The study team, led by Alper Tahmaz and colleagues in the Department of Infectious Diseases and Clinical Microbiology at Antalya Training and Research Hospital, designed the analysis around a single admission per patient. When a patient had been hospitalized more than once during the study window, the researchers selected the chronologically latest admission, irrespective of whether the patient survived. This approach ensured that each individual contributed only one observation to the dataset, avoiding the statistical distortion that repeated admissions can introduce when the same severely ill patients dominate hospital records. The investigators then combed retrospectively through demographic characteristics, immune status, viral load measurements, comorbidities, and the recorded indications for hospitalization, which were treated as non-mutually exclusive categories, meaning a single admission could carry several simultaneous reasons for care.

The demographic and clinical profile of the cohort was striking. The median age of admitted patients was 45 years, and nearly nine in ten participants, 89.8 percent, were male. More revealing were the immunological numbers: at admission, 56.3 percent of patients had CD4 cell counts below 200 cells per cubic millimeter, the threshold that defines advanced immunosuppression and the level at which opportunistic infections become a dominant threat. Only 37.5 percent of the hospitalized patients had a previously established HIV diagnosis, and just 27.3 percent were receiving combined antiretroviral therapy at the time of admission. In other words, the majority of people ending up in hospital beds were either newly diagnosed in the course of their acute illness or had known HIV but were not on suppressive treatment, a pattern that echoes the persistent challenge of late diagnosis documented across many health systems.

The reasons these patients required hospitalization mapped closely onto the classical spectrum of HIV-related disease. Bacterial infections were the most frequently recorded indication, appearing in 58.6 percent of admissions, a reminder that even in the antiretroviral era, bacterial pneumonia, sepsis, and other common bacterial pathogens remain leading causes of serious illness among immunocompromised hosts. Pneumocystis jirovecii pneumonia, the fungal opportunistic infection that once defined the AIDS epidemic, was recorded in 28.9 percent of patients, while cytomegalovirus infection, another hallmark of severe cellular immune deficiency, appeared in 21.9 percent. Because the indications were not mutually exclusive, many patients carried multiple overlapping diagnoses at once, reflecting the compounded vulnerability of bodies whose CD4 defenses had collapsed.

Beyond the classic opportunistic infections, the study also captured the substantial burden of other medical conditions, which were recorded in 67 patients, or 52.3 percent of the cohort. Rather than forcing these into narrow diagnostic boxes, the researchers described them by organ system category, acknowledging that hospitalized people living with HIV frequently present with a tangle of concurrent problems affecting the respiratory tract, the gastrointestinal system, the nervous system, and beyond. This overlap of infectious and non-infectious conditions is one of the study’s central messages: the modern hospitalized HIV patient is rarely admitted for a single clean diagnosis, and clinical management must contend with simultaneous, interacting pathologies.

The severity of these admissions was underscored by intensive care utilization. Nearly a quarter of the cohort, 24.2 percent, required admission to the intensive care unit at some point during their hospital stay. That figure speaks to how far disease had progressed before these patients reached effective care, and it aligns with the broader clinical understanding that late presenters with CD4 counts below 200 cells per cubic millimeter face dramatically elevated risks of respiratory failure, septic shock, and central nervous system complications that demand critical care support.

The primary outcome of the study was documented in-hospital death, and the mortality figure was sobering: 20 of the 128 patients died, an in-hospital mortality rate of 15.6 percent, with a 95 percent confidence interval of 10.3 to 22.9 percent. To identify factors associated with this outcome, the researchers employed an exploratory Firth penalized logistic regression model, a statistical technique specifically designed for situations where the number of outcome events is small relative to the number of predictor variables. Ordinary logistic regression can fail or produce wildly unstable estimates in such sparse-data settings, and the Firth penalty shrinks coefficient estimates toward zero to reduce this small-sample bias. The model included three predictors: age, a CD4 count below 200 cells per cubic millimeter at admission, and a history of malignancy.

Of these three candidates, one emerged with a statistically clear signal. A history of malignancy was associated with roughly fourfold higher odds of in-hospital death, with an adjusted odds ratio of 4.00 and a 95 percent confidence interval of 1.25 to 12.37, yielding a p-value of 0.020. The authors are careful to frame this as an exploratory finding, and for good reason: with only 20 deaths in the entire cohort, the confidence interval is wide, spanning from just over one to more than twelve, which means the true strength of the association could plausibly range from modest to very large. The direction of the result, however, is biologically coherent. Cancer history in people living with HIV can reflect prior AIDS-defining malignancies such as lymphomas, the immunosuppressive effects of chemotherapy, and generally diminished physiological reserve, all of which plausibly compound the danger of an acute infectious admission.

The authors themselves are explicit about the limitations that should temper interpretation. The cohort was drawn from a single tertiary referral hospital, which selects for the most complex and severe cases in a region and limits generalizability to primary care settings or to the broader population of people living with HIV who never require admission. The retrospective design depends on the completeness and accuracy of medical records, and the regression model adjusted for only a small number of covariates, leaving open the possibility of confounding by unmeasured factors such as treatment adherence, nutritional status, or the specific pathogens involved. The selection of the latest admission per patient, while methodologically defensible, also means the analysis captures a particular snapshot of each patient’s trajectory rather than the full arc of their hospitalizations.

Even with those caveats, the study lands on a set of conclusions that resonate far beyond one Turkish hospital. The finding that more than half of hospitalized patients had CD4 counts below 200 cells per cubic millimeter, and that fewer than three in ten were on antiretroviral therapy, points to failures upstream of the hospital door: missed opportunities for earlier testing, gaps in linkage to care, and interruptions in treatment continuity. The authors argue that their findings support greater attention to timely HIV diagnosis, sustained continuity of care, and systematic comorbidity assessment in this population. As antiretroviral therapy transforms HIV into a manageable chronic condition for people who are diagnosed early and treated consistently, studies like this one document what happens in the gap between that promise and its delivery, and they quantify, in hard numbers, the cost of arriving at the hospital too late.

Subject of Research: Hospitalization indications, clinical course, and in-hospital mortality among people living with HIV/AIDS

Article Title: Indications for hospitalization, clinical course, and mortality analysis among patients with HIV/AIDS in a tertiary care hospital: a 5-year retrospective study (2021–2025)

Article References: Tahmaz, A., Yildiz Dikmen, M., Ersari, S. S., Dinç, E., & Seyman, D. (2026). Indications for hospitalization, clinical course, and mortality analysis among patients with HIV/AIDS in a tertiary care hospital: a 5-year retrospective study (2021–2025). BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14560-4

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14560-4

Keywords: HIV, AIDS, hospitalization, in-hospital mortality, CD4 count, opportunistic infections, Pneumocystis jirovecii pneumonia, cytomegalovirus, antiretroviral therapy, late diagnosis, malignancy, retrospective study

A new retrospective cohort study from the Department of Organ Transplantation at The Second Affiliated Hospital of Guangzhou Medical University, published in BMC Infectious Diseases, addresses that question with unusually detailed infection phenotyping. The research team, led by Rongxin Chen and Jialin Wu, with Luhao Liu and Zheng Chen as corresponding authors, followed 228 SPK recipients and 98 diabetic recipients of kidney transplantation alone, or KTA, who underwent surgery between January 2019 and June 2025 at a single center. The primary endpoint was infection-related hospitalization within 12 months of transplant, a measure chosen because it captures infections severe enough to disrupt recovery, not merely laboratory findings. Secondary endpoints included bloodstream infection, infections at specific anatomical sites, reactivation of cytomegalovirus, Pneumocystis jirovecii pneumonia, and one-year patient and graft survival.

The headline finding is a statistically robust increase in infection-related hospitalizations after SPK. Recipients of the combined transplant experienced 0.54 hospitalization episodes for infection per person-year in the first 12 months, compared with 0.31 episodes per person-year among kidney-alone recipients, an incidence rate ratio of 1.76 with a 95 percent confidence interval of 1.22 to 2.57 and a p-value of 0.003. In plain terms, SPK patients were hospitalized for infection roughly three-quarters more often than their kidney-alone counterparts. When the analysis was refined with multivariable Cox regression, accounting for differences in baseline characteristics between the two groups, the association persisted: SPK performed with rabbit anti-thymocyte globulin induction remained significantly more likely to result in infection-related hospitalization than KTA performed with basiliximab induction, with an adjusted hazard ratio of 1.6 and a p-value of 0.04.

The pattern of infections differed strikingly between the two operations, and that pattern is where the biology becomes visible. Surgical-site and intra-abdominal infections dominated after SPK, affecting 18.9 percent of those recipients compared with just 3.1 percent of kidney-alone recipients, an odds ratio of 7.36. This is precisely what one would expect from a procedure that opens the peritoneal cavity, places an additional vascularized organ, and creates two sets of anastomoses where leaks and collections can occur. By contrast, pulmonary infections were more common after kidney transplantation alone, at 25.5 percent versus 7.9 percent after SPK. The authors also documented a dramatic difference in bloodstream infection: bacteremia occurred at a rate of 0.10 episodes per person-year after SPK versus 0.01 after KTA, an incidence rate ratio of 9.4, indicating that the abdominal surgical burden of the double transplant translates directly into a far higher risk of organisms entering the circulation.

Viral complications added a second layer of risk. Cytomegalovirus DNAemia, detected by polymerase chain reaction in the blood, developed in 53.5 percent of SPK recipients, meaning that more than half of the cohort experienced reactivation of this herpesvirus within the first year. Cytomegalovirus is a well-known driver of indirect effects in transplant recipients: it is immunomodulatory, impairing host defenses well beyond its own direct tissue damage, and prior literature has identified it as a dominant risk factor for Pneumocystis jirovecii pneumonia, a fungal infection that can be devastating in immunosuppressed patients. This study provided a striking confirmation of that relationship. In every affected SPK recipient, cytomegalovirus DNAemia preceded the development of Pneumocystis pneumonia, and the authors report that extending prophylaxis with trimethoprim-sulfamethoxazole after documented DNAemia was followed by no subsequent cases of the fungal infection in the cohort.

That final observation deserves emphasis because it points toward a practical intervention. The authors are careful to describe it as preliminary, since a single-center retrospective series cannot establish causation the way a randomized trial could, and the number of patients who progressed to Pneumocystis pneumonia is necessarily small. Even so, the temporal chain they observed, in which cytomegalovirus reactivation consistently preceded Pneumocystis infection and prolonged prophylaxis appeared to interrupt that chain, is exactly the kind of signal that prospective studies should test. If validated, monitoring for cytomegalovirus DNAemia could become a trigger for extending anti-pneumocystis coverage, a low-cost strategy that might spare high-risk patients a life-threatening complication.

The most reassuring part of the study is what the extra infections did not do. One-year patient survival was statistically indistinguishable between the groups, at 96.3 percent for SPK recipients and 95.0 percent for kidney-alone recipients, with a p-value of 0.32. This suggests that although the combined operation generates more infectious complications, those complications were largely treatable and did not, within the first year, claim additional lives. Better still, death-censored kidney graft survival was actually higher after SPK, at 98.8 percent versus 93.0 percent, a difference that reached statistical significance with a p-value of 0.04. Pancreas graft survival at one year was 94.2 percent. The combined transplant, in other words, delivered its expected metabolic and renal benefits while weathering its own infectious storm.

The methodological architecture of the study strengthens confidence in these findings. The investigators used Kaplan-Meier estimation to characterize time-to-event patterns, multivariable Cox regression to adjust for confounders, and, critically, a Fine-Gray competing-risk sensitivity analysis. The latter is a technical detail that matters: when patients die, they can no longer experience infection, and naive analyses can distort infection rates by treating death as ordinary censoring. The Fine-Gray model treats death as a competing event and confirms that the infection signal is not an artifact of different mortality patterns between the groups. The use of infection-related hospitalization as the primary endpoint also avoids the common pitfall of counting asymptomatic viral detections as infections, anchoring the analysis in events that carry real clinical and economic weight.

The study’s limitations follow naturally from its design. It was conducted at a single center in Guangzhou, China, so induction and maintenance immunosuppression regimens, antimicrobial prophylaxis protocols, and local epidemiology of multidrug-resistant organisms may not generalize everywhere. The retrospective design means the two groups were not randomized, and although multivariable adjustment mitigated measurable imbalances, unmeasured differences between patients selected for a major double operation and those receiving a kidney alone may persist. Importantly, the comparison of induction agents, rabbit anti-thymocyte globulin in the SPK group versus basiliximab in the kidney-alone group, means that part of the adjusted hazard ratio reflects differences in induction strategy as well as the operation itself, a confounding that the authors acknowledge implicitly through their phrasing of the adjusted comparison. Rabbit anti-thymocyte globulin is a lymphocyte-depleting agent associated with deeper and more prolonged immunosuppression, which plausibly contributes to the infection excess.

For clinicians and patients weighing these two operations, the message is nuanced rather than alarming. The double transplant carries a real and quantifiable early infectious price, concentrated in surgical-site and intra-abdominal infections, bacteremia, and cytomegalovirus reactivation, roughly 76 percent more infection-related hospitalizations in the first year. But that price did not purchase worse outcomes; survival was equivalent and kidney graft survival was better, while the pancreas graft offered insulin independence for the vast majority of recipients. The practical implications are twofold: centers performing SPK should expect and surveil for the specific infection profile documented here, and the apparent protective effect of extending Pneumocystis prophylaxis after cytomegalovirus DNAemia is a hypothesis worth testing prospectively. As SPK volumes grow worldwide and donor organs remain scarce, studies like this one, which quantify the trade-offs rather than assume them, are what allow patients and their surgeons to make that choice with open eyes.

Subject of Research: Infection outcomes in the first year after simultaneous pancreas-kidney transplantation compared with kidney transplantation alone in diabetic recipients

Article Title: One-year infection outcomes in simultaneous pancreas-kidney versus kidney transplantation alone in diabetic recipients: a retrospective cohort study

Article References: One-year infection outcomes in simultaneous pancreas-kidney versus kidney transplantation alone in diabetic recipients: a retrospective cohort study. (n.d.). https://doi.org/10.1186/s12879-026-14532-8

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14532-8

Keywords: simultaneous pancreas-kidney transplantation, kidney transplantation, diabetes, organ transplantation, infection-related hospitalization, bacteremia, surgical site infection, cytomegalovirus, Pneumocystis jirovecii pneumonia, immunosuppression, graft survival, retrospective cohort study