How do PSA kinetics perform across different risk groups, treatments, and post-treatment settings (active surveillance vs post-prostatectomy)?

1. PSA after radiotherapy/SBRT: kinetics vary by pre‑treatment risk

Longitudinal data after stereotactic body radiotherapy (SBRT) show a rapid initial PSA fall then slower decline; patients without ADT and recurrence reached median nadirs and times to nadir that differed by risk group — low: nadir 0.075 ng/mL, 53.4 months; intermediate: 0.23 ng/mL, 46.4 months; high: 0.13 ng/mL, 50.1 months — and the per‑month decline slopes were statistically different across groups (p = 0.011) with the steepest slope in the high‑risk group (−0.253 ng/mL/month) ^{[1] [2]}. Meta‑analysis and scoping reviews similarly highlight heterogeneity in PSA kinetics after SBRT across risk strata, fractionation, and ADT use, and caution that study heterogeneity limits direct comparisons ^[8].

2. PSA kinetics after definitive local therapy: time‑to‑nadir matters

Older radiotherapy literature and pooled analyses emphasize that early post‑RT PSA kinetics (first‑year rate of change and minima) are prognostic for survival and can identify patients who might need early salvage therapy; first‑year PSA minima and slope were predictive of overall survival in historic cohorts ^[9]. Modern series of systemic and localized treatments continue to analyze PSA nadir and time‑to‑nadir as outcome correlates ^[10], but available sources show variation by treatment modality and patient selection ^{[8] [10]}.

3. After prostatectomy: PSA behavior is categorical, not gradual

Post‑radical prostatectomy practice treats any confirmed PSA above a low threshold as biochemical recurrence rather than tracking a slow downward slope; the literature notes lack of consensus on the exact cutpoint but stresses validated nomograms incorporating PSA kinetics to stratify progression and mortality risk ^[11]. Available reporting in the provided set does not give numeric post‑prostatectomy nadir kinetics comparable to the SBRT data; current sources focus on definitions and prognostic use of kinetics rather than typical numeric nadirs after surgery ^[11].

4. PSA kinetics in oligorecurrence and PSMA‑RGS: limited predictive value

In a multicenter series of 374 patients undergoing PSMA‑radioguided surgery for oligorecurrent disease, EAU BCR risk classification and PSA kinetics (doubling time, velocity) did not predict complete biochemical response (cBR), BCR‑free survival, or therapy‑free survival; low‑ and high‑risk BCR groups achieved cBR at essentially the same rates (62% vs 60%) and PSA‑DT/PSA‑V showed no association with outcomes in this setting ^{[3] [4]}. That suggests PSA kinetics that help in other contexts may have less value when salvage is applied at very low absolute PSA and imaging‑guided metastasis‑directed therapy is used ^{[3] [4]}.

5. Active surveillance: PSA is a monitoring tool, not a standalone trigger

Active surveillance protocols universally include serial PSA but frequency and thresholds differ across programs; PSA will fluctuate during surveillance and is interpreted alongside DRE, MRI and repeat biopsies, with triggers for treatment including grade/upgrading, extent of cores involved, PSA‑DT and imaging changes rather than PSA alone ^{[6] [7] [5]}. Guideline and institutional series emphasize that surveillance is appropriate for low‑risk disease and that most men on properly executed AS do well long term; however, the literature documents variable monitoring intensity and conversion rates to active treatment up to ~50% at five years in some series ^{[5] [12] [6]}.

6. Practical implications and contested areas

Clinicians treating localized disease should expect different PSA kinetics after radiation (including SBRT) than after surgery; time‑to‑nadir and nadir magnitude carry prognostic information after RT ^{[1] [9]}. But in the oligorecurrent, PSMA‑guided salvage context, traditional PSA‑based BCR risk groups and kinetics may not guide selection or predict short‑term biochemical outcomes ^{[3] [4]}. Active surveillance relies on integrating PSA trends with imaging and biopsy, since PSA alone fluctuates and can mislead if taken out of context ^{[7] [6]}.

Limitations and open questions: most SBRT and kinetics studies exclude patients receiving ADT or with recurrence to isolate PSA curves ^[1]; meta‑analyses note heterogeneity in cohorts, ADT use and follow‑up ^[8]. Available sources do not report uniform numeric PSA‑kinetic thresholds that apply across all treatments/settings; they emphasize context — modality, imaging, biopsy, and timing — when interpreting kinetics ^{[8] [11]}.