The research team, led by investigators from Helsinki University Hospital, Turku University Hospital, Tampere University Hospital, and the data analytics firm Medaffcon, leveraged a uniquely Finnish advantage: near-complete longitudinal health records. By linking the Finnish Kidney Transplant Registry with regional hospital data lakes, the national inpatient and outpatient register (HILMO), pharmacy purchase records from the Social Insurance Institute, and mortality data from Statistics Finland, the researchers assembled a dataset covering approximately half of the Finnish population. All transplantations occurred between 2013 and 2022, and patients were followed for clinical outcomes during the first 18 months and for healthcare resource utilization up to four years after surgery.

The cohort was stratified by cytomegalovirus serostatus, a critical distinction in transplant medicine. Roughly 73 percent of recipients were CMV-seropositive before transplantation (the R+ group), about 21 percent received a kidney from a seropositive donor while being seronegative themselves (the high-risk D+/R− group), and just over 6 percent were seronegative with seronegative donors (D−/R−). This distribution reflects Finland’s CMV seroprevalence of approximately 70 percent, meaning roughly one in five Finnish transplant recipients falls into the highest-risk category for primary CMV infection after surgery.

The headline finding is stark: post-transplant leukopenia or neutropenia, abbreviated PTLN in the study, occurred in 34.5 percent of all recipients within the first year. But the risk was far from evenly distributed. Among D+/R− recipients, 51.5 percent developed PTLN by 12 months, compared with 31.7 percent of R+ recipients and only 10 percent of D−/R− recipients, a difference that remained highly significant after statistical adjustment. In a multivariable logistic regression model, D+/R− serostatus carried 2.42-fold higher odds of PTLN within 18 months, while D−/R− status was actually protective relative to the R+ reference group.

Beyond serostatus, several other risk factors emerged. Female sex was independently associated with PTLN, a finding the authors attribute in part to sex differences in drug pharmacokinetics that may lead to higher plasma drug exposures in women receiving standard doses. Polycystic kidney disease as the primary diagnosis also increased risk, consistent with prior reports that patients with autosomal dominant polycystic kidney disease frequently have leukopenia even before transplantation, possibly related to splenic sequestration or intrinsic immune dysregulation. Delayed graft function, meaning the transplanted kidney did not immediately work, was another independent risk factor. Perhaps most strikingly, induction therapy with anti-thymocyte globulin (ATG) was associated with a seven-fold increase in PTLN risk, a finding the authors note was unsurprising given ATG’s well-known myelosuppressive effects but clinically important given its increasing use in solid organ transplantation.

The relationship between PTLN and CMV infection proved more nuanced than a simple cause-and-effect story. CMV DNAemia, detectable viral DNA in the blood, occurred at broadly similar frequencies in R+ and D+/R− recipients, roughly half of each group. But the timing differed dramatically. In R+ recipients, the median time to first CMV DNAemia was 66 days, with most episodes occurring within the first six months after transplantation. In D+/R− recipients, the median time was 239 days, with most episodes occurring after the six-month mark, coinciding with the end of their standard six-month valganciclovir prophylaxis. This temporal pattern reflects the different prophylactic strategies: 95 percent of D+/R− patients started valganciclovir prophylaxis at transplantation, compared with only 28 percent of R+ patients, who were instead monitored for CMV DNAemia and treated if it appeared.

Using a multistate model that tracked the sequence of events over time, the researchers uncovered a striking asymmetry. In D+/R− recipients, PTLN tended to precede CMV DNAemia, whereas in R+ recipients, CMV DNAemia was more often detected first. By six months post-transplant, 34.5 percent of D+/R− patients had developed PTLN, only 6 percent had CMV DNAemia, and 7.5 percent had experienced both. Among R+ patients, the pattern was nearly reversed: 14.4 percent had PTLN, 31.3 percent had CMV DNAemia, and 11.9 percent had both. The authors caution that these observational findings do not establish causality, and that in R+ patients it was impossible to reliably distinguish CMV-driven cytopenia from valganciclovir-induced myelosuppression because the registry data lacked complete information on drug dosing and indications. Nevertheless, the temporal patterns are clinically plausible given the different prophylactic regimens each group receives.

The economic dimension of the study may prove to be its most consequential contribution. Patients who developed PTLN had substantially higher healthcare resource utilization across virtually every metric measured. Hospital readmission rates at 12 months were 75.3 percent among R+ patients with PTLN versus 64.6 percent among those without, and 78.9 percent versus 72.9 percent in the D+/R− group. ICU admission rates were also elevated, particularly among R+ patients with PTLN, at 13.8 percent versus 6 percent. The cost differences were even more pronounced: during the first year after transplantation, excluding the initial 30 days, inpatient costs averaged 14,028 euros per patient among those with PTLN compared with 5,716 euros among those without, while outpatient costs were 11,695 euros versus 9,045 euros respectively. These differences persisted into the second year of follow-up.

In a multivariable gamma regression model adjusting for demographics, comorbidities, and transplant characteristics, both D+/R− serostatus and PTLN remained independently associated with higher total healthcare costs over four years. The authors emphasize that these cost estimates should be interpreted conservatively, since PTLN may function as a marker of overall clinical complexity rather than a direct cause of increased spending. Many PTLN episodes are managed in outpatient settings through intensified laboratory monitoring and medication adjustments that do not generate inpatient costs, and the exclusion of the first 30 days after transplantation means early PTLN-related events were not captured in the primary cost model.

Notably, the study did not find statistically significant associations between PTLN and graft loss or mortality, though the authors attribute this partly to the limited number of events and note that prior studies have yielded conflicting results on this question. The five-year patient survival rate for the entire cohort was 87.7 percent, and five-year graft survival was 84.7 percent, with no significant differences by CMV serostatus or PTLN status. Advanced recipient age and diabetes as the primary kidney disease were associated with higher mortality and graft loss risk, while female sex and polycystic kidney disease were associated with better graft survival.

The proportion of patients experiencing PTLN also increased over the study period, from 3.6 percent of those transplanted in 2014–2015 to 8.6 percent of those transplanted in 2020–2022. The authors suggest this trend may reflect changes in clinical practice during the decade, including increasing use of ATG induction, greater reliance on tacrolimus-based immunosuppression, and a moderate expansion of valganciclovir prophylaxis, partly driven by more ABO-incompatible transplants and ATG induction protocols. As transplant populations grow older and frailer, the cumulative immunosuppressive burden from multiple concomitant therapies may further elevate PTLN risk, reinforcing the importance of strategies aimed at mitigating both its clinical and economic consequences.

Subject of Research: Post-transplant leukopenia, neutropenia, and cytomegalovirus infection in kidney transplant recipients

Article Title: The frequency and timing of leukopenia and CMV infections in kidney transplant recipients in Finland – a retrospective observational study

Article References: Helanterä, I., Ortiz, F., Havula, E., Tuominen, S., Hakamäki, M., Hellman, T., Mäkelä, S., & Korhonen, R. (2026). The frequency and timing of leukopenia and CMV infections in kidney transplant recipients in Finland – a retrospective observational study. Transplant International, 39, Article 16893. https://doi.org/10.3389/ti.2026.16893

Image Credits: AI Generated

DOI: 10.3389/ti.2026.16893

Keywords: kidney transplantation, leukopenia, neutropenia, cytomegalovirus, valganciclovir, CMV DNAemia, healthcare resource utilization, transplant immunosuppression, Finland, registry study, donor-recipient serostatus, myelosuppression

The new research, conducted at Rabin Medical Center, the largest solid organ transplant center in Israel, and published in Archives of Osteoporosis, followed 39 adults who received teriparatide, a recombinant analogue of human parathyroid hormone, after kidney, lung, or liver transplantation. The investigators report that patients treated with the drug for a median of more than 22 months gained significant bone mineral density at the lumbar spine, femoral neck, and total hip, while clinicians observed acceptable metabolic safety and no episodes of graft rejection during therapy. The findings offer some of the most detailed evidence to date on anabolic osteoporosis treatment in a population that has long been underrepresented in bone research.

The scale of the skeletal problem after transplantation is difficult to overstate. In this cohort, 90 percent of patients had already suffered at least one fragility fracture before starting teriparatide, and 79 percent had multiple broken bones. The immune-suppressing glucocorticoids that nearly all transplant recipients take, at an average dose of around 7 milligrams of prednisone-equivalent per day in this study, directly impair the bone-forming cells called osteoblasts while accelerating bone resorption. Combined with pre-existing organ dysfunction, vitamin D deficiency, and the metabolic upheaval of end-stage organ disease, the result is a skeleton under relentless attack in patients who often cannot tolerate standard therapies.

Teriparatide works differently from the antiresorptive drugs, such as bisphosphonates, that are usually the first line of defense against post-transplant bone loss. Rather than slowing bone breakdown, it stimulates new bone formation by mimicking intermittent pulses of parathyroid hormone, a signal that activates osteoblasts when delivered in daily injections. This anabolic mechanism has made it a first-line option for severe glucocorticoid-induced osteoporosis in the general population. But transplant medicine has harbored a persistent worry: laboratory and clinical studies have suggested that bones in chronic kidney disease and after transplantation may become resistant to parathyroid hormone signaling, a condition linked to adynamic bone disease in which the cellular machinery for building bone falls silent. Skeptics questioned whether an anabolic drug could overcome that resistance.

The new data argue that, in many patients, it can. Among the subset of participants with paired bone density scans taken at the start and end of therapy, lumbar spine bone mineral density rose by an average of 11 percent, femoral neck density by 8 percent, and total hip density by 11 percent, gains that the authors note are comparable to responses reported in non-transplant populations and exceed what antiresorptive drugs typically achieve in transplant recipients. Statistically, the increases reached significance at all three skeletal sites. Treatment was started a median of 36 months after transplantation, once graft function and immunosuppressive regimens had often stabilized, and continued for a median of 22.3 months, a longer exposure than in most previous reports.

Fracture outcomes, though limited by small numbers, added a reassuring note. Six patients broke bones after starting teriparatide, but only two of those fractures occurred while the drug was actively being taken; the other four happened months to years after treatment had stopped. Given that nearly every participant entered the study with an already shattered fracture history, the apparent stabilization of fracture incidence during therapy is clinically meaningful, even though the retrospective design and small sample size prevented the study from formally demonstrating fracture reduction.

Safety, particularly for the transplanted organ itself, was a central question. Kidney function, measured by estimated glomerular filtration rate, declined modestly during the first six months of therapy, from an average of 73 to 64 milliliters per minute per 1.73 square meters, and then stabilized through the remainder of treatment and follow-up. Crucially, a contemporaneous matched group of transplant recipients who never took teriparatide showed a broadly similar decline over the same period, suggesting the change reflected the natural course of post-transplant kidney function rather than a drug effect. No patient progressed to end-stage kidney disease or required dialysis, and metabolic complications were rare: a single case of hypercalcemia, which resolved when the drug was stopped, and no cases of significant hypercalciuria despite most patients taking calcium and vitamin D supplements.

The study’s authors are careful to frame these results within the limits of a single-center, retrospective design. Patients were not randomly assigned; teriparatide was reserved for those with the most severe disease, often after failure of or intolerance to bisphosphonates, a selection reinforced by national reimbursement criteria in Israel. The matched control group was used only to contextualize kidney function trends, not to compare treatment effects, and causality cannot be inferred. Yet the very severity of the treated cohort strengthens the clinical signal: these were patients whose skeletons had already failed, and they still built substantial new bone. Only one randomized trial has previously tested teriparatide after transplantation, a short six-month study in kidney recipients begun during the intense immunosuppression of early recovery, which found no density gains but did prevent bone loss compared with placebo.

By including lung and liver recipients alongside kidney patients, the new study extends the evidence base to populations for which no dedicated osteoporosis treatment guidelines exist, in contrast to the organ-specific guidelines published for heart, kidney, and liver transplant care. The results align with recent observational work showing that teriparatide outperformed alendronate in renal transplant recipients and produced meaningful density gains in patients with low bone turnover, and they add histological and clinical weight to case reports of improved bone formation in heart transplant patients. Taken together, the picture emerging is that skeletal resistance to parathyroid hormone after transplantation, while a real phenomenon, is not an insurmountable barrier when therapy is timed after graft stabilization and sustained for nearly two years.

For clinicians, the message is one of selective optimism rather than blanket prescription. Teriparatide is expensive, requires daily injections, and carries a limited treatment duration, so it is unlikely to become a universal post-transplant remedy. But for the growing population of transplant survivors with severe osteoporosis, prior fractures, and few remaining options, the study suggests a viable path: an anabolic window that can rebuild what immunosuppression has torn down, administered with routine monitoring of calcium and kidney function. The authors call for prospective trials to define the optimal timing, duration, and sequencing of anabolic therapy after transplantation, questions that will only grow more urgent as transplant medicine continues to extend survival and shifts its focus toward the long-term quality of the lives it saves.

Subject of Research: Teriparatide treatment of severe osteoporosis in solid organ transplant recipients

Article Title: Teriparatide treatment of osteoporosis in solid organ transplant recipients—a single-center experience

Article References: Diker Cohen, T., Shraga-Slutzky, I., Kaminer, K., Gorshtein, A., Dotan, I., & Tsvetov, G. (2026). Teriparatide treatment of osteoporosis in solid organ transplant recipients—a single-center experience. Archives of Osteoporosis, 21(1), Article 136. https://doi.org/10.1007/s11657-026-01751-4

Image Credits: AI Generated

DOI: 10.1007/s11657-026-01751-4

Keywords: teriparatide, osteoporosis, solid organ transplantation, bone mineral density, fragility fractures, glucocorticoid-induced osteoporosis, anabolic therapy, kidney transplant, lung transplant, liver transplant, kidney function, transplant immunosuppression