Testosterone therapy increases lean mass and can improve muscle strength in men with hypogonadism. This review examines the relationship between testosterone therapy, tendon adaptation, and tendon injury, including the possibility of a mismatch between changes in muscle strength and tendon capacity. This narrative review critically evaluates the clinical and experimental evidence relating testosterone exposure to tendon injury. The present review focuses specifically on tendon-related safety and is not intended to assess the overall benefit-risk profile of testosterone therapy. Prescription-based studies have identified associations with distal biceps, rotator cuff, quadriceps, patellar, and Achilles tendon injuries. The magnitude of association varies considerably, with modest elevations in broad analyses and larger relative estimates in some site-specific studies. Absolute event rates are generally low, and the available studies cannot establish causation. Important limitations include incomplete information about treatment indications, testosterone concentrations, dosage, adherence, formulation, physical activity, pre-existing tendinopathy, and undisclosed anabolic-androgenic steroid use. Evidence from supraphysiologic androgen exposure provides greater biological plausibility but cannot be directly extrapolated to physiologic testosterone replacement. Potential biological mechanisms involving collagen synthesis, matrix remodelling, and tendon mechanical properties are also examined. No clinical evidence establishes a dose-response relationship or demonstrates that topical treatment, smaller injections, or more frequent dosing reduces tendon risk. Testosterone improves bone mineral density and estimated bone strength, but fracture prevention has not been demonstrated. Overall, a small increase in tendon injury risk with testosterone therapy is plausible, particularly in highly active individuals undergoing rapid increases in loading, but the evidence remains observational and substantially confounded. Clinicians should provide proportionate counselling without discouraging appropriately indicated treatment.

Thyrotoxic periodic paralysis (TPP) is a rare but life-threatening cause of acute flaccid paralysis associated with hypokalemia. Although more common in males and individuals of Asian descent, it may present atypically in young females and be easily misdiagnosed. We report a case of a 30-year-old female who presented with acute quadriparesis. Extensive neuromuscular evaluation initially pointed toward Guillain-Barré syndrome (GBS), but subsequent investigations revealed profound hypokalemia. Further workup confirmed thyrotoxicosis as the underlying cause. Prompt potassium replacement and initiation of antithyroid therapy led to complete clinical recovery. This case highlights the importance of considering both endocrine disorders and electrolyte disturbances, such as hypokalemia, in the differential diagnosis of acute paralysis.

Acute liver failure (ALF) due to hepatitis A virus (HAV) can lead to multi-organ dysfunction with a high mortality. Extracorporeal therapies like therapeutic plasma exchange (TPE) and continuous renal replacement therapy (CRRT) often have a central role in the management of ALF. Thirteen patients admitted with HAV-related ALF between August 2024 and July 2025 were included in the study. All patients underwent standard-volume TPE (SV-TPE) followed by continuous veno-venous haemodiafiltration (CVVHDF) with an effluent dose target of 45 mL/kg/hour. Nine patients (69.2%) had hyperacute liver failure, and four (30.7%) had ALF. Seven patients met the King's College criteria for liver transplantation. The median number of TPE sessions was one. The median duration and dose of CRRT were 76 hours and 44 mL/kg/hour, respectively. There was sustained improvement in serum bilirubin, lactate, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels with the offered treatment. The mean serum ammonia also reduced from 336.68 to 205.91 μmol/L after TPE, and to 123.81, 95.94, and 87.43 μmol/L after 24, 48, and 72 hours of CRRT, respectively. The mean duration of mechanical ventilation was 3.7 days. The mean ICU length of stay was 7.1 days, and the mean hospital length of stay was 13.5 days. Six patients had secondary infections. None of the patients needed liver transplantation at 21 days. The ICU-, in-hospital-, and 28-day mortality was zero; however, three patients were found to have hyperbilirubinemia at 28 days. SV-TPE followed by high-dose CRRT could significantly improve transplant-free survival in HAV-related ALF.

A man in his 50s with long-standing learning difficulties and schizophrenia currently treated with clozapine presented with gynaecomastia and a new right testicular mass. He was noted to have a severe tremor interfering with activities of daily living treated with combination levodopa + benserazide, primidone and topiramate. Investigations revealed elevated prolactin, gonadotropins, sex hormone binding globulin, total testosterone and oestradiol. Right orchidectomy revealed Leydig cell hyperplasia. Karyotyping diagnosed Klinefelter syndrome. Testosterone replacement therapy (TRT) was commenced, with subsequent marked improvement in his debilitating tremor. Tremor is a potentially disabling complication of Klinefelter syndrome with fewer than 50 cases reported in the literature. The pathophysiology of tremor in Klinefelter syndrome is unclear. Tremor in Klinefelter syndrome is often refractory to anti-tremor medical therapy; however, as reported in this case, testosterone therapy may improve tremor in Klinefelter syndrome. It is rare for TRT to significantly improve tremor as reported in this case.

Transcatheter aortic valve replacement has become an established therapy for severe aortic stenosis across the surgical-risk spectrum. Although procedural safety has improved, transcatheter valve embolization or migration remains an uncommon but high-impact complication that may require immediate rescue under conditions of severe acute aortic regurgitation, hemodynamic instability, coronary compromise, or branch-vessel risk. Existing evidence is derived primarily from registries, observational cohorts, technical reviews, systematic reviews, and case-based reports rather than prospective comparative trials. Building on prior descriptions of device-embolization mechanisms and location-based management, this review synthesizes contemporary evidence into an operator-oriented phenotype-based framework. We classify transcatheter valve embolization or migration into left ventricular/left ventricular outflow tract migration, annular malposition with instability, ascending aortic embolization, distal aortic embolization, and delayed migration, while emphasizing that these phenotypes may overlap or evolve during the procedure. For each phenotype, we summarize reported mechanisms, platform-specific considerations, hemodynamic hazards, and commonly described bailout strategies. Because comparative data are lacking, the proposed framework should be interpreted as an evidence-informed practical decision aid rather than recommendation-level guidance. Standardized reporting and contemporary multicenter data are needed to refine risk prediction, define procedural success, and validate phenotype-specific rescue pathways.

For individuals who are partially edentulous, fixed dental prostheses (FDPs), such as single crowns and fixed partial dentures, are crucial for restoring function, aesthetics, and structural continuity. Accurate marginal and internal fit are crucial for the long-term success of these restorations because inconsistencies can lead to cement disintegration, plaque buildup, microleakage, secondary caries, periodontal breakdown, and pulpal irritation. These issues can eventually lead to restorative failure, which can include loss of retention or debonding of the restoration, fracture or chipping of the restoration or supporting tooth structure, recurrent infection necessitating restoration replacement, and, in extreme circumstances, the need for more involved procedures like endodontic therapy or tooth extraction. From a therapeutically relevant prosthodontic standpoint, this narrative review sought to assess how alloy composition and fabrication methods affected the marginal and internal fit of FDPs. Databases like PubMed, Medical Literature Analysis and Retrieval System Online (MEDLINE), and EBSCOhost were used to search the literature for English-language research published between 1990 and 2025. Included were pertinent comparative studies, randomized and non-randomized trials, observational studies, validation studies, in vitro investigations, and review articles assessing titanium, nickel-chromium (Ni-Cr), and cobalt-chromium (Co-Cr) alloys made using direct metal laser sintering (DMLS) and conventional casting methods. According to the examined data, titanium alloys often exhibit less predictable marginal adaptation than Co-Cr and Ni-Cr alloys. Due to numerous technique-sensitive laboratory procedures, conventional lost-wax casting techniques demonstrated higher variability but produced clinically acceptable results. On the other hand, while internal fit varied based on workflow factors and post-processing procedures, available literature suggests that, especially DMLS and additive manufacturing techniques, may improve reproducibility and marginal accuracy in numerous tests. Clinically, better internal and marginal adaptation may eliminate chairside adjustments, increase the durability of restorations, and lessen biological problems. Overall, rather than being the product of a single material or fabrication method, restoration fit should be viewed as the consequence of an integrated interplay between alloy composition, fabrication workflow, and laboratory precision.

In this editorial, we comment on the study by Puri et al published in the World Journal of Nephrology, which highlights a neglected gap in preventive care at dialysis initiation: Inadequate protection against vaccine-preventable and endemic infections in advanced chronic kidney disease. In an incident hemodialysis cohort from a tertiary centre in North India, the authors report major deficiencies in adult vaccination against hepatitis B virus, pneumococcus, and influenza at dialysis entry, with more than half of patients having received none of the recommended immunizations. Concurrently, a substantial burden of tuberculosis - predominantly extrapulmonary - was observed, underscoring a dual infectious vulnerability at the outset of renal replacement therapy in endemic, resource-constrained settings. Importantly, vaccination uptake aligned with markers of health-system engagement rather than patient characteristics or presumed biological limitations: Prior nephrology follow-up and structured pre-transplant evaluation were associated with higher vaccination rates and indicators of anticipatory care, including permanent vascular access. These findings suggest that impaired immunogenicity may not be the sole barrier to vaccination in advanced kidney disease and are consistent with an association between delayed referral, fragmented care pathways, and avoidable infectious risk. Although limited by its single-centre, cross-sectional design, this study supports viewing dialysis initiation as a sentinel checkpoint for infection prevention. We argue for integrating vaccination assessment, delivery, serologic monitoring, and tuberculosis screening into pre-dialysis and dialysis-start workflows to operationalize preventive nephrology in routine practice.

Alcohol-associated lactic acidosis (AALA) is a rare but potentially life-threatening complication of acute or chronic alcohol exposure. Severe hyperlactataemia attributed primarily to alcohol is uncommon and should prompt careful evaluation for alternative or co-existing causes, including sepsis, hypoperfusion, toxic ingestion, seizures and ischaemia. We report the case of a 42-year-old man who presented to the emergency department with generalised malaise and vomiting following one week of heavy alcohol consumption involving whisky and beer. He had a history of recurrent hospital admissions related to alcohol intoxication but no significant documented medical comorbidities. Initial venous blood gas analysis revealed profound high anion gap metabolic acidosis, with a pH of 6.86, bicarbonate of 5.9 mmol/L, anion gap of 40 mmol/L, and lactate greater than 20 mmol/L. Serum ethanol concentration was elevated at 297 mg/dL, and blood ketones were markedly elevated at 6.5 mmol/L. Initial investigations showed mild leucocytosis, a normal C-reactive protein level, mildly elevated serum creatinine with preserved estimated glomerular filtration rate, and transaminitis with aspartate transaminase predominance. Paracetamol and salicylate levels were negative, methanol was within the laboratory reference range, and contrast-enhanced computed tomography of the chest, abdomen, and pelvis did not identify an infective, ischaemic, or intra-abdominal cause. The patient was admitted to the intensive care unit and managed supportively with intravenous fluids, intravenous thiamine supplementation, and close biochemical monitoring. He showed rapid clinical and metabolic improvement, with lactate decreasing to 4.6 mmol/L by 10 hours and normalising by 16 hours. He remained stable without vasopressor support, ventilatory support, or renal replacement therapy and was discharged home on day four. This case highlights the importance of considering AALA with concomitant ketoacidosis in patients with severe high anion gap metabolic acidosis and significant alcohol exposure. Early recognition, systematic evaluation for life-threatening alternative diagnoses, and supportive treatment with fluid resuscitation and thiamine replacement may be associated with rapid clinical and biochemical recovery.

Kidney transplantation is the preferred kidney replacement therapy for eligible patients with kidney failure; however, early allograft function remains vulnerable to potentially modifiable events across the perioperative continuum. Delayed graft function (DGF), hemodynamic instability, electrolyte and acid-base disturbances, vascular compromise, and surgical complications can adversely affect early recovery, prolong hospitalization, and influence subsequent graft outcomes. This narrative review summarizes evidence-based perioperative strategies designed to reduce preventable contributors to DGF and optimize early kidney allograft function, spanning recipient preparation before surgery, intraoperative anesthetic and surgical management, and structured surveillance during the immediate postoperative period. Preoperative optimization includes assessment of cardiovascular reserve, volume status, frailty, anemia, electrolyte and acid-base abnormalities, timing of dialysis, anticoagulant and antiplatelet therapy, and immunologic risk, including crossmatch and donor-specific antibody status. Donor and graft-related determinants, particularly deceased-donor status, ischemia times, donation after circulatory death, and donor quality, should be integrated into perioperative risk stratification and monitoring intensity. During transplantation, avoidance of sustained hypotension, individualized fluid administration, use of balanced crystalloids where appropriate, early vasopressor support for vasodilatory hypotension, temperature and glucose control, and proactive management of hyperkalemia and metabolic acidosis are central to perfusion protection. Reperfusion should be treated as a critical diagnostic interval requiring prompt assessment for arterial or venous thrombosis, graft malposition, anastomotic compromise, and inadequate perfusion. Immediate postoperative care should incorporate structured handoff, serial assessment of urine output and biochemical parameters, early Doppler ultrasonography when graft dysfunction is suspected, and timely differentiation of DGF from reversible vascular, urological, or hemodynamic complications. Enhanced Recovery After Surgery pathways may facilitate consistent multidisciplinary communication, early mobilization, analgesic optimization, and protocolized escalation. The ultimate clinical goal of this coordinated, risk-adapted perioperative strategy is to reduce preventable DGF, accelerate recognition of reversible complications, and support early allograft recovery.

Kidney failure is a common complication in recipients of nonkidney solid organ transplants (NKSOT), often stemming from prolonged calcineurin inhibitor (CNI) exposure or perioperative insults. Although haemodialysis (HD) remains the predominant renal replacement therapy (RRT), peritoneal dialysis (PD) offers advantages such as better quality of life, haemodynamic stability and preservation of residual renal function. Concerns about infection risk, technical feasibility and respiratory complications have curtailed its broader use. We present the first reported case of successful PD in a liver and double-lung transplant recipient. The patient, a 30-year-old male with cystic fibrosis, extensive abdominal surgery and immunosuppression, was initially deemed unsuitable for PD due to surgical complexity and potential complications in a transplant recipient. A multidisciplinary team (MDT) review at our liver and kidney transplant specialist centre ultimately supported PD based on clinical suitability and lifestyle preferences. Laparoscopic catheter insertion was achieved despite significant intra-abdominal adhesions, and the patient remained on PD for 18 months without complications. This case underscores that with meticulous surgical planning and MDT input, PD can be a safe and viable option in complex NKSOT recipients. It challenges prevailing biases against PD in this population and suggests that prior transplantation should not preclude its consideration.

Acute kidney injury (AKI) is a major cause of preventable morbidity and mortality worldwide, with a disproportionate burden in low-resource settings. In these regions, AKI is commonly community-acquired, affects younger patients, and is frequently related to sepsis, hypovolemia, obstetric complications, nephrotoxins, and infections. Kidney replacement therapy (KRT) is a cornerstone of supportive care for severe AKI, but its use is strongly shaped by local infrastructure, cost, workforce, and supply chains. Current evidence does not show consistent superiority of continuous KRT, intermittent hemodialysis (IHD), prolonged intermittent KRT, or peritoneal dialysis (PD) in broad AKI populations with respect to survival or kidney recovery. Accordingly, modality choice should be individualized according to patient characteristics and local feasibility. In many African and other low-resource settings, IHD and PD remain the dominant modalities because they are more accessible and scalable than continuous therapies. This review discusses how resource limitations shape AKI KRT practice, with emphasis on Africa, and outlines pragmatic strategies to improve equitable access to life-saving renal support.