AIM:In 2012, the Australian state of Victoria introduced a 6-monthly reportable renal quality indicator (QI) for the proportion of patient's waitlisted or pre-emptively transplanted by set time points after beginning kidney replacement therapy (KRT). This prospective cohort study aimed to determine if the QI influenced timeliness of transplant waitlisting for Victorians, compared to the rest of Australia as a control group. METHODS:Patients aged 18-70 commencing KRT between 2007 and 2020 were extracted from the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA) and divided into three time eras. The primary outcome was the percentage of patients waitlisted or transplanted at 6, 12 and 24 months from starting KRT. Given the systematic disadvantage reported, specific analysis was performed to examine the QI's effect on Aboriginal and Torres Strait Islander people living in Victoria. RESULTS:Of 25 836 (14.7% Indigenous) patients starting dialysis, one third (8587, 5.7% Indigenous) were listed for transplant. Following implementation of the QI, the proportion of Victorian patients waitlisted within 6, 12 and 24-months of starting KRT increased (adjusted OR [aOR] 1.85, 1.67 and 1.55 respectively; all p < 0.001). There was no significant change in Australian (non-Victorian) rates at 6 and 12 months but a small increase was observed at 24 months. CONCLUSION:Following introduction of the Victorian renal QI, the proportion of Victorian patients waitlisted at key timepoints improved more than patients in Australian states without QIs.
Ultrafiltration during hemodialysis is the most hemodynamically stressful intervention dialysis patients endure, yet its prescription relies on interdialytic weight gain and clinical gestalt. Rates exceeding 13 mL/kg/h carry substantially higher cardiovascular mortality, and recurrent intradialytic hypotension drives myocardial stunning, accelerated loss of residual kidney function, and progressive cardiac dysfunction. Existing volume management tools, including bioimpedance spectroscopy, relative blood volume monitoring, and even lung ultrasound, address fragments of this problem but none integrates the two questions that should govern every prescription: how much volume can be removed, and how fast? This review synthesizes principles from critical care hemodynamics and nephrology to propose an integrated ultrasound-guided framework. We apply the Frank-Starling relationship to volume removal, translating the principles of active fluid removal to maintenance hemodialysis. We approach the safety of fluid removal in terms of preload responsiveness: removal is best tolerated when the patient is preload-unresponsive, operating on the flat portion of the cardiac function curve. The framework uses a rapid screen (inferior vena cava diameter and lung ultrasound) to identify patients near dry weight versus those requiring further assessment. When congestion is present, a two-axis decision matrix combines venous congestion quantification (portal vein pulsatility) with preload dependence testing (passive leg raising with a stroke volume surrogate) to guide both volume target and removal rate. Preload responsiveness is defined by a rise of at least 10% to 12% in the left ventricular outflow tract velocity-time integral after passive leg raising, and significant venous congestion by an inferior vena cava diameter of 2 cm or greater with portal vein pulsatility; preload-unresponsive patients without congestion may tolerate rates toward the 13 mL/kg/h safety ceiling, whereas preload-responsive or severely congested patients warrant slower removal over extended or additional sessions. We propose a two-tiered protocol adaptable to diverse practice settings. This integrated framework has not been tested prospectively and should be regarded as hypothesis-generating; that said, the individual components are validated and the physiological rationale is sound, and the potential to reduce ultrafiltration-related morbidity, from intradialytic symptoms to myocardial stunning and residual function loss, is substantial.
BACKGROUND:While sex disparities in access to transplant have been shown in a number of countries, the ways additional measures of disadvantage, such as intersectional and clinical disadvantage, influence sex-based disparities is less well understood. Access to transplant by sex or intersectional disadvantage has not been studied in Australia. METHODS:We conducted a population-based cohort study of incident dialysis patients (2006-2023) using Australia & New Zealand Dialysis and Transplant Registry data. Cox proportional hazards models, interaction analyses and competing-risk approaches were used to evaluate associations between sex, waitlisting and deceased donor transplantation, adjusting for intersectional and clinical characteristics. RESULTS:Among 47 884 incident dialysis patients contributing 147 510 person-years of follow-up, females were 19% less likely to be waitlisted than males (aHR 0.81, 95% CI 0.77-0.84). Sex-based disparities were greatest among females with intersectional disadvantage, including ethnic minority status (Aboriginal & Torres Strait Islander: aHR 0.57, 95% CI 0.49-0.66), diabetic kidney disease (aHR 0.61, 95% CI 0.56-0.67), having ≥ 3 comorbidities (aHR 0.66, 95% CI 0.56-0.79) and obesity (aHR 0.69, 95% CI 0.65-0.75), compared to male peers. Once waitlisted, females and males had similar likelihood of deceased donor transplantation (aHR 1.04, 95% CI 0.99-1.10) and comparable waitlist mortality (aHR 0.91, 95% CI 0.76-1.08). CONCLUSIONS:Females in Australia experience substantially reduced access to the kidney transplant waitlist, with the greatest inequities affecting those facing overlapping social and/or clinical disadvantage. The absence of sex-disparity after waitlisting indicates that inequities arise earlier in the referral and evaluation pathway. Interventions to improve equity must target these upstream stages and address intersecting drivers of disadvantage.
AIM:To report a case of nephrogenic syndrome of inappropriate antidiuresis (NSIAD) caused by a de novo hemizygous hotspot variant (c.409C>T p.R137C) in the AVPR2 gene in a young male child, and to discuss the diagnostic approach, therapeutic management, and follow-up of NSIAD. METHODS:A 3-year and 2-month-old male child presenting with intermittent convulsions persisting for over one year and chronic hyponatremia was clinically evaluated. Genetic testing was performed to identify potential causative variants. Water restriction therapy was implemented, with the patient spontaneously limiting water intake to prevent infections and regulating fluid intake during illnesses. Follow-up evaluations were conducted at 3 and 6 months. RESULTS:Genetic testing identified a de novo hemizygous hotspot variant, c.409C>T (p.R137C), in the AVPR2 gene. The patient adhered to spontaneous water restriction and regulated fluid intake during illnesses. Follow-up evaluations at 3 and 6 months demonstrated normal serum sodium levels, with no recurrence of convulsions or other symptoms. CONCLUSION:NSIAD should be included in the differential diagnosis of hyponatremia of unknown etiology. Genetic testing is crucial for achieving an early diagnosis, optimizing treatment regimens, and enhancing treatment compliance. Water restriction therapy, under careful monitoring, remains a safe and effective treatment modality, particularly during periods of illness.
Fibronectin glomerulopathy (FNG) is a rare renal disorder characterized by excessive glomerular fibronectin deposition, often associated with variants in the fibronectin 1 (FN1) gene. Clinically, FNG presents with proteinuria, hematuria, and hypertension, and may progress to end-stage kidney disease. However, its long-term clinical course and optimal management remain incompletely defined. We report a sporadic case of FNG in a 26-year-old woman carrying an FN1 variant, c.2918A > G (NM_212482.4). Seventeen years after initial detection of proteinuria, she developed nephrotic syndrome with generalized edema. Supportive therapy, including renin-angiotensin system inhibitors and diuretics, was insufficient, and prednisolone and cyclosporine A were initiated for management of nephrotic syndrome. The patient subsequently achieved partial remission, with urinary protein decreasing to < 1 g/gCr and no major adverse events. During tapering of immunosuppression, a sodium-glucose cotransporter 2 (SGLT2) inhibitor was added as adjunct therapy. This case suggests a potential role for immunosuppressive therapy in management of late-onset nephrotic syndrome associated with FNG, with SGLT2 inhibition potentially contributing to maintenance of remission.
Nintedanib (NIB), a small-molecule tyrosine kinase inhibitor (TKI), is approved for idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease. Although nephrotoxicity is uncommon, cases of nephrotic syndrome (NS), acute kidney injury (AKI) and glomerular lesions including thrombotic microangiopathy (TMA) and anti-glomerular basement membrane (GBM) nephritis have been reported. However, the optimal management of NIB-associated glomerular disease remains undefined. We report a 69-year-old man with IPF, hypertension, diabetes and underlying chronic kidney disease who developed persistent NS and renal dysfunction 16 months after initiation of NIB. Kidney biopsy demonstrated glomerular endothelial injury with microangiopathic features, accompanied by secondary collapsing focal segmental glomerulosclerosis (FSGS) and background diabetic kidney disease. Despite discontinuation of NIB and intensification of renin-angiotensin system inhibition and mineralocorticoid receptor blockade, nephrotic-range proteinuria persisted. Subsequent initiation of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) dapagliflozin was temporally associated with a gradual and sustained reduction in proteinuria, with partial remission achieved while preserving the estimated glomerular filtration rate. To our knowledge, this is the first report of NIB-associated glomerular endothelial injury with secondary collapsing FSGS in which SGLT2i initiation was temporally associated with sustained proteinuria reduction under concomitant supportive therapy. TKIs may induce both endothelial and podocyte injury and therapeutic options beyond drug withdrawal remain limited. In this context, SGLT2 inhibition may represent a potential adjunctive therapeutic strategy in selected cases with underlying chronic kidney disease and warrants further systematic evaluation.
AIM:Nephrotic-range proteinuria in patients with Type 2 diabetes mellitus (T2DM) may result from diabetic nephropathy or non-diabetic glomerular disease (NDGD). Kidney biopsy risks and limited accessibility complicate patient selection. We aimed to identify predictors of NDGD and develop a score to guide biopsy decisions. METHODS:We conducted a single-center retrospective study of T2DM patients undergoing native kidney biopsy for nephrotic-range proteinuria at a tertiary hospital in Thailand between 2014 and 2022. Biopsy findings were classified according to the presence or absence of NDGD. Independent predictors were identified using multivariable logistic regression, and a weighted clinical prediction score was derived. Discrimination was evaluated using the area under the receiver operating characteristic curve (AUROC). RESULTS:Among 289 patients, 142 (49.1%) had NDGD with or without concomitant DN. The most frequent diagnosis was IgA nephropathy. Independent predictors of NDGD included older age, shorter duration of T2DM, absence of diabetic retinopathy, absence of prior hypertension, higher estimated glomerular filtration rate, and hematuria. Higher haemoglobin was retained in the prediction model despite its borderline statistical association. The prediction score demonstrated good discrimination (AUROC, 0.85; 95% confidence interval, 0.80-0.89). At a threshold of ≥ 3 points, the score had 96.5% sensitivity and 40.8% specificity, whereas a threshold of ≥ 7 points had 66.9% sensitivity and 84.4% specificity. CONCLUSION:NDGD is common among T2DM patients with nephrotic-range proteinuria. The proposed clinical prediction score showed good discrimination in this cohort but requires external validation before it can be used to support biopsy decision-making in clinical practice.
AIM:Rabbit anti-thymocyte globulin (rATG) is widely used for induction immunosuppression in kidney transplantation, but conventional dosing is largely weight based and may not reflect dynamic interindividual immune responses. We aimed to evaluate a predefined, individualized dosing strategy guided by peripheral CD4-to-total lymphocyte (CD4/TLC) and CD8-to-total lymphocyte (CD8/TLC) ratios and to assess its feasibility and 1-year outcomes. METHODS:In this single-center retrospective cohort study conducted in Taiwan from 2018 to 2024, 76 adult kidney transplant recipients received rATG titrated by serial flow cytometry to a predefined target of both CD4/TLC and CD8/TLC ratios < 10%. We evaluated cumulative rATG exposure, lymphocyte-subset response, for-cause biopsy-proven acute rejection (BPAR), graft function, graft loss, hospitalization-requiring infections, and mortality over 1 year. RESULTS:The median cumulative rATG dose was 1.2 mg/kg (IQR, 1.1-1.5; maximum, 3.8). Thirty-eight recipients (50.0%) reached the immunologic target after a single intraoperative dose (1-1.5 mg/kg). At 1 year, for-cause BPAR occurred in 1 recipient (1.3%), mean serum creatinine was 1.20 mg/dL, and no graft loss occurred. Seventeen recipients experienced hospitalization-requiring infections, accounting for 22 episodes. No CMV disease or biopsy-proven BK virus nephropathy was observed. Four recipients (5.3%) died, including two deaths related to opportunistic fungal infections. CONCLUSION:CD4/TLC- and CD8/TLC-guided rATG dosing was feasible and achieved predefined immunologic targets with low cumulative rATG exposure in this cohort. These findings support prospective controlled studies to evaluate the clinical utility, safety, and comparative effectiveness of this individualized dosing strategy.
AIM:Despite growing recognition of chronic kidney disease (CKD) as a major health threat in Asia, its subregional variations are often overlooked. This study aimed to assess the CKD burden across five Asian subregions. METHODS:This study analysed data from the Global Burden of Disease Study 2023 to estimate the burden of CKD in Asia. CKD cases were classified using International Classification of Diseases codes. Age-standardized mortality rates (ASMRs) and age-standardized disability-adjusted life-year (DALY) rates (ASDRs) per 100 000 population were estimated from 1990 to 2023 across 34 Asian countries, which were grouped into five subregions: Central, East, South, Southeast Asia and high-income Asia Pacific. Estimates were stratified by age, sex and underlying causes and reported with 95% uncertainty intervals (UIs), along with an assessment of major risk factors. RESULTS:In 2023, Southeast Asia experienced the heaviest CKD burden, with the highest ASMR (24.73 [95% UI, 19.98-29.83] per 100 000 population) and ASDR (816.37 [695.11-964.14]). Females under 35 years in South and Southeast Asia had a higher DALY burden than males. In Southeast Asia, type 1 diabetes contributed significantly to CKD deaths (ASMR, 3.18 [95% UI, 2.38-4.18] per 100 000 population), whereas CKD deaths in Central Asia were primarily due to other causes (7.48 [6.51-8.49]). High fasting plasma glucose levels were the leading risk factor across most regions, except in Central Asia. CONCLUSION:Although CKD is often considered uniform in Asia, our findings reveal distinct subregional drivers. Effective CKD control requires a shift from aggregated targets to precision- and region-specific strategies.
AIM:Haematuria is frequently present in podocytopathies, but its significance and prognostic value are not well described. This study aimed to determine the prevalence and association between persistent haematuria and kidney survival in patients with membranous nephropathy (MN), minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS). METHODS:We conducted a retrospective cohort study of 236 adults with biopsy-proven primary podocytopathies. Persistent haematuria was defined as ≥ 5 red blood cells per high-power field in ≥ 3 consecutive urine specimens within 3 months post-biopsy. The primary outcome was end-stage kidney disease (ESKD) requiring chronic renal replacement therapy. Kaplan-Meier analysis and Cox proportional hazards regression were performed. RESULTS:Among 236 participants (114 MN, 76 MCD, 46 FSGS), 73 (31%) had persistent haematuria. Participants with haematuria had higher proteinuria (5.3 vs. 3.2 g/g, p = 0.01) and were more likely to have hypertension (55% vs. 36%, p = 0.007). During a median follow-up of 96 months, 38 patients (16%) reached ESKD. ESKD incidence was significantly higher in patients with persistent haematuria (32% vs. 9%, p < 0.001). After adjusting for diagnosis, eGFR, proteinuria, Charlson comorbidity score and histological chronicity score, persistent haematuria remained independently associated with ESKD (hazard ratio: 3.55; 95% CI: 1.78-7.05; p < 0.001). CONCLUSION:Persistent haematuria is prevalent among patients with podocytopathies and is significantly and independently associated with ESKD. Urinalysis, including microscopic haematuria assessment, is widely available and inexpensive, providing a valuable data point to help formulate patient prognosis.
BACKGROUND:To investigate whether miR-145-5p regulates high-glucose-induced ferroptosis and injury in renal tubular epithelial cells through the KLF4/SIRT3/GPX4 signaling axis. Ferroptosis, a regulated form of iron-dependent cell death, has been increasingly implicated in DKD pathogenesis. The present investigation was designed to explore the functional significance and underlying molecular mechanisms of the miR-145-5p/KLF4/SIRT3/GPX4 signalling cascade in ferroptotic cell death of renal tubular epithelial cells during DKD. METHODS:A high-glucose-stimulated in vitro DKD model was constructed using human renal tubular epithelial cells (HK-2) exposed to 25.0 mmol/L glucose. Gene and protein expression profiles were characterised through RT-qPCR, Western blotting and immunofluorescence staining. Cellular viability, apoptotic rates and ferroptosis-associated biomarkers were quantified using CCK-8 assay, flow cytometric analysis, ELISA and JC-1 mitochondrial probe, respectively. Molecular binding interactions were confirmed through dual luciferase reporter assays and co-immunoprecipitation experiments. Intracellular reduced glutathione (GSH) content and GPX4 enzymatic activity were additionally measured to evaluate the functional status of the antioxidant arm of ferroptosis. RESULTS:High glucose exposure triggered time-dependent cellular damage and ferroptotic responses in HK-2 cells, characterised by elevated miR-145-5p levels alongside diminished KLF4, SIRT3 and GPX4 expression. Forced expression of miR-145-5p aggravated cellular damage and ferroptotic phenotypes, whilst its functional suppression conferred cytoprotection. Mechanistic analyses demonstrated that miR-145-5p directly engages the 3'-UTR of KLF4 to repress its expression. Restoring KLF4 expression attenuated high-glucose-mediated cellular injury and enhanced SIRT3 and GPX4 levels. Co-immunoprecipitation assays verified a physical protein-protein association between KLF4 and SIRT3. Functionally, HG stimulation reduced intracellular GSH content and GPX4 enzymatic activity. These changes were aggravated by miR-145-5p overexpression but were partially reversed by miR-145-5p inhibition or KLF4 overexpression. CONCLUSION:In the context of hyperglycemia, miR-145-5p facilitates ferroptotic cell death in renal tubular epithelial cells through KLF4 suppression, consequently attenuating the SIRT3/GPX4 signalling cascade and worsening DKD-related cellular injury. This regulatory axis may constitute a promising molecular intervention target for DKD treatment.
AIM:Develop and evaluate a chronic kidney disease (CKD) electronic (e-) phenotype to identify and risk-stratify CKD patients at scale using electronic health record (EHR) data. METHODS:Patient encounter and laboratory data determining kidney function and proteinuria from a four-year period (2021-2024) at a large Australian tertiary referral hospital was extracted from the hospital EHR. Following exclusion of kidney transplant recipients and patients on dialysis, eligible patients were classified as having CKD based on ICD-10 codes, decreased estimated glomerular filtration rate (eGFR, < 60 mL/min per 1.73 m2) and/or albuminuria (urine albumin-to-creatinine ratio [uACR] ≥ 3 mg/mmol, A2/A3 equivalent) for a minimum of 3 months. Patients with sufficient laboratory data were also staged according to the Kidney Disease Improving Global Outcomes (KDIGO) A-by-G grid. RESULTS:From a total undifferentiated hospital cohort of n = 342 146, the CKD e-phenotype algorithm identified n = 17 908 likely CKD cases (5.2%). Algorithm-detected CKD cases were validated against blinded manual chart review (n = 200), revealing sensitivity and specificity for CKD by ICD-10 codes (0.85 and 0.83), eGFR (0.62 and 0.98) and proteinuria criteria (0.33 and 0.75). The proportion of patients that were ICD-10-coded for CKD increased significantly (p < 0.001) with increasing G-stage (odds ratio [OR] 3.05) and A-stage (OR 2.31). CONCLUSION:Incorporating eGFR and proteinuria data into the e-phenotype algorithm appears to identify novel CKD cases with high specificity, particularly in the earlier stages of CKD progression. However, overall sensitivity is limited when compared to ICD-10 CKD codes alone.
BACKGROUND:Iron deficiency is common in patients receiving haemodialysis and contributes to adverse outcomes. Conventional iron biomarkers, including ferritin and transferrin saturation (TSAT), have limitations and may be less accessible in some settings. Reticulocyte haemoglobin equivalent (RET-He) is a lower-cost, potentially more accessible marker for detection of iron deficiency. This study evaluated whether RET-He-guided intravenous iron supplementation is non-inferior to TSAT-guided supplementation in haemodialysis patients. METHODS:In this randomized non-inferiority trial, 160 haemodialysis patients were randomized to a TSAT-guided group (n = 79) or RET-He-guided group (n = 81). Intravenous iron was administered in both groups according to prespecified protocols. The primary outcome was the erythropoietin resistance index (ERI) at 3 and 6 months. RET-He guidance was considered non-inferior if the upper bound of the 95% confidence interval (CI) for the between-group mean difference was ≤ 160 units/week/g/dL. Secondary outcomes included all-cause mortality, hospitalization, cardiovascular events, blood transfusion, and infection. RESULTS:Baseline characteristics were comparable between groups. RET-He-guided supplementation was non-inferior to TSAT-guided supplementation for ERI at 3 months (mean difference, -35.92; 95% CI, -155.60 to 90.29; p = 0.001 for non-inferiority) and 6 months (mean difference, -39.68; 95% CI, -187.01 to 107.64; p = 0.004 for non-inferiority). The RET-He group received significantly lower cumulative intravenous iron doses. Secondary outcomes did not differ significantly, although the trial was not powered for these clinical outcomes. CONCLUSION:RET-He-guided intravenous iron supplementation was non-inferior to TSAT-guided supplementation for reducing ERI over 6 months. Use of RET-He may offer a lower-cost and more accessible strategy for anaemia management in haemodialysis patients, particularly in resource-limited settings.
AIM:Diabetic nephropathy (DN) is characterised by progressive renal tubular epithelial cell injury, yet underlying molecular mechanisms remain incompletely understood. METHODS:Differentially expressed genes (DEGs) in DN were identified through integrated GEO dataset analysis (GSE30529 and GSE175759). Protein-protein interaction networks identified hub genes. GO and KEGG enrichment analyses determined molecular mechanisms. Nephroseq v5 explored correlations between hub genes and clinical features. CORO1A expression was validated by immunohistochemistry and western blot in DN patients, diabetic db/db mice and high glucose-exposed HK-2 cells. Vps34 inhibition and CORO1A knockdown explored regulatory mechanisms in vesicular trafficking and ferroptosis. RESULTS:Bioinformatics identified CORO1A as a phagosome-related core gene significantly upregulated in DN renal tubulointerstitium and correlated with eGFR, proteinuria, serum creatinine, blood pressure and age. External validation and experiments confirmed CORO1A upregulation in DN patients, diabetic mice and high glucose-exposed cells. Vps34 inhibition impaired lysosomal degradation flux and increased tubular injury markers, ferroptosis, ferritinophagy and CORO1A expression. CORO1A knockdown attenuated ferroptosis and lipid peroxidation, while rescue experiments with Ferrostatin-1 and Erastin confirmed the functional link between CORO1A, vesicular trafficking and ferroptosis. CONCLUSION:CORO1A is elevated in diabetic renal tubular epithelial cells and regulates vesicular trafficking and ferroptosis. This mechanistic axis suggests CORO1A as a potential therapeutic target for mitigating tubular injury and diabetic nephropathy progression.
AIM:To compare four electronic health record (EHR)-based frailty tools-the Hospital Frailty Risk Score (HFRS), Johns Hopkins Adjusted Clinical Groups Frailty Indicator (CFI), Electronic Frailty Index (eFI) and a Laboratory-based Frailty Index (FI-Lab)-in predicting progression and all-cause mortality in hospitalised patients with chronic kidney disease (CKD). METHODS:This retrospective study evaluated the indices in two cohorts: a single-centre cohort (n = 5715) for CKD progression and the Medical Information Mart for Intensive Care (MIMIC) database (n = 2674) for mortality. We used Cox proportional hazards regression for association analyses. The incremental predictive value of adding frailty indices to established risk models was quantified using the area under the curve (AUC), net reclassification improvement (NRI) and integrated discrimination improvement (IDI). RESULTS:Correlations between the frailty indices were weak to moderate (Spearman's ρ = 0.205-0.451). In adjusted analyses, CFI, eFI and FI-Lab were associated with a higher risk of CKD progression, whereas HFRS was not. In the MIMIC cohort, all four indices were significantly associated with all-cause mortality. Notably, the CFI association was non-significant in patients < 65 years for both CKD progression and 28-day mortality. For predictive enhancement, adding FI-Lab and eFI to established CKD risk models significantly improved progression prediction (ΔAUC p < 0.05), yielding substantial reclassification (NRI: 0.376-0.498) and discrimination (IDI: 0.032-0.048). For mortality prediction, all indices improved baseline severity scores, with FI-Lab providing the greatest incremental value. CONCLUSION:Among the evaluated EHR-based frailty indices, FI-Lab offers the most robust utility for risk stratification in hospitalised patients with CKD, followed closely by eFI.
We describe a rare case of a 64-year-old man with acute renal failure secondary to paroxysmal cold haemoglobinuria (PCH), presenting with haemoglobinuria, jaundice, and fevers. PCH is an intravascular haemolytic anaemia with polyphasic IgG antibody binding of red blood cells at cold temperatures, with complement-mediated haemolysis on rewarming. Renal biopsy confirmed acute tubular necrosis without thrombotic microangiopathy. The patient received supportive management including intermittent haemodialysis with a warm circuit to prevent further haemolysis and achieved full renal recovery. Optimal therapy of PCH varies in the literature.
