Correction Of Metabolic Acidosis Research Articles

Chloride removal and bicarbonate replacement by isotonic sodium bicarbonate-based continuous hemodiafiltration: a novel method to correct severe metabolic acidosis.

Previous reports highlighted the efficacy of hemofiltration utilizing isotonic sodium bicarbonate solution as replacement fluid for severe metabolic acidosis. This approach corrects metabolic acidosis by eliminating chloride and supplementing bicarbonate. Here, we present the results of an in vitro study aimed at determining the effect of Isotonic sodium bicarbonate-based Continuous HemoDiafiltration (IBB-CHDF). Conventional Continuous HemoDiaFiltration (CHDF) and IBB-CHDF utilized aqueous solutions mimicking blood's electrolyte composition. To assess the efficacy and safety, we compared serial changes in pH, HCO3-, Na+, and K+ concentrations. Blood flow rate was 100mL/min, and the dialysis fluid flow rate maintained 1.0 L/h for both CHDF and IBB-CHDF. Replacement flow rates ranged from 0.5 to 1.5 L/h for CHDF and 0.1 to 1.5 L/h for IBB-CHDF. At a replacement flow rate of 0.5 L/h with IBB-CHDF, bicarbonate increased from 14.7 mEq/L to within the physiological range (25.9mEq/L), whereas in conventional CHDF, the post-treatment bicarbonate concentration did not increase (16.5mEq/L). The maximum bicarbonate concentration achieved was 22.0mEq/L at a replacement flow rate of 1.5 L/h in conventional CHDF. Notably, in IBB-CHDF, the sodium concentration remained constant at 150mEq/L, 10mEq/L higher than conventional CHDF, and did not escalate despite increasing the replacement flow rate. IBB-CHDF effectively corrects metabolic acidosis without inducing sodium and water overload by eliminating excess chloride while providing bicarbonate.

ABCs of base therapy in neonatology: role of acetate, bicarbonate, citrate and lactate.

Metabolic acidosis is common in preterm and term newborn infants and may be attributed to a variety of etiologies, potentially requiring base therapy such as acetate or bicarbonate. However, concerns exist regarding potential harm of sodium bicarbonate due to intracellular acidosis, fluctuations in cerebral blood flow, and osmolar load with rapid infusions, with no improvement in survival when used during resuscitation. Alternative approaches to correct metabolic acidosis include the addition of acetate in parenteral nutrition, intravenous lactated Ringer's (LR) solution, and use of oral citrate. Current guidelines focus on addressing the underlying cause of acidosis, reserving the use of sodium bicarbonate (NaHCO3) for severe cases requiring acute correction, LR instead of saline for volume boluses and using acetate or citrate for slow correction to stabilize acid-base status. Further research is necessary to better understand the efficacy and safety of acetate, NaHCO3, and other base sources in treating metabolic acidosis in neonates.

Urgent-Start Peritoneal Dialysis in Metformin-Associated Lactic Acidosis: A Critical Alternative When Immediate Hemodialysis is Unavailable.

Introduction Intermittent hemodialysis (IHD) is a preferable renal replacement therapy (RRT) option in metformin-associated lactic acidosis (MALA) due to rapid correct metabolic acidosis. However, IHD might not be started immediately. Immediate urgent-start peritoneal dialysis (iUSPD) is used as a life-saving dialysis option and then followed by IHD. The outcomes of iUSPD were compared with other extracorporeal dialysis in MALA. Methods In two tertiary hospitals in Thailand, the outcomes of patients with MALA who had received three different RRT modalities (iUSPD followed by IHD, IHD, and continuous renal replacement therapy [CRRT]) from January 2015 to December 2019 were compared. The primary outcome was 30-day mortality. The secondary outcomes were door-to-dialysis time and 90-day RRT dependence. Results 180 MALA cases that required dialysis were included (20 iUSPD, 120 IHD, and 40 CRRT). Their mean age was 64 years. Most of the patients had severe metabolic acidosis (mean pH 6.91, HCO3 6 mmol/L, and anion gap 40 mmol/L) and were critically ill. The 30-day mortality was 30% in iUSPD, 9.2% in IHD, and 32.5% in CRRT, p = 0.001). The mortality risk in the iUSPD group was not significantly different from those of the IHD and CRRT groups (adjusted HR 2.5, 95% CI 0.65-9.6 and adjusted HR 0.75, 95% CI 0.2-2.78, respectively). All dialysis modalities had comparable 90-day dialysis dependence. iUSPD exhibited the shortest door-to-dialysis time. Conclusion In MALA, iUSPD followed by IHD might be a viable RRT option to save patient lives if no other dialysis option are available.

Effect of Hydration with Bicarbonate Ringer's Solution on Cisplatin-induced Acute Kidney Injury in Patients with Esophageal Cancer: A Retrospective Cohort Study.

Cisplatin (CDDP) often causes acute kidney injury (AKI), and magnesium supplementation has been suggested to be important in preventing CDDP-induced AKI. Sodium bicarbonate Ringer's solution (BRS) is a crystalloid solution composed of various electrolytes, including Mg2+, and can be generally used to supplement missing extracellular fluid and correct metabolic acidosis; however, the clinical outcomes of hydration with BRS for CDDP-induced AKI remain unclear. In this study, we retrospectively compared the effects of BRS and normal saline for hydration in patients undergoing CDDP treatment. We analyzed the incidence rate of AKI (grade ≥ 1), the severity of AKI, the serum magnesium level, and the incidence rate of grade ≥ 3 hematological toxicities (leukopenia, neutropenia, anemia, or thrombocytopenia) following CDDP and fluorouracil (5-FU) administration in 131 in-patients who received CDDP and 5-FU for the first time to treat esophageal cancer. Fifty-six patients (43%) received saline alone, while 75 patients (57%) received BRS for hydration. The incidence rate of AKI (grade ≥ 1) was significantly lower in the BRS group (11%) than that in the saline group (39%, p < 0.001). Moreover, severe AKI (grade ≥ 2) was significantly less common in the BRS group than in the saline group. Although the serum magnesium levels before CDDP administration were not significantly different between the two groups (p = 0.939), the serum magnesium levels on days 2-3 after CDDP administration in the BRS group were significantly higher than those in the saline group (p < 0.001). In contrast, there were no significant differences in the incidence rates of hematological toxicity between the two groups. Multivariate analysis revealed that BRS use was an independent factor that significantly contributed to AKI prevention (odds ratio = 0.061, p < 0.001). Hydration with BRS could prevent CDDP-induced AKI in patients with esophageal cancer.

Administration of bicarbonates through percutaneous gastrostomy with continuous nocturnal infusion in a patient with Kearns-Sayre disease: a life changing therapeutical paradigm

BackgroundMitochondrial diseases (MDs) are systemic disorders that can affect multiple organs. Renal manifestations, including renal tubular acidosis, are common because kidneys are particularly vulnerable to energy deprivation. Treatment of MDs is often complex and electrolyte replacement can be difficult especially in pediatric patients, because large and repeated amounts of oral supplements are needed but are not well tolerated.Case presentationWe describe the case of a girl affected by Kearns-Sayre disease with severe renal tubular acidosis. The management of her metabolic acidosis was challenging because she showed persistent low levels of serum bicarbonates despite a progressive incrementation of oral bicarbonates. Furthermore, as a result to the ingestion of large amounts of alkali, the girl developed an aversion to oral supplementation. After positioning a percutaneous gastrostomy (PEG) and starting enteral administration of bicarbonates (with daily boluses and continuous nocturnal infusion), she finally obtained an adequate electrolyte control, with a significant increase in her quality of life.ConclusionsIn MDs, the combination of nocturnal continuous enteral administration of alkali plus diurnal boluses may represent a valid solution to correct metabolic acidosis. It can also result in an improved patients’ quality of life, particularly in pediatric settings, where compliance to oral therapy is often lacking due to the large and repeated amounts of unpalatable bicarbonates solutions required.

#2418 Effects of correction of acidosis on body composition and biochemical parameters in CKD patients on maintenance hemodialysis

Abstract Background and Aims Metabolic acidosis is a common problem in patients of chronic kidney disease and patients on maintenance hemodialysis. In resource poor countries, due to financial constraints frequency of dialysis and compliance to medication is adversely affected. This leads to worsening of clinical condition of patient and requirement of in hospital care, many times intensive care, further increasing cost of treatment. Metabolic acidosis has implications on bone and muscle health. Aim of our study was to assess the changes in body composition (fat percentage and lean body mass), changes in third space fluid, biochemical parameters, number of admissions and requirement of blood transfusions before and after correction of metabolic acidosis. Method This was a prospective, observational study. 25 patients on maintenance hemodialysis at our center were included in the study. Bio-impedance analysis (BIA), biochemical parameters (Complete blood counts, renal function tests, serum calcium and phosphorous, liver function tests, Blood gas analysis) were done at baseline before starting bicarbonate supplementation. Number of admissions and blood transfusions in 3 months prior to initiation of bicarbonate supplementation were noted. The oral bicarbonate supplementation was increased from baseline, based on the baseline blood gas analysis. The same parameters were assessed after 3 months and analyzed. Results At the end of 3 months we observed that there was significant reduction (p < 0.05) in total leucocyte counts (mean 8100/cumm to 6800/cumm), urea (mean 113.7 mg/dL to 83.72 ng/dL), creatinine (mean 7.87 mg/dL to 6.68 mg/dL), phosphorous (mean 5.18 mg/dL to 4.43 mg/dL), SGOT (mean 56.52 IU to 25.2 IU) and SGPT (mean 46.48 IU to 22.88 IU) with a trend of decrease (p ≤ 0.1) in percentage of extra cellular water (27.31% to 25.03%), lean body mass (44.27 kg to 43.0 kg) and trend of increase (p ≤ 0.1) in body fat composition (15.62 kg to 18.82 kg) and body fat percentage (26.924% to 31.90). There was a reduction in third space fluid (0.88 lit to 0.43 lit). The number of hospitalizations reduced (15 three months prior to initiation of therapy to 7 after initiation of therapy) and number of blood transfusions required also reduced (21 before initiation to 10 after initiation of therapy). Conclusion We concluded that correction of acidosis probably reduces the inflammation in patients of CKD on maintenance hemodialysis. This could be seen from the reduced total leucocyte counts, liver enzymes, urea and creatinine values. Changes in body composition with increased total fat mass, fat percentage and decreased lean mass was also noted. There was also a significant reduction in hospitalizations and number of blood transfusions.

Pharmacologic therapeutics in sarcopenia with chronic kidney disease.

Inflammation, metabolic acidosis, renin-angiotensin system activation, insulin resistance, and impaired perfusion to skeletal muscles, among others, are possible causes of uremic sarcopenia. These conditions induce the activation of the nuclear factor-kappa B and mitogen-activated protein kinase pathways, adenosine triphosphate ubiquitin-proteasome system, and reactive oxygen species system, resulting in protein catabolism. Strategies for the prevention and treatment of sarcopenia in chronic kidney disease (CKD) are aerobic and resistance exercises along with nutritional interventions. Anabolic hormones have shown beneficial effects. Megestrol acetate increased weight, protein catabolic rate, and albumin concentration, and it increased intracellular water component and muscle mass. Vitamin D supplementation showed improvement in physical function, muscle strength, and muscle mass. Correction of metabolic acidosis showed an increase in protein intake, serum albumin levels, body weight, and mid-arm circumference. The kidney- gut-muscle axis indicates that dysbiosis and changes in gut-derived uremic toxins and short-chain fatty acids affect muscle mass, composition, strength, and functional capacity. Biotic supplements, AST-120 administration, hemodiafiltration, and preservation of residual renal function are alleged to reduce uremic toxins, including indoxyl sulfate (IS) and p-cresyl sulfate (PCS). Synbiotics reversed the microbiota change in CKD patients and decreased uremic toxins. AST-120 administration changed the overall gut microbiota composition in CKD. AST-120 prevented IS and PCS tissue accumulation, ameliorated muscle atrophy, improved exercise capacity and mitochondrial biogenesis, restored epithelial tight junction proteins, and reduced plasma endotoxin levels and markers of oxidative stress and inflammation. In a human study, the addition of AST-120 to standard treatment had modest beneficial effects on gait speed change and quality of life.

Clinical efficacy of sodium bicarbonate in treating pediatric metabolic acidosis with varying level of acid–base balance parameters: a real-world study

BackgroundSodium bicarbonate (SB) infusion is commonly used to correct metabolic acidosis, but its clinical efficacy remains controversial. This study aims to investigate whether acid–base balance parameters should be a consideration for administering SB treatment.MethodsChildren with metabolic acidosis (pH < 7.35 and bicarbonate < 22 mmol/L) who were treated with or without 50 mg/ml SB injection were grouped and extracted from a retrospective cohort database of the Pediatric Intensive Care Unit. The interaction between acid–base balance parameters and SB treatment on mortality was analyzed through mortality curves and cross-effect models. Logistic regression was conducted to estimate the risk of death following SB treatment in the overall children as well as in subgroups, and potential confounding factors were adjusted for. After employing propensity score matching to account for confounding factors, further analysis was performed to evaluate the effectiveness of SB treatment within each chloride subgroup.ResultsA total of 5865 children with metabolic acidosis were enrolled, of which 2462 (42.0%) received SB treatment. In the overall population, it was found that SB treatment did not reduce hospital mortality or 28-day mortality. Interactions between acid–base balance parameters (chloride and anion gap) and SB treatment on mortality were observed. Subgroup analysis clarified that when chloride levels were below 107 mmol/L, children treated with SB had higher in-hospital mortality (29.8% vs 14.9%) and 28-day mortality (26.5% vs 13.4%), with adjusted ORs of 2.065 (95% CI, 1.435–2.97) and 1.947 (95% CI, 1.332–2.846), respectively. In contrast, when chloride levels were greater than or equal to 113 mmol/L, children treated with SB had a shorter stay in the PICU (median: 1.1 days vs 5.1 days, adjusted p = 0.004) and lower in-hospital mortality (4.3% vs 10.3%) and 28-day mortality (4.0% vs 8.4%), with adjusted ORs of 0.515 (95% CI, 0.337–0.788) and 0.614 (95% CI, 0.391–0.965), respectively. After controlling for confounding factors through matching, the impact of SB treatment on the risk of death in each chloride subgroup was consistent with the aforementioned results. However, treatment with SB did not significantly increase the risk of death in newborns or children with moderate to severe metabolic acidosis when chloride levels were below 107 mmol/L (p > 0.05).ConclusionsThe use of sodium bicarbonate for treating metabolic acidosis has been found to increase mortality in children with low chloride levels but decrease mortality in those with high chloride levels in this study. Further prospective multi-center clinical studies and basic research are needed to validate these findings.

Reversible acute blindness in suspected metformin-associated lactic acidosis: a case report

BackgroundMetformin is commonly used for the treatment of type 2 diabetes mellitus. Its multiple advantages include low risk of hypoglycemia, weight neutrality, low cost, and cardioprotective and anti-inflammatory effects. Renal insufficiency is one of the contraindications for its use. Inadvertent prescription in patients with renal insufficiency may lead to metformin-associated lactic acidosis, which brings a high risk of mortality. The early recognition and management of metformin-associated lactic acidosis are essential.Case reportWe present the case of a 58-year-old Hui woman with a history of type 2 diabetes mellitus with nephropathy and heart disease for which she was treated with metformin, insulin, and heart medications. She developed nausea, vomiting, anion gap metabolic acidosis due to hyperlactatemia, and acute kidney injury. She was hospitalized to receive intravenous hydration and correction of metabolic acidosis after she suddenly developed blindness. The diagnostic workup ruled out central causes and her symptoms resolved briefly after continuous venovenous hemodialysis was initiated, confirming the diagnosis of metformin-associated lactic acidosis.ConclusionsMetabolic disruption can cause acute blindness. Metabolic acidosis in a patient with a history of metformin intake should suggest the possibility of metformin-associated lactic acidosis, which must be treated immediately, without waiting for the results of other examinations, especially in patients with sudden blindness. Further study of reversible blindness-associated severe metabolic acidosis is needed.

Management of Hyperkalemia in Patients with Chronic Kidney Disease Using Renin Angiotensin Aldosterone System Inhibitors.

Use of renin-angiotensin-aldosterone system (RAAS) inhibiting medications is critical in the prevention of cardiovascular disease and kidney function decline in patients with chronic kidney disease (CKD); however, these agents can lead to hyperkalemia, an electrolyte disorder associated with risk of arrythmia, conduction disorders, and increased overall mortality. Discontinuation, or reduction of dose, of RAAS inhibitor therapy in hyperkalemic patients with CKD can lead to loss of kidney and cardiovascular protection afforded by these medications. Given the high prevalence of hyperkalemia among patients with CKD utilizing RAAS inhibitors, clear management principles are critical to minimize risk and maximize benefit when facing this clinical dilemma. Strategies to mitigate hyperkalemia that do not interfere with optimal RAAS inhibitor therapy should be prioritized when managing potassium elevation in patients with CKD. These strategies include discontinuing non-RAAS inhibitor medications known to cause hyperkalemia, correction of metabolic acidosis, and maximization of medication therapies that lower serum potassium, including diuretics and sodium-glucose cotransporter-2 (SGLT-2) inhibitors. Initiation of potassium exchange resins should also be considered to allow for sustained RAAS inhibitor utilization. An approach which employs multiple strategies concurrently is important to mitigate hyperkalemia and maintain long-term use of RAAS-inhibitors. Persistence of RAAS inhibitor use in patients with CKD is important to slow kidney function decline, delay onset of dialysis or the need for kidney transplant, and prevent adverse cardiovascular outcomes. When hyperkalemia develops among patients with CKD utilizing a RAAS inhibitor, a deliberate effort to reduce serum potassium levels using an approach that allows for continuation of maximally dosed RAAS inhibitor therapy is important. Patient education and engagement in the potassium management process is important for sustained success.

Effects of correcting metabolic acidosis on muscle mass and functionality in chronic kidney disease: a systematic review and meta-analysis.

Metabolic acidosis unfavourably influences the nutritional status of patients with non-dialysis dependent chronic kidney disease (CKD) including the loss of muscle mass and functionality, but the benefits of correction are uncertain. We investigated the effects of correcting metabolic acidosis on nutritional status in patients with CKD in a systematic review and meta-analysis. A search was conducted in MEDLINE and the Cochrane Library from inception to June 2023. Study selection, bias assessment, and data extraction were independently performed by two reviewers. The Cochrane risk of bias tool was used to assess the quality of individual studies. We applied random effects meta-analysis to obtain pooled standardized mean difference (SMD) and 95% confidence intervals (CIs). We retrieved data from 12 intervention studies including 1995 patients, with a mean age of 63.7±11.7years, a mean estimated glomerular filtration rate of 29.8±8.8mL/min per 1.73m2 , and 58% were male. Eleven studies performed an intervention with oral sodium bicarbonate compared with either placebo or with standard care and one study compared veverimer, an oral HCl-binding polymer, with placebo. The mean change in serum bicarbonate was +3.6mEq/L in the intervention group and +0.4mEq/L in the control group. Correcting metabolic acidosis significantly improved muscle mass assessed by mid-arm muscle circumference (SMD 0.35 [95% CI 0.16 to 0.54], P<0.001) and functionality assessed with the sit-to-stand test (SMD -0.31 [95% CI -0.52 to 0.11], P=0.003). We found no statistically significant effects on dietary protein intake, handgrip strength, serum albumin and prealbumin concentrations, and blood urea nitrogen. Correcting metabolic acidosis in patients with CKD improves muscle mass and physical function. Correction of metabolic acidosis should be considered as part of the nutritional care for patients with CKD.

The practices of intravenous sodium bicarbonate therapy in neonatal intensive care units: A multi-country survey.

A common occurrence in the neonatal intensive care unit (NICU) is metabolic acidosis. Sodium bicarbonate (SB) has been widely used, but there is insufficient evidence on how SB affects neonates in NICUs with metabolic acidosis. The worsening of intracellular acidosis, the impairment of myocardial function, fluctuations in cerebral blood flow, and intracranial hemorrhage are some of the unfavorable effects of SB treatment in neonates that have been documented in the literature. This study aimed to explore neonatologists' practices for using intravenous SB (ISB) in NICUs. A multi-country survey was carried out in 2022 using an online questionnaire sent to neonatologists in various countries in order to gather information about the use of ISB in NICUs. A previously validated questionnaire was adapted and used in this study. The response rate was 67%. The findings show that 91.2% of neonatologists were using SB to correct metabolic acidosis in the NICU; 71.4% did not have written guidelines for using sodium bicarbonate. The majority of them (78.9%) reported that dosage is included in their guidelines for the use of ISB. The findings of this study emphasize the critical importance of providing guidelines in using ISB for managing metabolic acidosis in NICU to standardize procedures and reduce the use of potentially unsuitable and unsafe treatments, as it has been shown that 71.4% of neonatologists worldwide use sodium bicarbonate without guidelines.

A Case Report of Metformin Related Lactic Acidosis

Metformin is an oral antidiabetic drug of the biguanide classused in type 2 diabetic patients with normal renal function. The mortality rate is high in cases of lactic acidos is developing in metformin intoxication. In the emergency department, metformin intoxication should be considered in the differential diagnosis of patients whouse metformin and have high anion gap metabolic acidosis (lactic acidosis). The most important and effective treatment with early diagnosis is correction of metabolic acidosis with hemodialysis or hemofiltration methods, bicarbonate treatment, adjustment of blood glucose level. Cardiovascular system support therapy significantly reduces morbidity/mortality. In this case report, we present the early diagnosis and successful treatment of a patient with lactic acidosis due to metformin intoxication.

#4238 UNEXPLAINED METABOLIC ACIDOSIS - A DIAGNOSTIC DILEMMA

Abstract Background and Aims Metabolic Acidosis is a common condition for which nephrology consult is sought. Most often the etiology is quite obvious like renal failure, diabetic ketoacidosis, lactic acidosis etc. We describe a case of high anion gap metabolic acidosis, unresponsive to medical management requiring hemodialysis, where finding the etiology became a diagnostic challenge because of medical and social reasons prevailing in this eastern part of India. Method A 55 year old obese gentleman came to emergency department at 3 am with complains of restlessness, pain abdomen and chest discomfort for last 4-6 hours. On clinical examination he had tachycardia with normal blood pressure and oxygen saturation. His sensorium was normal and systemic examination did not reveal any major abnormality. A possibility of acute cardiac event was considered but his ECG showed sinus tachycardia, echocardiography did not show any wall motion abnormality and Troponin I was less than 0.01 ng/mL. His blood gases showed an uncompensated metabolic acidosis with an anion gap of 21 (pH 7.19 / pCO2 44 / HCO3 15). The laboratory parameters showed a serum creatinine of 0.9 mg/dL, random blood sugar of 130 mg/dL. Any history of poisoning or drug overdose was denied by patient's attendants. Pending further workup patient was admitted in intensive care unit and correction of metabolic acidosis was started with intravenous sodium bicarbonate. Results The metabolic acidosis initially improved with medical management but within next 6 hours patient again had severe metabolic acidosis. Meanwhile patient's sensorium worsened and he had an episode of seizure. Patient was intubated and mechanical ventilation started. Within 30 minutes patient had status epilepticus which ultimately required intravenous thiopentone. Hemodialysis was started for correction of metabolic acidosis. Patient's history was re-evaluated. On persistent questioning his attendants admitted that patient had consumed alcohol 4-5 hours before the symptoms started. It is important to mention here that consumption of alcohol is a punishable offence in Bihar which a state in eastern part of India. Despite alcohol being completely banned in this part of country illicit alcohol is smuggled and consumed by some. Illicit alcohol is prone to be adulterated and sub-standard. It was because of this fact that patient's attendants suppressed the facts. Also alcohol consumption is a valid ground for rejection of medical insurance claims because of obvious reasons. After obtaining the complete history a possibility of consumption of alcohol adulterated with methyl alcohol was very likely. Serum methyl alcohol estimation was not available at our institute and patient had already received hemodialysis hence it was not done. With patient already having seizures MRI (Magnetic Resonance Imaging) of brain was done. MRI brain revealed altered hyperintense signal with cytotoxic edema in bilateral basal ganglia predominantly putamen. Subcortical white matter in bilateral cerebral hemisphere and bilateral optic nerve head showed restriction on diffusion weighted imaging. These typical features on MRI were highly suggestive of methanol toxicity. These MRI features along with the clinical scenario and history of illicit alcohol intake helped us reach the diagnosis of methanol toxicity. Patient was managed with hemodialysis sessions to remove methanol from blood until he improved clinically. Conclusion The etiology of the high anion gap metabolic acidosis turned out to be methanol toxicity. Typical MRI brain findings helped confirm the diagnosis. Our case highlights the importance of obtaining the correct medical history and how social and medicolegal issues sometimes become a hindrance to obtaining the same.

#5807 FACTORS ASSOCIATED WITH KALEMIA IN RENAL DISEASE

Abstract Background and Aims International recommendations promote a strict potassium diet in order to avoid hyperkalemia in chronic kidney disease patients. However, efficiency of such a dietary counseling has never been demonstrated. The objectives of this study were to define the relationship between kalemia, dietary potassium intake estimated by kaliuresis and renal function and to define the factors associated with kalemia in patients using artificial intelligence. Method To this extent, data from patients followed in a nephrology unit, included in the UniverSel study and whose kalemia (measured on the day of urine collection; n = 367) were analyzed. The association between kalemia and thirty-four variables concerning the patients' characteristics, their biological work-up, their medications and their answers to the UniverSel dietary self-questionnaire on kalemia were assessed using a Bayesian network. Results The patients included had a wide range of estimated glomerular filtration rate, but few had stage 5 chronic kidney disease (CKD). Kalemia was negatively and linearly correlated to estimated glomerular filtration rate (p&amp;lt;0.001) but was not correlated to kaliuresis (p = 0.55). Kaliuresis was not correlated to estimated glomerular filtration rate (p = 0.08). Factors associated with kalemia were analyzed using a Bayesian network. The 5 variables most associated with kalemia were, in descending order, estimated glomerular filtration rate, original nephropathy, age, diabetes, and plasma bicarbonate level. RAS-blockers prescription was also associated to kalemia. Consumption of potassium rich food were poorly associated to kalemia. Conclusion Our results do not support a strict control of potassium intake in stage 1 to 4 CKD patients. Our results reinforce the interest of a multidimensional management including personalized therapy and strict correction of metabolic acidosis. Lightning dietary restrictions in potassium would improve the quality of life of patients with CKD who are often multi-pathological and already subject to multiple dietary constraints.

The AE4 transporter mediates kidney acid-base sensing

The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na+-dependent Cl−/HCO3− exchanger AE4 (Slc4a9). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl−/HCO3− exchanger pendrin (Slc26a4) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status.

Effect of 3% Hypertonic Saline Resuscitation on Lactate Clearance and Its Comparison With 0.9% Normal Saline in Traumatic Injury Patients: A Prospective Randomized Control Trial.

Fluid resuscitation with normal saline (NS) can aggravate lactate production. The objective of this study was to evaluate the efficacy of small-volume resuscitation using 3% hypertonic sodium chloride (HS) and its comparison with NS in trauma patients.The primary endpoint was an increase in lactate clearance after 1 hr of fluid resuscitation.The secondary endpoint was the incidence of hemodynamic stability, the volume of transfusion, correction of metabolic acidosis, and complications such as fluid overload and abnormal serum sodium levels. It was a prospective, randomized, single-blind study. The study was conducted on 60patients who arrived at the trauma center for emergency operative intervention. Inclusion criteria for patient selection were trauma victims of age more than 18 years and the requirement of emergency operative intervention for trauma except for traumatic brain injury. Patients were divided into two groups: Group HS (hypertonic saline) and Group NS (normal saline). Patients were resuscitated with either 3% HS (4ml/kg) or 0.9% NS (20ml/kg). The HS group had higher lactate clearance at 1 hour compared to the NS group, and this difference was statistically significant with a p-value of <0.001. When hemodynamic parameters were compared at 30 and 60 minutes after resuscitation, the HS group had a significantly lower heart rate (p<0.05 at 30 minutes and <0.001 at 60 minutes, respectively), a higher mean arterial pressure at 60 minutes (p<0.001), a higher pH at 60 minutes (p< 0.05), and a higher bicarbonate concentration at 60 minutes (p<0.05). The HS and NS groups had significant differences in serum sodium levels at 60 minutes (p<0.001). Resuscitation with 3% hypertonic saline improved lactate clearance. Lower volumes of fluid infusion for resuscitation achieved better hemodynamic stability and correction of metabolic acidosis in the hypertonic saline group. Our study shows that hypertonic saline can be a promising fluid for small-volume resuscitation in trauma patients with compensated mild to moderate shock.

Elevation of Serum Amylase and Lipase Levels in Diabetic Ketoacidosis without Acute Pancreatitis: A Case Report and Literature Review

Serum amylase and lipase levels are commonly used as diagnostic markers for acute pancreatitis, but elevated levels of these enzymes can also occur in other conditions. We report a case of a 45-year-old male with a known history of type 2 diabetes who presented with nausea, vomiting, and abdominal pain. Laboratory investigations revealed hyperglycemia, ketonemia, metabolic acidosis, and elevated levels of serum amylase and lipase. However, imaging studies did not reveal any evidence of acute pancreatitis or other abdominal pathology. The patient was diagnosed with diabetic ketoacidosis and managed with fluid resuscitation, insulin therapy, and correction of metabolic acidosis. The serum amylase and lipase levels gradually normalized, supporting the diagnosis of diabetic ketoacidosis without complicated with acute pancreatitis. This case highlights the importance of considering alternative diagnoses in the setting of elevated serum amylase and lipase and appropriate management of diabetic complications to prevent the development of more severe conditions.

READINESS OF INTERPROFESSIONAL EDUCATION IN COMMUNITY MEDICINE: MEDICAL AND DENTISTRY STUDENTS

Systemic lupus erythematosus (SLE) is an autoimmune disease affecting several body systems with a variety of clinical manifestations, course of disease, and prognosis. Its clinical manifestations can involve almost all organ systems including musculoskeletal, skin and mucosa, kidney, neuropsychiatry, lung, heart, blood vessels, gastrointestinal, ocular, obstetric, endocrine, and haematology. SLE can occur with a variety of degrees of tubular abnormalities. Tubular inflammation, tubular atrophy, interstitial inflammation and fibrosis are reported in 50-70% of patients with SLE. We have reported a case of a 27-year-old female with renal tubular acidosis (RTA) type 1 who has systemic lupus erythematosus. RTA is a group of abnormalities of the renal function, characterized by renal impairment in the reabsorption of HCO3- and excreting acid (H+). The administration of corticosteroids and immunosuppressants, correction of metabolic acidosis with sodium bicarbonate, and potassium supplementation are the main modalities of therapy in patients with SLE with RTA type-1

Pathophysiology and clinical management of hyperkalemia in chronic kidney disease.

Adaptive increases in kidney and gastrointestinal excretion of K+ help to prevent hyperkalemia in patients with chronic kidney disease (CKD) as long as the glomerular filtration rate (GFR) remains >15-20 mL/min. K+ balance is maintained by increased secretion per functioning nephron, which is mediated by elevated plasma K+ concentration, aldosterone, increased flow rate, and enhanced Na+-K+-ATPase activity. Fecal losses of potassium also increase in CKD. These mechanisms are effective in preventing hyperkalemia if urine output is in excess of 600 mL/day and the GFR exceeds 15 mL/min. Development of hyperkalemia with only mild to moderate reductions in GFR should prompt a search for intrinsic disease of the collecting duct, disturbances in mineralocorticoid activity, and/or decreased delivery of sodium to the distal nephron. The initial approach to treatment is to review the patient's medication profile and whenever possible discontinue drugs that impair kidney K+ excretion. Patients should be educated on sources of K+ in the diet and should be strongly encouraged to avoid the use of K+ containing salt substitutes as well as herbal remedies since herbs may be a hidden source of dietary K+. Effective diuretic therapy and correction of metabolic acidosis are effective strategies to minimize the potential for hyperkalemia. Discontinuation or use of submaximal doses of renin-angiotensin blockers should be discouraged given the cardiovascular protective effect these drugs provide. Potassium binding drugs can be useful to enable use of these drugs and potentially allow liberalization of the diet in CKD patients.