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Potassium Shift With Insulin

Comparison Of Insulin Action On Glucose Versus Potassium Uptake In Humans

Comparison Of Insulin Action On Glucose Versus Potassium Uptake In Humans

Abstract Background and objectives Insulin has several physiologic actions that include stimulation of cellular glucose and potassium uptake. The ability of insulin to induce glucose uptake by cells is impaired in type 2 diabetes mellitus, but whether potassium uptake is similarly impaired is not known. This study examines whether the cellular uptake of these molecules is regulated in concert or independently. Design, setting, participants, & measurements Thirty-two nondiabetic and 13 type 2 diabetic subjects with normal GFR were given a similar, constant metabolic diet for 8 days. On day 9, they were subjected to a hyperinsulinemic euglycemic clamp for 2 hours. Serum and urinary chemistry were obtained before and during the clamp. Glucose disposal rate was calculated from glucose infusion rate during hyperinsulinemic euglycemia. Intracellular potassium and phosphate uptake were calculated by the reduction of extracellular potassium or phosphate content corrected for urinary excretion. Results Although glucose disposal rate tended to be lower in type 2 diabetics, cellular potassium uptake was similar between diabetics and nondiabetics. Additionally, although glucose disposal rate was lower with increasing body mass index (R2 = 0.362), cellular potassium (R2 = 0.052), and phosphate (R2 = 0.002), uptake rates did not correlate with body mass index. There was also no correlation between glucose disposal rate and potassium (R2 = 0.016) or phosphate uptake (R2 = 0.053). Conclusions Insulin-stimulated intracellular uptake of glucose and potassium are independent of each other. In type 2 diabetes, potassium uptake is preserved despite impaired glucose disposal. Introduction Insulin has a multitude of actions on a wide range of cellular processes. In terms of caloric and glucos Continue reading >>

Regulation Of Potassium Homeostasis

Regulation Of Potassium Homeostasis

Abstract Potassium is the most abundant cation in the intracellular fluid, and maintaining the proper distribution of potassium across the cell membrane is critical for normal cell function. Long-term maintenance of potassium homeostasis is achieved by alterations in renal excretion of potassium in response to variations in intake. Understanding the mechanism and regulatory influences governing the internal distribution and renal clearance of potassium under normal circumstances can provide a framework for approaching disorders of potassium commonly encountered in clinical practice. This paper reviews key aspects of the normal regulation of potassium metabolism and is designed to serve as a readily accessible review for the well informed clinician as well as a resource for teaching trainees and medical students. Introduction Potassium plays a key role in maintaining cell function. Almost all cells possess an Na+-K+-ATPase, which pumps Na+ out of the cell and K+ into the cell and leads to a K+ gradient across the cell membrane (K+in>K+out) that is partially responsible for maintaining the potential difference across the membrane. This potential difference is critical to the function of cells, particularly in excitable tissues, such as nerve and muscle. The body has developed numerous mechanisms for defense of serum K+. These mechanisms serve to maintain a proper distribution of K+ within the body as well as regulate the total body K+ content. Internal Balance of K+ The kidney is primarily responsible for maintaining total body K+ content by matching K+ intake with K+ excretion. Adjustments in renal K+ excretion occur over several hours; therefore, changes in extracellular K+ concentration are initially buffered by movement of K+ into or out of skeletal muscle. The regula Continue reading >>

Question Of The Week

Question Of The Week

Your answer is correct. The most appropriate treatment to reduce serum potassium by shifting potassium intracellularly is intravenous administration of insulin and dextrose. Detailed Feedback Intravenous insulin/dextrose is the most appropriate option for managing this patient's hyperkalemia. This treatment shifts potassium intracellularly within 3 to 5 minutes after administration, decreasing the serum potassium level by 0.6 to 1.0 mEq/liter after 30 minutes. Nebulized albuterol can also shift potassium intracellularly. The effective dose of albuterol to treat hyperkalemia, however, is much higher than that used for bronchospasm (10 to 20 mg instead of 2.5 mg). Many clinicians have reservations about using high-dose albuterol in patients with hyperkalemia for fear of producing a tachyarrhythmia. Although sodium bicarbonate would theoretically shift potassium intracellularly, the effect appears to be small, and data to support this practice are limited. Most clinicians reserve this strategy for patients who have a concomitant metabolic acidosis. Sodium polystyrene sulfate resin increases potassium excretion through the gastrointestinal tract, but it takes at least 4 hours to work and its efficacy is not supported by strong evidence. Furosemide effectively treats hyperkalemia in patients with preserved renal function, but its action is not as rapid as insulin/dextrose or albuterol and is unlikely to be effective in a patient with oliguric acute kidney injury. If volume resuscitation restores urine output, then furosemide can be used to increase potassium secretion. Calcium infusion does not lower the serum potassium level but makes cardiac tissue less excitable. This is critical for patients with an abnormal electrocardiogram but also reasonable in any patient with sever Continue reading >>

Treatment And Prevention Of Hyperkalemia In Adults

Treatment And Prevention Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem that is most often a result of impaired urinary potassium excretion due to acute or chronic kidney disease (CKD) and/or disorders or drugs that inhibit the renin-angiotensin-aldosterone system (RAAS). Therapy for hyperkalemia due to potassium retention is ultimately aimed at inducing potassium loss [1,2]. In some cases, the primary problem is movement of potassium out of the cells, even though the total body potassium may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled hyperglycemia (eg, diabetic ketoacidosis or hyperosmolar hyperglycemic state). In these disorders, hyperosmolality and insulin deficiency are primarily responsible for the transcellular shift of potassium from the cells into the extracellular fluid, which can be reversed by the administration of fluids and insulin. Many of these patients have a significant deficit in whole body potassium and must be monitored carefully for the development of hypokalemia during therapy. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Potassium replacement'.) The treatment and prevention of hyperkalemia will be reviewed here. The causes, diagnosis, and clinical manifestations of hyperkalemia are discussed separately. (See "Causes and evaluation of hyperkalemia in adults" and "Clinical manifestations of hyperkalemia in adults".) DETERMINING THE URGENCY OF THERAPY The urgency of treatment of hyperkalemia varies with the presence or absence of the symptoms and signs associated with hyperkalemia, the severity of the potassium elevation, and the cause of hyperkalemia. Our approach to therapeutic urgency is as follows (algorithm 1): Continue reading >>

Hypokalemia (low Potassium)

Hypokalemia (low Potassium)

What Is Hypokalemia? Hypokalemia is an electrolyte imbalance and is indicated by a low level of potassium in the blood. The normal adult value for potassium is 3.5-5.3 mEq/L. Potassium is one of many electrolytes in your body. It is found inside of cells. Normal levels of potassium are important for the maintenance of heart, and nervous system function. What Causes Hypokalemia? One way your body regulates blood potassium levels is by shifting potassium into and out of cells. When there is a breakdown or destruction of cells, the electrolyte potassium moves from inside of the cell to outside of the cell wall. This shift of potassium into the cells causes hypokalemia. Trauma or insulin excess, especially if diabetic, can cause a shift of potassium into cells (hypokalemia). Potassium is excreted (or "flushed out" of your system) by your kidneys. Certain drugs or conditions may cause your kidneys to excrete excess potassium. This is the most common cause of hypokalemia. Other causes of hypokalemia include: Increased excretion (or loss) of potassium from your body. Some medications may cause potassium loss which can lead to hypokalemia. Common medications include loop diuretics (such as Furosemide). Other drugs include steroids, licorice, sometimes aspirin, and certain antibiotics. Renal (kidney) dysfunction - your kidneys may not work well due to a condition called Renal Tubular Acidosis (RTA). Your kidneys will excrete too much potassium. Medications that cause RTA include Cisplatin and Amphotericin B. You may have hypokalemia from a loss of body fluids due to excessive vomiting, diarrhea, or sweating. Endocrine or hormonal problems (such as increased aldosterone levels) - aldosterone is a hormone that regulates potassium levels. Certain diseases of the endocrine system, s Continue reading >>

Hyperkalemia

Hyperkalemia

Definition Physiologic antagonists: 500 mg calcium chloride, or 1 gm calcium gluconate is enough to temporarily stabilize the heart from the effects of hyperkalemia Shift K+ from plasma back into the cell: intravenous glucose (25 to 50 g dextrose, or 1-2 amps D50) plus 5-10 U regular insulin will reduce serum potassium levels within 10 to 20 minutes, and the effects last 4 to 6 hours, hyperventilation, β-agonists. In the past, bicarbonate (1 mEq/kg, or 1-2 amps in a typical adult) was recommended, however keep in mind that bicarbonate rarely helps, and furthermore binds Ca++, which may be counterproductive. Note that in the setting of liver tranplantation, prophylactic insulin and glucose has been suggested. Increase renal excretion: diuretics (furosemide, 20-40 mg IV), resin exchange, dialysis, aldosterone agonists (fludrocortisone) Acute Hyperkalemia Treatment Membrane Stabilization: CaCl2 K+ Shift: glucose/insulin, induce alkalosis (bicarbonate, hyperventilation), β-agonists K+ Excretion: furosemide, resins, fludrocortisone, dialysis Causes of acute hyperkalemia: drugs (succinylcholine, ACE/ARB’s, mannitol, spironolactone, digitalis, non-selective beta blockers) that cause decreased renal K+ excretion, reperfusion of an organ/vascular bed after ischemia (usually greater than 4 hours), adrenal inhibition or decreased aldosterone levels, transcellular shifts (intracellular to extracellular), often caused by acidosis, acute renal failure Symptoms: mild elevation (6-7 mEq/L) can cause peaked T-waves on EKG tracing, 10-12 mEq/L can cause prolonged PR interval, widened QRS, VFib, Asystole. Clinical symptoms are muscle weakness and paralysis. Subspecialty Keyword history See Also: Sources PubMed M Allon, A Takeshian, N Shanklin Effect of insulin-plus-glucose infusion wi Continue reading >>

High Serum Potassium Levels And Cardiac Arrest

High Serum Potassium Levels And Cardiac Arrest

The amount of potassium (K+) in the blood determines the excitability of nerve and muscle cells, including the heart muscle or myocardium. When potassium levels in the blood rise, this reduces the electrical potential and can lead to potentially fatal abnormal heart rhythms. High serum potassium levels also called hyperkalemia can be life-threatening and requires immediate therapy. There are several conditions which can significantly affect serum potassium levels and cause them to rise. Metabolic acidosis causes a decrease in serum pH which has a direct effect on serum levels of potassium. When serum pH drops (metabolic acidosis) serum potassium rises, and potassium shifts from intracellular to extracellular (into the blood). Another condition that is a common cause of hyperkalemia is end-stage renal disease. When the kidneys fail, they can no longer remove excess potassium, and it accumulates in the blood. Signs and symptoms of hyperkalemia include weakness, ascending paralysis, and respiratory failure. There are some ECG signs that may suggest hyperkalemia. Mild hyperkalemia can cause peaked T waves. As potassium levels continue to rise, you may see flattened p-waves, prolonged PR-interval, and other anomalies. If hyperkalemia is left untreated you may see idioventricular rhythms and a sine-wave pattern. Severe hyperkalemia can lead to asystolic cardiac arrest. The treatment of hyperkalemia depends on the severity and the patient’s clinical presentation. For mild hyperkalemia removal of potassium from the body is achieved with diuretics which cause the release of potassium in the urine. One example of a diuretic which does not spare potassium is furosemide. Resins like Kayexalate can also be used to remove potassium from the body. Kayexalate can be administered oral Continue reading >>

Potassium Homeostasis

Potassium Homeostasis

Potassium: a critical cation Potassium (K+) is a main cation essential for many cellular functions. It is the most abundant cation in the body, with 98% in intracellular fluid and only 2% in extracellular fluid. Because of this delicate balance, even the slightest acute compartmental shifts can be fatal.1-3 The pathophysiology of serum potassium homeostasis Regulation of serum potassium is complex and involves appropriate distribution between intracellular and extracellular compartments, and a balance between dietary and supplemental intake and bodily excretion.3,4 (See a list of potassium-rich foods.) The kidney is central to this process, which also relies on several other regulators.4 In healthy individuals, homeostasis is maintained when cellular uptake and urinary or renal excretion naturally counterbalance a patient's dietary intake of K+.4 While values vary from person to person and day to day, the standard normal range of serum potassium is considered to be 3.5 mEq/L to 5.0 mEq/L.5,6 In healthy individuals, 90% of K+ is absorbed through the gut into the serum where the majority is taken up by cells. There is a delicate balance between intracellular and extracellular levels, with nearly 98% of K+ found in the intracellular compartment.7 The ratio of intracellular to extracellular K+, managed primarily by sodium-potassium ATPase, is important in determining the cell membrane potential.7 Other ion channels and transporters can also play a role in affecting this distribution.7 About 70% of the total intracellular content is distributed primarily in the muscles, with smaller amounts present in bone, red blood cells, liver, and skin.3 The kidney plays a major role in the maintenance of K+ balance by adjusting secretion in response to dietary intake, regulating about 9 Continue reading >>

Hyperkalaemia

Hyperkalaemia

Case Study of Hyperkalemia: George is a 72 year old male found collapsed at home on floor of his bedroom, incontinent of urine and faeces. He complained of significant pain in his right hip with shortening and rotation. George’s family last had contact with George 3 days prior to his collapse. Assessment: On arrival at ED he is confused and combative with a GCS 0f 13 Initial observations reveal BP 78/60; Pulse 74, RR 32, SPO2 91% (NRB 15L) ABG which shows a Potassium of 9.0, pH of 7.23 and a Blood Glucose Level of 32mmol Medical History: CCF Hypertension Type 2 DM Osteoarthritis Medication History: George is taking enlapril for hypertension; spironolactone & metoprolol for his CCF and celebrex for his osteoarthritis His diabetes is diet controlled. An ECG is performed on his arrival to the resuscitation area… You briefly review the ECG and confidently state (already knowing the ABG result) that this patient has sever hyperkalemia. Brilliant…now what? The 5 C’s of Metabolic Disturbances I use the 5 C’s approach to recognise, understand and manage metabolic disturbances in the ED. Causes – Understanding normal metabolic homeostatic mechanisms helps define potential causative events that lead to disruption of the sensitive pathophysiological milieu. Increased production; increased intake and decreased excretion are often the commonest causal factors in metabolic disruption. Clinical manifestations – evaluate, recognise and diagnose the problem Complications – what can go wrong in the short, medium and long term can define clinical manifestation, duration of illness and potentially affect management decisions Calculations – Calculate to Obviate Corrective measures – Call to action…how do you actually fix the problem! Potassium Pathophysiology Serum pot Continue reading >>

Potassium Shifts

Potassium Shifts

Snapshot A 22-year-old man presents to the emergency department after a crush injury to his lower extremities. He reports muscular pain, weakness, and palpitations and noticed that his urine is "tea-colored." On physical exam, there is tenderness upon palpation of his lower extremities and 4-/5 power in the same area. Urinalysis is heme positive. Laboratory testing is significant for a potassium level of 6.5 mEq/L and creatinine kinase level of 1,500 units/L. An electrocardiogram is shown. (Rhabdomyolysis resulting in hyperkalemia) Introduction The major intracellular cation is potassium and magnesium cells contain approximately 98% of the body's potassium the sodium-potassium-ATPase (Na+/K+ -ATPase) pump within the cellular membrane maintains this potassium distribution between the intracellular and extracellular compartments potassium is the major determinant of the resting membrane potential across the cell membrane normal potassium homeostasis is essential for proper action potential generation in muscle and neural tissue Normal potassium homeostasis determined by potassium intake intracellular and extracellular potassium distribution urinary excretion of potassium mainly accomplished by principal cells in the nephron Disruptions in potassium homeostasis can result in hyperkalemia or hypokalemia these disruptions can have a number of clinical consequences hyperkalemia defined as a potassium level in the blood that is > 5.0-5.5 mEq/L muscle and cardiac dysfunction muscular symptoms myalgias muscle paralysis chest pain cardiac symptoms arrhythmias and palpitations nausea and vomiting parasthesias hypokalemia defined as a potassium level in the blood that is < 3.5 mEq/L muscle and cardiac dysfunction muscular symptoms abdominal cramping muscle weakness and cramping car Continue reading >>

Hyperkalemia Management: Preventing Hypoglycemia From Insulin

Hyperkalemia Management: Preventing Hypoglycemia From Insulin

Insulin remains one of the cornerstones of early severe hyperkalemia management. Insulin works via a complex process to temporarily shift potassium intracellularly. Though insulin certainly lowers plasma potassium concentrations, we often underestimate the hypoglycemic potential of a 10 unit IV insulin dose in this setting. The purpose of this post is to highlight the need for proper supplemental glucose and blood glucose monitoring when treating hyperkalemia with insulin. Incidence of Hypoglycemia One of my favorite articles on the management of hyperkalemia was written by Dr. Weisberg in Critical Care Medicine.1 A 10 unit dose of IV regular insulin has an onset of action of about 5-10 minutes, peaks at 25-30 minutes, and lasts 2-3 hours (the Weisberg article actually lists subcutaneous kinetics). Herein lies the problem in that IV dextrose only lasts about an hour (at most). Allon et al reported up to 75% of hemodialysis patients with hyperkalemia developed hypoglycemia at 60 minutes after insulin administration.2 A retrospective review of 219 hyperkalemic patients reported an 8.7% incidence of hypoglycemia after insulin treatment.3 More than half of the hypoglycemic episodes occurred with the commonly used regimen of 10 units of IV insulin with 25 gm of dextrose. A more recent study of 221 end-stage renal disease patients who received insulin for treatment of hyperkalemia reported a 13% incidence of hypoglycemia.4 The overall incidence of hypoglycemia appears to be ~10%, but could be higher. Risk Factors for Developing Hypoglycemia The study by Apel et al identified three factors associated with a higher risk of developing hypoglycemia: No prior diagnosis of diabetes [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.0–5.1, P = 0.05] No use of diabetes medication Continue reading >>

Hyperkalaemia In Adults

Hyperkalaemia In Adults

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 Dietary Potassium article more useful, or one of our other health articles. Description Hyperkalaemia is defined as plasma potassium in excess of 5.5 mmol/L[1]. The European Resuscitation Guidelines further classify hyperkalaemia as: Mild - 5.5-5.9 mmol/L. Moderate - 6.0-6.4 mmol/L. Severe - >6.5 mmol/L. Potassium is the most abundant intracellular cation - 98% of it being located intracellularly. Hyperkalaemia has four broad causes: Renal causes - eg, due to decreased excretion or drugs. Increased circulation of potassium - can be exogenous or endogenous. A shift from the intracellular to the extracellular space. Pseudohyperkalaemia. Epidemiology The time of greatest risk is at the extremes of life. Reported incidence in hospitals is 1-10%, with reduced renal function causing a five-fold increase in risk in patients on potassium-influencing drugs[2]. Men are more likely than women to develop hyperkalaemia, whilst women are more likely to experience hypokalaemia. Renal causes Acute kidney injury (AKI). Chronic kidney disease (CKD): Normally all potassium that is ingested is absorbed and excretion is 90% renal and 10% alimentary. Most excretion by the gut is via the colon and in CKD this can maintain a fairly normal blood level of potassium. It seems likely that the elevated potassium levels in CKD trigger the excretion of potassium via the colon[3]. Patients with CKD must be careful of foods rich in potassium. Hyperkalaemic renal tubular acidosis. Mineralocorticoid deficiency. Medicines that interfere with potassium excretion - eg, amiloride, spironolac Continue reading >>

Potassium Disorders – Hyperkalemia And Hypokalemia

Potassium Disorders – Hyperkalemia And Hypokalemia

Hypokalemia will see flattened T waves and U waves on ekg RTAs 1 and 2, worry if <2.5. Can lead to rhabdomyolysis Causes: GI losses, ampho B, Insulin, Rta, Diet, Burns, Alkalosis, Timentin and other pcns, Hypomagnesaemia, Steroids. Diuretics, Cushing’s, Familial Periodic Paralysis, Hyperthyroidism Need ~40 mEq of K to increase 1 mEq/L A patient who is hypokalemic in the face of ACIDOSIS and is getting insulin to boot, may be another exception. Acidosis shifts K from the cell to the extracellular compartment. Serum K tends to rise. a K of 2.5 may be equivalent to a K of 1.5 in a patient with normal pH. The insulin will further drop his serum K. Yes, I would give KCl in this setting. The danger is giving potassium to a patient in ALKALOSIS where the observed hypokalemia is an effect of the pH. The most common setting for hyperkalemic arrest is in patients who are on chronic diuretics, have chronic mild hypokalemia because of chronic depletion, and their intracellular potassium is also low. The also have contraction alkalosis, and because the K gets artificially very low, are getting aggressive (20 mmol/h) K replacement. These patients may arrest at K levels of 5-6. and as their alkalosis is corrected may get there pretty darn quick. Your patient is the exact opposite example, and his hypokalemia should have been corrected. I never argued that one should never correct hypokalemia. In most cases, however, it should be corrected slowly, preferrably with oral potassium. Hypokalemia!Pearls to keep in mind: When treating significant hypokalemia with IV potassium replacement, initial therapy should consist of potassium administered in glucose-free solutions. Glucose may cause a further decrease in the serum potassium concentration, presumably caused by the enhanced insulin sec Continue reading >>

Insulin For The Treatment Of Hyperkalemia: A Double-edged Sword?

Insulin For The Treatment Of Hyperkalemia: A Double-edged Sword?

Potassium plays a critical role in cellular metabolism and normal neuromuscular function. Tightly regulated homeostatic mechanisms have developed in the process of evolution to provide primary defense against the threats of hyper- and hypokalemia. The kidney plays a primary role in potassium balance, by increasing or decreasing the rate of potassium excretion. Distribution of potassium between the intracellular and the extracellular fluid compartments is regulated by physiologic factors such as insulin and catecholamines which stimulate the activity of the Na+-K+ ATPase. Only about 10% of the ingested potassium is excreted via the gut under normal physiologic conditions [1]. End stage renal disease (ESRD) patients rely largely on extra-renal mechanisms and dialysis to maintain potassium homeostasis. Despite the availability of dialysis and the adaptive increase in colonic excretion of potassium in renal insufficiency, severe hyperkalemia (defined as serum potassium level > 6 mEq/L [6 mmol/L]) is observed in 5-10% of maintenance dialysis patients and is responsible for 0.7% of deaths in the dialysis population in the United States [2–4]. Several factors can explain the high incidence of hyperkalemia in this population. Tolerance for a rapid potassium load is impaired in ESRD, not only because of lack of renal excretion, but also as a result of impaired cellular distribution of potassium [5]. The latter may result from defect in the Na+-K+ ATPase and possibly elevated glucagon levels in uremia [5, 6]. High dietary potassium intake and missed dialysis treatments are common contributors to hyperkalemia in ESRD patients. Other factors such as constipation (decreased colonic excretion) and fasting state (relative lack of insulin) may also predispose ESRD patients to hyperka Continue reading >>

Hyperkalemia In Emergency Medicine

Hyperkalemia In Emergency Medicine

Practice Essentials Hyperkalemia can be difficult to diagnose clinically because symptoms may be vague or absent. The fact, however, that hyperkalemia can lead to sudden death from cardiac arrhythmias requires that physicians be quick to consider hyperkalemia in patients who are at risk for it. See the electrocardiogram below. See also Can't-Miss ECG Findings, Life-Threatening Conditions: Slideshow, a Critical Images slideshow, to help recognize the conditions shown in various tracings. Signs and symptoms Patients with hyperkalemia may be asymptomatic, or they may report the following symptoms (cardiac and neurologic symptoms predominate): Evaluation of vital signs is essential for determining the patient’s hemodynamic stability and the presence of cardiac arrhythmias related to hyperkalemia. [1] Additional important components of the physical exam may include the following: Signs of renal failure, such as edema, skin changes, and dialysis sites, may be present Signs of trauma may indicate that the patient has rhabdomyolysis, which is one cause of hyperkalemia See Clinical Presentation for more detail. Diagnosis Laboratory studies The following lab studies can be used in the diagnosis of hyperkalemia: Potassium level: The relationship between serum potassium level and symptoms is not consistent; for example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients; the rapidity of change in the potassium level influences the symptoms observed at various potassium levels Calcium level: If the patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances) Urinalysis: To look for evidence of glomerulonephritis if signs of renal insufficiency without a known cause are present Cortisol a Continue reading >>

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