Let's stop talking about 'citrate toxicity'.

PURPOSE OF REVIEW: Continuous renal replacement therapy (CRRT) is a vital medical intervention used in critically ill patients with acute kidney injury (AKI). One of the key components of adequate clearance with CRRT is the use of anticoagulants to prevent clotting of the extracorporeal circuit. Regional citrate anticoagulation is the most often recommended modality. The term 'citrate toxicity' is used to describe potential adverse effects of accumulation of citrate and subsequent hypocalcemia. However, citrate is itself not inherently toxic. The term and diagnosis of citrate toxicity are questioned in this review. RECENT FINDINGS: Citrate is being increasingly used for regional anticoagulation of the CRRT circuit. Citrate accumulation is infrequent and can cause hypocalcemia and metabolic alkalosis, which are potential adverse effects. Citrate itself, however, is not a toxic molecule. The term 'citrate toxicity' has been used to denote hypocalcemia and metabolic acidosis. However, citrate administration is well known to cause systemic and urinary alkalinization and under certain circumstances, metabolic alkalosis, but is not associated itself with any 'toxic' effects.We review the existing literature and debunk the perceived toxicity of citrate. We delve into the metabolism and clearance of citrate and question current data suggesting metabolic acidosis occurs as the result of citrate accumulation. SUMMARY: In conclusion, this article calls into question prevailing concerns about 'citrate toxicity'. We emphasize the need for a more nuanced understanding of its safety profile. We recommend discarding the term 'citrate toxicity' in favor of another frequently used, but more meaningful term: 'citrate accumulation'.

The effect of changing dialysate bicarbonate concentration on serum bicarbonate, body weight and normalized nitrogen appearance rate.

INTRODUCTION: Most hemodialysis machines deliver a fixed bicarbonate concentration. Higher concentrations may improve acidosis, but risk post-hemodialysis alkalosis, whereas lower concentrations potentially increase acidosis but reduce alkalosis. We reviewed the effects of lowering dialysate bicarbonate. METHODS: We reviewed peri-dialysis chemistries in patients switching to a lower bicarbonate dialysate at 4 time points over 19 months. RESULTS: We studied 126 patients, mean age 63.7 ± 16.3 years, 57.9% males. Post-hemodialysis alkalosis fell from 1.6 to 0.3% sessions, but pre-hemodialysis acidosis increased from 11.9 to 23.8% sessions (p = 0.005) reducing dialysate bicarbonate from 32 to 28 mmol/L. After 3 months, pre-hemodialysis serum bicarbonate fell (21.1 ± 2.3 to 19.8 ± 2.2 mmol/L), and post-hemodialysis (24.9 ± 2.1 to 22.5 ± 2.0 mmol/L, p < 0.001) with a fall in pre-hemodialysis weight from 74.6 ± 20.7 to 71.7 ± 18.2 kg, normalized protein nitrogen accumulation rate 0.8 ± 0.28 to 0.77 ± 0.2 g/kg/day, p < 0.05, and serum albumin 39.7 ± 4.2 to 37.7 ± 4.9 g/L, p < 0.001. Thereafter, apart from pre- and post-hemodialysis serum bicarbonate, weight and normalized protein nitrogen accumulation stabilized, although albumin remained lower (37.6 ± 4.0 g/L, p < 0.001). On multivariate logistic analysis, serum bicarbonate increased more with lower pre-hemodialysis bicarbonate standardized coefficient ß 0.5 (95% confidence interval -0.6 to -0.42), increased normalized protein nitrogen accumulation ß 0.2 (0.96 to 2.38), p < 0.001, and session time ß 0.09, (0.47 to 5.98), p < 0.022, and less with lower dialysate bicarbonate 0.0-0.23 (-1.54 to -0.74), p < 0.001. CONCLUSION: Increases in SE-Bic with hemodialysis, depend on the bicarbonate gradient, session time and nPNA. Lower D-Bic reduces post-hemodialysis alkalosis but increases pre-hemodialysis acidosis and may initially have adverse effects on weight and normalized protein nitrogen accumulation.

Milk-Alkali Syndrome: A Century-old Cause of Hypercalcemia Requires the Addition of Venous Blood Gas in Hypercalcemia Workup.

The Milk-Alkali syndrome (MAS) is identified by the triad of high serum levels of calcium, metabolic alkalosis, and acute kidney injury, usually caused by consuming excessive amounts of calcium and absorbable alkali. If not treated promptly, the syndrome can result in rapid hypercalcemia, acute renal failure, and metastatic calcification. Notably, an increasing number of cases of MAS have been observed, potentially due to the rampant use of calcium-based over-the-counter supplements for the prevention and treatment of osteoporosis in postmenopausal women. Herein, we report a case of severe hypercalcemia due to prolonged intake of calcium carbonate supplements in the absence of any alkali. The case report highlights the importance of including venous blood gas (VBG) analysis as a part of the workup for hypercalcemia, as metabolic alkalosis can help clinch the diagnosis of MAS in the setting of severe hypercalcemia. How to cite this article: Sahu U, Trivedi T, Gupta R. Milk-Alkali Syndrome: A Century-old Cause of Hypercalcemia Requires the Addition of Venous Blood Gas in Hypercalcemia Workup. J Assoc Physicians India 2023;71(9):104-105.

A Case of Milk-Alkali Syndrome Caused by Diuretic-Induced Alkalosis and Polypharmacy.

Milk-alkali syndrome, which is characterized by hypercalcemia, metabolic alkalosis, and renal dysfunction, typically results from the ingestion of large amounts of calcium and absorbable alkaline products. However, these symptoms can also manifest when alkalosis and calcium loading occur simultaneously, owing to other factors. We report a case of milk-alkali syndrome caused by loop-diuretic-induced alkaline load and polypharmacy in an 85-year-old Japanese woman with multiple comorbidities, including osteoporosis, hypertension, type 2 diabetes, dyslipidemia, and Parkinson's disease. The patient regularly took 14 drugs, including calcium L-aspartate, eldecalcitol, celecoxib, and a fixed-dose combination of losartan and hydrochlorothiazide. Immediately before admission, furosemide was administered for the treatment of edema. The patient presented with chest discomfort, general malaise, and clinical signs of dehydration, hypercalcemia, hypophosphatemia, hypokalemia, and hypomagnesemia, accompanied by electrocardiogram abnormalities, renal dysfunction, and chloride-resistant metabolic alkalosis. The hypercalcemia was specifically induced by calcium L-aspartate and eldecalcitol. The hypomagnesaemia and hypophosphatemia were caused by diuretics and hypercalcemia. Thus, all the oral medications were discontinued, and rehydration and electrolyte correction therapy were administered. The final diagnosis was milk-alkali syndrome caused by the concomitant use of loop diuretics and other medications, without absorbable alkaline preparation use. This case underscores the importance of considering drug-related factors, checking concomitant medications, and being aware of the benefits, harmful effects, and side effects of polypharmacy in older adults with multimorbidity.

Acid-base effects of continuous infusion furosemide in clinically stable surgical ICU patients: an analysis based on the Stewart model.

OBJECTIVES: We sought to test the strength of correlation between predicted and observed systemic acid-base status based on the Stewart model equations during continuous infusion (CI) furosemide therapy. DESIGN, SETTING AND PARTICIPANTS: This was a prospective, single-center, observational study conducted in the Surgical ICU of a large academic medical center. Ten critically ill patients who received CI furosemide were included. MAIN OUTCOMES AND MEASURES: The primary purpose was to characterize the relationship between changes in serum electrolyte and acid-base status and the excretion of electrolytes in the urine during infusion of CI furosemide in critically ill patients. As a secondary endpoint, we sought to evaluate the predictive application of the Stewart model. Over 72-h, intake and output volumes, electrolyte content of fluids administered, plasma and urine electrolytes, urine pH, and venous blood gases were collected. Predicted and observed changes in acid-based status were compared for each day of diuretic therapy using Spearman's correlation coefficient. RESULTS: The mean (SD) strong ion difference (SID) increased from 45.2 (3.2) at baseline to 49.6 (4.0) after 72 h of continuous infusion furosemide. At Day 1, the mean SID (observed) (SD) was 47.5 (3.5) and the predicted SID was 49.5 (5.8). Day 1 observed plasma SID was positively correlated with the predicted SID (rs = 0.80, p = 0.01). By Days 2 and 3, the correlations of observed and predicted SID were no longer statistically significant. CONCLUSIONS AND RELEVANCE: Using the Stewart model, increases in SID as an indicator of metabolic alkalosis due to the chloruretic effects of furosemide were observed. Predicted and observed SID correlated well over the first 24 h of treatment.

An unusual cause of metabolic alkalosis: hiding in plain sight.

BACKGROUND: Sodium bicarbonate, in the form of baking soda, is widely used as a home remedy, and as an additive for personal and household cleaning products. Its toxicity has previously been reported following oral ingestion in the setting of dyspepsia. However, its use as a non-ingested agent, like a toothpaste additive, has not been reported as a potential cause of toxicity. CASE PRESENTATION: We are reporting a case of an 80-year-old woman who presented with chronic metabolic alkalosis and hypokalemia secondary to exogenous alkali exposure from baking soda as a toothpaste additive, which might have represented an underreported ingestion of the substance. CONCLUSIONS: Considering that one teaspoon of baking soda provides approximately 59 m-equivalents (mEq) of bicarbonate, specific questioning on its general use should be pursued in similar cases of chloride resistant metabolic alkalosis.

Effect of Bicarbonate-Buffered Dialysate on Ventricular Arrhythmias in Hemodialysis Patients.

BACKGROUND: The etiology of sudden cardiac death in patients with end-stage renal disease (ESRD) on hemodialysis (HD) is largely unknown, though there is evidence to suggest that metabolic alkalosis induced by HD with a high-bicarbonate dialysate/prescription may play a role. METHODS: We investigated the effects of metabolic alkalosis induced by HD with an acetate-containing bicarbonate-buffered dialysate on frequency of ventricular arrhythmia in 47 patients with ESRD on chronic HD using 48-h Holter monitoring in 3 phases: intra-HD, post-HD day 1, and post-HD day 2. Serum levels of bicarbonate, calcium, and potassium along with hemodynamics were measured pre-HD, post-HD, 20-h post-HD, and 44-h post-HD. Correlations were performed to verify the association between bicarbonate prescription and change in serum bicarbonate levels post-HD and to determine if the HD-induced change in serum bicarbonate level (metabolic alkalosis) had any direct association with ambient ventricular arrhythmia (premature ventricular contractions per hour) or indirect associations with ambient ventricular arrhythmia by affecting electrolytes or hemodynamics that are known to increase the risk of ventricular arrhythmia. RESULTS: Mean pre-HD serum bicarbonate level was 21.3 mEq/L. Dialysate bicarbonate prescription (mean of 36.4 mEq/L) correlated with changes in serum bicarbonate levels immediately post-HD 26.7 mEq/L (r = 0.46, p < 0.01), 20-h post-HD 25.2 mEq/L (r = 0.38), and 44-h post-HD 23.2 mEq/L (r = 0.35, p = 0.01). No statistically significant correlations were found between the post-HD change in serum bicarbonate levels (metabolic alkalosis) with ambient ventricular arrhythmia, changes in serum calcium, potassium, or hemodynamics in any phase. CONCLUSIONS: High-bicarbonate dialysate prescription is associated with metabolic alkalosis following the HD procedure. A mild metabolic alkalosis induced by HD with an acetate-containing bicarbonate-buffered dialysate solution had no direct association with ambient ventricular arrhythmia on Holter monitoring and was not associated with changes in hemodynamics or changes in serum total calcium or potassium levels. This study helps to provide guidance for the safe use of high bicarbonate dialysate/prescription in patients with ESRD on HD.

An unexpected cause of acute kidney injury in a patient with ANCA associated vasculitis.

Diagnostic kidney biopsies sometimes yield clinically unsuspected diagnoses. We present a case of a 69-year-old woman with established ANCA-associated vasculitis (AAV) of 4 years duration who was in clinical remission following cytotoxic therapy and was on maintenance immunosuppression. She presented to the hospital with acute kidney injury (AKI), symptoms suggestive of a systemic vasculitis, and in addition had hypercalcemia, metabolic alkalosis. A relapse in the AAV was suspected but a diagnostic kidney biopsy showed acute tubular necrosis, patchy interstitial inflammation, and calcium phosphate deposits. It was found that the patient recently started consuming large doses of over-the-counter calcium-containing antacids and vitamin Dcontaining multivitamin supplements. Cessation of these drugs led to improvement of renal function to baseline. This case highlights several teaching points: (1) the kidney biopsy can prove to be critically important even in cases where there appears to be a more obvious clinical diagnosis, (2) AK due to calcium-alkali syndrome has characteristic histopathological changes, and (3) that the triad of hypercalcemia, metabolic alkalosis, and AKI is exclusively associated with the ingestion of excessive quantities of calcium-containing antacids. The physician should keep this in mind, and pro-actively seek pertinent medication history from the patient. A brief review of calcium-alkali syndrome is given.

Gitelman-like Syndrome with Kanamycin Toxicity.

A 22 year-old lady with multi-drug-resistant pulmonary tuberculosis was on Kanamycin, Cycloserine, Ethionamide, Pyrazinamide and Moxifloxacin since more than two months. She presented with muscle cramps and carpopedal spasm. Investigation revealed hypokalemia and metabolic alkalosis. She also had hypomagnesemia, hypochloremia and hypocalciuria. Serum urea and creatinine levels were normal. Patient was treated with intravenous and oral potassium chloride. Kanamycin was stopped. Metabolic alkalosis and hypokalemia improved gradually over one month. Biochemical parameters were like Gitelman's syndrome but it reversed with stoppage of Kanamycin. Gitelman-like syndrome with Kanamycin toxicity has not been reported in literature previously.

Safety and efficacy of regional citrate anticoagulation in continuous venovenous hemodialysis in the presence of liver failure: the Liver Citrate Anticoagulation Threshold (L-CAT) observational study.

INTRODUCTION: Regional citrate anticoagulation (RCA) for continuous renal replacement therapy is widely used in intensive care units (ICUs). However, concern exists about the safety of citrate in patients with liver failure (LF). The aim of this study was to evaluate safety and efficacy of RCA in ICU patients with varying degrees of impaired liver function. METHODS: In a multicenter, prospective, observational study, 133 patients who were treated with RCA and continuous venovenous hemodialysis (RCA-CVVHD) were included. Endpoints for safety were severe acidosis or alkalosis (pH ≤7.2 or ≥7.55, respectively) and severe hypo- or hypercalcemia (ionized calcium ≤0.9 or ≥1.5 mmol/L, respectively) of any cause. The endpoint for efficacy was filter lifetime. For analysis, patients were stratified into three predefined liver function or LF groups according to their baseline serum bilirubin level (normal liver function ≤2 mg/dl, mild LF >2 to ≤7 mg/dl, severe LF >7 mg/dl). RESULTS: We included 48 patients with normal liver function, 43 with mild LF, and 42 with severe LF. LF was predominantly due to ischemia (39 %) or multiple organ dysfunction syndrome (27 %). The frequency of safety endpoints in the three patient strata did not differ: severe alkalosis (normal liver function 2 %, mild LF 0 %, severe LF 5 %; p = 0.41), severe acidosis (normal liver function 13 %, mild LF 16 %, severe LF 14 %; p = 0.95), severe hypocalcemia (normal liver function 8 %, mild LF 14 %, severe LF 12 %; p = 0.70), and severe hypercalcemia (0 % in all strata). Only three patients showed signs of impaired citrate metabolism. Overall filter patency was 49 % at 72 h. After censoring for stop of the treatment due to non-clotting causes, estimated 72-h filter survival was 96 %. CONCLUSIONS: RCA-CVVHD can be safely used in patients with LF. The technique yields excellent filter patency and thus can be recommended as first-line anticoagulation for the majority of ICU patients. TRIAL REGISTRATION: ISRCTN Registry identifier: ISRCTN92716512 . Date assigned: 4 December 2008.

Severe alkalosis and hypokalemia with stanozolol misuse.

Stanozolol is a popular androgenic anabolic steroid, used by body builders and athletes for physical performance enhancement. There are few data on its potential adverse effects and no documented cases of it causing severe electrolyte imbalance. Here, we report a patient presenting to a tertiary care emergency department with reduced conscious level, profound hypokalemia, and severe metabolic alkalosis, resulting from stanozolol misuse. This is the first such case reported.

[Intraperitoneal irrigation for pseudomyxoma peritonei-a case of critical metabolic alkalosis precipitated by irrigation with 101 of sodium bicarbonate--].

Pseudomyxoma peritonei causes marked accumulation of jelly-like ascites in the peritoneal cavity. Removal of much mucinous ascites by irrigating the cavity appears to be an effective treatment. We describe a patient who underwent the irrigation with sodium bicarbonate solution and developed critical alkalemia. A 68-year-old woman with normal renal function was operated on for recurrent pseudomyxoma peritonei. Fol- lowing the excision of primary lesion, her intraperitoneal cavity was irrigated with 10 1 of 7% sodium bicarbonate in about 45 minutes. Thirty minutes after irrigation, blood gas analysis revealed severe metabolic alkalosis (pH 7.714, BE 25.6 mmol x l-1 ) with electrolyte disorder (Na 157.8 mmol x l-1 K 2.31mmol x l-1, Ca 0.73 mmol x l-1). Hypotension (<60 mmHg) and sinus tachycardia (>130 beats x min -1) supervened 75 minutes later. Transferring to the ICU, she was given KC1 solution intravenously based on serial blood analysis while on mechanical ventilation. The next day acid-base disturbance returned spontaneously to normal (pH 7.45, BE 8.0mmol x l-1), leading to endotracheal extubation. Electrolyte imbalance was gradually resolved on 2nd POD and she was discharged from the ICU. Intraperitoneal irrigation with sodium bicarbonate requires special perioperative considerations for lifethreatening alkalemia, especially in a patient with renal impairment.

Predicting the safety and efficacy of buffer therapy to raise tumour pHe: an integrative modelling study.

BACKGROUND: Clinical positron emission tomography imaging has demonstrated the vast majority of human cancers exhibit significantly increased glucose metabolism when compared with adjacent normal tissue, resulting in an acidic tumour microenvironment. Recent studies demonstrated reducing this acidity through systemic buffers significantly inhibits development and growth of metastases in mouse xenografts. METHODS: We apply and extend a previously developed mathematical model of blood and tumour buffering to examine the impact of oral administration of bicarbonate buffer in mice, and the potential impact in humans. We recapitulate the experimentally observed tumour pHe effect of buffer therapy, testing a model prediction in vivo in mice. We parameterise the model to humans to determine the translational safety and efficacy, and predict patient subgroups who could have enhanced treatment response, and the most promising combination or alternative buffer therapies. RESULTS: The model predicts a previously unseen potentially dangerous elevation in blood pHe resulting from bicarbonate therapy in mice, which is confirmed by our in vivo experiments. Simulations predict limited efficacy of bicarbonate, especially in humans with more aggressive cancers. We predict buffer therapy would be most effectual: in elderly patients or individuals with renal impairments; in combination with proton production inhibitors (such as dichloroacetate), renal glomular filtration rate inhibitors (such as non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors), or with an alternative buffer reagent possessing an optimal pK of 7.1-7.2. CONCLUSION: Our mathematical model confirms bicarbonate acts as an effective agent to raise tumour pHe, but potentially induces metabolic alkalosis at the high doses necessary for tumour pHe normalisation. We predict use in elderly patients or in combination with proton production inhibitors or buffers with a pK of 7.1-7.2 is most promising.

Advances in continuous renal replacement therapy: citrate anticoagulation update.

Because of the potential side effects of heparin, methods of regional citrate anticoagulation (RCA) for continuous renal replacement therapy (CRRT) have been gaining wider acceptance with the development of simplified and safer protocols. Advantages of RCA include the avoidance of systemic anticoagulation and heparin-induced thrombocytopenia. The disadvantage is that citrate can add complexity and labor intensity to CRRT. Frequent monitoring of electrolytes, ionized calcium, and acid-base status is required, due to the potential for hypernatremia, metabolic alkalosis, and systemic ionized hypocalcemia. If properly monitored, complications associated with RCA are uncommon. A variety of methods of delivering RCA are described in the literature. Overall, studies of RCA, as compared to unfractionated heparin, report better filter survival times and less bleeding. In this section, we summarize the characteristics of citrate as an anticoagulant and provide an update of citrate use in CRRT.

A patient with foot ulcer and severe metabolic alkalosis.

We report a case of triple acid-base disorder with metabolic alkalosis as the primary disorder in a 65-year-old man due to ingestion and application to leg ulcers of baking soda (calcium bicarbonate). The blood pH was 7.65 with hypochloremia, hypokalemia, and prerenal azotemia. He was treated with isotonic saline with K replacement, and the patient improved without any adverse clinical consequences. We discuss the causes, mechanisms, and management of Cl-responsive (depletion) metabolic alkalosis.

Practical recommendations for coaches and athletes: a meta-analysis of sodium bicarbonate use for athletic performance.

Sodium bicarbonate (NaHCO3) is a buffering agent that is suggested to improve performance by promoting the efflux of hydrogen ions from working cells and tissues. Research surrounding its efficacy as an ergogenic aid is conflicting, making it difficult to draw conclusions as to its effectiveness for training and competition. This study performed a meta-analysis of relevant research articles to allow the development of concise practical recommendations for coaches and athletes. The overall effect size for the influence of NaHCO3 on performance was moderate, and was significantly lower for specifically trained as opposed to recreationally trained participants.

Sodium bicarbonate supplementation and ingestion timing: does it matter?

Although a considerable amount of literature exists on the ergogenic potential of ingesting sodium bicarbonate (NaHCO3) before short-term, high-intensity exercise, very little exists on optimal loading times before exercise. The purpose of this study was to determine the influence of NaHCO3 supplementation timing on repeated sprint ability (RSA). Eight men completed 3 (randomized and counterbalanced) trials of ten 10-second sprints separated by 50 seconds of active recovery (1:5 work-to-rest) on a nonmotorized treadmill. Before each trial, the subjects ingested 0.3 g·kg(-1) body weight of NaHCO3 at 60 (H1), 120 (H2), or 180 (H3) minutes before exercise. Additionally, the subjects were assessed for any side effects (gastrointestinal [GI] discomfort) from the NaHCO3 ingestion via a visual analog scale (VAS). Blood buffering was assessed using a 2-way analysis of variance (ANOVA) with repeated measures, whereas repeated sprint performance and GI discomfort were assessed via a 1-way ANOVA with repeated measures. Blood-buffering capacity was not different at preexercise times (HCO3(-) [millimoles per liter] H1: 30.2 ± 0.4, H2: 30.9 ± 0.6, H3: 31.2 ± 0.6; p > 0.74). Average speed, average power, and total distance covered progressively declined over the 10 sprints; however, there was no difference between conditions (p > 0.22). The incidence of GI discomfort was significantly higher (p < 0.05) from preingestion at all time points with the exception of 180 minutes, whereas severity was only different between 90 and 180 minutes. Ingestion times (between 60 and 180 minutes) did not influence the blood buffering or the ergogenic potential of NaHCO3 as assessed by RSA. However, VAS scores indicated that at 180 minutes postingestion, an individual is less prone to experiencing significant GI discomfort.

Life-threatening alkalosis from baking soda pica in an end stage renal disease hemodialysis patient.

Severe metabolic alkalosis is rarely seen in end stage renal disease (ESRD) patients on long-term hemodialysis. This can be life threatening and mortality is exponentially increased when the pH exceeds 7.60. Persistent vomiting, ingestion of alkali for dyspepsia and pica behavior are all potential causes of such severe metabolic alkalosis. The prevalence of pica is increased in chronic kidney disease and ESRD patients, with ice being the most commonly ingested substance. It can cause a myriad of complications including death, but the diagnosis may be elusive unless the pica behavior is witnessed firsthand by others since patients do not typically disclose their behavior. We present the case of a hemodialysis patient with severe alkalemia, hypernatremia, and excessive interdialytic weight gains resulting in recurrent hospitalizations for fluid overload due to baking soda pica behavior.

Comparison of different modalities of continuous renal replacement therapy with regional sodium citrate anticoagulation in paediatric patients.

BACKGROUND: To evaluate the efficacy and safety of continuous renal replacement therapy (CRRT) modalities with regional sodium citrate anticoagulation (RCA) in children. METHODS: This retrospective study was conducted at the paediatric intensive care unit of Hunan Children's Hospital in China. Medical records of paediatric patients hospitalised for RCA-CRRT between April 2017 and March 2021 were reviewed. Patients received continuous venovenous haemodialysis, continuous venovenous haemofiltration (CVVH), or continuous venovenous haemodiafiltration (CVVHDF). RESULTS: Patients on continuous venovenous haemodialysis (n = 2) were excluded because of their small sample size. The remaining participants were divided into CVVH and CVVHDF groups; 80 patients received CRRT, with 40 and 62 sessions in the CVVH and CVVHDF groups, respectively. The filtre lifespan was longer in the CVVHDF group than in the CVVH group (median value [interquartile range]; 47 [15] hours vs. 35 [17.5] hours; p = 0.029). Compared with the CVVHDF group, the hazard ratio for filtre lifespan in the CVVH group was 3.023 (95% confidence interval 1.820-5.023, p < 0.001). There were no significant differences in ionised calcium levels of the circuits between the two groups at different time points (p < 0.05). Metabolic alkalosis, hyperlactataemia, hypocalcaemia, and hypercalcaemia occurred in both groups, with metabolic alkalosis being the most common complication. No patients in either group experienced sodium citrate accumulation or hypernatraemia. Inter-group differences in the incidence of these complications were not statistically significant (p > 0.05). CONCLUSIONS: Our results suggest that CVVHDF is a better option for RCA-CRRT than CVVH.