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Books on the topic 'Urine collection'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Rabinovitch, Albert. Urinalysis and collection, transportation, and preservation of urine specimens: Approved guideline. 2nd ed. Wayne, Pa: NCCLS, 2001.

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2

Crumrine, Paul. Navigating the yellow stream: A voyage into the cesspool of urine collection for drug testing. Palm Harbor, FL: Nest Egg Press, 1991.

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3

Pangmulgwan, Sŏul Yŏksa. Urine saramdŭl ŭi mŏt kwa pʻungnyu. [Seoul]: Sŏul Yŏksa Pangmulgwan, 2006.

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4

Associations, American Trucking, ed. The Correct collection of urine samples. Alexandria, VA (2200 Mill Rd., Alexandria 22314-4677): American Trucking Associations, 1989.

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5

Routine Analysis and Collection Transportion Preservation Urine Specimins. Natl Committee for, 1992.

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6

Quinlan, Joan W. Urine Specimen Collection Handbook For Federal Workplace Drug Testing Programs. Diane Pub Co, 1996.

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7

Daly, Donna, and Christopher Chapple. Anatomy, neurophysiology, and pharmacological control mechanisms of the bladder. Edited by Christopher R. Chapple. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0034.

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The lower urinary tract has two main functions; the collection and low pressure storage of urine and periodical controlled elimination of urine at an appropriate time. In order to achieve continence during bladder filling and storage and produce efficient and effective bladder emptying, there is accurate coordination between opening and closing of the urethral sphincters and contraction of the detrusor smooth muscle. The process of micturition has two phases: the storage/filling phase and the voiding phase. The analogy for the transition between these two phases has been described as an on-off circuit, rather akin to flicking a light switch, between synchronous bladder contraction and urethral outlet relaxation, and vice versa. These phases are regulated by a complex, integration of somatic and autonomic efferent and afferent mechanisms that coordinate the activity of the bladder and urethra. This chapter provides an overview of our current understanding of these complex mechanisms.
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8

Olaziregi, MariJose, and Amaia Elizalde. Kirmen Uribe: Life and Fiction. Center for Basque Studies, 2022.

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9

Inc. National Safety Compliance Services. Urine Specimen Collections: A Complete Training Manual for the Proficient Collector. Kendall Hunt Pub Co, 2001.

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10

Saunders. Saunders Clinical Skills for Medical Assistants: Disk Six: Collecting and Testing Urine and Microbiology Specimens. Saunders, 2006.

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11

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 albumin is the major component of excess glomerular proteinuria. Even small amounts of proteinuria are associated with increased cardiovascular risk and long-term renal risk. In patients with renal disease, regardless of type, proteinuria is a strong predictor of loss of glomerular filtration rate and proteinuria at levels higher than an equivalent of 1 g/24 hours can be considered high renal risk. This limit should be lowered in young patients, and if microscopic haematuria is also present. For both cardiovascular and renal outcomes, risk is graded with severity of proteinuria. In routine clinical practice, ratios of albumin or total protein to creatinine level (ACR or PCR) in spot urine samples are usually more pragmatic and useful than 24-hour collections. ACR is more sensitive as a screening test (normal range up to 2.5 mg/mmol in men, 3.5 mg/mmol in women).
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12

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 themselves is invaluable. Analysis may include X-ray diffraction, infrared spectroscopy and a number of other techniques. .Dietary evaluation is valuable in recurrent stone formers.
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13

Kennish, Steven. Intervention. Edited by Christopher G. Winearls. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0012_update_001.

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Imaging technology allows complex yet minimally invasive diagnostic and therapeutic interventions in the genitourinary tract. It provides precise targeting for tissue biopsy to allow accurate diagnosis. Percutaneous nephrolithotomy is invaluable in the treatment of complex stone disease and percutaneous nephrostomy insertion preserves normal renal tissue in the patient with malignant or benign urinary tract obstruction. (Percutaneous nephrolithotomy and percutaneous nephrostomy are very different.) Antegrade ureteric procedures allow strictures, stones, and tumours to be dealt with, often with much greater ease than the retrograde approach. Collections and leaks can be drained and urine can be diverted to facilitate healing. Minimally invasive endovascular techniques can arrest iatrogenic or trauma-related haemorrhage from the renal tract. Although interventional radiological procedures are generally safe, they do come with risks of specific complications that the nephrologist needs to be aware of. Nephrologists need to be familiar with interventional uroradiological techniques to allow appropriate counseling and care of patients who require these procedures.
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14

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 concentration depends on age, gender and muscle mass. Cystatin C is an alternative marker of GFR, but estimation is more expensive and it is not clear that it has a useful place in routine practice. The MDRD Study equation was validated in the framework of the Modification of Diet in Renal Diseases study. It is superior to the Cockcroft and Gault formula for estimating Creatinine Clearance in most people. In 2009, the CKD Epidemiology Collaboration (CKD-EPI) formula was introduced, which provides a more accurate estimation for patients with GFR values between 60 and 90 mL/min. In children, the Schwartz formula is frequently used. Some urinary markers of kidney disease are also discussed.
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15

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 low colloid osmotic pressure as a consequence of loss of serum proteins, leading to egress of extracellular fluid from the intravascular compartment. It was hypothesized that this led to underfilling of the circulation and a drive to sodium retention. While low osmotic pressure may play a part in the clinical picture of nephrotic syndrome, a variety of observations suggest that underfilling is not a common feature except in the most severe nephrotic syndrome. Furthermore the gradient in colloid osmotic pressure between serum and interstitium tends to be preserved in nephrotic syndrome. The distribution of excess extracellular fluid is markedly different in patients with nephrotic syndrome from that seen in patients who have reduced glomerular filtration rate as the cause of sodium retention. This is not fully understood but hypotheses centre on capillary permeability and colloid osmotic pressure effects.
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