A couple of years ago I came across an initiative that has been generating some genuinely interesting conversations in the urology world. It is called the "Defenders of the Detrusor", born from the work of Dr. Wayne Kuang in the United States, and its central message is as simple as it is provocative: we are treating the prostate and forgetting about the bladder.

I will admit the idea felt refreshing. And also incomplete. Both things at once, without contradiction.

The idea worth listening to

BPH — benign prostatic hyperplasia — affects virtually every man who ages. For decades, the dominant paradigm has been pharmacological: alpha-blockers to relax the bladder neck, 5-alpha reductase inhibitors to shrink the prostate, and wait. The AUA and EAU clinical guidelines reflect this, for good reasons backed by clinical trial data.

But Dr. Kuang and his colleagues point to something those same guidelines only acknowledge in passing: the prostate is not the only organ at stake. In 2023 they published an editorial in Prostate Cancer and Prostatic Diseases with a title that captures it perfectly: "When you say 'Prostate', don't forget to say 'Bladder'!" [1]. The bladder, forced to work against rising resistance for years, undergoes a silent remodelling. First it hypertrophies in compensation, then destabilises, and finally — in the most advanced cases — its muscle fibres are progressively replaced by collagen.

The molecular science of recent years confirms this process with a precision we did not previously have. A single-cell transcriptomics study published in 2024 showed that chronic obstruction triggers a cascade running from initial inflammation to smooth muscle hypertrophy, excessive extracellular matrix accumulation and eventual fibrosis — with a urodynamic pattern that shifts from "high pressure, low flow" to "low pressure, low flow" [2]. That is solid science. That matters. And there is every reason to say it more loudly.

The "Five Stages of Bladder Health" model proposed by Kuang is, in essence, a pedagogical tool: a way of explaining to a patient that their symptoms have a direction, that direction may be irreversible, and that the timing of intervention matters.

Where the evidence does not hold up

Here comes the part a critically minded physician cannot overlook — even if delivered with goodwill.

The problem of medications framed as mere "band-aids". The initiative tends to describe BPH medications as nothing more than temporary measures masking symptoms while silent damage accumulates. This narrative is an oversimplification. The MTOPS trial — 3,047 patients, 4.5 years of follow-up — demonstrated that combination therapy with doxazosin and finasteride significantly reduced the risk of overall BPH clinical progression more than either drug alone, and that both the combination and finasteride alone reduced the long-term risk of acute urinary retention and the need for prostatic surgery [3]. They do not "cure" the anatomical obstruction — granted — but they are not passive placebo while the bladder quietly fails.

The five-stage model still lacks prospective validation. The fact that something has pathophysiological logic does not mean it predicts what will happen in the individual patient in front of you. The most recent review developing the concept — published in Current Urology in 2025 — explicitly describes itself as a "hypothesis-generating review" [4]. That is a scientific starting point, not a finishing line.

The "window of curability" does not yet have a clock. The concept is intuitively powerful. There is observational evidence to support it — we know that patients operated on after episodes of acute urinary retention have worse outcomes, with a significantly higher 10-year treatment failure risk when surgical delay exceeds 12 months [5]. But we still do not have data answering the practical question with precision: when exactly? With which biomarkers? At what threshold of post-void residual, bladder wall thickness, or maximum flow rate? Without those answers, the "window" remains an illuminating metaphor rather than an actionable clinical guide.

Early surgery is not without risk. The literature documents that endoscopic prostatic surgery carries ejaculatory dysfunction in a significant proportion of patients, postoperative retention in 3–9% of cases, urethral stricture in 2–9%, and iatrogenic incontinence in around 0.5% [6]. For a 60-year-old man with moderate symptoms and still-preserved bladder function, the risk-benefit equation of early surgery versus active surveillance with medication is unresolved.

A note on the editorial's origins. The initiative's reference editorial in Prostate Cancer and Prostatic Diseases [1] is, by its own nature, an opinion piece. One of its three authors is Dr. Kuang himself — founder of ManVsProstate and author of the book the editorial reviews. This overlap does not invalidate the arguments, but it does call for the careful reading that any publication with a declared interest deserves.

The research we actually need

The real problem is not that the "Defenders of the Detrusor" are wrong about their concern — they are not. The problem is that they are asking us to change how we practise medicine without yet having the evidence to make that change safely. So what would it take?

  • 1 Prospective validation of the five-stage model. Recruit a large cohort of men with BPH, classify them according to the model with strict operational criteria and follow them for at least five years measuring urodynamic bladder function, quality of life and progression to detrusor underactivity or retention. Until that is done, the five stages remain useful pedagogy, but not clinical staging [4].
  • 2 Define the thresholds of the "window of curability". A randomised controlled trial — or at minimum a prospective cohort study with propensity score analysis — comparing early surgical intervention guided by objective biomarkers versus protocolised medical management with active surveillance, with long-term detrusor function as the primary endpoint.
  • 3 Studies of damage reversibility. How far along the remodelling pathway can bladder function recover after deobstruction? A 2024 meta-analysis of TURP in patients with preoperative detrusor underactivity showed significant improvements in maximum flow rate, IPSS, and bladder contractility index [7], and a molecular study showed that deobstruction partially reverses transcriptional changes [8]. We need larger cohorts and longer follow-up to define what is reversible, in whom, and for how long.
  • 4 Cost-effectiveness analysis of the proposed objective diagnostics. If we are going to recommend routine cystoscopies and bladder wall thickness measurements across the BPH population, we need to know the cost to the health system, the risks those procedures carry, and whether the information they generate genuinely changes clinical decisions and patient outcomes.

A strength worth highlighting: technological agnosticism

Something the initial analysis did not adequately capture: the initiative does not advocate for any specific surgical technology. The book mentions no device by name — no Urolift, no Rezum, no iTind, no Aquablation. It acknowledges the explosion of minimally invasive surgical options (MISTs) and uses them as a favourable point of comparison against medication, but deliberately leaves the technical choice to an individualised shared decision-making process — what Dr. Kuang calls the Trifecta: prostate size, prostate shape, and the detrusor function of each specific patient.

This technological agnosticism is intellectually honest and makes the paradigm more robust. This is not a device looking for a market — it is a philosophy of timely intervention with the best available tool for each case. In a field where many "initiatives" have a commercial technology behind them, that deserves explicit recognition.

A closing thought

The "Defenders of the Detrusor" have done something genuinely difficult: they have put an uncomfortable question on the table that urology has been skirting for years. Are we letting the bladder deteriorate while we busy ourselves controlling symptoms? That question deserves a serious scientific answer — not a hasty one in either direction.

The initiative deserves credit for identifying the problem and for creating accessible language to communicate it with patients. What it still needs is the evidence that converts a clinically coherent hypothesis into a safe medical recommendation.

And that, fortunately, is something that can be built. It just requires someone to do it with the rigour that the bladder — that silent, forgotten muscle — deserves.