Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. Hematologic malignancies are known precipitants of disseminated intravascular coagulation (DIC), and the coexistence of these conditions is associated with poor outcomes; however, large-scale data specifically examining concurrent DLBCL and DIC are limited. We performed a retrospective cohort study using the National Inpatient Sample (NIS) to evaluate in-hospital mortality among adult hospitalizations with DIC and/or DLBCL identified using ICD-10 codes. Adults aged ≥ 18 years with a diagnosis of DLBCL and/or DIC were included. In-hospital mortality among patients with concurrent DLBCL and DIC was 54.1%, significantly higher than mortality observed in patients with either condition alone (p < 0.001). In multivariable analysis restricted to patients with both DLBCL and DIC, independent predictors of increased mortality included HIV/AIDS (aOR 4.266, 95% CI: 1.886-9.649; p < 0.001), septic shock (aOR 3.201, 95% CI: 2.305-4.443; p < 0.001), mechanical ventilation (aOR 2.948, 95% CI: 2.175-3.995; p < 0.001), vasopressor use (aOR 2.759, 95% CI: 1.789-4.255; p < 0.001), chronic kidney disease (aOR 2.523, 95% CI: 1.596-3.989; p < 0.001), acute kidney injury (aOR 1.884, 95% CI: 1.347-2.637; p < 0.001), Black race (aOR 2.221, 95% CI: 1.418-3.477; p < 0.001), and Asian or Pacific Islander race (aOR 2.383, 95% CI: 1.329-4.271; p = 0.004) compared to White patients. Bleeding events, thromboembolic complications, stem cell transplantation, and CAR-T therapy were not independently associated with mortality. These findings demonstrate that among patients with DLBCL, the development of DIC is associated with markedly elevated in-hospital mortality, driven predominantly by critical illness, organ dysfunction, and comorbidity burden rather than bleeding or thrombosis alone. Racial disparities in outcomes were independently observed after adjusting for illness severity and comorbidities, warranting further investigation. Early recognition of DIC in patients with DLBCL and aggressive management of systemic complications, particularly septic shock, respiratory failure, and renal dysfunction, may help mitigate disease severity and improve outcomes.

Renal disease in people living with HIV extends beyond classical HIV-associated nephropathy to include immune-mediated and vasculitic lesions, of which pauci-immune crescentic glomerulonephritis is among the rarest and most easily missed. We describe two biopsy-proven cases with anti-myeloperoxidase anti-neutrophil cytoplasmic antibody positivity. The first, established on antiretroviral therapy, presented with a pulmonary-renal syndrome after empirical anti-tubercular treatment had failed; biopsy showed cellular crescents without chronic change, and corticosteroids with rituximab achieved sustained clinical, biochemical and serological remission. The second, antiretroviral-naive, had glomerular haematuria and proteinuria documented at HIV diagnosis and an ischaemic stroke soon afterwards, but declined nephrological assessment; biopsy 3 years later was dominated by global glomerulosclerosis and interstitial fibrosis and he remained dialysis-dependent. The divergence turned on the histological stage at diagnosis rather than antiretroviral status and argues for early biopsy whenever unexplained renal decline with an active urinary sediment occurs in HIV.

Introduction. End-stage renal disease exhibits a disproportionate prevalence among Black individuals and older adults within the United States and worldwide. A significant genetic contributor to this disparity is the Apolipoprotein L1 (APOL1) gene, found exclusively in populations of African ancestry. Materials and Method. We aim to perform a narrative review regarding the current understanding of APOL1 and its complex role in kidney disease pathogenesis. Results. The G1 and G2 APOL1 risk alleles are strongly associated with an elevated risk for non-diabetic chronic kidney disease (CKD), including hypertensive nephropathy, focal segmental glomerulosclerosis, and HIV-associated nephropathy, in individuals who are homozygous or compound heterozygous for these variants. While 10-15% of African Americans carry two APOL1 risk alleles, approximately 80% remain disease-free, suggesting incomplete penetrance and the involvement of additional risk factors. In this condition, renal damage could be induced through different mechanisms such as altered cellular ion transport, mitochondrial dysfunction, and the requirement for additional stressors or "second hits". Conclusion. The increased susceptibility to end-stage renal disease (ESRD) in individuals of African ancestry is influenced by variations in the APOL1 gene.

BACKGROUND: Globally, AIDS-related opportunistic infections complicated by multiple organ dysfunction syndrome (MODS) are associated with high mortality and are difficult to treat. This article summarizes the resuscitation experience of a patient with AIDS-related opportunistic infections-induced multiple MODS and explores the multidisciplinary collaborative treatment strategies. METHODS: A retrospective analysis was conducted on a 37-year-old female patient withImmune Deficiency Syndrome (AIDS) who was admitted to the hospital due to “oliguria for 2 months and fever accompanied by dyspnea for 4 days”. She had a 10-year history of HIV infection without regular antiretroviral therapy. Complications such as renal failure, Co-infection of the lungs, respiratory failure, heart failure, liver injury, and cardiac arrest occurred. Multidisciplinary collaboration was carried out to promptly initiate comprehensive treatments including advanced life support and targeted anti-infection therapy. Rapid initiation of Antiretroviral Therapy (Rapid ART) was started after the patient’s condition stabilized. RESULTS: After 2 months of comprehensive treatment, the patient regained consciousness, was weaned off the ventilator, and showed improvement in liver and kidney functions and inflammatory markers, achieving clinical cure. CONCLUSION: Early recognition, strong advanced life support, targeted anti-infection therapy, and timely initiation of Rapid ART are the keys to the successful treatment of MODS caused by AIDS-related opportunistic infections. It suggests that for patients with AIDS-related opportunistic infections complicated by multiple organ failure, active comprehensive treatment can still lead to a good prognosis.

INTRODUCTION: Crystal-induced acute kidney injury (AKI) is caused by the intratubular precipitation of crystals, which results in obstruction. Crystal-induced AKI mostly occurs as a result of acute uric acid nephropathy and following the administration of drugs or toxins that are poorly soluble. CASE DESCRIPTION: A 23-year-old man presented with AIDS and 1 week history of right sided weakness. Brain MRI showed bilateral ring enhancing lesions. Patient was empirically started on pyrimethamine, sulfadiazine and leucovorin. Brain biopsy confirmed the diagnosis of toxoplasmosis. Hospital course was complicated by AKI and labs showed serum creatinine 2.0 mg/dL (baseline 0.8 mg/dL). Urinalysis showed no hematuria or pyuria with urine pH of 6. Examination of urine sediments under polarized light revealed multiple yellow brown asymmetric rosette shaped crystals (sulfonamide crystals). Sulfadiazine was discontinued and patient was switched to clindamycin. Patient was treated with IV fluids (sodium bicarbonate) for urinary alkalinization. The patient’s serum creatinine returned to baseline within 8 days. DISCUSSION: Sulfadiazine induced crystalluria is a serious complication in patients with AIDS who are treated for toxoplasmosis. Predisposing factors include high dose of sulfadiazine and volume depletion. It usually presents with AKI within 3 weeks of starting the medication. Treatment requires stopping the offending agent, aggressive IV hydration (urine output at least 1.5 L/day) and bicarbonate infusion for urinary alkalinization (goal pH > 7). CONCLUSION: This case highlights sulfadiazine-induced crystal nephropathy as a reversible cause of AKI. Early drug withdrawal, aggressive hydration, and urinary alkalinization are crucial for recovery. Preventive measures, especially hydration and urine pH monitoring, can significantly reduce risk.

BackgroundChronic kidney disease (CKD) is a frequent non-communicable complication in people living with HIV (PLHIV), influenced by antiretroviral therapy (ART), comorbidities, and healthcare setting. The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) CKD risk score is widely applied internationally, while the Thai CKD risk score, developed for the general Thai population, has not been validated in HIV cohorts. This study compared the predictive accuracy of the DAD models and the Thai CKD risk score in Thai people living with HIV receiving ART.MethodsA retrospective cohort analysis was conducted using electronic medical records of adults (≥18 years) living with HIV at Warinchamrap Hospital between January 2020 and May 2024. Patients with pre-existing CKD or incomplete data were excluded. CKD was defined per Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Model calibration was assessed with the Hosmer-Lemeshow test, and discrimination with the C-statistic.ResultsAmong 901 PLHIV receiving ART, 104 (11.5%) developed incident CKD during a median follow-up of approximately 4 years. Patients who developed CKD were more likely to be male and have a lower baseline estimated glomerular filtration rate, and higher prevalence of proteinuria and comorbidities. All evaluated models stratified CKD risk; however, the full and short DAD scores showed moderate discrimination (C-statistics ≈0.76) with evidence of risk underestimation and suboptimal calibration. The Thai CKD risk score demonstrated higher discrimination (C-statistic 0.93), sensitivity (88.5%), and better calibration in this cohort.ConclusionsIn this Thai HIV cohort, all evaluated risk models provided CKD risk stratification, but the Thai CKD risk score showed more reliable discrimination and calibration than the DAD models. These findings highlight the importance of population-specific validation when applying CKD risk prediction tools in HIV care.

Biktarvy, a once-daily combination of bictegravir, emtricitabine, and tenofovir alafenamide (TAF), is a highly effective antiretroviral therapy for HIV management. Although well-tolerated, rare but serious complications such as lactic acidosis can occur, particularly in patients on nucleoside reverse transcriptase inhibitors. We present the case of a 36-year-old male with HIV/AIDS and chronic kidney disease, who was admitted with altered mental status and acute hypoxic respiratory failure. Imaging confirmed atypical pneumonia. Initial labs revealed elevated lactate and creatinine. He was treated with broad-spectrum antibiotics, and after clinical improvement, Biktarvy was resumed. Within 24 h, his lactate spiked to 21.8 mmol/L. Suspecting TAF-induced lactic acidosis, Biktarvy was discontinued. Continuous renal replacement therapy, along with L-carnitine and thiamine, was initiated based on a literature review. The patient's condition improved significantly. Upon discharge, lactate and creatinine returned to baseline. At outpatient follow-up, he remained clinically stable on Dolutegravir-Rilpivirine and Entecavir.