The consensus documents in question represent a genuine milestone. They establish standardized protocols for cDCDD across Europe, including detailed recommendations for abdominal NRP (a-NRP) and, more recently, thoraco-abdominal NRP (TA-NRP), in which donor blood is circulated via extracorporeal membrane oxygenation (ECMO) to reanimate abdominal organs and even the heart itself. In both scenarios, abdominal and cardiac graft management follows rigorous, written procedures. The lungs, however, are treated almost as an afterthought. Current clinical practice typically alternates between regional perfusion and immediate static cold storage, delaying lung reinflation until sternotomy and pulmonary artery cannulation in the operating room, long after the critical post-mortem window has closed.

The physiological argument at the heart of the Forum is elegant and, the authors insist, conceptually decisive. Unlike other solid organs, lung parenchyma does not depend on continuous blood perfusion to sustain aerobic cellular metabolism. Instead, the alveolus functions as its own oxygen delivery system: direct alveolar oxygen diffusion into the interstitial space and vascular endothelium is sufficient to prevent ATP depletion and ischemic cell collapse. This mechanism, sometimes described as the so-called pulmonary privilege, means the only truly effective way to preserve cellular metabolism during the immediate post-mortem period is alveolar oxygenation, achieved either through protective mechanical ventilation or continuous positive airway pressure (CPAP) with a high fraction of inspired oxygen. Framing lung preservation strategy exclusively around the a-NRP versus TA-NRP debate is, from a pulmonary perspective, conceptually flawed, because the lung’s preservation needs are met through the airway, not the vasculature.

Timing, however, is everything, and this is where the bioethical safeguards become inseparable from the physiology. The mandatory post-mortem observation or no-touch period, during which no intervention is permitted after cardiac arrest, varies internationally from 3 to 20 minutes, with a global average of 5 minutes. From both ethical and physiological standpoints, a minimum of 5 minutes must be respected to avoid auto-resuscitation of the heart. Initiating mechanical ventilation prematurely within this window is strictly forbidden, because hypoxic cardiac arrest might otherwise be reversed in the donor, or residual cerebral oxygenation could be compromised, violating the dead donor rule that underpins the entire ethical framework of donation after circulatory death.

Once the mandatory standoff period has been fully respected and death has been legally declared, the authors argue that initiating mechanical ventilation or CPAP represents minute zero of lung preservation. This early alveolar recruitment must not be deferred until chest opening in the operating room. Pathophysiological principles strongly support the strategy, international donor procurement guidelines advise it, and current ethical and legal regulations fully permit it as a post-mortem preservation maneuver. In other words, the simplest, cheapest, and most physiologically rational intervention available, reconnecting the ventilator or applying CPAP with a high fraction of inspired oxygen the moment death is declared, is already ethically sanctioned and guideline-endorsed, yet remains unrecognized as a standardized frontline maneuver in cDCDD protocols.

The authors insist that the lung cannot remain an overlooked organ in global DCD standards. In cDCDD cases managed with abdominal NRP, the overall preservation environment should be recognized as a dual-temperature preservation: abdominal normothermia combined with thoracic hypothermic or ischemic oxygenated preservation. Rather than relying solely on hypothermia to slow metabolic rates, early alveolar oxygen supply delivers what the authors call true oxygenated ischemia, which preserves pneumocyte viability and allograft quality over extended periods. This approach has been successfully demonstrated in uncontrolled donation after circulatory death, where long ischemic times have been managed with simple normothermic ventilation and ex vivo lung perfusion assessment, offering a template for what controlled donation protocols could achieve.

Technical standardization in cDCDD managed with TA-NRP, however, must extend beyond ventilatory parameters to address pulmonary hydrostatic safety, and here the picture becomes considerably more complex. Reanimating the donor heart inherently exposes the pulmonary vasculature to active perfusion. The ESOT Bucharest Consensus explicitly acknowledges the threat of lung congestion and cardiac distension during TA-NRP, and its guidelines rely on indirect right-sided decompression by optimizing venous return to the ECMO circuit via a centrally inserted dual-stage venous cannula. This approach, however, fails to prevent post-capillary congestion caused by left ventricular stunning or transient contractility failure. When antegrade perfusion is restored, blood pools retrogradely into the left heart while the ventricular apparatus is still arrested or stunned, causing devastating post-capillary damage if an active outflow tract is not provided.

To address this, Van Raemdonck and colleagues argue that direct and immediate venting of the left atrium, by inserting a venting catheter via the interatrial groove at the initiation of TA-NRP, is required to prevent hydrostatic pulmonary edema. This direct approach, however, introduces significant surgical complexity and suffers from a profound lack of standardization. The 2024 American Association for Thoracic Surgery (AATS) Expert Consensus confirms that clinical utilization of lungs after TA-NRP remains highly controversial and data are limited, pointing directly to inconsistent venting practices as the primary cause of hydrostatic edema and variable graft outcomes. To date, there is no high-quality clinical evidence confirming that this in situ surgical maneuver increases the rate of valid donors. On the contrary, its technical difficulty in an unstable donor, combined with the absence of a uniform protocol, frequently deters transplant teams from accepting these grafts altogether out of fear of acute hydrostatic edema.

How to reliably protect the pulmonary vascular bed during TA-NRP therefore remains a poorly standardized frontier, as current guidelines fail to offer a clear, consensus-driven protective roadmap. Within this gap, inconsistent venting practices represent a critical technical failure and a lapse in procedural leadership that acts as a powerful deterrent for transplant teams, unnecessarily limiting lung graft utilization. The authors also raise the strategic allocation of high-cost healthcare resources: while ex vivo lung perfusion (EVLP) is an indispensable, vital safety net to evaluate and rescue borderline grafts, particularly those with suspected hydrostatic edema, it must never serve as a routine, high-cost bypass for suboptimal in situ preservation. Shifting the burden of graft protection from the donor’s bedside to ex situ platforms is both logistically and financially unsustainable, and clinical priority must remain focused on rigorous, proactive in situ donor care.

Ultimately, the Forum delivers a pointed challenge to the transplant community. While current consensus guidelines remain heavily focused on complex hepatic or cardiac preservation protocols, they frequently overlook simple, cost-effective, and highly viable maneuvers to safeguard the lung graft. While the community debates highly invasive and poorly standardized in situ surgical venting procedures to mitigate hydrostatic injury, the simplest protective strategy of all, early in situ alveolar oxygenation via ventilation or CPAP immediately following the mandatory 5-minute no-touch period, remains unrecognized as a standardized frontline maneuver. A paradigm shift is urgently required, the authors conclude: transitioning from static cold storage toward early in situ oxygenated preservation, as successfully demonstrated in uncontrolled donation after circulatory death. The lung, they insist, must no longer be the forgotten organ in regional perfusion strategies and cDCDD consensus guidelines.

Subject of Research: Transplantation

Article Title: Don’t forget to safeguard the lungs during DCD multi-organ retrieval! Early in situ oxygenated preservation matters

Article References: Jordá Aragón, C., & Fontana Bellorín, A. (2026). Don’t forget to safeguard the lungs during DCD multi-organ retrieval! Early in situ oxygenated preservation matters. Transplant International, 39, Article 17507. https://doi.org/10.3389/ti.2026.17507

Image Credits: AI Generated

DOI: 10.3389/ti.2026.17507

Keywords: lung transplant, DCD donation, normothermic regional perfusion, organ preservation, ESOT consensus, transplant surgery, forget, safeguard, lungs, during, multi-organ, retrieval

Oscillometry, also called the forced oscillation technique, works by superimposing small, multi-frequency pressure oscillations on a person’s ordinary tidal breathing. Unlike spirometry, which demands forceful, coordinated blows, oscillometry is effort-independent and requires only passive cooperation, making it attractive for children, elderly patients, and people who cannot perform forced maneuvers. The technique reports two fundamental quantities: respiratory resistance, which reflects how hard it is for air to move through the airways, and respiratory reactance, which captures the elastic and inertive properties of the lungs and chest wall. Both are derived from respiratory system impedance, measured across a spectrum of frequencies from 5 to 37 hertz in modern devices.

The Toronto team compared the Tremoflo C-100, made by Thorasys Medical Systems in Canada, with the Resmon Pro, made by Restech srl in Italy. Their cohort of 76 participants included 49 patients with chronic lung disease and 27 healthy volunteers. Among the patients were 37 double-lung transplant recipients, 10 people with interstitial lung disease, one with chronic obstructive pulmonary disease, and one with lymphangioleiomyomatosis. Standard pulmonary function tests classified the group into 36 people with normal lung function, 26 with restriction, 8 with obstruction, and 5 with mixed patterns. Participants completed paired oscillometry with both devices in alternating order, each calibrated daily and performed according to European Respiratory Society technical standards.

The results were unambiguous. For all five primary oscillometry parameters, resistance at 5 hertz (R5), the resistance difference between 5 and 19 hertz (R5-19), reactance at 5 hertz (X5), resonant frequency (Fres), and the area of reactance (AX), the differences between devices reached statistical significance at p at or below 0.001. The Resmon Pro consistently reported lower R5, R5-19, Fres, and AX, and a less negative X5 than the Tremoflo C-100. In practical terms, the Resmon Pro painted a rosier picture of airway mechanics than the Tremoflo did for the same pair of lungs on the same day.

Statistical agreement analysis told a similar story. Intraclass correlation coefficients ranged from 0.59 to 0.85, and Spearman correlations were strong, between 0.779 and 0.920, meaning the devices rank-ordered patients similarly. But correlation is not agreement. Bland-Altman analysis, which plots the difference between paired measurements against their average, revealed systematic bias with wide limits of agreement for every parameter. The bias for AX, a reactance-derived index that integrates the frequency-dependent behavior of reactance, was minus 4.10 centimeters of water per liter, with limits of agreement stretching from minus 14.99 to plus 6.80. For Fres, the limits spanned from minus 6.46 to plus 4.75 hertz. Cohen’s d effect sizes were large for R5, R5-19, X5, and AX, confirming that the differences were not merely statistically detectable but substantively meaningful.

One of the study’s most clinically important findings concerned where the disagreement mattered most. When the researchers applied per-patient Oostveen reference limits, they found that agreement between devices was excellent, 91 to 100 percent within the Bland-Altman limits, when measurements fell within the normal reference range. But when measurements fell outside that range, agreement dropped to 81 to 92 percent. In other words, the systematic bias does little harm when a patient’s lungs are clearly normal, but becomes clinically consequential precisely when the lungs are abnormal, which is when monitoring decisions are being made.

The researchers also tested whether the inter-device differences translated into different patient classifications. They applied two schemes: a two-step decision tree the team had previously developed and validated in over 1,800 patients, and recently published Delphi consensus thresholds for asthma and COPD. Neither device showed clearly superior agreement with the pulmonary-function-test-derived gold standard, with kappa values of roughly 0.30 for the decision tree and only 0.09 to 0.12 for the Delphi thresholds. More concerning, individual participants could be classified differently depending on which device was used, meaning the same patient might be labeled normal by one machine and abnormal by the other.

Why do two devices measuring the same physical quantity disagree so much? The authors point to several technical factors. Hardware differences in oscillation waveform and amplitude can influence the measured signal. The two devices also handle mouthpiece dead space differently and use different calibration procedures: the Tremoflo completes an 8-second calibration against a 15-centimeter-water-second-per-liter reference load, while the Resmon Pro performs an 86-second calibration against a manufacturer-supplied load with distinct resistance and reactance characteristics. Signal processing differs too. The Tremoflo records for 20 seconds with 9 frequencies, while the Resmon Pro records for 60 seconds with 10 frequencies. The longer Resmon recording may improve low-frequency reactance estimation but increases susceptibility to drift and within-test changes in lung mechanics. Tidal volume was also higher during Tremoflo testing in this study.

The study is notable for extending device comparison beyond the healthy volunteers and asthma or COPD populations that dominated earlier work. Prior studies, including work by Dandurand and colleagues using mechanical test loads, Ducharme and colleagues in children, Soares and colleagues with a 3D-printed airway model, and De’s 2026 comparison of the same two devices in 97 symptomatic adults, all found systematic inter-device bias. But the Toronto cohort is the first to directly compare two commercial forced oscillation devices across normal, restrictive, obstructive, and mixed lung function patterns, including patients with interstitial lung disease and stable lung transplant recipients. The restrictive group showed the largest AX discrepancy, with a median Tremoflo value of 13.70 versus 8.23 on the Resmon Pro, a difference the authors note is particularly relevant because reactance abnormalities are the primary oscillometric signature of restrictive disease.

The practical message for clinicians is straightforward: stick with one device when following a patient over time. Changes in oscillometry parameters could otherwise be misattributed to disease progression or treatment response when they actually reflect device-specific differences. The authors also call for standardization of signal generation and processing across manufacturers, which they argue is necessary for cross-device comparability in both clinical practice and multi-center research. Participant feedback added a human dimension: of the 51 people who completed a survey, 61 percent had no preference, but some found the longer Resmon recordings fatiguing, while others preferred the handheld Tremoflo for its easier positioning. As oscillometry moves toward wider clinical adoption, particularly for early detection of lung disease and monitoring of transplant recipients, the Toronto findings make clear that the technology’s promise depends on the field first solving a problem that is less glamorous than the physics itself: getting the machines to speak the same language.

Subject of Research: Agreement between two commercial respiratory oscillometry devices across normal, obstructive, restrictive, and mixed lung function patterns

Article Title: Comparison of two respiratory oscillometers in patients with a broad range of lung function patterns

Article References: Binnie, M., Wu, J. K. Y., & Chow, C.-W. (2026). Comparison of two respiratory oscillometers in patients with a broad range of lung function patterns. Frontiers in Allergy, 7, Article 1896281. https://doi.org/10.3389/falgy.2026.1896281

Image Credits: AI Generated

DOI: 10.3389/falgy.2026.1896281

Keywords: oscillometry, forced oscillation technique, lung function, respiratory resistance, respiratory reactance, Bland-Altman analysis, pulmonary function testing, interstitial lung disease, lung transplant, device standardization, Tremoflo C-100, Resmon Pro

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