Hypomagnesaemia, a common complication ranging from 20% to over 90%, depending on the diagnostic criteria and population studied, significantly contributes to adverse outcomes, including new-onset diabetes after transplantation, cardiovascular complications, neurological dysfunction and increased infection risk. A total serum magnesium below 0.70 mmol/L is commonly used to define deficiency. In kidney transplant recipients, calcineurin inhibitors downregulate TRPM6 in the distal nephron, leading to early and persistent hypomagnesaemia with links to adverse metabolic and cardiovascular outcomes. Arrhythmia risk rises steeply at total magnesium of <0.50 mmol/L, while neuromuscular irritability and neuropsychiatric symptoms may appear at levels below 0.70 mmol/L. Severe manifestations, such as seizures or tetany, usually occur at ≤0.50 mmol/L and coma at <0.30 mmol/L. Normal ionised magnesium is typically ~0.48–0.65 mmol/L; transplant-specific intervention thresholds remain unvalidated. This narrative review addresses critical diagnostic gaps and explores emerging therapeutic strategies. It highlights three areas: the diagnostic accuracy of ionised magnesium over total magnesium, the critical role of pharmacogenomics in individualising immunosuppression to mitigate tacrolimus-induced hypomagnesaemia and the promising link between gut microbiome modulation and magnesium homeostasis. The implications of these insights are profound: enabling more precise diagnosis and personalised management, reducing the incidence and severity of hypomagnesaemia-related complications, and ultimately supporting more precise diagnosis and personalised management; prospective validation in transplant cohorts is required before outcome claims can be made. This review exposes current diagnostic and therapeutic limitations, advocating for more precise and personalised strategies to address this critical electrolyte imbalance. Identifying hypomagnesaemia as a mechanistically complex and clinically undertreated complication, this review proposes a thematic roadmap that serves as a scientific and clinical framework for advancing personalised electrolyte care in renal transplantation. It is emphasised that while these approaches appear promising, most remain under-evaluated or hypothesis-generating. Addressing hypomagnesaemia through validated thresholds, new research is required to test novel diagnostics and personalised strategies to improve patient and graft outcomes.

Background: Uraemic cardiomyopathy (UCM), the cardiac manifestation of chronic kidney disease, represents a significant clinical challenge that is often underdiagnosed despite being one of the strongest predictors of mortality in the chronic kidney disease (CKD) population. It develops through pathophysiological mechanisms unique to the uraemic state—left ventricular hypertrophy, myocardial fibrosis, and diastolic dysfunction—that often progress silently, sometimes even without traditional cardiovascular risk factors. Purpose: This review synthesises nephrology-centric mechanisms with clinical phenotypes and contemporary imaging (including CMR T1/T2 mapping and ECV), and proposes a CKD-stage–tailored diagnostic–therapeutic framework. It offers a distinct perspective by integrating the complex pathophysiology of UCM with practical diagnostic approaches and evolving management strategies, differentiating it from prior cardiology-focused overviews. Methods: A comprehensive literature search was conducted across Ovid MEDLINE, Embase, PubMed, Google Scholar, BMJ Best Practice, and UpToDate for studies published up to March 2025. Key findings were extracted from the final evidence set and manually verified for relevance. This review introduces a patho-mechanical cascade model of uraemic cardiomyopathy, integrating toxin-driven, metabolic, and haemodynamic axes. Nephrology-led screening protocols are proposed, leveraging proteomics and strain echo, and advocate mineralocorticoid receptor antagonists with sodium–glucose co-transporter-2 (SGLT2) inhibitor initiation at CKD Stage 3a. Cardiorenal clinics are essential for improved outcomes. Key Insights: UCM develops from a multifactorial process. This involves neurohormonal activation, oxidative stress, chronic inflammation, and exposure to toxins such as indoxyl sulfate and p-cresyl sulfate, arising from uraemia. Diagnosis is challenging, masked by overlapping features of fluid overload and anaemia. SGLT2 inhibitors, non-steroidal mineralocorticoid antagonists, and renin–angiotensin–aldosterone system modulation offer promising interventions. The effect of the dialysis modality, its timing, and renal transplantation on cardiac remodelling also emerging from recent studies. Conclusions: UCM sits at the intersection of two failing organ systems. Managing it effectively requires a paradigm shift to incorporate pharmacological and early diagnostic interventions and the integration of cardiology and nephrology care, and the timely implementation of interventions.

The case is presented of an elderly patient (DCP) with extensive medical history, including osteoporosis, who developed hypocalcaemia and hypophosphataemia whilst treated with denosumab, while prescribed concomitant calcium and vitamin D therapies. The management of this complex case involved a multidisciplinary team (MDT) approach, incorporating the patient’s wishes. It included discontinuation of denosumab and intravenous (IV) and oral mineral supplementation that yielded gradual amelioration of calcium and phosphate levels. This case demonstrates the importance of vigilant monitoring and appropriate management in patients receiving denosumab, particularly those with multiple comorbidities. It carries important considerations for using denosumab for osteoporosis treatment in patients with complex medical backgrounds. Ethical clearance waiver was granted by the Trust Research Ethics Committee on 18/01/2024.

Anaphylaxis is a severe, potentially life-threatening allergic reaction that requires urgent and effective management. The UK Resuscitation Council updated its advanced life support (ALS) guidelines for anaphylaxis in 2021, emphasising early and repeated adrenaline administration, intravenous (IV) fluid use, and reduced reliance on antihistamines and steroids. A retrospective audit was carried out to compare the management of anaphylaxis at two English NHS hospitals, namely the University Hospital of North Midlands (UHNM) and the Shrewsbury and Telford Hospital (SATH), before (2018) and after (2022/23) the ALS guideline implementation. Adherence to NICE anaphylaxis guidance was also assessed. Data from 272 patients revealed significant improvements in recognition of anaphylaxis in 2022 compared with 2018 (70.8% vs. 50%; p=0.001). The use of adrenaline and IV fluids increased, whereas the use of antihistamines and steroids declined, aligning with the new guidance. Tryptase measurement (checked in 45% of patients) and specialist referral rates (67% at UHNM vs. 3% at SATH; p=0.0001) remained suboptimal at both centres. A case example highlights the risks of misdiagnosis and adrenaline overuse in patients with recurrent urticarial presentations. Anaphylaxis management in these centres has changed in keeping with the new ALS guidelines, although antihistamines and steroids were still used in the acute management of around 50% of the patients. Adrenaline overuse may be an unintended consequence of the guideline, which needs monitoring. There may have been some improvement in anaphylaxis recognition, but serum tryptase measurement and referral to allergy specialists remain poor.

Background: Diabetic ketoacidosis (DKA) in patients with kidney failure receiving dialysis presents a formidable clinical challenge. Standard DKA protocols, designed for patients with preserved renal function, often fail in this cohort and can be unsafe when applied without modification. Patients are at risk of iatrogenic fluid overload, dyskalaemia, and hypoglycaemia due to altered insulin kinetics, impaired gluconeogenesis, and the absence of osmotic diuresis. Purpose: This narrative review aims to synthesise current understanding of DKA pathophysiology in dialysis patients, delineate distinct clinical phenotypes, and propose individualised management strategies grounded in physiology-based reasoning, comparative guideline insights, and consensus-supported literature. Methods: We searched PubMed/MEDLINE, Embase, and Google Scholar (January 2004–June 2024) for adult dialysis populations, using terms spanning DKA, kidney failure, insulin kinetics, fluid balance, and cerebral oedema. Reviews, observational cohorts, guidelines, consensus statements, and physiology papers were prioritised; case reports were used selectively for illustration. Evidence was weighted by physiological plausibility and practice relevance. Nephrology-led authors aimed for a pragmatic, safety-first synthesis, seeking and integrating contradictory recommendations. Conclusions: Our findings highlight the critical need for a nuanced approach to fluid management, a tailored insulin strategy that accounts for glucose-insulin decoupling and prolonged insulin half-life, and careful consideration of potassium and acidosis correction. We emphasise the importance of recognising specific volume phenotypes (hypovolaemic, euvolaemic, hypervolaemic) to guide fluid therapy, and advocating the judicious use of variable-rate insulin infusions (‘dry insulin’) to mitigate fluid overload. We also show that service-level factors are critical. Dialysis-specific pathways, interdisciplinary training, and quality improvement metrics can reduce iatrogenic harm. By linking physiology with workflow adaptations, this review provides a physiologically sound, bedside-oriented map for navigating this complex emergency safely and effectively. In doing so, it advances an individualised model of DKA care for dialysis-dependent patients.

Background: Hyponatraemia is a rare but potentially life-threatening complication of terlipressin therapy. Case history: In the current case, a 39-year-old female with decompensated liver cirrhosis (Child-Pugh C) and acute variceal bleeding experienced a precipitous decline in serum sodium—from 136 mmol/L to 115 mmol/L—within 48 h of initiating terlipressin therapy. This was accompanied by marked fluid retention, reduced urine output, and symptoms of confusion and agitation. Laboratory tests confirmed dilutional hyponatraemia, characterized by urinary sodium <20 mmol/L and urine osmolality <100 mOsm/kg, indicating excessive free water reabsorption. Outcomes: The prompt discontinuation of terlipressin, fluid restriction and the cautious administration of hypertonic sodium chloride solution (2.7% NaCl) achieved a gradual normalization of sodium levels and resolution of symptoms. Fluid balance monitoring revealed a marked diuretic response following terlipressin cessation. This case aligns with existing reports, emphasizing the dual vasopressin receptor activity of terlipressin and its capacity to induce hyponatraemia, particularly in cirrhotic patients with preserved renal function and higher baseline sodium levels. Conclusions: This case and a literature review underscored the critical need for early fluid balance monitoring to detect retention. This case highlights the importance of individualized risk assessment, multidisciplinary management, and vigilant sodium correction to avoid complications. Practical recommendations are outlined to aid clinicians in the recognition and management of terlipressin-induced hyponatraemia.