Rising creatinine after kidney transplantation: interpreting the resistive index
A 48-year-old man is 10 days out from a deceased-donor kidney transplant. Serum creatinine has risen from 1.4 to 2.9 mg/dL over 48 hours and urine output is falling. Tacrolimus trough is 11 ng/mL. Ultrasound shows an 11 cm graft with no hydronephrosis and a patent main renal artery. Spectral Doppler of an interlobar artery in the upper pole gives a resistive index of 0.85; a second sample in the lower pole gives 0.62. The patient has just received a bolus of intravenous fluid and is pressing on the site because of discomfort.
1. How do you interpret the resistive indices and the difference between the two poles?
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The resistive index is (peak systolic velocity − end-diastolic velocity)/peak systolic velocity, so it is angle-independent but still depends on the quality of the waveform.
- Normal renal RI is usually below about 0.70–0.80.
- An RI of 0.85 suggests increased parenchymal resistance, but it is not specific. Causes include acute tubular necrosis, rejection, calcineurin-inhibitor toxicity, obstruction, venous thrombosis, and external compression.
- A normal RI (0.62 here) does not exclude rejection or ATN.
- A difference of more than 0.10 between poles suggests either a focal abnormality or a sampling error. Before calling focal ischaemia, repeat sampling in multiple interlobar and arcuate arteries in both poles and check the waveform quality.
Interpret the numbers alongside the clinical picture: early post-transplant ATN is common, and the tacrolimus trough of 11 ng/mL could be contributing to toxicity.
2. What technical and patient factors can falsely elevate the resistive index?
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Technical and physiological confounders:
- Excessive transducer pressure on a tender graft - the patient is already pressing the site.
- Valsalva, breath-holding, or pain, which raise intra-abdominal and renal venous pressure.
- Sampling a vein or a poorly filled vessel instead of an interlobar artery.
- Wall filter too high, low colour gain, or an inadequate waveform.
- Wrong sample site or a single sample in one pole.
- Very low heart rate or high systemic vascular resistance.
- The recent fluid bolus may lower the RI, so timing matters.
To improve reliability: use a low wall filter, a small sample volume, obtain at least three good waveforms per pole, avoid heavy pressure, let the patient breathe quietly, and document heart rate and blood pressure. Repeat after the graft has settled.
3. What is your differential and what should happen next?
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Differential for a rising creatinine at day 10 with no hydronephrosis:
- Acute tubular necrosis - common in deceased-donor grafts, often delayed function.
- Acute rejection - possible at this time; RI may be normal or elevated.
- Calcineurin-inhibitor toxicity - tacrolimus 11 ng/mL may be in the toxic range depending on target.
- Renal vein thrombosis - check venous flow carefully.
- Renal artery stenosis or kinking - assess the whole artery, not just patency.
- Perinephric collection (haematoma, lymphocele, urinoma) compressing the graft.
- Urinary obstruction - less likely with no hydronephrosis, but not excluded early.
Next steps: complete the Doppler study including the renal vein and vein, search for collections, review the tacrolimus level and target range, check urine output and fluid balance, and involve the transplant team. If the cause remains unclear, a percutaneous biopsy is the definitive way to distinguish rejection from ATN and drug toxicity. The RI should guide, not decide.