapy, then treat promptly. The culture result refines therapy; it should not be a reason to postpone initial coverage.

Case 14 — Acute allograft dysfunction after a tacrolimus interaction

A 39-year-old man received a deceased-donor kidney transplant 18 months ago. His usual creatinine is 1.2 mg/dL. He develops sinusitis and is prescribed clarithromycin at an urgent-care clinic. Four days later, he reports tremor and headache. Creatinine is 2.1 mg/dL, potassium is 5.8 mmol/L, blood pressure is 154/92 mmHg, and a timed tacrolimus trough is markedly above his individual target range. He is afebrile, has no graft tenderness, and reports taking all immunosuppressive medication as prescribed.

Which is the most appropriate next step?

Option Answer
A Assume acute cellular rejection and give empiric high-dose glucocorticoids without a medication review or graft assessment.
B Reassure the patient that a high tacrolimus trough cannot explain AKI if adherence is good.
C Urgently contact the transplant team to stop or replace the interacting drug and make transplant-guided tacrolimus adjustment/temporary withholding decisions; repeat a properly timed drug level and simultaneously evaluate other reversible causes of allograft dysfunction, including obstruction, infection, hemodynamic injury, and rejection.
D Permanently discontinue tacrolimus and all other immunosuppression to eliminate nephrotoxicity.

Correct answer: C. Clarithromycin can markedly increase tacrolimus exposure through metabolic interaction. The high trough, tremor, hypertension, hyperkalemia, and AKI make acute calcineurin-inhibitor toxicity a leading concern. However, it remains a diagnosis within a broader allograft-dysfunction evaluation. The immediate action is transplant-center coordination to reverse the interacting exposure and adjust tacrolimus safely, with repeated timed levels and parallel assessment for obstruction, infection, volume/hemodynamic injury, rejection, and thrombotic microangiopathy. [3] [5]

Why the other options are less appropriate: A treats an unconfirmed diagnosis while missing an obvious reversible interaction. B is false; drug interactions, diarrhea, and other factors can substantially alter tacrolimus exposure despite adherence. D exposes the patient to rejection and is not an independent outpatient decision.

Clinical pearl: A high tacrolimus level is important—but it should not prematurely close the differential diagnosis. Allograft dysfunction may have more than one contributor.

Case 15 — Rising creatinine with de novo donor-specific antibody

A 52-year-old woman received a kidney transplant 5 years ago. Her creatinine has risen from 1.1 to 1.8 mg/dL over 6 weeks and urine protein–creatinine ratio is now 0.9 g/g. Ultrasound shows no hydronephrosis and patent major vessels. BK plasma nucleic-acid testing is negative. Testing identifies a new donor-specific anti-HLA antibody. She has not missed doses but recently had a medication change that may have reduced mycophenolate exposure.

Which is the most appropriate next step?

Option Answer
A Treat donor-specific antibody positivity alone as definitive antibody-mediated rejection and begin a fixed antirejection regimen without biopsy.
B Expedite transplant-nephrology assessment and allograft biopsy, while confirming drug exposure/adherence and reviewing infection, obstruction, hemodynamic, recurrent/de novo disease, and drug-toxicity possibilities; biopsy findings should direct any specific antirejection therapy.
C Ignore the donor-specific antibody because ultrasound is normal.
D Stop maintenance immunosuppression to reduce the risk of infection while awaiting repeat creatinine in 3 months.

Correct answer: B. New donor-specific antibody with graft dysfunction and proteinuria raises concern for antibody-mediated rejection, but DSA is a risk marker rather than a biopsy-equivalent diagnosis. Contemporary consensus guidance supports allograft biopsy to assess the pathogenicity and prognostic impact of de novo DSA, while maintenance therapy, adherence, and alternate causes of dysfunction are evaluated. Specific treatment should be driven by histology, clinical severity, infection status, and transplant-center protocol. [4] [5]

Why the other options are less appropriate: A can expose the patient to intense immunosuppression without defining the pathology. C ignores both functional deterioration and a high-risk immunologic signal. D risks precipitating or worsening rejection.

Clinical pearl: In transplant medicine, DSA plus dysfunction is a biopsy problem. Serology, drug levels, imaging, virology, urinalysis, and histology often answer different parts of the same question.

Advanced takeaways

Presentation Action that should not be delayed Key pitfall to avoid
Loss of fistula thrill Urgent access-team assessment for thrombosis/salvage Repeated traumatic cannulation or routine delay
Rigors during catheter dialysis Sepsis assessment, cultures, prompt empiric therapy, and source-control planning Assuming every catheter can—or must—be managed identically
Cloudy PD effluent Effluent studies and protocol-based empiric intraperitoneal therapy Waiting for culture before starting treatment
High tacrolimus trough with AKI Transplant-guided reversal of interaction and parallel allograft assessment Attributing all dysfunction to tacrolimus or independently stopping immunosuppression
Dysfunction plus de novo DSA Timely allograft biopsy and transplant review Treating DSA alone as a histologic diagnosis

References

[1] National Kidney Foundation. KDOQI Vascular Access Guidelines and Clinical Tools.

[2] Li PKT, et al. ISPD peritonitis guideline recommendations: 2022 update on prevention and treatment. Peritoneal Dialysis International.

[3] Hansen CM, et al. Calcineurin Inhibitor Associated Nephrotoxicity in Kidney Transplantation—A Transplant Nephrologist’s Perspective. Acta Physiologica.

[4] van den Broek DAJ, et al. The Clinical Utility of Post-Transplant Monitoring of Donor-Specific Antibodies in Stable Renal Transplant Recipients: A Consensus Report. Transplant International.

[5] KDIGO. Transplant Recipient Guideline Hub.

Advanced Self-Assessment

Complete the 10-question Advanced self-assessment below. Detailed explanations are provided after submission.

Advanced Self-Assessment: Dialysis Complications and Kidney Transplant Management

1 / 10

A 58-year-old man receives maintenance hemodialysis through a left brachiocephalic arteriovenous fistula. Before today’s session, he notices that the usual palpable thrill has disappeared. The dialysis nurse cannot obtain an adequate blood flow. He has no fever, hand pain, or bleeding. Examination shows a firm fistula with no thrill or bruit. His potassium is 5.4 mmol/L, he is euvolemic, and he has no urgent dialysis indication.

Which is the most appropriate next step?

2 / 10

A 71-year-old woman with limited vascular-access options has a right internal-jugular tunnelled hemodialysis catheter. Forty minutes into dialysis, she develops rigors, temperature 39.2°C, and blood pressure 102/64 mmHg. The exit site is mildly erythematous but there is no obvious purulent drainage. She is alert and has no focal back pain, new murmur, or pulmonary symptoms. Her pre-dialysis white-cell count is 15,000/µL.

Which management approach is most appropriate?

3 / 10

A 46-year-old man on automated peritoneal dialysis reports diffuse abdominal pain and cloudy drainage fluid since this morning. He is afebrile, blood pressure is stable, and the exit site appears clean. His PD effluent has 620 leukocytes/µL with 84% neutrophils after an adequate dwell. The nephrology service is available by phone, but microbiology results will not return for at least 24 hours.

Which is the best immediate management step?

4 / 10

A 39-year-old man received a deceased-donor kidney transplant 18 months ago. His usual creatinine is 1.2 mg/dL. He develops sinusitis and is prescribed clarithromycin at an urgent-care clinic. Four days later, he reports tremor and headache. Creatinine is 2.1 mg/dL, potassium is 5.8 mmol/L, blood pressure is 154/92 mmHg, and a timed tacrolimus trough is markedly above his individual target range. He is afebrile, has no graft tenderness, and reports taking all immunosuppressive medication as prescribed.

Which is the most appropriate next step?

5 / 10

A 52-year-old woman received a kidney transplant 5 years ago. Her creatinine has risen from 1.1 to 1.8 mg/dL over 6 weeks and urine protein–creatinine ratio is now 0.9 g/g. Ultrasound shows no hydronephrosis and patent major vessels. BK plasma nucleic-acid testing is negative. Testing identifies a new donor-specific anti-HLA antibody. She has not missed doses but recently had a medication change that may have reduced mycophenolate exposure.

Which is the most appropriate next step?

6 / 10

A 64-year-old woman on hemodialysis through a recently created brachial-based AV fistula develops severe pain, numbness, and coolness of the access-side hand during dialysis. The radial pulse is diminished compared with the contralateral side. There is no fever, erythema, or loss of access thrill.

Which is the most appropriate next step?

7 / 10

A 54-year-old man on continuous ambulatory peritoneal dialysis is treated with culture-directed intraperitoneal antibiotics for PD-associated peritonitis. After 5 days of appropriate treatment, he still has abdominal pain and cloudy effluent with persistently elevated effluent leukocytes. He is hemodynamically stable, but repeated cultures and exit-site assessment are in progress.

Which approach is most appropriate now?

8 / 10

A 33-year-old kidney-transplant recipient has a creatinine increase from 1.0 to 1.7 mg/dL over 10 days. Timed tacrolimus trough is within the individual target range. Ultrasound shows no hydronephrosis, BK testing is negative, and urine culture is negative. She has no diarrhea, volume depletion, or recent medication changes. The transplant team considers acute rejection a leading possibility, and she is clinically stable.

Which is the most appropriate next step?

9 / 10

A 47-year-old kidney-transplant recipient with stable prior graft function develops 4 days of profuse diarrhea from viral gastroenteritis. She continues her usual tacrolimus dose. She now has tremor and creatinine has increased from 1.1 to 1.6 mg/dL. There is no new antimicrobial or azole exposure.

Which interpretation and action are most appropriate?

10 / 10

At a routine 1-year post-transplant visit, a 41-year-old kidney-transplant recipient has stable creatinine, no proteinuria, and a newly detected de novo donor-specific anti-HLA antibody. She reports several recently delayed tacrolimus doses because of a medication-access problem. She has no symptoms of infection.

Which is the most appropriate management principle?

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Level: Advanced — nephrology trainees and nephrologists

Educational disclaimer: This fictional case is for postgraduate education and does not replace clinical judgment, local protocols, multidisciplinary review, current prescribing information, or individual patient factors.

Learning objectives

After completing this case, learners should be able to diagnose and stage primary IgA nephropathy (IgAN), distinguish prognostic information from a treatment mandate, optimize kidney-protective care, and discuss an APRIL-directed treatment option using current evidence, regulatory limitations, infection precautions, and shared decision-making.

Stage 1 — Establishing the diagnosis and excluding secondary causes

A 34-year-old man is referred for persistent microscopic hematuria and proteinuria discovered during a routine occupational assessment. He reports no edema, purpura, arthralgia, chronic abdominal symptoms, or recurrent gross hematuria. He has treated hypertension and no known diabetes. His father developed kidney failure in his early sixties of an uncertain cause. He drinks alcohol infrequently and has no history of inflammatory bowel disease, chronic liver disease, hepatitis, HIV infection, or systemic autoimmune disease.

Investigation Result
Serum creatinine / eGFR 1.70 mg/dL / 48 mL/min/1.73 m²
First-morning urine protein–creatinine ratio (UPCR) 2.4 g/g on two measurements
Urine sediment Dysmorphic erythrocytes; no red-cell casts
Serum albumin 3.8 g/dL
Blood pressure 142/88 mmHg
HbA1c 5.4%
Hepatitis B, hepatitis C, HIV testing Negative
Liver tests and abdominal ultrasonography No evidence of chronic liver disease

A kidney biopsy contains 18 glomeruli. Immunofluorescence shows dominant mesangial IgA deposition. Light microscopy and electron microscopy support IgAN. The revised Oxford score is M1 E0 S1 T1 C0, with mild interstitial fibrosis/tubular atrophy and no necrotizing lesion. There is no evidence of infection-related glomerulonephritis, monoclonal gammopathy-related disease, or a superimposed podocytopathy.

Decision point 1

Which interpretation is most appropriate?

Option Interpretation
A Serum galactose-deficient IgA1 confirms primary IgAN, so a kidney biopsy is optional.
B A biopsy is required to diagnose IgAN; after biopsy confirmation, secondary causes should be assessed and the MEST-C score documented for prognosis.
C The S1 lesion proves that immediate systemic glucocorticoids are required in every patient.
D The absence of edema excludes clinically meaningful risk of progressive kidney disease.

Preferred decision: B. KDIGO states that IgAN can be diagnosed only by kidney biopsy, because there are no validated serum or urine biomarkers for diagnosis. Once IgAN is diagnosed, clinicians should assess for secondary causes and determine the MEST-C score. MEST-C, eGFR, proteinuria, blood pressure, and other biopsy-era clinical data contribute to risk assessment; no histologic component alone prescribes one universal treatment.[1]

Stage 2 — Quantifying risk and completing foundational care

The International IgAN Prediction Tool is reviewed with the patient using his biopsy-era data. The result supports a meaningful risk of progressive kidney-function loss over the next several years. The team emphasizes that the tool informs a discussion; it does not replace longitudinal assessment of eGFR slope, proteinuria, blood pressure, adverse effects, medication adherence, and the patient’s preferences.

Over the next six months, lisinopril is titrated to the maximally tolerated dose and dapagliflozin is added. Sodium intake, smoking avoidance, cardiovascular risk, vaccination history, body weight, and exercise are reviewed. His blood pressure becomes 126/76 mmHg. He tolerates both drugs without hyperkalemia, symptomatic hypotension, or recurrent genitourinary infection. Despite this optimized kidney-protective strategy, first-morning UPCR remains 2.1 g/g and eGFR is 47 mL/min/1.73 m².

Decision point 2

Which conclusion now best reflects current guidance?

Option Interpretation
A Persistent proteinuria is not relevant once an ACE inhibitor and an SGLT2 inhibitor have been started.
B A patient with proteinuria of at least 0.5 g/day or equivalent is at risk of progressive kidney-function loss; treatment or additional treatment should be considered while kidney-protective care continues.
C The only meaningful goal is immediate normalization of the eGFR.
D Sparsentan can be layered on top of the ACE inhibitor because both lower intraglomerular pressure.

Preferred decision: B. KDIGO identifies proteinuria of at least 0.5 g/day or equivalent as a marker of risk for progressive kidney-function loss, whether the patient is on or off IgAN therapy. The broader treatment goal is to reduce the rate of kidney-function loss; urine protein is the validated early biomarker used to guide decisions and should be minimized, ideally below 0.3 g/day when achievable.[1] If sparsentan is selected, it replaces rather than accompanies ACE inhibitor or ARB therapy because it already incorporates angiotensin-receptor blockade.[1]

Stage 3 — Discussing a newer APRIL-directed option

The patient wants to avoid systemic glucocorticoids if a suitable disease-directed alternative is available. Targeted-release budesonide, sparsentan, and current U.S. options are reviewed in light of his disease features, tolerance of ACE inhibition, treatment burden, reproductive plans, local availability, insurance coverage, and the limits of direct comparative evidence. He has no active infection, has completed an age-appropriate vaccination review, and does not use systemic immunosuppressants.

The multidisciplinary team also discusses sibeprenlimab-szsi (Voyxact), a monoclonal antibody that inhibits APRIL. In the United States, it has accelerated approval to reduce proteinuria in adults with primary IgAN at risk for progression. This does not yet establish that it slows long-term kidney-function decline.[2]

In the VISIONARY phase 3 interim analysis, adults with biopsy-confirmed IgAN receiving sibeprenlimab 400 mg subcutaneously every four weeks had a 50.2% reduction in 24-hour UPCR at nine months, compared with a 2.1% increase with placebo; the placebo-adjusted relative difference was 51.2%.[3] The key eGFR-slope outcome is reported at trial completion, so the proteinuria signal must not be overstated as definitive long-term kidney protection.[3]

Decision point 3

Which counseling statement is most appropriate before starting sibeprenlimab in this patient?

Option Interpretation
A Because it is approved for IgAN, sibeprenlimab should replace all supportive therapy.
B It is a reasonable U.S. option to discuss after optimized supportive therapy, but accelerated approval is based on proteinuria reduction; assess active infection, review vaccines, avoid live vaccines shortly before and during treatment, and discuss the uncertainty about long-term eGFR benefit.
C It can be combined indiscriminately with systemic immunosuppression because its safety is fully established in such combinations.
D It is contraindicated when eGFR is below 90 mL/min/1.73 m².

Preferred decision: B. Sibeprenlimab is an APRIL blocker, not a substitute for optimized kidney-protective care or individualized treatment selection. The U.S. label recommends assessment for active infection before treatment, monitoring for infection during treatment, and avoidance of live vaccines within 30 days before starting and during therapy. It also notes limited clinical data with concomitant systemic immunosuppressants.[2]

Domain Educational management plan
Foundational therapy Maintain tolerated kidney-protective therapy, blood-pressure management, cardiovascular-risk assessment, and longitudinal surveillance.
New option If selected in the relevant jurisdiction, sibeprenlimab is administered as 400 mg subcutaneously every four weeks according to current prescribing information.[2]
Infection and vaccination Assess for active infection before initiation; monitor during therapy; revisit vaccination status and avoid live vaccines within 30 days before initiation or during treatment.[2]
Treatment framing Explain accelerated-approval status, proteinuria-based evidence, the pending long-term eGFR outcome, administration burden, access, and the absence of head-to-head evidence proving universal superiority.
Alternatives Compare targeted-release budesonide, sparsentan, and other locally available options using disease phenotype, contraindications, reproductive considerations, treatment burden, and patient values.[1]

Stage 4 — Longitudinal response, intercurrent infection, and reassessment

After nine months of sibeprenlimab alongside continued kidney-protective therapy, the patient’s UPCR has fallen from 2.1 g/g to 0.92 g/g. eGFR is 46 mL/min/1.73 m². His blood pressure remains controlled and he has had no injection-site reaction. He now develops fever, productive cough, and focal crackles on examination one week before his next planned injection.

Decision point 4

Which response is most appropriate?

Option Interpretation
A Administer the scheduled injection immediately because proteinuria has improved.
B Treat the improved UPCR as a complete durable remission and discontinue kidney follow-up.
C Evaluate the respiratory illness urgently and consider interrupting sibeprenlimab if infection is serious until the infection is controlled; continue a structured assessment of kidney trajectory, proteinuria, blood pressure, and treatment safety.
D Add a live vaccine immediately to reduce future infection risk while continuing treatment.

Preferred decision: C. New infection symptoms require timely clinical evaluation. The label advises consideration of treatment interruption if a serious infection develops until it is controlled.[2] The improvement in proteinuria is encouraging but remains above the ideal proteinuria target. It should prompt continued follow-up, rather than premature declaration of cure or indefinite continuation without reassessment.[1]

Expert synthesis

Primary IgAN requires diagnosis by kidney biopsy, active exclusion of secondary causes, structured risk assessment, and concurrent treatment of both immune-complex-mediated injury and chronic nephron-loss consequences. MEST-C contributes to prognosis and shared decision-making but should not be converted into an automatic drug-selection rule.

This patient has persistent high-risk proteinuria despite optimized kidney-protective therapy. Sibeprenlimab offers a newer APRIL-directed option in the United States, with an accelerated-approval indication based on proteinuria reduction. Its decision framework must explicitly include the unresolved long-term eGFR question, infection and immunization precautions, drug access, alternative disease-directed options, and the patient’s preferences. The result is a reasoned therapeutic discussion rather than a universal prescription.

References

[1] [inline_viewer url="https://kdigo.org/wp-content/uploads/2026/04/KDIGO-2025-IgAN-IgAV-Guideline.pdf"]

[2] [inline_viewer url="https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/761434s000lbl.pdf"]

[3] Perkovic V, et al. Sibeprenlimab in IgA Nephropathy — Interim Analysis of a Phase 3 Trial. New England Journal of Medicine. 2026;394:635–646.

[4] FDA Drug Trials Snapshot: VANRAFIA (atrasentan)

Advanced self-assessment

Complete the 10-question Advanced self-assessment below. Detailed explanations are provided after submission.

Advanced Self-Assessment: IgA Nephropathy and APRIL-Directed Therapy

1 / 10

A 34-year-old adult has persistent microscopic hematuria, UPCR 2.4 g/g, and eGFR 48 mL/min/1.73 m². Which statement is most accurate?

2 / 10

Which finding most strongly requires reconsideration of whether apparent IgA-dominant glomerular disease represents primary IgAN rather than a secondary process?

3 / 10

Which is the most appropriate use of the International IgAN Prediction Tool in adults with biopsy-confirmed primary IgAN?

4 / 10

After optimized supportive therapy, a patient has eGFR 47 mL/min/1.73 m² and persistent UPCR 2.1 g/g. Which statement best reflects the current treatment framework?

5 / 10

Which is the most appropriate foundational pharmacologic step in an adult with IgAN at risk of progression, absent a contraindication?

6 / 10

If sparsentan is selected for a patient with IgAN at risk of progression, which statement is correct?

7 / 10

Which statement best describes KDIGO 2025’s position on targeted-release budesonide (Nefecon) in IgAN?

8 / 10

Which counseling statement is most accurate regarding sibeprenlimab-szsi (Voyxact) in the United States?

9 / 10

Which action is most appropriate before starting sibeprenlimab-szsi?

10 / 10

At nine months, UPCR has fallen from 2.1 g/g to 0.92 g/g and eGFR is stable, but the patient develops fever, productive cough, and focal crackles before the next sibeprenlimab dose. What is the best next step?

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Level: Advanced — nephrology trainees and nephrologists

Educational disclaimer: This fictional case is for postgraduate education and does not replace clinical judgment, local protocols, multidisciplinary review, current prescribing information, or individual patient factors.

Learning objectives

After completing this case, learners should be able to recognize high-risk active lupus nephritis (LN), interpret a mixed proliferative and membranous biopsy pattern, distinguish supportive care from disease-directed treatment, and weigh a newly approved B-cell-directed add-on option against its safety, reproductive, and access considerations.

Stage 1 — Presentation and diagnostic framing

A 31-year-old woman with systemic lupus erythematosus (SLE), diagnosed six years earlier, is referred urgently with progressive edema, foamy urine, hypertension, and fatigue. Her SLE history includes photosensitivity, inflammatory arthritis, and immune thrombocytopenia. She has continued hydroxychloroquine but discontinued mycophenolate mofetil (MMF) eighteen months ago after a sustained period of low disease activity. She is not pregnant, would like to consider pregnancy in approximately two years, and agrees to effective contraception while active disease is treated.

During the preceding three weeks, she has gained 4 kg and developed ankle edema, arthralgia, and lower exercise tolerance. Her blood pressure is 166/102 mmHg. Examination identifies 2+ bilateral ankle edema but no fever, murmur, livedo, focal neurological deficit, or active synovitis.

Investigation Result
Serum creatinine 1.23 mg/dL; prior 0.68 mg/dL
Estimated GFR 57 mL/min/1.73 m²
Urine protein–creatinine ratio (UPCR) 5.8 g/g
Urine microscopy Dysmorphic red cells and red-cell casts
Serum albumin 2.6 g/dL
Complement C3/C4 Both low
Anti-dsDNA antibody Markedly increased from baseline
Hemoglobin / platelets 9.8 g/dL / 178 × 10⁹/L
Pregnancy test and urine culture Negative

Decision point 1

Which interpretation is most appropriate?

Option Interpretation
A The proteinuria can be observed while renin–angiotensin system blockade is optimized.
B The combination of rising creatinine, active urinary sediment, nephrotic-range proteinuria, hypocomplementemia, and increased anti-dsDNA makes active glomerular inflammation highly likely and warrants urgent kidney biopsy and specialist-led treatment planning.
C The normal platelet count excludes active lupus nephritis.
D The negative urine culture excludes all causes of acute kidney injury, so biopsy is unnecessary.

Preferred decision: B. This is a high-risk renal presentation. Supportive treatment for blood pressure and edema is necessary, but cannot substitute for establishing the renal lesion and directing immunosuppression. Kidney biopsy remains central to classification and to separating potentially reversible active injury from chronic damage.[1]

Stage 2 — Biopsy, differential refinement, and immediate risks

Kidney biopsy shows ISN/RPS Class IV-G (A) diffuse proliferative LN with a membranous Class V component. The activity index is 13/24 and chronicity index 2/12. Approximately 20% of glomeruli contain cellular crescents. There is no thrombotic microangiopathy (TMA), no anti-GBM pattern, and only mild interstitial fibrosis/tubular atrophy.

The treating team should now address blood pressure, edema, kidney-protective therapy, thrombosis risk in nephrotic syndrome, infection exclusion, adherence, and reproductive counseling in parallel with immunosuppression planning. The low chronicity score and active lesions make the possibility of recovery clinically meaningful, but do not eliminate the risk of irreversible nephron loss if control is delayed.

Decision point 2

Which statement best guides the next step?

Option Interpretation
A Cellular crescents automatically require plasma exchange as routine initial treatment for LN.
B The Class V component means that proliferative-LN therapy is no longer relevant.
C The biopsy confirms active mixed proliferative/membranous LN. Plasma exchange is not a routine response to crescents alone; a separate indication, such as a concomitant process, must be demonstrated.
D The absence of TMA makes blood-pressure management and antiphospholipid-antibody assessment unnecessary.

Preferred decision: C. The biopsy supports prompt combination immunosuppression in addition to supportive management. It also provides important negative findings: if TMA, antiphospholipid-associated nephropathy, or anti-GBM disease is suspected clinically, those diagnoses require separate evaluation and may change the rescue strategy. They should not be presumed from crescents alone.[1]

Stage 3 — Selecting an initial regimen and discussing a newer option

The multidisciplinary team proposes pulse intravenous glucocorticoids followed by a planned oral taper and MMF, while continuing hydroxychloroquine unless contraindicated and implementing kidney-protective care. Because of severe proteinuria, high histologic activity, and the goal of limiting ongoing glucocorticoid exposure, the team discusses obinutuzumab as an add-on to standard therapy.

Obinutuzumab is a type II anti-CD20 B-cell-depleting antibody. In the United States it is FDA-approved for adults with active LN who are receiving standard therapy.[3] It should not be framed as monotherapy or as a universal replacement for MMF, glucocorticoids, belimumab, or voclosporin. The selection of an add-on must be individualized: renal function and proteinuria trajectory, extrarenal disease, prior response, infection history, infusion burden, reproductive plans, access, cost, and patient preferences all matter.[1] [2]

In REGENCY, participants receiving obinutuzumab or placebo also received MMF and a structured glucocorticoid taper. At week 76, complete renal response occurred in 46.4% of participants given obinutuzumab and 33.1% given placebo.[4] The trial supports the option but does not establish superiority over other modern add-on strategies, because direct comparative trials are lacking.

Decision point 3

Which approach best describes an appropriate discussion of obinutuzumab in this case?

Option Interpretation
A Use obinutuzumab alone so MMF and glucocorticoids can be stopped immediately.
B Defer all treatment until the patient has finished future pregnancy plans.
C Add obinutuzumab to standard therapy only after infection, hepatitis B, hematologic, vaccination, reproductive, and infusion-risk considerations have been reviewed; incorporate the patient’s values and local access.
D Use the drug only after every other modern therapy has failed, irrespective of disease severity or labeling.

Preferred decision: C. Current U.S. labeling specifies obinutuzumab for active LN in adults receiving standard therapy. It carries important safety warnings, including hepatitis B reactivation and PML, and requires appropriately supervised intravenous administration.[5]

Domain Educational management plan
Disease-directed therapy Use glucocorticoids and MMF as standard therapy, with an add-on chosen by individualized shared decision-making.
Obinutuzumab regimen The U.S. label specifies 1,000 mg intravenously initially, at week 2, week 24, week 26, and then every six months. Premedication and infusion monitoring are required.[5]
Infection and vaccine planning Exclude active infection; complete hepatitis B screening before treatment; review vaccinations and avoid live-virus vaccines during treatment and until B-cell recovery.[5]
Kidney protection Address blood pressure, sodium and edema management, renin–angiotensin system blockade when clinically appropriate, and cardiovascular/thrombotic risk.
Reproductive care Confirm non-pregnancy, provide contraception during active therapy, and revisit a planned conversion to a pregnancy-compatible regimen only after disease control and specialist review.

Stage 4 — Longitudinal reassessment and possible escalation

At three months, the patient reports better energy and less edema. Her creatinine is 0.95 mg/dL and UPCR is 3.3 g/g. She has not had an infusion reaction, fever, respiratory symptoms, or recurrent urinary infection. Her prednisone dose is being reduced according to the team’s protocol. She asks whether the residual proteinuria means therapy has failed.

Decision point 4

What is the most appropriate response?

Option Interpretation
A Declare treatment failure immediately and switch all immunosuppression without further assessment.
B Stop monitoring because the serum creatinine has improved.
C Continue longitudinal assessment of proteinuria, kidney function, urine sediment, blood pressure, treatment tolerance, adherence, infection, and glucocorticoid toxicity; reassess the diagnosis or consider repeat biopsy if the trajectory becomes discordant or unexpectedly worsens.
D Increase glucocorticoids indefinitely until proteinuria is absent.

Preferred decision: C. Improvement in kidney function and proteinuria is reassuring but not equivalent to complete response. Response assessment is trajectory-based and must include safety and adherence. KDIGO emphasizes structured reassessment of an unsatisfactory response before reflexively escalating therapy.[1]

Expert synthesis

This case illustrates a young adult with severe, active mixed proliferative and membranous LN. The renal biopsy defines the lesion and helps balance urgency against reversibility. A new treatment should be presented as an add-on to standard therapy, never as a substitute for informed clinical judgment, infection screening, kidney-protective measures, reproductive planning, or serial reassessment.

Obinutuzumab is a relevant new U.S. option for adults with active LN receiving standard therapy. Its benefit in REGENCY must be interpreted in the context of the study population and background therapy; there is no direct trial evidence establishing that it is the preferred add-on for every patient. The best choice is therefore individualized and multidisciplinary.

References

[1] [inline_viewer url="https://kdigo.org/wp-content/uploads/2024/01/KDIGO_2024_Lupus_Nephritis_Guideline.pdf"]

[2] Sammaritano LR, et al. 2024 American College of Rheumatology Guideline for the Screening, Treatment, and Management of Lupus Nephritis. Arthritis & Rheumatology. 2025.

[3] Lupus Foundation of America. FDA Approves Gazyva (obinutuzumab) for the Treatment of Adults with Lupus Nephritis. October 20, 2025.

[4] Furie RA, et al. Efficacy and Safety of Obinutuzumab in Active Lupus Nephritis. New England Journal of Medicine. 2025;392:1471–1483.

[5] [inline_viewer url="https://www.gene.com/download/pdf/gazyva_prescribing.pdf"]

Advanced self-assessment

Complete the 10-question Advanced self-assessment below. Detailed explanations are provided after submission.

Advanced Self-Assessment: Complex Lupus Nephritis

1 / 10

A 31-year-old woman with SLE has a serum creatinine increase from 0.68 to 1.23 mg/dL, UPCR 5.8 g/g, low C3/C4, rising anti-dsDNA titres, dysmorphic erythrocytes, and red-cell casts. Which interpretation is most appropriate?

2 / 10

Biopsy demonstrates Class IV-G (A) lupus nephritis with a Class V component, activity index 13/24, chronicity index 2/12, and 20% cellular crescents. Which conclusion is best supported?

3 / 10

The biopsy shows 20% cellular crescents but no thrombotic microangiopathy and no anti-GBM pattern. Which management statement is most appropriate?

4 / 10

Which statement best describes the appropriate role of obinutuzumab in this educational case?

5 / 10

In the phase 3 REGENCY trial, what was the principal renal-response finding at week 76?

6 / 10

Before the first planned obinutuzumab infusion, which action is most important because it is specifically emphasized in the product warning?

7 / 10

For adults with active lupus nephritis, which obinutuzumab schedule matches current U.S. prescribing information?

8 / 10

At three months, creatinine has improved from 1.23 to 0.95 mg/dL and UPCR has fallen from 5.8 to 3.3 g/g. The patient is clinically better and has no infection symptoms. What is the most appropriate next step?

9 / 10

The patient wants to conceive in approximately two years but is not currently pregnant. Which approach is most appropriate?

10 / 10

Six months into therapy, the patient reports new confusion and focal weakness. Which response is most appropriate?

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Level: Advanced — nephrology trainee or nephrologist
Topic: Acute electrolyte emergencies in CKD
Educational disclaimer: This case is for postgraduate education only. It does not replace clinical judgment, local monitored-care protocols, specialist consultation, or current prescribing information. Treatment choices and doses must be individualized to the patient, available monitoring, and institutional policy.

Learning objectives

By the end of this case, learners should be able to recognize and prioritize immediately life-threatening hyperkalemia; classify hypotonic hyponatremia when diuretic therapy confounds urine indices; distinguish correction goals from correction ceilings; identify and respond to emerging overcorrection; and integrate acute medication review with a plan for safe reintroduction of disease-modifying CKD and heart-failure therapy.

Clinical scenario

A 68-year-old man with CKD G4 (baseline serum creatinine 2.8 mg/dL), heart failure with reduced ejection fraction, type 2 diabetes, and hypertension is brought to the emergency department because of progressive weakness and confusion. He has had poor oral intake and profuse diarrhea for three days. His medications include lisinopril, spironolactone, and furosemide. He reports no potassium supplements or salt substitute use.

On examination, he is confused but arousable. Blood pressure is 92/58 mmHg, heart rate 110 beats/minute, respiratory rate 22 breaths/minute, and temperature 37.2 °C. He has dry mucous membranes, cool extremities, no pulmonary crackles, and no peripheral edema. A 12-lead ECG shows tall peaked T waves and QRS widening.

Initial tests show serum sodium 118 mmol/L, potassium 6.8 mmol/L, bicarbonate 12 mmol/L, blood urea nitrogen 98 mg/dL, serum creatinine 4.2 mg/dL, glucose 110 mg/dL, magnesium 1.4 mg/dL, phosphate 5.8 mg/dL, and arterial blood gas pH 7.22 with PaCO₂ 28 mmHg. The patient is oliguric.

Decision point: What must be addressed first, and why? Consider which abnormality has the most immediate risk of sudden death and which treatments only stabilize, shift, or remove potassium.

Stage 1 — First-hour priorities: electrical instability before biochemical elegance

The combination of potassium 6.8 mmol/L, QRS widening, and peaked T waves represents an immediate monitored-care emergency. The initial priority is continuous cardiac monitoring, urgent senior and renal/critical-care involvement, and treatment according to the institution’s severe-hyperkalemia protocol. Intravenous calcium is used to stabilize the myocardium in the presence of ECG changes; it does not remove potassium. Insulin–glucose and adjunctive beta-agonist therapy can shift potassium intracellularly, while repeat potassium and glucose measurements are necessary to identify rebound hyperkalemia and treatment-related hypoglycemia. Definitive removal depends on the clinical context and may include renal excretion when feasible, a locally approved potassium binder as an adjunct, or kidney replacement therapy. [6] [7] [8]

Bicarbonate is not a default potassium-shifting intervention. In this patient with marked metabolic acidemia, its role should be discussed with senior clinicians in the context of sodium load, fluid tolerance, and the overall resuscitation plan rather than used reflexively. [6] [7] [8]

Preferred decision: Initiate the local ECG-positive hyperkalemia pathway immediately, stabilize the myocardium, begin monitored intracellular-shift therapy with a hypoglycemia-prevention plan, seek urgent renal input, and repeat ECG, potassium, and glucose at protocol-defined intervals.

Debrief: Hyponatremia is clinically important, but the ECG-positive hyperkalemia creates a more immediate arrhythmic threat. The learner should be able to separate membrane stabilization from potassium redistribution and definitive potassium removal. [6] [7]

Stage 2 — Define the sodium problem without overtrusting a diuretic-confounded urine sodium

After immediate hyperkalemia treatment, the ECG improves and potassium falls transiently to 6.1 mmol/L. Serum sodium is 119 mmol/L. Measured serum osmolality is 260 mOsm/kg, urine osmolality is 480 mOsm/kg, and urine sodium is 52 mmol/L. The patient remains oliguric. There are no seizures, coma, or focal neurological deficits.

The sodium disorder is hypotonic hyponatremia. The likely duration is unknown, which should be treated cautiously as chronic until proven otherwise. The presentation strongly suggests reduced effective circulating volume from gastrointestinal losses and acute kidney injury, with reduced kidney function and concurrent diuretic therapy complicating the interpretation of urinary sodium. A spot urine sodium alone cannot reliably assign volume status after recent loop-diuretic exposure. Serial bedside reassessment, urine output, response to carefully selected therapy, and the broader clinical context matter more than a single urine electrolyte value. [3] [5]

Because severe neurological symptoms are absent, the immediate objective is not to normalize serum sodium. The team should use frequent serum-sodium and urine-output surveillance while correcting the reversible hemodynamic insult in a way that respects the patient’s heart-failure history and current fluid tolerance. If severe symptoms emerge, a monitored 3% saline bolus protocol is used to obtain a limited initial serum-sodium rise, followed by reassessment; the goal is symptom relief, not rapid normalization. [3] [4] [5]

Decision point: Is the patient’s elevated urine sodium proof of SIADH? What information would you seek before committing to a volume-directed or antidiuretic-directed plan?

Preferred decision: Treat urine sodium as confounded by loop diuretic exposure. Reassess history, examination, serum and urine osmolality, medication timeline, renal trajectory, urine output, and response to carefully monitored treatment. Avoid routine maintenance fluid prescriptions and avoid vasopressin-antagonist therapy as an emergency rescue maneuver in an unstable, potentially hypovolemic patient.

Debrief: Correction goals and correction ceilings are not interchangeable. The exact safety ceiling depends on chronicity and risk factors; high-risk patients warrant especially conservative correction and close surveillance. [4] [5]

Stage 3 — The hidden inflection point: water diuresis and overcorrection risk

Six hours later, the patient’s perfusion has improved, urine output abruptly increases to 250 mL/hour, and serum sodium has risen from 118 to 124 mmol/L. Potassium is 5.7 mmol/L after shift therapy. The patient is more alert but remains weak.

A sudden dilute water diuresis can raise serum sodium faster than anticipated, particularly when the underlying stimulus for antidiuresis resolves. The critical response is to recognize the changing physiology promptly. Stop or revise contributors to the unintended sodium rise, intensify sodium and urine-output monitoring, and involve nephrology/critical care to consider a local rescue strategy using electrolyte-free water and/or desmopressin when correction is exceeding the patient’s safe trajectory. This is a safety intervention, not a failure of care. [3] [4] [5]

Preferred decision: Escalate monitoring immediately and use a protocolized overcorrection-rescue plan rather than allowing the serum sodium to continue rising because the patient appears clinically improved.

Debrief: A large water diuresis, not simply an excessive saline dose, is a common mechanism of overcorrection. In chronic or unknown-duration hyponatremia, biochemical improvement can coexist with emerging neurologic risk if sodium rises too fast. [4] [5]

Stage 4 — Definitive clearance and kidney replacement therapy with sodium safety in mind

Despite initial improvement, potassium rebounds to 6.4 mmol/L, bicarbonate remains low, and the patient remains oliguric with worsening azotemia. The care team is concerned that repeated redistribution therapy will not provide durable control. At the same time, routine intermittent dialysis could accelerate sodium correction if the prescription is not planned carefully.

This is an urgent multidisciplinary decision. Refractory or recurrent severe hyperkalemia with persistent acidosis and oliguria may require kidney replacement therapy. The dialysis prescription and monitoring plan must explicitly account for the concurrent hyponatremia, including the desired sodium trajectory, serial measurement, and local capability for controlled correction. [6] [7] [8]

Preferred decision: Arrange urgent renal replacement therapy with a sodium-aware prescription and continuous clinical, ECG, potassium, glucose, and serum-sodium surveillance. Avoid framing dialysis as an isolated treatment for potassium while ignoring the sodium-correction risk.

Debrief: Potassium shifting buys time; it does not eliminate total body potassium. Dialysis is a definitive removal strategy when medical management is inadequate or when associated acidosis, kidney failure, or oliguria makes durable control unlikely. [6] [7]

Stage 5 — Recovery, medication stewardship, and recurrence prevention

Over the following days, kidney function and urine output improve. Potassium normalizes, sodium is corrected cautiously without neurological deterioration, and the patient is transitioned from monitored care. Before discharge, the team reviews precipitating factors: gastrointestinal losses, reduced intake, acute kidney injury, lisinopril, spironolactone, and the patient’s limited understanding of sick-day medication management.

The acute medication holds should not become permanent by inertia. The discharge plan should specify which drugs are temporarily withheld, what laboratory and clinical criteria are needed before reintroduction, who will review the plan, and how the patient will access early outpatient testing. KDIGO emphasizes addressing contributing factors and treating hyperkalemia where possible rather than reflexively abandoning disease-modifying RAAS inhibition; however, reintroduction must be individualized after recovery of hemodynamics, kidney function, and potassium control. [1] [2]

Preferred decision: Document a time-limited medication plan, laboratory follow-up, renal and heart-failure coordination, individualized dietary counseling after non-dietary contributors are addressed, and clear return precautions for weakness, palpitations, reduced urine output, vomiting, or diarrhea. [1] [2] [7]

Expert synthesis

This case illustrates the hierarchy of acute electrolyte care. ECG-positive hyperkalemia requires immediate monitored treatment because of arrhythmic risk. Concurrent hypotonic hyponatremia must then be classified by tonicity, symptoms, chronicity, and context—not by an isolated urine sodium in a diuretic-treated patient. The trajectory of urine output is a major safety signal: recovery from antidiuresis can cause abrupt sodium overcorrection, so rescue capability must accompany treatment. Finally, renal replacement therapy can solve refractory potassium and acid-base problems but must be prescribed with the sodium trajectory in mind. Acute medication holds require a structured reassessment plan, not indefinite discontinuation by default. [1] [2] [3] [4] [5] [6] [7] [8]

Sources

  1. KDIGO 2024 CKD Guideline
  2. KDIGO 2024 CKD guideline primer
  3. Hyponatraemia—treatment standard 2024
  4. Treatment Guidelines for Hyponatremia: Stay the Course
  5. Treatment of hyponatremia: comprehension and best clinical practice
  6. KDIGO acute hyperkalemia conference summary
  7. BNF/NICE Hyperkalaemia treatment summary
  8. GGC Medicines acute hyperkalaemia guidance

Advanced Self-Assessment

Complete the 10-question Advanced self-assessment below. Detailed explanations are provided after submission.

Advanced Self-Assessment: Electrolyte Collapse in CKD

1 / 10

A 68-year-old patient with CKD G4 has potassium 6.8 mmol/L, QRS widening, and peaked T waves. He is confused and has serum sodium 118 mmol/L. Which action has the highest immediate priority?

2 / 10

In the same patient, which statement best describes the purpose of intravenous calcium administered for hyperkalemia with ECG changes?

3 / 10

After a local insulin–glucose protocol is given for severe hyperkalemia, which monitoring plan is most appropriate?

4 / 10

A patient with hypotonic hyponatremia received high-dose loop diuretics before arrival. Urine sodium is 52 mmol/L. Which interpretation is most appropriate?

5 / 10

A patient with confirmed hypotonic hyponatremia develops a seizure. Which statement best reflects the immediate therapeutic objective?

6 / 10

Six hours after initial treatment, serum sodium has increased from 118 to 124 mmol/L and urine output abruptly rises to 250 mL/hour. The patient is more alert. What is the best next action?

7 / 10

After emergency stabilization, a patient with CKD G4 remains on an ACE inhibitor for proteinuric kidney disease. Which longitudinal plan is best?

8 / 10

Despite membrane stabilization and potassium-shifting treatment, the potassium concentration remains 6.6 mmol/L with recurrent ECG abnormalities in a patient with advanced CKD and oliguria. What is the best next step?

9 / 10

Which diagnostic approach is most appropriate for a patient with suspected hypotonic hyponatremia and complex cardiorenal disease?

10 / 10

Which discharge and follow-up plan best reduces recurrent electrolyte emergencies after this admission?

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Supporting presentation

The slide deck is provided as a supporting learning resource after the self-assessment.

Download the Electrolyte Disorders supporting presentation (PPTX)

NEPHROHUB • ADVANCED INTERACTIVE CASE

Educational disclaimer: This postgraduate case is for education and does not replace bedside assessment, local vascular-access protocols, multidisciplinary judgment, current prescribing information, or patient-specific evaluation.

Difficulty and format

Difficulty: Advanced. Format: Four-stage branching hemodialysis access case focused on clinically significant AV fistula dysfunction, endovascular treatment, recurrence, and access succession planning.

Learning objectives

By the end of this case, learners should be able to recognize clinical indicators of AV fistula dysfunction, integrate physical examination with dialysis-treatment trends, distinguish clinical monitoring from device-based surveillance, select evidence-aligned intervention for clinically significant stenosis, monitor after angioplasty, and plan recurrent stenosis management within the patient’s individualized ESKD Life-Plan.

Stage 1 — Bedside assessment of a failing access

Presentation

Mrs. Maria Gonzalez is a 58-year-old woman with kidney failure requiring hemodialysis because of diabetic nephropathy. She has used a left radiocephalic AV fistula for 18 months; it was created two years ago. During the last three treatments, the dialysis technician has reported difficult cannulation and lower achievable blood-flow rates. Her history includes diabetes, hypertension, peripheral vascular disease, and a right-arm AV graft that thrombosed after eight months.

For two weeks, she has noticed that the fistula feels different, with a weaker thrill and a change in the bruit. She has no pain, swelling, fever, erythema, drainage, or hand ischemic symptoms. The radial pulse and capillary refill are preserved. The fistula has a diminished thrill, and the bruit is high-pitched and localized rather than the expected continuous machinery murmur.

Decision point 1 — Is this clinically significant access dysfunction?

Preferred decision: Treat the findings as suspected AV fistula dysfunction and arrange prompt access evaluation. Examine the entire access circuit, including inspection for aneurysm, skin change, edema, collateral veins, and infection; palpation of the thrill and pulse augmentation; auscultation of the bruit; assessment of inflow and outflow; distal perfusion; and review of recent cannulation, pressures, blood-flow rates, recirculation, bleeding time, and delivered dialysis dose.

The change in thrill and bruit plus difficult cannulation and reduced blood flow are clinical indicators. A high-pitched, localized bruit suggests a hemodynamically important stenosis, but physical findings do not determine its exact location. Do not intervene based only on an isolated surveillance measurement in an asymptomatic access.

Stage 2 — Integrate dialysis trends and targeted imaging

Treatment records

Blood-flow rates have fallen from her usual 350–400 mL/min to 250–280 mL/min. Venous pressures have risen from 120–140 mmHg to 180–200 mmHg. Arterial pressures are more negative, and the dialysis team needs higher pump speeds to approach the prescribed blood flow. Kt/V has fallen from 1.4–1.5 to 1.2–1.3. These trends should prompt evaluation of delivered dialysis, treatment time, sampling, recirculation, cannulation, and access function rather than being interpreted in isolation.

Imaging

Targeted duplex ultrasound demonstrates a significant venous-outflow lesion with approximately 70% narrowing and a velocity ratio of 3.5 across the segment. Arterial inflow appears satisfactory, and there is no evidence of central venous obstruction on the available study. The access-flow measurement is 800 mL/min, but this value should be interpreted in context; no single flow threshold replaces clinical assessment and the overall dialysis picture.

Decision point 2 — Is intervention indicated?

Preferred decision: Because the patient has multiple clinical indicators plus a significant lesion, arrange timely fistulography and endovascular treatment planning. KDOQI implementation guidance supports intervention when a clinically significant indication is present together with a significant stenosis, generally at least 50%. The indication is not the Doppler percentage alone.

Before the procedure, review the ESKD Life-Plan, prior access procedures and imaging, cannulation zones, contrast and allergy history, bleeding and anticoagulation issues, cardiopulmonary risk, and the contingency plan if the access thromboses or cannot be salvaged.

Stage 3 — Treat and monitor the clinically significant lesion

Decision point 3 — Initial treatment

Preferred decision: Use percutaneous transluminal angioplasty as first-line endovascular therapy in most situations, performed by the appropriate interventional team under local protocol. Procedural access route, sedation, balloon type, inflation pressure, and duration should be individualized to anatomy and patient risk. Assess technical result by residual stenosis, restoration of access function, and resolution of clinical indicators; do not rely on a single post-procedure flow value.

If the lesion responds inadequately, the team may consider prolonged inflation or an ultrahigh-pressure balloon according to local expertise. Selective stent-graft use requires attention to lesion location, future cannulation zones, the ESKD Life-Plan, and whether the device would compromise future access. Stent grafts are not a universal default.

Post-intervention monitoring

After angioplasty, document the access examination, blood pressure, puncture-site status, bleeding, distal perfusion, and any signs of rupture, dissection, thrombosis, embolization, or infection. On the next dialysis treatment, review cannulation, achievable blood flow, venous and arterial pressures, recirculation, treatment completion, and delivered adequacy. Report loss of thrill, prolonged bleeding, new swelling, hand pain or coldness, fever, or sudden access failure urgently.

Stage 4 — Recurrence, revision, and access succession

Clinical response

The patient returns to dialysis the next day with an improved thrill. Blood flow reaches 380 mL/min, venous pressure returns to 135 mmHg, and Kt/V improves to 1.45. These changes support restoration of access function, but they do not guarantee durable patency.

Clinical monitoring remains primary. The dialysis team continues routine examination and tracks access-related indicators at each treatment. Targeted duplex or fistulography is obtained when new clinical changes arise; a fixed monthly duplex schedule is not mandatory for every patient and asymptomatic preemptive angioplasty is not recommended solely to improve patency.

Recurrence at six months

At six months, difficult cannulation, a weaker thrill, rising venous pressures, and a similar duplex lesion recur. Repeat angioplasty restores function, but the recurrence prompts a multidisciplinary review.

Decision point 4 — What is the next best strategy?

Preferred decision: Do not assume that one recurrence automatically requires surgery. Review lesion location, cannulation-zone involvement, prior angioplasty results, residual stenosis, access anatomy, patient preferences, and the ESKD Life-Plan. Options may include another PTA, selected stent graft when the lesion and future access plan permit, surgical revision, or planned creation of the next access. Surgical consultation is particularly important when endovascular treatment repeatedly fails, anatomy is unfavorable, or revision can preserve useful access while protecting future sites.

In this patient, recurrent venous-anastomotic disease outside the intended cannulation zone leads the access team to discuss surgical revision with creation of a new proximal venous anastomosis, while documenting a contingency and succession plan if the revised fistula later fails. The choice is individualized and should be made by the patient and multidisciplinary access team.

Expert synthesis

This case illustrates that AV access management is a clinical-monitoring and Life-Plan process rather than a sequence of isolated Doppler measurements. A changed thrill or bruit, difficult cannulation, pressure changes, falling achievable blood flow, recirculation, prolonged bleeding, or declining delivered dialysis should trigger structured assessment. When clinical indicators coexist with significant stenosis, PTA is usually the initial endovascular treatment. Recurrent disease requires review of anatomy, prior interventions, cannulation zones, future access options, and the patient’s ESKD Life-Plan. Selective stent grafting, surgical revision, repeat PTA, or access succession may each be appropriate in different circumstances.

Advanced Self-Assessment

Complete the 10-question Advanced assessment below. Detailed explanations are provided after submission.

NephroHub assessment: Advanced level • 10 questions • vascular-access clinical reasoning

Advanced Self-Assessment: Comprehensive Vascular Access Management

1 / 10

What is the most appropriate long-term planning principle for this patient with recurrent access disease?

2 / 10

After technically successful PTA, the same clinically significant stenosis recurs at six months. What is the best next approach?

3 / 10

When might a stent graft be considered for recurrent AV fistula stenosis?

4 / 10

Which statement best reflects the surveillance principle after successful angioplasty?

5 / 10

Which post-angioplasty plan is most appropriate?

6 / 10

What is the most appropriate initial treatment for this patient’s clinically significant venous-outflow stenosis?

7 / 10

Which finding combination best meets the principle for intervention on an AV fistula lesion?

8 / 10

How should the fall in Kt/V from 1.4–1.5 to 1.2–1.3 be used in this case?

9 / 10

What is the best interpretation of the high-pitched, localized bruit and diminished thrill?

10 / 10

Which combination most strongly indicates clinically significant AV fistula dysfunction in this patient?

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References

  1. NKF KDOQI. 2019 Vascular Access Guideline and implementation tools.
  2. NKF KDOQI. [inline_viewer url="https://www.kidney.org/sites/default/files/vait-15a_management_clinically_significant_av_fistula_lesions.pdf"].
  3. Lok CE, Yuo T, Lee T. Hemodialysis Vascular Access: Core Curriculum 2025.

NephroHub — postgraduate clinical education in nephrology

Advanced Real-Life Case

Learning objectives: Apply a structured approach to recurrent hyperkalaemia in CKD G4; identify reversible contributors; preserve kidney-protective therapy when safe; and plan monitoring using shared clinical decisions.

Clinical Scenario

A 67-year-old man with diabetic CKD G4 (eGFR 24 mL/min/1.73 m²; UACR 650 mg/g) attends renal clinic after an outpatient potassium of 6.8 mmol/L. He takes losartan 100 mg daily, dapagliflozin 10 mg daily, and several over-the-counter medicines. He is clinically stable but reports intermittent muscle weakness.

Clinic Approach

Begin with immediate safety: repeat a non-haemolysed sample, obtain an ECG, assess symptoms and renal function, and escalate urgently if there are ECG changes, severe symptoms, or rapidly worsening biochemical abnormalities. Then move through medication reconciliation, dietary review, acid–base assessment, and a plan to reduce recurrence without reflexively abandoning albuminuria and cardiovascular protection.

Interactive Decision Stages

This case is designed as a sequential decision exercise. Each stage changes the clinical context: acute safety, long-term preservation of RAAS therapy, reversible contributor review, and follow-up after treatment optimization.

Complete the four decision points below. Detailed explanations are displayed at the end of the assessment.

Advanced Renal Clinic: Recurrent Hyperkalaemia — Branching Decision Case

1 / 4

A 67-year-old man with diabetic CKD G4 (eGFR 24 mL/min/1.73 m²; UACR 650 mg/g) is taking losartan 100 mg daily and dapagliflozin 10 mg daily. At a nephrology clinic review, potassium is 6.1 mmol/L on a non-haemolysed repeat sample, bicarbonate is 18 mmol/L, and ECG shows peaked T waves. He is haemodynamically stable and has no muscle weakness. What is the most appropriate immediate management?

2 / 4

After emergency treatment, the patient’s potassium is 5.2 mmol/L, ECG is normal, and creatinine is near baseline. He has persistent albuminuria and blood pressure 148/82 mmHg. Which is the best longer-term nephrology plan?

3 / 4

At a 2-week review, potassium is again 5.9 mmol/L, bicarbonate 19 mmol/L, and eGFR is stable. The patient reports using ibuprofen for back pain and a salt substitute containing potassium. Which next step most directly addresses reversible contributors while preserving diagnostic accuracy?

4 / 4

Two weeks after stopping ibuprofen, removing the potassium-containing salt substitute, and starting a potassium binder, potassium is 4.8 mmol/L, bicarbonate is 21 mmol/L, and eGFR has fallen from 24 to 21 mL/min/1.73 m². He is euvolaemic and blood pressure is 132/76 mmHg. What is the most appropriate next step?

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Advanced Real-Life Case

Learning objectives: Recognize TMA from thrombocytopenia, hemolysis, and kidney injury; use timing and response to delivery; and coordinate urgent multidisciplinary management.

Clinical Scenario

A 32-year-old at 31 weeks gestation presents with headache, hypertension, thrombocytopenia, anemia, rising creatinine, dark urine, high LDH, undetectable haptoglobin, and schistocytes. ADAMTS13 activity is pending.

Clinical Reasoning

The differential includes preeclampsia with severe features or HELLP, TTP, complement-mediated TMA, and secondary causes. Stabilize the mother, involve maternal-fetal medicine, hematology, nephrology, and critical care, and use the post-delivery trajectory to refine the diagnosis.

Interactive Checkpoints

Complete the case questions to test your clinical reasoning. Detailed explanations are revealed after completion.

Pregnancy-Associated Thrombotic Microangiopathy

Advanced real-life nephrology case. Distinguish pregnancy-associated TMA syndromes using hemolysis, platelet trends, timing, and multidisciplinary priorities.

1 / 5

Which combination establishes a clinical TMA syndrome?

2 / 5

Which test is most urgent when TTP is a serious possibility?

3 / 5

Which feature favors complement-mediated TMA over isolated preeclampsia-spectrum disease?

4 / 5

What is the immediate management principle in severe maternal disease?

5 / 5

Which blood-film finding is most characteristic of microangiopathic hemolysis?

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Advanced Real-Life Case

Learning objectives: Recognize pulmonary–renal syndrome, use serology and biopsy appropriately without delaying urgent care, and apply supportive management principles.

Clinical Scenario

A 48-year-old man develops sinus symptoms, hemoptysis, edema, and rapidly rising creatinine. Urinalysis shows dysmorphic erythrocytes and red-cell casts; CT chest demonstrates bilateral ground-glass opacities; PR3-ANCA is strongly positive.

Clinical Reasoning

Consider infection, anti-GBM disease, lupus, and other vasculitides while urgently evaluating the pulmonary hemorrhage and kidney injury. Obtain cultures and targeted testing, send relevant serology, and pursue biopsy when safe.

Interactive Checkpoints

Complete the case questions to test your clinical reasoning. Detailed explanations are revealed after completion.

Pulmonary–Renal Syndrome from ANCA-Associated Vasculitis

Advanced real-life nephrology case. Recognize pulmonary–renal syndrome and reason through urgent diagnostic and treatment priorities.

1 / 5

Which urine finding most strongly indicates glomerular inflammation?

2 / 5

Which diagnosis best unifies hemoptysis, diffuse alveolar opacities, and rapidly progressive GN?

3 / 5

Which test is essential before committing to immunosuppression when clinically feasible?

4 / 5

What is the role of kidney biopsy in this setting?

5 / 5

Which clinical feature most warrants escalation to an intensive care setting?

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Advanced Real-Life Case

Learning objectives: Treat severe hyperkalemia according to ECG risk, identify medication and acid-base contributors, and plan definitive potassium removal.

Clinical Scenario

A 62-year-old woman with diabetic kidney disease, heart failure, and eGFR 24 mL/min/1.73 m² presents with weakness after starting spironolactone and trimethoprim-sulfamethoxazole. Potassium is 7.1 mmol/L and the ECG shows QRS widening with sine-wave evolution.

Clinical Reasoning

Give intravenous calcium for membrane stabilization, shift potassium with appropriate emergency therapy, and arrange urgent potassium removal because redistribution is temporary and ECG toxicity is present.

Interactive Checkpoints

Complete the case questions to test your clinical reasoning. Detailed explanations are revealed after completion.

Life-Threatening Hyperkalemia in Diabetic Kidney Disease

Advanced real-life nephrology case. Work through ECG toxicity, medication triggers, potassium shifting, and definitive potassium removal.

1 / 5

What is the first pharmacologic priority with QRS widening and potassium 7.1 mmol/L?

2 / 5

Which combination most plausibly precipitated this episode?

3 / 5

Why is insulin-glucose therapy not definitive treatment?

4 / 5

Which finding most strongly supports urgent dialysis consultation?

5 / 5

Which medication review is most appropriate after stabilization?

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