Our findings show that even a modest rise in CRP (≥ 5 mg L⁻¹) has clear implications across the diagnostic pathway. Complicated stones or alternative non urolithic conditions (Groups C and D) accounted for 44.8% of all presentations, and 65.5% with a raised CRP fell into these higher risk categories, compared with about one quarter of those whose CRP was normal (p = 0.002).

At a threshold of 5 mg L⁻¹, CRP had a sensitivity of 73% and a negative predictive value of 76% for detecting any complicated calculus or alternative diagnosis. These correspond to likelihood ratio positive 2.34 and likelihood ratio negative 0.39, which are clinically interpretable for first-line imaging selection. Thus, patients with a low CRP are unlikely to harbour an urgent finding and can, in most cases, proceed directly to low dose CT KUB without the need for further imaging.

A clear gradient of risk was observed: a raised CRP tripled the odds (OR 3.1, p = 0.04) of any acute finding (Groups B, C or D) and increased the odds (OR 6.0, p = 0.002) of a severe acute finding (Groups C or D) six fold. Despite this, CRP did not predict the need for repeat imaging within seven days, suggesting its utility lies chiefly in the initial imaging decision rather than in follow-up planning. This may also reflect radiologists’ reluctance to repeat imaging unless necessary. White cell count offered no such discrimination (p = 0.38), underscoring CRP as the more informative inflammatory marker for triage. Alternative diagnoses were more frequent in the elevated-CRP cohort (Table 1). Within Group D, the pattern was predominantly gastrointestinal (diverticulitis/appendicitis) with smaller numbers of renal non-urolithic, tumor and other entities (Table 2); this is consistent with CRP tracking inflammatory pathology, while neoplastic/other categories show greater heterogeneity in CRP.

No previous study has evaluated CRP expressly to guide the choice between low dose CT KUB and contrast enhanced CT of the abdomen and pelvis (CTAP). Angulo et al. [15] employed a higher cut off (28 mg L⁻¹) to predict the need for ureteric stenting, reporting 76% sensitivity and 89% specificity [15]. Our lower threshold, matching clinical practice, is geared towards sensitivity so that clinically significant disease is not missed; future work could explore tiered values, for example < 5, 5–20 and >20 mg L⁻¹, to refine specificity without compromising safety.

Our findings are consistent with ED literature showing that low CRP (0–5 mg/L) does not exclude positive abdomino-pelvic CT findings and that higher CRP increases yield (Coyle et al. [13]). Accordingly, prospective renal-colic studies should model CRP continuously and evaluate clinically anchored tiers (e.g., < 5, 5–20, >20 mg/L) within pre-specified multivariable frameworks, rather than re-deriving a single optimal cut-off in a small dataset. All cases of acute gastro-intestinal pathology in our series occurred in the CRP high cohort, mirroring surgical data that link elevated CRP with appendicitis and diverticulitis [10]. A “CRP first” algorithm could therefore stream low CRP patients straight to low dose CT KUB whilst directing those with a raised CRP to single phase CTAP. Such an approach shortens diagnostic delay, reduces cumulative radiation exposure (≈ 4.7 mSv versus ≈ 16 mSv) and limits contrast administration to the patients most likely to benefit [16,17,18]. The small number of clinically mild false negatives suggests that a CRP-first approach is safe only when integrated with clinical review: imaging should still proceed if pain persists, infection is suspected or examination findings are concerning.

Strengths of our study include a prespecified threshold informed by preliminary audit data, blinded CT classification using clearly defined categories, and standardised imaging protocols, all of which support internal validity.

Several limitations should be noted. CRP testing was performed at clinician discretion rather than universally so the analyzed cohort may over-represent diagnostically complex or higher-risk presentations. This case mix could inflate apparent specificity and PPV relative to an unselected population. CRP is a non-specific marker that rises with chronic inflammatory conditions and advancing age [19, 20]. Because we did not capture exact time interval between CRP sampling and CT, evolving inflammation could lead to misclassification. This uncertainty likely attenuates associations between CRP and imaging outcomes.

We did not fit data-driven thresholds or multivariate models owing to overfitting risk in this small retrospective cohort. Prospective validation should model CRP continuously within pre-specified multivariate frameworks (with adequate events-per-variable) to obtain transportable estimates. Generalizability is therefore to similar ED workflows and CRP practices. A prospective pathway with universal CRP sampling or random sampling, pre-specified imaging triggers and blinded interpretation would be needed to obtain unbiased accuracy estimates. Cost-effectiveness and radiation-dose modelling were beyond the scope of the present work. However, we have shown that utilizing the laboratory assay thresholds to determine choice of imaging is effective.

Diagnostic performance cannot be extrapolated to pregnancy. Physiological variation in CRP during pregnancy may reduce specificity at a 5 mg/L threshold, so any CRP-first approach would require pregnancy-specific validation. Whilst pregnancy is not an absolute contraindication to CT imaging therefore non-ionizing imaging techniques should be employed thus making CRP thresholds less important in this cohort. CRP is non-specific and may be elevated at baseline in chronic inflammatory conditions, malignancy, chronic infection and with increasing age. We did not adjust for comorbidities or age, which may reduce specificity of a 5 mg/L threshold.

A multicenter prospective study using the described methodology could validate the 5 mg L⁻¹ cut off and investigate stratified thresholds. Integrating clinical features such as fever, urinalysis or point-of-care ultrasound, and where appropriate, existing stone-risk scores adds incremental value over CRP alone. Future research should also address economic outcomes, including length of stay and time to definitive therapy, to quantify clinical and economic value.

In summary, a “CRP-first” imaging algorithm aligns diagnostic resources with clinical risk. Even a modest elevation (≥ 5 mg L⁻¹) increases the likelihood of pathology caused by complicated renal stones or conditions that are non-urological in origin, while a low CRP identifies patients who can begin, and often end, the diagnostic pathway with low dose CT KUB.