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Books on the topic 'Urine excretion'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Klosterman, Lorrie. The excretory system. Marshall Cavendish Benchmark, 2010.

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2

Richman, Josh. "What's my pee telling me?". Chronicle Books, 2009.

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3

Klosterman, Lorrie. Excretory system. Marshall Cavendish Benchmark, 2010.

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4

Hollingbery, Patsy Whitmer. Acute effects of dietary caffeine, aspirin and sucrose on urinary mineral excretion in adult women and adolescents. 1986.

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5

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Polyuria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0057.

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Polyuria describes the passage of more than 3 l of urine a day. This is an arbitrary definition, and the term is commonly applied to patients who are complaining of passing larger than normal volumes of urine. As water excretion is tightly regulated by the body to maintain normal osmolality, water excretion varies greatly depending on intake. Polyuria may be physiological or pathological. A patient with polyuria often presents with nocturia, urination overnight that disturbs sleep. It is usually accompanied by polydipsia (to maintain normal fluid balance). In hospital the commonest causes of p

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6

The relationship between exercise-induced delayed muscle soreness and the excretion of urine metabolites creatinine, 3-methylhistidine, and hydroxyproline. 1986.

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7

World Health Organization (WHO). Basic Methods for Assessment of Renal Fluoride Excretion in Community Programmes in Oral Health. World Health Organization, 2014.

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8

Bushinsky, David A., and Orson Moe. Calcium stones. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0201.

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Key predisposing factors in calcium stone formation are idiopathic hypercalciuria, primary hyperparathyroidism, and hyperoxaluria (dietary, enteric, idiopathic, sometimes genetic). These are described in detail. Other predisposing conditions include renal tubular acidosis, and risk factors identified in epidemiological studies such as hypocitraturia, increased urinary urate. is defined as an excess of urine calcium excretion without a discernible metabolic cause.

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9

Turney, Ben, and John Reynard. Prevention of idiopathic calcium stones. Edited by John Reynard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0015.

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The main principles of idiopathic calcium oxalate stone prevention are to maintain dilute urine through increasing fluid intake and to reduce calcium and oxalate excretion. The influence of various urinary factors on the risk of stone formation has been quantified mathematically. Urine volume and urinary oxalate concentration are most influential on the risk of stone formation, while magnesium concentration contributes a small amount to risk. It is estimated that around 50% of stone formers will form another stone within five years. Some stone formers have frequent recurrences. Most stone form

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10

Turner, Neil. Postural proteinuria (benign orthostatic proteinuria). Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0051.

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Postural proteinuria, synonymous with the condition known as benign orthostatic proteinuria, describes increased levels of protein excretion associated with normalization first thing in the morning. It is usually diagnosed in children, for whom it is the most common explanation for proteinuria picked up incidentally on dipstick testing. In children, it generally resolves with age and is thought to have a benign long-term prognosis, with the caveat that numbers with very long follow-up times are few. It is also seen in teenagers but becomes much less common in early adulthood. Its aetiology is

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11

The effect of acute and endurance exercise on endogenous 3-methylhistidine excretion in female runners and non-runners. 1986.

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12

The effect of acute and endurance exercise on endogenous 3-methylhistidine excretion in female runners and non-runners. 1988.

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13

Duran, Marinus, and Isabel Tavares de Almeida. Interpretation of Organic Acid Analysis Results. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0084.

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The analysis of organic acids in urine will detect more than 60 inherited conditions, most of which have clinical significance. Some of the abnormalities that are found represent non-diseases or artefacts of dietary/drug manipulations. Not all inherited organic acidemias are associated with excessively high excretion levels; some patients excrete the characteristic organic acids just above the upper normal level. This makes a quantitative analysis of organic acids a prerequisite. Approximately half of the organic acids will form acylcarnitines, therefore the analysis of carnitine and its ester

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14

Daudon, Michel, and Paul Jungers. Cystine stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0203_update_001.

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Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine st

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15

Federico, Antonio, and Silvia Palmeri. Oligosaccharidoses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0057.

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Oligosaccharidoses are a group of lysosomal diseases, also called glycoproteinoses, biochemically characterized by storage of protein-bound oligosaccharides within lysosomes and excretion with urine of corresponding sugars. Storage of oligosaccharides results from absence or defective function of a specific lysosomal enzyme. Classification includes α‎ and β‎ mannosidosis, fucosidosis, sialidosis types I and II, Schindler disease, and aspartylglycosaminuria. Galactosialidosis characterized by deficiency of β‎-galactosidase and α‎-neuraminidase with presence in patient urine of oligosaccharides

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16

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of acid–base balance. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0178.

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Normal metabolism results in a net acid production of approximately 1 mmol/kg day−1. Physiological pH is regulated by excretion of this acid load (as carbon dioxide) by the kidneys and the lungs. A series of buffers in the body reduces the effects of metabolic acids on body and urine pH. For acid–base disorders to occur, there must be excessive intake (or loss) of acid (or base) or, alternatively, an inability to excrete acid. For these changes to result in a substantially abnormal pH, the various buffer systems must been overwhelmed. The pH scale is logarithmic, so relatively small changes in

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17

¡No tires de la cadena!: Secretos científicos sobre la caca y el pis. Blume, 2013.

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18

Hendriksz, Christian J., and Francois Karstens. Mucopolysaccharidosis in Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0054.

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There are 8 different types of diseases of the mucopolysaccharides, each caused by a deficiency in one of 10 different enzymes involved in the degradation of glycosaminoglycans (GAGs). Partially degraded GAGs accumulate within the lysosomes of many different cell types and lead to clinical symptoms and excretion of large amounts of GAGs in the urine. Heritability is autosomal recessive except for MPS type II, which is X-linked. The disorders are chronic and progressive and, although the specific types all have their individual features, they share an abundance of clinical similarities. All inv

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19

Daudon, Michel, and Paul Jungers. Uric acid stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0202_update_001.

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Uric acid (UA) stones are typically red-orange and often appear as sand/ gravel though they may be large. They are totally radiolucent. They account for about 10% of all kidney stones in most countries, and up to 20% in some populations. It is twice as frequent in males, prevalence increases with age, and it is two to three times higher in patients with type 2 diabetes or with features of the metabolic syndrome. Factors that induce the formation of UA stones are a low urine volume, hyperuricosuria, and, more importantly, a permanently low urine pH (< 5). Indeed, below its pKa of 5.35 at 37°

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20

Berlot, Giorgio, and Ariella Tomasini. Management of tricyclic antidepressant poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0321.

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Tricyclic antidepressants (TCAs) are still prescribed worldwide for the treatment of major depression and other disorders. Unfortunately, the safety margin of these agents is rather narrow and TCA-related intoxication is associated with a number of potentially life-threatening side effects. The symptoms being rather unspecific, a high index of suspicion is warranted in order to identify promptly the intoxicated patients and to provide the appropriate care, even before the detection and dosage of TCAs and related metabolites in the blood and/or urine. In the absence of a specific antidote, the

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21

Murer, Heini, Jürg Biber, and Carsten A. Wagner. Phosphate homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.

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Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanc

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22

Turner, Neil, and Stewart Cameron. Proteinuria. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0050.

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Excess protein in the urine almost always comes from the kidney. Proteinuria up to 150 mg/day in an adult (protein:creatinine ratio (PCR) up to 15 mg/mmol) is considered normal. Daily average excretion is 80 mg, of which about 30 mg is albumin that has been filtered and not reabsorbed. Other components comprise low-molecular-weight filtered proteins that have escaped reabsorption, and proteins secreted or lost into urine from cells of the nephron. Increased permeability of the glomerulus to high-molecular-weight proteins is the most common cause of the clinically detected proteinuria, and albu

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23

Rabier, Daniel. Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0083.

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Amino acids present in the different biological fluids belong to two groups: the protein group, with the 21 classical amino acids constituting the backbone of the protein, and the nonprotein group, appearing in different metabolic pathways as intermediate metabolites. It is important to know and to be able to recognize the latter, as they are the markers of many inherited metabolic diseases. Three kinds of pathways must be considered: the catabolic pathways, the synthesis pathways, and the transport pathways. A disorder on a catabolic pathway induces an increase of all metabolites upstream and

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24

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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25

Radović, Milan, and Adalbert Schiller. Balkan endemic nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.

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Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmet

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26

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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27

Schechter, Marcos. Viral Hemorrhagic Fevers (Ebola, Lassa, Hantavirus). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0066.

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Viral hemorrhagic fever (VHF) designates diseases caused by enveloped, single-stranded RNA viruses belonging to the families Ebola, Lassa, Hantavirus, and yellow fever. Unifying features include fever, capillary leak, and coagulation defects. These viruses can affect all organ systems; transmission occurs via contact with rodent excretions, either by ingestion or through mucosa or non-intact skin. Aerosolized rodent urine and saliva are also infectious. Person-to-person spread has been documented in Lassa and Machupo viruses, both by direct contact with bodily fluids and by airborne transmissi

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