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.
[5] KDIGO. Transplant Recipient Guideline Hub.
Advanced Self-Assessment
Complete the 10-question Advanced self-assessment below. Detailed explanations are provided after submission.