Presentation of mixed diabetic ketoacidosis and metabolic acidosis due to ileal neobladder reconstruction

Diabetic ketoacidosis (DKA) is one of the most serious acute metabolic complications of diabetes mellitus. It is characterised by the biochemical triad of hyperglycaemia, ketonemia/ketonuria, and an increased anion gap metabolic acidosis. In this case, a 40-year-old male patient presented to the emergency department, with vomiting, nausea, polydipsia, polyuria and weight loss. He was found to have an elevated plasma glucose, despite having no known history of diabetes mellitus. His medical history was significant for spina bifida and ileal neobladder reconstruction. The plasma glucose level was 38 mmol/L. Blood gas analysis showed normal anion gap metabolic acidosis with high chloride and low bicarbonate. His plasma ketone level was 4.5 mmol/L. No significant reason for hyperchloraemia was identified. On initiation of DKA regimen, his condition improved and serum ketones normalised. Due to persistent hyperchloraemic metabolic acidosis, bicarbonate infusion was administered and his metabolic acidosis resolved.

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High Anion Gap Metabolic Acidosis due to Euglycemic Diabetic Ketoacidosis Caused by Sodium-Glucose Co-transporter 2 inhibitor

10.31227/osf.io/zbw26 ◽

2019 ◽

Author(s):

Awad Magbri ◽

Eusera El-Magbri ◽

Mariam El-Magbri ◽

Brar Balhinder ◽

Shauket Rashid

Keyword(s):

Metabolic Acidosis ◽

Vital Signs ◽

Blood Gas Analysis ◽

Gas Analysis ◽

Anion Gap ◽

Urine Ph ◽

History Of ◽

Lactate Levels ◽

Breathing Room ◽

Work Up

The case is that of 58 year-male with type 2 diabetes mellitusfor 7 years, hypertension, hypercholesterolemia, who was admittedto the hospital with left lower limb cellulitis over the past 8 days.On work-up he was found to have high anion-gap metabolic acidosis(AGMA) with anion gap of 25, his lactate levels were normal (Dand L-lactate). He denies overdosing with any medications and histoxicology screen for methanol, ethanol, aspirin, and ethylene glycolwere negative. He has no psychiatric history of note. He denies usingover the counter medications like acetaminophen. No bowel surgerycould be elicited. He felt dehydrated and nauseous but otherwisefine.His medications includes; carvedalol 25mg twice daily,hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeksago to control his blood sugar level and A1C.Physical examination of the patient revealed, slightly dehydratedbut well-nourished man, his vital signs; heart rate of 78 BPM andregular, BP 143/85 mmHg, temperature 98.7 F, and his oxygensaturation while breathing room air was 92%. Examination of theheart, abdomen, and chest were unremarkable. He had left lower legcellulitis but no edema or tenderness.His work-up including chemistry-7 which showed sodium of142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L,bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78mg/L respectively. His blood glucose level was 178 mg/L with A1Cof 8.2. His serum osmolality was 312 mosm/L, and his arterial bloodpH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of32mmHg. His calculated anion gap was 25 given his normal albuminlevel. His investigation also showed positive ketones in the serumand urine. His urine PH was 5.5 and the urine contain >800 mg ofglucose

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Euglycemic Diabetic Ketoacidosis in a Diabetic Patient Treated with SGLT2 Inhibitor

10.26420/austinendocrinoldiabetescaserep.2021.1018 ◽

2021 ◽

Vol 6 (1) ◽

Author(s):

Lavrynenko O ◽

◽

Santos H ◽

Garza A ◽

Qazi R ◽

...

Keyword(s):

Metabolic Acidosis ◽

Diabetic Ketoacidosis ◽

Glucose Transporter ◽

Sglt2 Inhibitor ◽

Anion Gap ◽

Laboratory Evaluation ◽

Intravenous Insulin ◽

Glucose Transporter 2 ◽

Life Threatening ◽

History Of

Diabetic Ketoacidosis (DKA) is a life - threatening complication and must be diagnosed and treated promptly and aggressively. The classic triad of DKA is hyperglycemia (Blood Glucose (BG) >250mg/dl; anion gap metabolic acidosis (pH <7.30 and bicarbonate <18mEq/L); and ketonemia. With Food and Drug Administration (FDA) approval of the sodium - glucose transporter 2 inhibitors (SGLT2i), DKA can occur with BG levels below 200mg/dl and has been defined as Euglycemic DKA (EuDKA). Due to the absence of hyperglycemia, the diagnosis of EuDKA is challenging and often delayed. This 60-year-old diabetic male, treated with Empagliflozin and pioglitazone, presented with diarrhea and abdominal pain, which started 20 days ago. He was admitted with dehydration and diagnosis of colitis. On admission laboratory evaluation revealed metabolic acidosis with elevated anion gap of 18mEq/L, bicarbonate of 19mEq/L, and BG of 146mg/dL. There was no history of ingestion of alcohol, salicylates, methanol, ethylene glycol and nothing to suggest lactic acidosis. The plasma creatinine was 0.79mg/dl. On the following day, he developed an increase in the anion gap to 22mEq/L and further decrease in bicarbonate to 13mEq/L, and serum ketones were detected. The patient was treated for EuDKA in ICU with intravenous insulin, dextrose (to prevent hypoglycemia), and normal saline with resolution of his symptoms and EuDKA in 3 days. With the widespread use of SGLT2i, physicians need to have a high suspicion of EuDKA in patients who present with an unexplained anion gap acidosis without or only modest elevation in BG concentration.

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Hypochloremia in cats – prevalence and associated diseases

Tierärztliche Praxis Ausgabe K Kleintiere / Heimtiere ◽

10.15654/tpk-150647 ◽

2016 ◽

Vol 44 (04) ◽

pp. 237-244 ◽

Cited By ~ 1

Author(s):

Maximilian Pagitz ◽

Mona Sarah Friedrich ◽

Florian K. Zeugswetter

Keyword(s):

Diabetes Mellitus ◽

Medical Records ◽

Inverse Correlation ◽

Blood Gas Analysis ◽

Gas Analysis ◽

Anion Gap ◽

Control Group ◽

Blood Gas ◽

Acid Base ◽

Correction Formula

SummaryObjective: To describe the prevalence and possible causes of hypochloremia in the local hospital cat population. Material and methods: Retrospective study consisting of two parts. Data were collected from the local electronic medical records database using the search terms „chloride“ and „cats“ (part A), and „blood gas analysis“ and „cats“ (part B). The medical records of the hypochloremic cats were then reviewed to determine prior treatment or infusions and to identify major underlying disease processes. Part A included an age and gender matched non-hypochloremic control group, whereas in part B acid-base status was assessed. Results: Hypochloremia was detected in 367 (27%) of 1363 blood samples. The application of a correction formula to adjust for free water changes decreased the number of hypochloremic cats to 253 (19%). Only a minority had received glucocorticoids or loop diuretics and the prevalence of vomiting was 44%. Common associated disorders were gastrointestinal and respiratory diseases, as well as azotemia and diabetes mellitus. Polyuria/ polydipsia, dehydration, prednisolone or furosemide pretreatment, azotemia and diabetes mellitus increased, whereas fluid therapy and the diagnosis of neoplasia decreased the prevalence of hypochloremia. An inverse correlation was found between corrected chloride and standar dized base excess (rs = –0.597, p = 0.001) as well as anion gap (rs = –0.4, p = 0.026). 99% of the hypochloremic cats had derangements of acid-base balance. Conclusion: Hypochloremia is a common electrolyte disorder in the local cat population. The correction formula is ne cessary to adjust for changes in plasma osmolality. Although associated with metabolic alkalosis, most of the hypochloremic cats have a normal or decreased pH. The inverse correlation of chloride and anion gap als well as the high proportion of azotemic or diabetic animals support the concept of compensatory acidosis induced hypochlor emia. Clinical relevance: Hypochloremia should prompt the clinician to performe blood-gas analysis. Diabetes mellitus (especially ketoacidosis) and renal disease should be included in current algorithms for the evaluation of hypochloremic patients.

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Euglycemic Diabetic Ketoacidosis With SGLT-2 Inhibitor

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.777 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A381-A382

Author(s):

F N U Manas ◽

Barbara L Mols-Kowalczewski ◽

Shobha Mandal

Keyword(s):

Blood Glucose ◽

Diabetic Ketoacidosis ◽

Side Effect ◽

Blood Gas Analysis ◽

Gas Analysis ◽

Anion Gap ◽

Blood Gas ◽

Glucose Levels ◽

Beta Hydroxybutyrate ◽

Euglycemic Diabetic Ketoacidosis

Abstract Introduction: The SGLT-2 inhibitors (SGLT-2i) are a newer anti-diabetic drugs. Their use has tremendously increased due to their favorable profile but they are also the focus of attention because of their side effect of euglycemic diabetic ketoacidosis (euDKA), which is challenging to diagnose because of its rarity and normal or mildly elevated blood glucose levels. SGLT2i decrease blood glucose independently of insulin secretion, by reversibly inhibiting SGLT2 protein which is responsible for reabsorbing glucose from the proximal renal tubule. Beside glycemic control with reduced glycated hemoglobin, they also decrease all-cause mortality, cardiovascular mortality, and hospitalization for heart failure. The major side effect is genitourinary infections, euDKA and volume depletion. EuDKA is characterized by blood glucose <200mg/dl, anion gap metabolic acidosis and positive serum ketones. It can, therefore, present without hyperglycemia and the symptoms of dehydration, making it challenging to identify. DKA is rarely seen in DM-2 and the normal glucose levels can cause misinterpretation of the patient’s condition, causing a delay in treatment. The beta-hydroxybutyrate and arterial pH should be checked in suspected SGLT2i associated euDKA. The mainstay of treatment of euDKA is immediately stopping SGLT2i and traditional DKA treatment protocol. Patient should be educated regarding adequate hydration and adequate calorie intake while using SGLT2i and physician should avoid using SGLT2i in patients with poor oral intake, alcohol dependence or pregnancy. Case Presentation: A 52-year-old male with uncontrolled type 2 diabetes, on Metformin and Sitagliptin, presented to clinic. Canagliflozin (SGLT-2i) was added to his oral hypoglycemic regimen. Six days later he presented with blurred vision, lightheadedness, nausea, vomiting, and abdominal pain. On examination, he had tachycardia and tachypnea. Labs were significant for glucose levels of 131mg/dL, bicarbonate 12meq/l, anion gap 20, creatinine 0.7mg/dl, normal lactic acid. Serum ketones were positive with elevated beta-hydroxybutyrate of 5.9mmol/l. Blood gas analysis showed a pH of 7.14. The patient was admitted to ICU and managed according to the guidelines for DKA. The symptoms resolved within 24 hours, with a reduction of anion gap to 12. Canagliflozin was discontinued indefinitely and the patient was discharged with the diagnosis of SGLT2i-induced euDKA. Conclusion: SGLT2i-induced euDKA can present without the classical laboratory findings of DKA. The patients, with a history of SGLT2i use and, signs and symptoms of DKA, even in the absence of hyperglycemia, should be suspected of euDKA. The complete lab work with blood gas analysis, blood and urine ketones including beta-hydroxybutyrate level must be done to ensure that the diagnosis is not missed and timely interventions are made to manage this serious condition.

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An Atypical Presentation of Hyperosmolar Hyperglycemic State Induced by SARS CoV 2

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.746 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A366-A367

Author(s):

Ivan Augusto Rivera Nazario ◽

Arnaldo Nieves Ortiz ◽

Jose Ayala Rivera ◽

Kyomara Hernandez Moya ◽

Arnaldo Rojas ◽

...

Keyword(s):

Diabetes Mellitus ◽

Metabolic Acidosis ◽

Cell Function ◽

De Novo ◽

Vital Signs ◽

Anion Gap ◽

Severe Illness ◽

Metabolic Complications ◽

Early Management ◽

Hyperosmolar Hyperglycemic State

Abstract Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2. We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms. SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.

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New-Onset Diabetic Ketoacidosis Secondary to Nivolumab Therapy in a Patient with Primary Central Nervous System Lymphoma

Osteopathic Family Physician ◽

10.33181/13037 ◽

2021 ◽

pp. 40-43

Author(s):

Christine Feng ◽

Pavel Kibrik ◽

Christian Castañeda ◽

Gurdeep Singh

Keyword(s):

Diabetes Mellitus ◽

Central Nervous System ◽

Nervous System ◽

Diabetic Ketoacidosis ◽

Checkpoint Inhibitors ◽

Central Nervous System Lymphoma ◽

Anion Gap ◽

Prior History ◽

Life Threatening ◽

History Of

Introduction: Inhibitors of programmed cell death receptor (PD-1) and its ligand (PD-L1), such as nivolumab and pembrolizumab, confer anti-autoimmune activities and are therefore approved for anti-cancer therapy. Their mode of action removes autoimmunity checkpoints, thus increasing the risk of immune-related adverse events. Case Presentation: This report describes a clinical case of life-threatening diabetic ketoacidosis (DKA) in a patient after long-term nivolumab administration to treat primary central nervous system lymphoma (PCNSL). The patient presented to the emergency department (ED) with symptoms of fatigue, along with nausea and vomiting for two days; laboratory testing revealed significant hyperglycemia (glucose 673 mg/dL), elevated anion gap (>27), metabolic acidosis, ketonemia, glucosuria and ketonuria, findings of which were consistent with DKA. Given no personal history of diabetes mellitus or other autoimmune conditions and additional tests ruling out alternative causes, the patient was suspected of having newly-onset DKA secondary to nivolumab treatment. Management & Outcome: The patient was treated with fluids, electrolytes replenishments and insulin drip, which closed the anion gap and normalized electrolytes. She was transitioned to subcutaneous insulin. The patient recovered well and was discharged on Metformin and longacting insulin, with close follow-up with endocrinology and oncology. Discussion: Autoimmune endocrinopathies induced by checkpoint inhibitors for cancer treatment have been reported in the past. Newly-onset hyperglycemia and DKA are common autoimmunemediated side effects of checkpoint inhibitor uses in patients without prior history of diabetes mellitus. Clinicians should be aware to prevent this potentially life-threatening condition.

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High Anion Gap Metabolic Acidosis due to Euglycemic Diabetic Ketoacidosis Caused by Sodium-Glucose Co-transporter 2 inhibitor

10.31219/osf.io/eyv5b ◽

2019 ◽

Author(s):

Awad Magbri ◽

Eusera El-Magbri ◽

Mariam El-Magbri ◽

Brar Balhinder ◽

Shauket Rashid

Keyword(s):

Metabolic Acidosis ◽

Vital Signs ◽

Blood Gas Analysis ◽

Albumin Level ◽

Gas Analysis ◽

Anion Gap ◽

Urine Ph ◽

Bowel Surgery ◽

Arterial Blood ◽

Work Up

7 years, hypertension, hypercholesterolemia, who was admitted to the hospital with left lower limb cellulitis over the past 8 days. On work-up he was found to have high anion-gap metabolic acidosis (AGMA) with anion gap of 25, his lactate levels were normal (D and L-lactate). He denies overdosing with any medications and his toxicology screen for methanol, ethanol, aspirin, and ethylene glycol were negative. He has no psychiatric history of note. He denies using over the counter medications like acetaminophen. No bowel surgery could be elicited. He felt dehydrated and nauseous but otherwise fine. His medications includes; carvedalol 25mg twice daily, hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin 81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeks ago to control his blood sugar level and A1C. Physical examination of the patient revealed, slightly dehydrated but well-nourished man, his vital signs; heart rate of 78 BPM and regular, BP 143/85 mmHg, temperature 98.7 F, and his oxygen saturation while breathing room air was 92%. Examination of the heart, abdomen, and chest were unremarkable. He had left lower leg cellulitis but no edema or tenderness. His work-up including chemistry-7 which showed sodium of 142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L, bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78 mg/L respectively. His blood glucose level was 178 mg/L with A1C of 8.2. His serum osmolality was 312 mosm/L, and his arterial blood pH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of 32mmHg. His calculated anion gap was 25 given his normal albumin level. His investigation also showed positive ketones in the serum and urine. His urine PH was 5.5 and the urine contain >800 mg of glucose.

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High Anion Gap Metabolic Acidosis due to Euglycemic Diabetic Ketoacidosis Caused by Sodium-Glucose Co-transporter 2 inhibitor

10.31221/osf.io/f4xub ◽

2019 ◽

Author(s):

Awad Magbri ◽

Eusera El-Magbri ◽

Mariam El-Magbri ◽

Brar Balhinder ◽

Shauket Rashid

Keyword(s):

Metabolic Acidosis ◽

Vital Signs ◽

Blood Gas Analysis ◽

Albumin Level ◽

Gas Analysis ◽

Anion Gap ◽

Urine Ph ◽

Bowel Surgery ◽

Arterial Blood ◽

Work Up

The case is that of 58 year-male with type 2 diabetes mellitus for 7 years, hypertension, hypercholesterolemia, who was admitted to the hospital with left lower limb cellulitis over the past 8 days. On work-up he was found to have high aniongap metabolic acidosis (AGMA) with anion gap of 25, his lactate levels were normal (D and L-lactate). He denies overdosing with any medications and his toxicology screen for methanol, ethanol, aspirin, and ethylene glycol were negative. He has no psychiatric history of note. He denies using over the counter medications like acetaminophen. No bowel surgery could be elicited. He felt dehydrated and nauseous but otherwise fine. His medications includes; carvedalol 25mg twice daily, hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin 81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeks ago to control his blood sugar level and A1C. Physical examination of the patient revealed, slightly dehydrated but well-nourished man, his vital signs; heart rate of 78 BPM and regular, BP 143/85 mmHg, temperature 98.7 F, and his oxygen saturation while breathing room air was 92%. Examination of the heart, abdomen, and chest were unremarkable. He had left lower leg cellulitis but no edema or tenderness. His work-up including chemistry-7 which showed sodium of 142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L, bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78 mg/L respectively. His blood glucose level was 178 mg/L with A1C of 8.2. His serum osmolality was 312 mosm/L, and his arterial blood pH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of 32mmHg. His calculated anion gap was 25 given his normal albumin level. His investigation also showed positive ketones in the serum and urine. His urine PH was 5.5 and the urine contain >800 mg of glucose.

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MON-690 Euglycemic Diabetic Ketoacidosis Associated with SGLT-2 Inhibitors- an Under-recognized Diagnosis

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.612 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Sarah Chhabra ◽

Alex Manzano ◽

Neha Garg

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Diabetic Ketoacidosis ◽

Urine Analysis ◽

Kidney Injury ◽

Anion Gap ◽

History Of ◽

Euglycemic Diabetic Ketoacidosis

Abstract Background Sodium glucose cotransporter-2 inhibitors (SGLT-2i) are a promising class of oral anti-hyperglycemic agents with mounting evidence of reduced cardiovascular risk and renal failure, in patients with type 2 diabetes mellitus. Recent increase in their use has led to identification of hitherto unknown side effects of these drugs. Euglycemic Diabetic Ketoacidosis (eDKA), found to be associated with SGLT-2i use, is a life-threatening condition and commonly goes unrecognized due to absence of the cardinal sign of hyperglycemia. Clinical Case We describe a 47 year old male with history of coronary artery disease and recently diagnosed type 2 diabetes mellitus who presented to our hospital with one week history of nausea, lethargy, progressive fatigue, and shortness of breath. He was diagnosed with type 2 diabetes three weeks prior, with HBA1c of 12%. His regimen included basal insulin and recent transition to empagliflozin due to severe GI intolerance with metformin use. On arrival he was noted to be tachycardic with a heart rate of 113/min, afebrile and normotensive. Physical exam was mostly unremarkable except for dry oral mucous membranes. Serum chemistry was consistent with high anion gap metabolic acidosis with bicarbonate of 6.9 mmol/L (21-32 mmol/L), anion gap of 29 mmol/L (10-20 mmol/L), mildly elevated blood glucose of 132 mg/dl (74-106 mg/dl), acute kidney injury with creatinine of 1.47 mg/dl (0.7- 1.3 mg/dl), and a beta hydroxybutyrate level of 82.7 mg/dl (0.20- 5.63 mg/dl). Urine analysis showed ketonuria. This was consistent with a clinical and biochemical diagnosis of eDKA. He was treated with IV D5%NS-20mEq/L KCL and an insulin drip. Upon resolution of his acidosis and normalization of the anion gap he was switched to subcutaneous Insulin Glargine and Lispro. Empagliflozin was held as it was thought to be contributing to the diagnosis of eDKA. Conclusion Our case yet again illustrates the importance of recognition of EDKA to aid prompt management, especially with the rising popularity of SGLT-2 inhibitors. It is also important to educate patients about this condition, mostly notable in the first two months of starting the medication, to recognize the concerning symptoms and precipitating factors like dehydration, improper insulin dosing, low calorie diet, alcohol, infection, surgery. An acceptable alternative to SGLT-2i can be glucagon like peptide receptor (GLP- 1) agonists, also associated with good cardiovascular outcomes.

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Renal Tubular Acidosis in Patients with Systemic Lupus Erythematosus

Kidney & Blood Pressure Research ◽

10.1159/000509841 ◽

2020 ◽

Vol 45 (6) ◽

pp. 883-889

Author(s):

Necmi Eren ◽

Ozkan Gungor ◽

Feyza Nur Sarisik ◽

Fatih Sokmen ◽

Didem Tutuncu ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Metabolic Acidosis ◽

Lupus Erythematosus ◽

Blood Gas Analysis ◽

Gas Analysis ◽

Anion Gap ◽

Blood Gas ◽

Systemic Lupus ◽

The Mean ◽

Renal Tubular

Objective: Renal tubular acidosis (RTA) is a clinical manifestation that occurs with insufficiency in restoring bicarbonate or disruption in hydrogen ion elimination as a result of a disruption in tubulus functions, causing normal anion gap-opening metabolic acidosis. In the present study, we aimed to investigate the prevalence of RTA in the largest systemic lupus erythematosus (SLE) patient population to date. Materials and Methods: SLE patients, who were followed up in 2 different healthcare centers, were included. Patients with metabolic acidosis (pH <7.35 and HCO3 <22 mEq/L) in venous blood gas analysis were determined. The serum and urine anion GAP of these patients were estimated, and the urine pH was assessed. RTA presence was evaluated as metabolic acidosis with a normal serum anion gap and a positive urine anion GAP. Results: A total of 108 patients were included in the present study. The mean age of the patients was 41.5 ± 1.2 and 87% were female. The SLE diagnosis duration was 75 ± 5 months. The mean creatinine value was 0.6 ± 0.1 mg/dL and the mean eGFR was 111 ± 2 mL/min. According to the blood gas analysis, 18 patients (16.7% of the total) had RTA. Sixteen of these patients had type 1 RTA and 2 had type 2 RTA; type 4 RTA was not determined in any of the patients. Conclusion: RTA should be considered in SLE patients even if they have normal eGFR values. This is the largest study to examine the prevalence of RTA in SLE patients in the literature.

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