Sex Hormones and Sexual Health in Chronic Kidney Disease Before and After Kidney Transplantation

65% of women with advanced CKD had sexual dysfunction; hormones improved after transplant but sexual dysfunction persisted

Journal: Journal of Nephrology | Published: 2026-06-04 | Type: Journal Article | PMID: 41774595 Authors: Lobo AS et al. (University of Minnesota, Mayo Clinic, Harbor-UCLA) Funding/COI: NIH on Aging (3K12AR084223-18S1); no conflicts declared

Summary

Advanced chronic kidney disease wreaks havoc on female reproductive hormones, and this prospective study quantifies how bad it is: nearly two-thirds of premenopausal women with CKD stages 3b–5 met the clinical threshold for sexual dysfunction. Kidney transplantation normalized prolactin and DHEAS levels, but sexual dysfunction stubbornly remained at the 6-month mark. The unexpected villain of the piece is DHEAS — an adrenal androgen precursor not typically discussed in this context — which showed the strongest statistical association with impaired sexual function.

Claims

• 65.8% of enrolled women (25/38) had sexual dysfunction, defined as FSFI total score < 26.55
• 44.7% (17/38) had menstrual irregularities
• Majority had abnormally elevated luteinizing hormone during the follicular phase
• Prolactin was negatively associated with FSFI score after adjusting for age (β = −0.26, P = 0.03)
• DHEAS was negatively associated with FSFI score after adjusting for age (β = −0.07, P = 0.01)
• Post-transplant: both prolactin and DHEAS levels improved significantly
• Post-transplant: sexual dysfunction persisted despite hormonal normalization

Study Quality

This is a small single-arm prospective cohort — 38 women recruited from outpatient CKD clinics and dialysis units, with data collected at enrollment and again 6 months after transplant. The FSFI is a validated, widely-used instrument for measuring female sexual function, which is a methodological plus. Exclusion of pregnant, menopausal, post-hysterectomy, and hormonally-contracepted women tightens the population but reduces generalizability. The regression analyses controlling for age are appropriate given the sample's age range (18–51).

The critical limitation is that 6 months is an arbitrary and short post-transplant window — sexual function after transplant is influenced by immunosuppression regimens, graft function trajectory, and psychological recovery, none of which are reported here. Without a healthy control group or a longer follow-up, it's impossible to say whether the persistent dysfunction reflects residual hormonal disruption, psychosocial factors, or medication effects.

Red Flags

• N = 38 total; only a subset received transplants — regression findings in this sample size are underpowered and exploratory at best
• No control group — comparison to healthy premenopausal women is absent
• No data on immunosuppressant type or dose, which directly affects hormone levels post-transplant
• 6-month follow-up is too short to assess whether sexual function eventually recovers
• No baseline FSFI data reported pre-CKD; the dysfunction's chronology is unknown
• Cross-sectional hormonal associations don't establish causality

Strengths

• Prospective design with pre/post transplant measurements in the same patients
• Validated instrument (FSFI) with an established clinical cutoff
• NIH-funded with no industry conflicts — a clean funding picture in a space where that matters
• Measured a broad hormone panel (LH, prolactin, DHEAS) rather than testosterone alone
• Practical exclusion criteria that reduce confounding from exogenous hormones

Verdict

A well-intentioned pilot study that raises an interesting question about DHEAS in CKD-related sexual dysfunction — but 38 patients is a sample size that can only generate hypotheses, not conclusions. The finding that transplantation corrects hormones without correcting sexual function is clinically useful context, but without longer follow-up or a control arm, readers can't know what "persisted at 6 months" actually means for these women's long-term outcomes. Treat this as preliminary data that justifies a larger, better-powered study, not as settled evidence about the role of DHEAS.