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Why Is Creatinine High In Diabetic Ketoacidosis?

Falsely-elevated Serum Creatinine Values In Diabetic Ketoacidosis -- Clinical Implications.

Falsely-elevated Serum Creatinine Values In Diabetic Ketoacidosis -- Clinical Implications.

Falsely-elevated serum creatinine values in diabetic ketoacidosis -- clinical implications. Unusual elevations of serum creatinine (S-CR) out proportion to increases in serum urea nitrogen (S-UN) are frequently observed in patients with diabetic ketoacidosis when S-CR is measured by the Jaffe end-point reaction. This has been ascribed to interference from acetoacetate but this is not however observed with kinetic DuPont ACA methodology. Eighteen patients with diabetic ketoacidosis were studied: SCR measurements were done using the end point Technicon SMA 6/60 method (Group a, 10 patients) or the kinetic DuPont ACA method (Group B, 8 patients). The values for S-CR in Group A patients (mean value and S-D were 3.3 +/- 1.1 mg/dl) were significantly different from Group B patients (1.6 +/- 0.24 mg/dl) (P less than 0.01). A significant positive correlation was obtained between the "excess anion gap" and S-CR in Group A patients (r = + 0.81, p less than 0.01). The results from two patients in whom serial measurements of S-UN, S-CR and the anion gap were carried out further demonstrate the analytical interference. The study demonstrates that in diabetic ketoacidosis elevated creatinine values measured by an end-point method should not necessarily be interpreted as evidence of significant renal impairment and if possible should be verified by a kinetic method which is free of "ketone" interference. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

Measure Electrolyte And Ketone Levels And Determine Anion Gap In Patients With Diabetes And Normal Sugar Levels

Measure Electrolyte And Ketone Levels And Determine Anion Gap In Patients With Diabetes And Normal Sugar Levels

DIABETIC KETOACIDOSIS DX: Diabetic Ketoacidosis (DKA) when the blood glucose is >=250 mg/dL, arterial pH <=7.30, serum bicarbonate <=15 mEq/L, and positive serum ketones. (Hyperglycemia, ketonemia, ketonuria, metabolic acidosis) Screening for Diabetic Ketoacidosis - Consider DKA if hyperglycemia, acidosis, or ketonemia are present. Screen all patients with moderate to severely elevated blood sugars (glucose >350 mg/dL). Measure electrolytes, glucose, ketones, and blood gases to determine whether anion gap metabolic acidosis is present in patients with positive ketones, constitutional symptoms, or suspicion of DKA. in patients with an anion gap metabolic acidosis. Measure serum glucose in patients with metabolic acidosis. in diabetes patients with infection, CVA, MI, or other illness. Measure serum glucose and if glucose >250 mg/dL, check the patient's electrolyte and ketone levels and anion gap. in diabetic patients with symptoms of nausea and vomiting (with polyuria, polydipsia), even if blood glucose is <250 mg/dL. if symptoms suggest DKA despite normal blood sugar levels. in patients on atypical antipsychotics who present with hyperglycemia. Measure anion gap and ketones in patients on atypical antipsychotics who present with moderate to severe hyperglycemia. SX: Dehydration with hypotension, hyperventilation with fruity "acetone" odor, polyphagia, polydipsia, polyuria, altered mental status, N&V. History and Physical Examination Elements for Diabetic Ketoacidosis History Type 1 diabetes - DKA is a frequent complication of type 1 diabetes Constitutional symptoms - DKA may show vague symptoms of lethargy, diminished appetite, and headache Polyuria, polydipsia - May precede the development of DKA by 1 or 2 days, especially if intercurrent illness (infection) is present Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Department of Obstetrics and Gynaecology Diabetic ketoacidosis is an acute metabolic and obstetric emergency that can jeopardize both mother and fetus. Normally treated in ICU. Fetal mortality as high as 50%. The clinical features of DKA are due to: Marked dehydration Acidosis Electrolyte disturbance Presenting signs and symptoms of DKA: Vomiting Polydipsia Polyuria Weakness Abdominal pain Weight loss Hyperventilation Dry mucus membranes Tachycardia Hypotension Disorientation Coma Underlying infection Laboratory Findings: Pregnant patient can develop DKA with glucose level less than 20 mg/dl. Diabetic Plasma glucose >16 mmol/l Keto Serum Acetone 1,2 or more Acidosis Arterial pH S-HCO3 Anion Gap less than 7,4 <15,1 [Na+ - (Cl- +HCO-3)] > 12 Diagnostic criteria for diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) DKA DKA DKA HHS Mild Moderate Servere . Plasma glucose (mg/dL) >250 >250 >250 >600 Arterial pH 7.25-7.30 7.00-7.24 <7,00 >7,30 Serum bicarbonate (mEq/L) 15-18 10-15 <10 >15 Urine ketones* Positive Positive Positive Small Serum ketones* Positive Positive Positive Small Effective serum osmolality (mOsm/kg) Variable Variable Variable >320 Anion gap >10 >12 >12 <12 Alteration in sensoria or mental obtundation Alert Variable/drowsy Stupor/coma Stupor/coma * Nitroprusside reaction method. Calculation: 2[measured Na (mEq/L)] + glucose (mg/dL)/18. Calculation: (Na+) - (Cl- + HCO3-) (mEq/L). See text for details. Copyright © 2006 American Diabetes Association From Diabetes Care Vol 29, Issue 12, 2006. Reprinted with permission from the American Diabetes Association. Additional Laboratory Findings Glucosuria Leukocytosis Ketonuria Elevated CPK Metabolic acidosis Elevated amylase Hyperosmolarity Elevated transaminase Hypokalemia Elevated BUN Hypomagne Continue reading >>

Creatinine Is Falsely Elevated In Diabetic Ketoacidosis Patients: A Comparison Of 4 Jaffe Assays With An Enzymatic Method. Asn Events

Creatinine Is Falsely Elevated In Diabetic Ketoacidosis Patients: A Comparison Of 4 Jaffe Assays With An Enzymatic Method. Asn Events

Creatinine is Falsely Elevated in Diabetic Ketoacidosis Patients: A Comparison of 4 Jaffe Assays with an Enzymatic Method. ASN Events Creatinine is Falsely Elevated in Diabetic Ketoacidosis Patients: A Comparison of 4 Jaffe Assays with an Enzymatic Method. Azni Abdul-Wahab 1 , Hanh Nguyen 2 , Mervyn Kyi 3 , Wei Ling Chiu 3 , Que Lam Lam 4 , Cherie Chiang 1 3 Pathology/ Endocrinology, Royal Melbourne Hospital, Melbourne Endocrinology, Royal Melbourne Hospital, Melbourne Endocrinology, Austin Hospital , Melbourne Falsely elevatedplasma creatinine due to glucose and ketone interference is well documented inroutine Jaffe assay (1,2). Although Jaffe assays have been recentlystandardised since the introduction of eGFR, the effect of this interference isunknown since the alignment process. Weassessed plasma creatinine in DKA patients using 4 Jaffe assays against anenzymatic method as the gold standard. Samples were collected from DKA patients presenting to the EmergencyDepartment and ten outpatients with normal glucose and bicarbonate.Aliquots were frozen, transported on dry ice, and analysed on 4 Jaffe assays (Architect,Roche, Beckman Coulter and Siemens) and the Vitros Enzymatic assay. Assay bias (Jaffecreatinine enzymatic creatinine)/ enzymatic creatinine x 100%) was correlatedwith pH, glucose, ketone and baseline creatinine. Of the 22 episodes ofDKA from 20 patients (16 M, 4 F, age 32.4 13.4 years), admission venous pHwas 7.14 0.15, bicarbonate was 9.4 5.5 mmol/L, glucose was 35.9 14.9mmol/L and capillary ketone was 5.9 1.1 mmol/L. The average enzymaticcreatinine value was 111.5 64.1 mol/L. All Jaffe creatinine results weresignificantly higher (p <0.001), in order of magnitude: Abbott (154.6 68.2mol/L), Beckman Coulter (147.1 70.5 mol/L), Roche (128.0 56.4 mol/L) andSieme Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia, ketonuria, acidosis, and dehydration. Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel. Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver. Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to the hyperglycemia caused by insulin deficiency, accelerates the development of DKA. Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water. Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL. Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon dioxide is decreased as a respiratory compensation mechanism. Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and dehydration, despite total body depletion. Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic diuresis and dehydration. Observe for cardiac changes reflecting dehydration, metabolic acidosis, and electrolyte imbalance- hypotension; tachycardia; weak pulse; electrocardiographic changes, including elevated P wave, flattened T wave or inverted, prolonged QT interval. Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb some insulin and the initial solution may contain decreased concentration of insulin. Continue reading >>

The Impact Of Hyperglycemic Emergencies On The Kidney And Liver

The Impact Of Hyperglycemic Emergencies On The Kidney And Liver

Copyright © 2013 Feng Bai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Studies on the alterations of liver and kidney function parameters in patients with diabetic ketoacidosis (DKA) and diabetic ketosis (DK) were limited. Participants with DKA, DK, non-DK, and healthy controls were enrolled in the current study. Parameters of liver and kidney function were measured and evaluated. The patients with DKA had higher levels of plasma glucose, hemoglobin A1c (HbA1c), uric acid, and creatinine but lower levels of transferases and protein compared with the other three groups ( for all). The patients with DK had higher levels of plasma glucose and HbA1c but lower levels of glutamyl transpeptidase and protein compared with the non-DK and control groups (). Prealbumin levels were significantly reduced in the severe DKA patients compared with the mild/moderate DKA patients. Serum prealbumin levels were correlated with albumin levels (, ), HCO3 (, ), and arterial pH (, ) in the DKA patients. A diagnostic analysis showed that lower prealbumin levels significantly reflected the presence of hyperglycemic emergencies (). Liver and kidney function parameters deteriorated, especially in DKA. Prealbumin levels can be of value in detecting the presence of hyperglycemic crisis. This clinical trial is registered with ChiCTR-OCH-12003077. 1. Introduction Diabetic ketoacidosis (DKA) and diabetic ketosis (DK) are common and serious complications of diabetes mellitus. DKA most often occurs in patients with type 1 diabetes (T1D). However, increasing evidence indicates that DKA and DK are also common features of ketosis-pr Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Diabetic ketoacidosis (DKA) is an acute, life‐threatening metabolic complication of diabetes mellitus. Hyperglycaemia, ketosis (ketonaemia or ketonuria) and acidosis are the cardinal features of DKA [1]. Other features that indicate the severity of DKA include volume depletion, acidosis and concurrent electrolyte disturbances, especially abnormalities of potassium homeostasis [1,2]. We describe a type 2 diabetic patient presenting with severe generalized muscle weakness and electrocardiographic evidence of severe hyperkalaemia in association with DKA and discuss the related pathophysiology. A 65‐year‐old male was admitted because of impaired mental status. He was a known insulin‐treated diabetic on quinapril (20 mg once daily) and was taking oral ampicillin 500 mg/day because of dysuria which had started 5 days prior to admission. He was disoriented in place and time with severe generalized muscle weakness; he was apyrexial (temperature 36.4°C), tachycardic (120 beats/min) and tachypneic (25 respirations/min) with cold extremities (supine blood pressure was 100/60 mmHg). An electrocardiogram (ECG) showed absent P waves, widening of QRS (‘sine wave’ in leads I, II, V5 and V6), depression of ST segments and tall peaked symmetrical T waves in leads V3–V6 (Figure 1). Blood glucose was 485 mg/dl, plasma creatinine 5.1 mg/dl (reference range (r.r.) 0.6–1.2 mg/dl, measured by the Jaffe method), urea 270 mg/dl (r.r. 11–54 mg/dl), albumin 4.2 g/dl (r.r. 3.4–4.7 g/dl), sodium 136 mmol/l (r.r. 135–145 mmol/l), chloride 102 mmol/l (r.r. 98–107 mmol/l), potassium 8.3 mmol/l (r.r. 3.5–5.4 mmol/l), phosphorus 1.6 mmol/l (r.r. 0.8–1.45 mmol/l) and magnesium 0.62 mmol/l (r.r. 0.75–1.25 mmol/l). A complete blood count revealed leukocytosis (12 090/µl with Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

Many Children In Dka Experience Acute Kidney Injury

Many Children In Dka Experience Acute Kidney Injury

A study finds more than half of children with Type 1 exhibit the symptoms. Kidney disease is often viewed as a potential long-term complication for Type 1 diabetes. A new study suggests, however, that even a single bout of diabetic ketoacidosis (DKA) may injure the kidneys of children. sponsor For the study, researchers with the University of British Columbia and British Columbia Children’s Hospital reviewed the medical records of 165 children with Type 1 diabetes who had been hospitalized for DKA. Out of this group, 106 children were found to also have experienced acute kidney injury, with two children needing dialysis to treat the condition, according to findings published in JAMA Pediatrics. Acute kidney injury was diagnosed using a blood test to measure the buildup of creatinine, a waste product expelled by the kidneys. Learn more about DKA by reading the article “How DKA Happens and What to Do About it.” According to the National Kidney Foundation, acute kidney injury can be asymptomatic or have a variety of symptoms. Potential symptoms can include a decrease in urination, swelling around legs, ankles, and eyes, fatigue, and chest pain. While acute kidney injury often can be effectively treated in the hospital, it’s considered a risk factor for future stroke, heart disease, and kidney disease; acute kidney injury even ups the risk of future acute kidney injury. The National Kidney Foundation recommends that those who experience acute kidney injury should inform their healthcare providers about it so they can screen kidney health and function. To do this, though, the injury must be properly diagnosed at the time it occurs. sponsor An audit found the risk of DKA during hospitalization was too high. Read more here. DKA taxes the kidneys in a number of ways. Hi Continue reading >>

Diabetic Ketoacidosis Linked To Higher Risk For Aki In Youth

Diabetic Ketoacidosis Linked To Higher Risk For Aki In Youth

High rates of acute kidney injury (AKI) were reported among youth in the hospital for diabetic ketoacidosis (DKA), researchers reported. A low serum bicarbonate level (<10 mEq/L) among hospitalized children with type 1 diabetes and DKA was associated with a significant increase in the risk for stage 2 or 3 AKI (aOR 5.22; 95% CI; 1.35-20.22), according to Brenden E. Hursh, MD, of the University of British Columbia, and colleagues. In the study, published in JAMA Pediatrics, stage 1 acute kidney injury for children with DKA was also linked to an initial corrected sodium level of 145 mEq/L or more (aOR 3.29; 1.25-8.66). Using a multinomial logistic regression model, the researchers also reported a linear relationship between heart rate and severe AKI, with a 22% increase in risk for AKI associated with each increase of five beats per minute in initial heart rate (aOR 1.22; 1.07-1.39). In an interview with MedPage Today, the senior author, Constadina Panagiotopoulos, MD, also of the University of British Columbia, noted, "While I thought we would detect more cases of AKI than that previously represented by the two isolated case reports in the literature, I was surprised by the high proportion -- 64.2% -- of AKI in pediatric DKA documented in our study." The team explained that they predicted that the risk level of hospitalized children with DKA is actually higher than previous case studies have reported, and therefore aimed to identify a more accurate depiction of AKI rates for this high-risk population. Panagiotopoulos said that inspired by a lack of large-scale, systematic studies regarding AKI in youth with DKA when caring for patients affected, the researchers "decided to conduct this study to better understand the magnitude of the problem and any associated risk factor Continue reading >>

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