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Books on the topic 'Serum and urine electrolytes'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

International Symposium on Circulating Nucleic Acids in Plasma/Serum (5th 2007 Moscow, Russia). Circulating nucleic acids in plasma and serum V. Edited by Gahan Peter B, Swaminathan R. Professor, and New York Academy of Sciences. Blackwell Pub. on behalf of the New York Academy of Sciences, 2008.

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2

J, Wald N., National Co-ordinating Centre for HTA (Great Britain), and Health Technology Assessment Programme, eds. First and second trimester antenatal screening for Down's syndrome: The results of the serum, urine and Ultrasound Screening Study (SURUSS). Core Research on behalf of the NCCHTA, 2003.

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3

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Prevention of kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0345.

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A number of factors are known to predispose to renal disease, such as diabetes mellitus, hypertension, and exposure to certain drugs or substances (e.g. mercury and other heavy metals). In people who are at risk for these reasons, renal function should be regularly monitored as part of routine care. Kidney diseases are identified by elevations in the serum creatinine; the presence in the urine of blood, protein, or elevated levels of certain electrolytes; or evidence of anatomical abnormalities. Due to the large functional reserve of the kidneys, symptoms of impaired renal function usually occ

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4

Hibbs, Clair M. Transaminase Activity in Serum, Urine, and Cerebrospinal Fluid of Normal and Diseased Dogs. Creative Media Partners, LLC, 2021.

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5

Quinlan-Murphy, Lonnie J. Influence of age, condition, nutrition and season on serum and urine chemistry in Rocky Mountain elk. 1998.

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6

Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.

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The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves spec

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7

Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.

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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as

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8

Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.

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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as

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9

Lehmann, Paul, Wolf Rüdiger Külpmann, and H. K. Stummvoll. Electrolytes, Acid-Base Balance and Blood Gases: Clinical Aspects and Laboratory. 2nd ed. Springer, 2007.

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10

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Diagnosis in suspected renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0156.

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Renal dysfunction can be easily and, in most cases, unambiguously diagnosed from an elevation in serum creatinine and/or abnormal urinalysis. The clinical challenges lie in first suspecting that renal dysfunction is present and therefore requesting the appropriate test (e.g. serum creatinine/urine analysis), and then identifying the underlying etiology. A major clue to renal dysfunction in the hospitalized patient can be a reduction in urine output. Therefore, urine output should be carefully monitored in those patients who are at risk, which includes most significantly ill hospitalized patien

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11

Raine, Tim, James Dawson, Stephan Sanders, and Simon Eccles. Interpreting results. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199683819.003.0017.

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Blood testsFull blood count (FBC)ClottingCardiac markersInflammatory responseUrea and electrolytes (U+E)Liver function tests (LFT) and amylaseCalcium and phosphateEndocrine testsCardiologyElectrocardiogram (ECG)RespiratoryChest X-ray (CXR)Arterial blood gases (ABGs)Respiratory function testsGastrointestinalAbdomen X-ray (AXR)Urine tests...

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12

Raine, Tim, James Dawson, Stephan Sanders, and Simon Eccles. Fluids and renals. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199683819.003.0012.

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Acute kidney injuryChronic renal failureHaematuriaProteinuriaGlomerular diseaseUrological disordersLow urine outputIV fluidsPotassium emergenciesElectrolyte imbalanceAcute rise from baseline of serum urea and creatinine ±oliguria ( Table 12.1);1there are three basic mechanisms:•Prerenal hypoperfusion of kidney due to eg ↓BP, hypovolaemia, renal artery occlusion (mass, emboli)...

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13

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy diagnosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0067_update_001.

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The defining histological hallmark of immunoglobulin A (IgA) nephropathy is the presence of IgA in the mesangium as the sole or dominant immunoreactant. Light microscopy appearances vary very widely. The most common appearance is mesangial cell proliferation and an increase in mesangial matrix. However, this is not diagnostic in the absence of immunohistology. Focal segmental proliferative or necrotizing glomerulonephritis may be seen in ‘vasculitic’ disease with or without the skin changes of Henoch–Schönlein purpura. Extracapillary proliferation and crescent formation may occur. Occasionally

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14

Palevsky, Paul M. Monitoring renal function in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0209.

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Renal function needs to be monitored in critically-ill patients to detect changes in glomerular filtration rate (GFR) and promptly diagnosis acute kidney injury (AKI). In the absence of reliable bedside techniques for the assessment of GFR, continuous monitoring of urine output and frequent assessment of serum creatinine levels remain the cornerstone of renal functional monitoring. Calculated estimations of GFR should not be relied upon in critically-ill patients, particularly if kidney function is not stable. The role of serum cystatin C as a marker of GFR and biomarkers of tubular injury in

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15

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Clinical approach. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0001.

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History taking in patients with haematological disease - Physical examination - Splenomegaly - Lymphadenopathy - Unexplained anaemia - Patient with elevated haemoglobin - Elevated white blood cell (WBC) count - Reduced WBC count - Elevated platelet count - Reduced platelet count - Easy bruising - Recurrent thromboembolism - Pathological fracture - Raised ESR - Serum or urine paraprotein - Anaemia in pregnancy - Thrombocytopenia in pregnancy - Prolonged bleeding after surgery - Positive sickle test (HbS solubility test)

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16

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Hassan Al-Sader. Clinical approach. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0001_update_001.

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History taking in patients with haematological disease - Physical examination - Splenomegaly - Lymphadenopathy - Unexplained anaemia - Patient with elevated haemoglobin - Elevated white blood cell (WBC) count - Reduced WBC count - Elevated platelet count - Reduced platelet count - Easy bruising - Recurrent thromboembolism - Pathological fracture - Raised ESR - Serum or urine paraprotein - Anaemia in pregnancy - Thrombocytopenia in pregnancy - Prolonged bleeding after surgery - Positive sickle test (HbS solubility test)

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17

Raman, Vidya T. Perioperative Management of Diabetes Mellitus Type 1 and 2. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0046.

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Diabetes management offers unique challenges in children and adolescents versus adults especially in the perioperative environment. The obvious challenges of monitoring dietary intake plus possible communication barriers with increased risk of diabetic ketoacidosis and hypoglycemia. Adding the catabolic stressors from surgery also add challenges to the perioperative physician managing the patient’s glycemic control. It is important to work with endocrinology in order to manage their diabetes. Lengthier procedures also complicate glycemic control. It involves sometimes close monitoring of not o

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18

Henry, Mark A., and Avinash B. Kumar. Cerebral Salt Wasting. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0068.

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Human survival (on a biochemical level) depends on the body’s critical ability to regulate the osmolality and salinity of extracellular fluid. When functioning in a normal state, the osmoregulatory system stringently maintains the serum sodium in a narrow range. Alterations in the serum sodium and water balance have significant and sometimes life-threatening impact on patients—especially when they occur in conjunction with serious intracranial pathology. This chapter, including the case discussion, illustrates the conundrum of hyponatremia and high urine output states complicating neurological

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19

Fervenza, Fernando C. Evaluation of Kidney Function, Glomerular Disease, and Tubulointerstitial Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0472.

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Several measures are used to evaluate kidney function: serum creatinine, urinalysis, renal clearance, and renal imaging. Creatinine is an end product of muscle catabolism and is commonly used as a filtration marker. Dysmorphic erythrocytes in the urinary sediment indicate bleeding in the upper urinary tract. A urine pH less than 5.5 excludes type 1 renal tubular acidosis. A pH greater than 7 suggests infection. Acidic urine is indicative of a high-protein diet, acidosis, and potassium depletion. Alkaline urine is associated with a vegetarian diet, alkalosis and urease-producing bacteria. Clear

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20

Kuypers, Dirk R. J., and Morie A. Gertz. Light-chain deposition disease. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0154_update_001.

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Light-chain deposition disease (LCDD) is characterized by extracellular tissue deposition of non-amyloid monoclonal immunoglobulin light chains (predominantly kappa light chains) in various organs including kidneys, heart, and liver. It is a rare cause of renal insufficiency. In two-thirds of cases it is associated with multiple myeloma, while in the remainder their monoclonal B cell proliferation does not meet the criteria for that diagnosis.Renal involvement occurs almost invariably and dominates the clinical course of the disease: greater than 90% of patients with LCDD have renal functional

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21

Kellum, John A. Diagnosis of oliguria and acute kidney injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0212.

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Diagnosis and classification of acute pathology in the kidney is major clinical problem. Azotemia and oliguria represent not only disease, but also normal responses of the kidney to extracellular volume depletion or a decreased renal blood flow. Clinicians routinely make inferences about both the presence of renal dysfunction and its cause. Pure prerenal physiology is unusual in hospitalized patients and its effects are not necessary benign. Sepsismay alter renal function without the characteristic changes in urine indices. The clinical syndrome known as acute tubular necrosis does not actuall

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22

Dalbeth, Nicola. Imaging in gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0007.

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Identification of monosodium urate (MSU) crystals is the gold standard for gout diagnosis. Serum urate is an important test for both gout diagnosis and effective management. For all people with gout on urate-lowering therapy, the target urate concentration is less than 0.36 mmol/L (6 mg/dL). Blood tests may also assist with screening for co-morbid conditions in gout. Spot urine tests may assist in determining the basis for hyperuricaemia in people with gout. Microscopically, the tophus represents a chronic inflammatory granulomatous response to MSU crystal aggregates.

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23

Speeckaert, Marijn, and Jopis Delanghe. Assessment of renal function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0007.

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Glomerular filtration rate (GFR) can be measured as the clearance of exogenous or endogenous filtration markers. Practical formulas permit estimation of creatinine clearance or GFR without timed urine collections in many stable patients with CKD. Standardization of serum creatinine is important for all of these estimation methods and implementing traceability of the assays to the new global SRM 967 standard has led to changes in clinical decision-making criteria. Calibration to an IDMS reference produces a lowering of serum creatinine values by 10–30% for most methods. Serum creatinine concent

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24

Hodgkiss, Andrew. Opportunities for prevention, or early detection, of psychopathology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0010.

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The value of informing patients and carers about the possible psychiatric consequences of specific cancers and cancer treatments is emphasized. Eight examples follow, of cancer treatments where formal consent concerning possible adverse psychiatric effects is indicated. Modest modifications of certain oncological treatments can reduce the incidence of psychopathology—seven examples are offered. Proactive monitoring of endocrine status, serum electrolytes, or vitamin B12 levels during or after particular treatments is advocated to prevent psychopathology. The chapter closes with practical recom

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25

Turner, Neil, and Premil Rajakrishna. Pathophysiology of oedema in nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0053.

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The mechanism by which loss of serum proteins into the urine causes expansion of extracellular fluid volume and oedema has become clearer. A key initiating abnormality is avid sodium retention by the kidney, leading to increased whole-body sodium and increased extracellular fluid volume. This appears to be driven primarily by overactivation of the amiloride-sensitive epithelial sodium channel (ENaC) in the collecting duct, activated proteolytically through abnormal filtration of plasminogen, and its activation to plasmin in the nephron. Conventional explanations for nephrotic oedema focused on

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26

Keshav, Satish, and Alexandra Kent. Chronic diarrhoea. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0029.

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Four to five per cent of the Western population suffers from chronic diarrhoea (defined as the passage of >3 stools per day, for >4 weeks), with irritable bowel syndrome (IBS) being the commonest cause in 20–40-year-old patients. It is the commonest reason for referral to secondary care gastroenterology clinics. The list of possible causes of chronic diarrhoea is long but, in the absence of rectal bleeding, loss of weight, or abnormal blood tests, it is unlikely to be due to a serious illness. Laboratory investigations should include serum glucose, electrolytes, renal and liver tests, fu

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27

Chopra, Bhavna, and Stanley Goldfarb. Approach to the patient with kidney stones. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0200.

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A detailed history can identify some risk factors and narrows down the potential causes of kidney stone formation. Radiological investigations confirm the diagnosis and give information on likely stone type. Urine and serum biochemistry is invaluable, but a more comprehensive investigation is reserved for recurrent stone formers. In that case at least two 24h collections, remote from any acute event are recommended, measuring volume, pH, calcium, oxalate, citrate, uric acid and phosphate. Urinary crystals can shed light on some stone types.For single or recurrent stones, analysis of stones the

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28

Farmer, Brenna M., and Neal Flomenbaum. Management of salicylate poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0317.

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Salicylates are weak acids that work as neurotoxins. The goal of management is to keep salicylates out of the brain and enhance elimination. Acute salicylate toxicity manifests as tinnitus, nausea, vomiting, and hyperventilation in a patient who takes a single large ingestion. Chronic salicylate toxicity is associated with long-term use, has a more insidious onset, and symptoms tend to be less severe, resulting in delayed diagnosis. It is more commonly seen in elderly patients. Therapeutic interventions for toxicity include gastrointestinal decontamination, serum and urine alkalinization, and

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29

Jörres, Achim, Dietrich Hasper, and Michael Oppert. Electrolyte and acid–base disorders in AKI. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0230.

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Electrolyte disturbances are common in patients with acute kidney injury (AKI) and should be corrected. In particular, hyperkalaemia above 6–6.5 mmol/L (especially with electrocardiogram changes) constitutes a medical emergency and warrants immediate intervention. Both hypo- and hypernatraemia may occur during AKI. Chronic changes in serum sodium need to be corrected bearing in mind the underlying pathology; however, when severe and evolving rapidly they should be corrected faster, irrespective of the cause. Acid–base disorders are also common in AKI and need to be treated in the context of un

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30

Burdmann, Emmanuel A. Leptospirosis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0191.

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Leptospirosis is one of the most prevalent zoonotic diseases worldwide. Pathogenic spirochaetes are shed in the urine of infected mammals to the environment. Humans are infected through contact with contaminated material. Leptospirosis is more prevalent in tropical and subtropical areas, but exists in all continents except Antarctica. The disease is difficult to diagnose and hence frequently neglected. Its clinical picture ranges from a mild flu-like disease to a life-threatening form with pulmonary haemorrhage, liver failure and acute kidney injury (AKI), called Weil disease, which may affect

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31

Langer, Thomas, and Pietro Caironi. Pathophysiology and therapeutic strategy of respiratory alkalosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0114.

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Respiratory alkalosis is a condition characterized by low partial pressure of carbon dioxide and an associated elevation in arterial pH caused by an imbalance between CO2 production and removal, in favour of the latter. Conditions that cause increased alveolar ventilation, without having a reduction in pH as input stimulus, will cause hypocapnia associated with a variable degree of alkalosis. The major effect of hypocapnia is the increase in pH (alkalosis) and the consequent shift of electrolytes that occurs in relation to it. As a general law, in plasma, anions will increase, while cations wi

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32

Neligan, Patrick J., and Clifford S. Deutschman. Pathophysiology and causes of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0255.

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Critical illness is typically characterized by changes in the balance of water and electrolytes in the extracellular space, resulting in the accumulation of anionic compounds that manifests as metabolic acidosis. Metabolic acidosis manifests with tachypnoea, tachycardia, vasodilatation, headache and a variety of other non-specific symptoms and signs. It is caused by a reduction in the strong ion difference (SID) or an increase in weak acid concentration (albumin or phosphate). Increased SID results from hyperchloraemia, haemodilution or accumulation of metabolic by-products. A reduction in SID

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33

Stewart, Douglas, Gaurav Shah, Jeremiah R. Brown, and Peter A. McCullough. Contrast-induced acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0246.

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Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a tr

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34

Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy

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35

Prowle, John, and Rinaldo Bellomo. Acute kidney injury in severe sepsis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0244_update_001.

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Septic acute kidney injury (S-AKI) accounts for close to 50% of all cases of AKI in ICU and, in its various forms, affects between 15% and 20% of ICU patients. Patients typically present with clinical evidence of severe sepsis and septic shock, developing oliguria or anuria, and rapidly rising serum creatinine concentration. The pathophysiology of S-AKI is poorly understood. Although haemodynamic factors might play a role in the loss of glomerular filtration rate, this may not be through the induction of renal ischaemia. Inflammation, microvascular shunting, and changes in glomerular arteriola

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36

Hoste, Eric A. J., John A. Kellum, and Norbert Lameire. Definitions, classification, epidemiology, and risk factors of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0220_update_001.

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The lack of a precise biochemical definition of acute kidney injury (AKI) resulted in at least 35 definitions in the medical literature, which gave rise to a wide variation in reported incidence and clinical significance of AKI, impeded a meaningful comparison of studies.The first part of this chapter describes and discusses different definitions and classification systems of AKI. Patient outcome and the need for renal replacement therapy are directly related to the severity of AKI, an observation that supports the use of a categorical staging system rather than a simple binary descriptor. The

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37

Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.

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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistrie

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