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Books on the topic 'Proteinurie'

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Published: 4 June 2021
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1

Avram, M. M., ed. Proteinuria. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2477-5.

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2

1946-, Smith Michael C., ed. Proteinuria and the nephrotic syndrome. Chicago: Year Book Medical Publishers, 1986.

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3

Parker, James N., and Philip M. Parker. The official patient's sourcebook on proteinuria. Edited by Icon Group International Inc and NetLibrary Inc. San Diego, Calif: Icon Health Publications, 2002.

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4

Blaine, Judith, ed. Proteinuria: Basic Mechanisms, Pathophysiology and Clinical Relevance. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43359-2.

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5

H, Brouhard Ben, and Kalia Alok, eds. An approach to the child with hematuria and proteinuria. Norwalk, Conn: Appleton-Century-Crofts, 1985.

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6

D, Bianchi Claudio M., ed. Kidney and proteins in health and disease: Fifth International Symposium of Nephrology at Montecatini, Montecatini Terme, July 21-23, 1987. Basel: Karger, 1988.

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7

D, Bianchi Claudio M., ed. Kidney, proteins, and drugs: 6th International Symposium of Nephrology at Montecatini, Montecatini Terme, June 1-3, 1989. Basel: Karger, 1990.

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8

D, Bianchi Claudio M., ed. Kidney, proteins, and drugs: An update : 7th International Symposium of Nephrology at Montecatini, Montecatini Terme, October 14-16, 1991. Basel: Karger, 1993.

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9

Wheeler, Linda A. Maternal assessment: Blood pressure. Edited by Raff Beverly S, Albers Lolita, and March of Dimes Birth Defects Foundation. 2nd ed. White Plains, N.Y: March of Dimes Birth Defects Foundation, 1988.

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10

Wheeler, Linda A. Maternal assessment: Urine evaluation. Edited by Raff Beverly S, Albers Lolita, and March of Dimes Birth Defects Foundation. 2nd ed. White Plains, N.Y: March of Dimes Birth Defects Foundation, 1987.

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11

National Kidney and Urologic Diseases Information Clearinghouse (U.S.) and National Institute of Diabetes and Digestive and Kidney Diseases (U.S.), eds. Proteinuria. [Bethesda, Md.]: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 2000.

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12

1929-, Avram Morrell M., ed. Proteinuria. New York: Plenum Medical Book Co., 1985.

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13

Avram, M. M. Proteinuria. Springer, 2011.

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14

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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15

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 not well understood, although patients with pathological causes for proteinuria and patients with physiological levels of total protein excretion have been shown to exhibit similar diurnal variation. Using currently published limits for daily protein excretion the diagnosis is common. Some examples have been attributed to nutcracker syndrome (compression of the left renal vein), although that is more commonly associated with macroscopic haematuria, and the association remains uncertain. The condition is best diagnosed by comparing first-in-morning urine samples paired with afternoon samples on several occasions. In childhood, if proteinuria levels are in the normal range in morning samples, and within moderately increased limits later in the day, probably no investigation beyond observation is required. Most will resolve; very few will evolve into serious renal disease. The simplest mode of long-term monitoring is to measure protein:creatinine or albumin:creatinine ratios in first-in-morning urine samples.
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16

(Editor), Shaul G. Massry, P. Mene (Editor), and G. A. Cinotti (Editor), eds. Proteinuria: American Journal of Nephrology, Suppl. 1 (Proteinuria). S. Karger AG (Switzerland), 1990.

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17

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
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18

Blaine, Judith. Proteinuria: Basic Mechanisms, Pathophysiology and Clinical Relevance. Springer, 2018.

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19

Turner, Neil. Mechanisms of glomerular injury. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0045.

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Proteinuric diseases, historically termed ‘nephrosis’, are characterized by subtle abnormalities in podocytes or by abnormal glomerular matrix, including the scarring laid down by inflammatory diseases. Angiotensin blockers, corticosteroids, calcineurin inhibitors, and a wide range of other drugs known or believed to be effective in different renal diseases, appear to have direct effects on podocytes that reduce proteinuria that may be important to their effectiveness. Several of these have previously been assumed to work via haemodynamic, immune or other modes. Haematuric diseases are characterized by inflammatory disruption of the glomerular basement membrane (GBM) (‘nephritis’), or less commonly by fragile GBM without inflammation. The majority of haematuric conditions are slowly or rapidly destructive diseases associated with infiltration of inflammatory cells, and proliferation of endogenous cells of the glomerulus, probably in attempts at repair. With time, many haematuric diseases are associated with the development of proteinuria, possibly as a consequence of scarring and its effects on podocyte function.
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20

Burdmann, Emmanuel A. Syphilis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0192.

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Syphilis is an infectious disease caused by the bacterium Treponema pallidum. The transmission route is usually sexual, but prenatal contamination (congenital syphilis) and transmission by infected blood can also occur. The most frequent presentation of syphilis nephropathy is proteinuria, and the most common form of associated glomerular disease is membranous glomerulopathy. Kidney disease usually reverts with antibiotic therapy. Syphilis must always be considered in proteinuric HIV-infected patients. Renal biopsy is necessary to differentiate between HIV-associated nephropathy and syphilis-induced glomerulopathies, since both kidney diseases have analogous clinical presentations, but syphilis-induced glomerulopathies may recover with syphilis successful treatment.
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21

Network, Scottish Intercollegiate Guidelines, ed. Investigation of asymptomatic proteinuria in adults: A national clinical guideline recommended for use in Scotland by the Scottish Intercollegiate Guidelines Network. Edinburgh: Scottish Intercollegiate Guidelines Network, 1997.

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22

Niaudet, Patrick, and Alain Meyrier. Pathogenesis of proteinuria in minimal change disease and focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0059_update_001.

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It is now well established that the podocyte, and in particular the slit diaphragm structure, are critical to the barrier to serum albumin entering glomerular filtrate in large quantities. In minimal change disease there is proteinuria without podocyte death, whereas in focal segmental glomerulosclerosis there is not only podocyte dysfunction but also podocyte loss.
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23

(Editor), Rosanna Coppo, and Licia Peruzzi (Editor), eds. Moderately Proteinuric IgA Nephropathy in the Young (Biomedical and Health Research, V. 44). Ios Pr Inc, 2000.

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24

Publications, ICON Health. The Official Patient's Sourcebook on Proteinuria: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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25

(Editor), P. W. Mathieson, and J. H. Miner (Editor), eds. Glomerular Proteinuria and Hematuria: Crossing the Bridge from Molecules to Man, Special Issue, Nephron Physiology 2007. S Karger Pub, 2007.

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26

Kaysen, George A. The Nephrotic Syndrome: Pathogenesis and Consequences : The Homeostatic and Pathogenic Consequences of Proteinuria (American Journal of Nephrology,). S Karger Pub, 1994.

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27

Rascher, Wolfgang. Treatment of hypertension in children. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0219_update_001.

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Management of hypertension is dependent on the underlying cause and the magnitude of the blood pressure abnormality. Healthy behavioural changes are the primary management tool for treating primary hypertension in adolescents and other cardiovascular risk factors and obesity. In children and adolescents with renal hypertension, high blood pressure requires pharmacological treatment. There is randomized controlled trial evidence to support a blood pressure target for those with proteinuria of not higher than the 50th centile for age. The use of angiotensin-converting enzyme inhibitors is safe in patients with proteinuria, and assumed to be equally beneficial. For those without proteinuria, less stringent targets may be acceptable. Often a combination of two or three drugs is required to lower arterial blood pressure to the target blood pressures. In children and adolescents at or near end-stage renal failure, fluid removal by dialysis may be necessary to control hypertension.
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28

Rajakrishna, Premil, Stewart Cameron, and Neil Turner. Nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0052.

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Nephrotic syndrome is the constellation of manifestations seen in patients with such severe proteinuria that serum albumin falls below normal levels. Its severity and the risk of complications are graded by the severity of the protein loss. The risks of some complications begin to rise at levels of proteinuria below those conventionally associated with nephrotic syndrome. The main manifestation, oedema, is characterized by avid sodium retention and managed by sodium restriction and diuretics. A pronounced thrombotic tendency is particularly apparent within the first 6 months of diagnosis and in patients with the most severe proteinuria. Venous thromboembolism may be a presenting feature. Prophylactic full anticoagulation may be considered for those at highest risk. Hyperlipidaemia is severe and justifies lipid-lowering therapy in patients with sustained nephrotic syndrome. There is a marked increased risk of bacterial infection, particularly from Streptococcus pneumoniae. The causes of nephrotic syndrome are diseases affecting the podocyte, either directly or through an effect on glomerular matrix (e.g. through scarring). Identification of a cause is important for management and often requires a renal biopsy.
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29

Ferro, Charles J., and Khai Ping Ng. Recommendations for management of high renal risk chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0099.

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Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.
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30

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Nephrotic syndrome. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0161.

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Nephrotic syndrome is a clinical syndrome of heavy proteinuria (greater than 3.5 g per 24 hours), oedema, and hypoalbuminaemia, which is associated with hyperlipidaemia and a procoagulant state. Causes of nephrotic syndrome are traditionally classified by their histopathological descriptions. In most cases, the histological picture can have a primary (idiopathic) or secondary cause. Minimal change, membranous nephropathy, and focal segmental glomerulosclerosis account for over 60% of cases. Diabetic nephropathy and renal amyloidosis are common secondary causes of nephrotic syndrome. Nephrotic-range proteinuria will show up as at least 3+ protein on urinalysis. The diagnosis is confirmed by a urinary protein-to-creatinine ratio over 300 mg/mmol, and hypalbuminaemia. In adults, renal biopsy is the diagnostic test. This chapter addresses the causes, diagnosis, and management of nephrotic syndrome in adults.
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31

Meyrier, Alain, and Patrick Niaudet. Primary focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0058_update_001.

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The proportion of cases of primary focal segmental glomerulosclerosis responsive to treatment with corticosteroids is variable and depends on histological type, patient age and duration, and dose of steroid treatment, but overall complete remission rate is estimated at 20–25% in white and Asian patients, and lower in black patients. Partial response dependent on a high dose of steroids is common. Despite anxieties about nephrotoxicity, there may be justification for adding calcineurin inhibitors to control nephrotic syndrome if it is severe. Data for additional agents is not very encouraging. Plasma exchange appears to remove a circulating factor that causes proteinuria in focal segmental glomerulosclerosis, as illustrated by responses to this treatment when proteinuria recurs acutely after kidney transplantation. This is rarely pursued clinically except after transplantation, in advance of severe glomerular injury.
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32

Davenport, Dr Andrew. Renal diseases and emergencies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00011.

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Chapter 11 discusses diseases and emergencies involving renal medicine, including investigation of the renal tract, acute kidney injury (AKI), haematuria and proteinuria, urinary tract infection (UTI), urinary tract obstruction, tumours of the renal tract, chronic kidney disease (CKD), and renal transplant patients.
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33

O’Neal, M. Angela. Postpartum Visual Disturbance. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0017.

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Preeclampsia (PE) is a multi-organ system disorder defined as hypertension with blood pressures greater than 140/90 on two occasions and proteinuria of more than 300 mg/24 hours. Eclampsia is defined as when seizures occur in a woman with preeclampsia. The pathophysiology of preeclampsia/eclampsia is felt to be related to incomplete penetration of the cytotrophoblasts of the placenta into the myometrium, leading to local ischemia, propagation of ischemic factors causing hypertension, resulting in endothelial dysfunction. The clinical features are related to which end organ is involved: in the kidney, proteinuria; in the liver, coagulopathy; and in the brain, posterior white matter dysfunction. The involvement of the parietal and occipital lobes explains the associated neurological features of confusion and visual changes. MRI reflects the white matter changes associated with eclampsia in posterior reversible encephalopathy syndrome (PRES). Eclampsia is treated with blood pressure control and magnesium to treat the seizures.
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34

Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0338_update_001.

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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide (Gb3), which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. Proteinuria and estimated glomerular filtration rate (eGFR) are strongly associated with risk of progression, but this may be reduced by treatment with angiotensin-converting enzyme inhibitors as well as by enzyme replacement therapy (ERT). ERT was approved in 2001; it improves pain and other neuropathic symptoms, and well-being, and has been proven to clear deposits of Gb3 from tissues, at variable speeds. There is limited randomized controlled trial data but protective effects have been proven for renal outcomes, death, and better outcomes in some other organ systems. Renal function may be protected if ERT is commenced before there is heavy proteinuria or substantial loss of GFR. It is recommended to start ERT as soon as the diagnosis is made in those with very low or absent enzyme. For those with intermediate levels it is recommended to commence treatment only when signs or symptoms appear. Proteinuria and eGFR give most information from a renal point of view, but renal biopsy is also useful for confirming the renal diagnosis and staging the disease as well as monitoring progress in selected cases. Management should include regular screening for complications including myocardial and neurological assessments. It is likely that registries will show progressive rises in median survival with this condition.
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35

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0062_update_001.

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A common rule of thumb in primary membranous glomerulonephritis (MGN) is that one-third of patients improve spontaneously, one-third progress, and one-third continue to have substantial proteinuria. The rate of spontaneous recovery may be near the truth, but MGN is usually an indolent condition and few studies have run long enough to give accurate outcomes for the remainder. However MGN is an important cause of end-stage renal failure. Treatment regimens that include cyclophosphamide or chlorambucil can improve the outcome of patients at greatest risk of deterioration, but their toxicity has limited their use in randomized studies to the highest risk patients. Steroids alone, and ciclosporin, do not improve long-term outcomes in these studies. Whether anti-B-cell antibodies offer additional benefits requires randomized studies. After confirming the diagnosis of primary MGN it is recommended to maximize supportive therapy and monitor for at least 6 months to give a clear picture of the long-term risk. For patients at lowest risk, supportive management and monitoring alone is recommended. Patients at medium risk (nephrotic range proteinuria but normal and stable glomerular filtration rate), or high risk (very heavy proteinuria, greater than 8 g/day or deterioration of glomerular filtration rate) may justify specific treatment directed at the immune response. For the medium-risk group it is not certain that it is required; for some in the high-risk group it may come too late. Overall outcomes in the high-risk group remain quite poor even with aggressive treatment.
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36

Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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37

Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.

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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.
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38

Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.

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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.
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39

Turner, Neil. Exercise-related pseudonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0049.

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Vigorous and prolonged physical exercise can produce a range of urinary abnormalities which would normally be considered alarming. They include haematuria, haemoglobinuria, the appearance in urine of red cells in urine, some fragmented in a ‘glomerular’ manner, red cell cast formation, and proteinuria. A variety of names have been given to these syndromes, including march haematuria and march haemoglobinuria. Mostly these changes seem benign and self-limiting. Rarely they are associated with acute kidney injury but this is often in the context of other renal insults, extreme dehydration, or hyperpyrexic conditions. Vigorous exercise is also commonly associated with various electrolyte changes related to both over- and under-hydration. These can complicate assessment. Transient proteinuria in the absence of haematuria appears to be a physiological response to even short-term exercise, its degree related to the intensity of the exercise. Causation of these syndromes is mixed and not fully explained. There is good evidence for physical trauma to red cells being a significant part, but this cannot explain the appearance of glomerular red cells and red cell casts. Exercise-related changes mostly resolve within less than a day, and almost all by 72 hours.
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40

Woywodt, Alexander, and Diana Chiu. Drug-induced and toxic glomerulopathies. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0082.

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Glomerulopathies induced by particular exogenous compounds or molecules include those attributable to toxicity, and those caused by inducing an immune or autoimmune response. Tubules are more commonly the target of toxicity as they absorb and concentrate components of filtrate. Damage to endothelial cells may account for thrombotic microangiopathy in response to calcineurin inhibitors. Endothelial cells are also likely to be the target in drug-induced small vessel vasculitis. Toxicity to podocytes accounts for focal segmental glomerulosclerosis caused by pamidronate and other agents. Chloroquine can cause a remarkable pseudo-storage disorder with inclusions in podocytes that resemble those seen in Fabry disease. The mechanism by which drugs cause minimal change disease, another podocyte disorder, is not known. Membranous nephropathy may be caused by exposure to gold, mercury, and some other drugs; this is antibody mediated and presumably the targets are altered podocyte surface molecules. Inhibitors of the mammalian target of rapamycin (mTOR) cause proteinuria, possibly through effects on vascular endothelial growth factor, inhibitors of which are associated with not only proteinuria (an expected podocyte effect) but also thrombotic microangiopathy (endothelial cell effect). This latter may be through disturbing podocyte-endothelium cross-signaling.
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41

Burdmann, Emmanuel A., and Vivekanad Jha. Rickettsiosis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0193.

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Rickettsiae are obligate intracellular bacteria transmitted by arthropods to a vertebrate host. Clinically relevant rickettsioses have a similar clinical pattern, manifesting as an acute febrile disease accompanied by headache, articular and muscle pain, and malaise.Epidemic typhus is a worldwide distributed disease caused by the Rickettsia prowazekii, with a human louse as a vector. Data on epidemic typhus-related renal injury is extremely scarce.Murine typhus is caused by the Rickettsia typhi and has a rodent flea as the vector. It is one of the most frequent rickettsioses, and is usually a self-limited febrile illness. Proteinuria, haematuria, elevations in serum creatinine (SCr) and/or blood urea nitrogen (BUN) and AKI have been reported. The real frequency of renal involvement in murine typhus is unknown. Renal abnormalities recover after the infectious disease resolution.Scrub typhus, caused by the Orientia tsutsugamushi, has the Leptotrombidium mite larva as vector. It is endemic in the Tsutsugamushi triangle delimited by Japan, Australia, India, and Siberia. It can manifest either as a self-limiting disease or as a severe, life-threatening multiorgan illness. Early administration of adequate antibiotics is essential to prevent adverse outcomes. Proteinuria, haematuria, and acute kidney injury (AKI) are frequent.Tick-borne rickettsioses are caused by bacteria from the spotted fever group and have ticks as vectors. Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii. It is the most severe of the spotted fever rickettsial diseases, causing significant morbidity and lethality. RMSF occurs in North, Central, and South America. Renal impairment is frequent in severe forms of RMSF. Mediterranean spotted fever is caused by Rickettsia conorii, and is endemic in the Mediterranean area. It is usually a benign disease, but may have a severe course, clinically similar to RMSF. Haematuria, proteinuria, increased serum creatinine, and AKI may occur. Japanese spotted fever is caused by Rickettsia japonica. Lethal cases are reported yearly and AKI has occurred in the context of multiple organ failure.
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42

Heidet, Laurence, and Marie Claire Gubler. Nail patella syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0326_update_001.

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Nail patella syndrome can be recognized by its characteristic nail dystrophy and symmetrical skeletal abnormalities. Proteinuric renal disease is a variable part of the syndrome, usually mild but causing end-stage renal failure in up to 10%. An association with glaucoma has been recognized and this should be screened for. Underlying gene mutations are in a LIM homeodomain-containing transcription factor LMX1B, which seems to influence production of basement membrane proteins and other podocyte gene products.
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43

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 symmetrically shrunken, smooth-shaped kidneys, with interstitial fibrosis, mild interstitial inflammation, and tubular atrophy. Diagnosis is usually based upon positive family history of BEN, past or current residence in endemic regions, tubular proteinuria, tubular dysfunctions (such as urine acidification defects, salt wasting, and impaired excretion of ammonia, uric acid, and phosphate), scant urinary sediment, bilateral and symmetrically reduced kidney size, accompanied by severe anaemia, disproportionate to the degree of GFR reduction. There is no specific therapy for BEN; patients should therefore be treated as all patients with chronic kidney disease, in general. The use of distant water supplies or moving to another residence area should be advised to affected families. Careful evaluation for urothelial cancers is mandatory in patients with haematuria.
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44

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0068_update_001.

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Immunoglobulin A nephropathy is characteristically slowly evolving, and studies from autopsies and kidney donors show that deposition of immunoglobulin A is quite common and not necessarily associated with overt disease. However, series of biopsy-diagnosed patients that extend to 20 or 30 years report rates of end-stage renal failure of up to 40–50%. A very approximate overall rate of end-stage renal disease of 1% per year has been suggested. Proteinuria, glomerular filtration rate (GFR), and possibly some features on renal biopsies enable risk stratification, but all patients need long-term monitoring. Treatment is based on the use of angiotensin converting-enzyme inhibitors for patients with proteinuria, and blood pressure control, and of course during most of the previous long-term studies patients would not have been treated with these agents or to modern blood pressure standards. For patients who show loss of GFR despite this, or other markers of high risk, the best evidence is for treatment with high-dose corticosteroids over a limited period of months. There is little convincing evidence for additional benefit from cytotoxic or other immunomodulatory agents, except possibly in the most aggressive disease, when there is weak evidence for cyclophosphamide. Some studies claim benefit from tonsillectomy, but this is not clear, and most nephrologists only recommend this for patients with recurrent tonsillitis.
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45

Bissell, Lesley-Anne, Dwomoa Adu, and Paul Emery. The patient with rheumatoid arthritis, mixed connective tissue disease, Sjögren syndrome, or polymyositis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0166.

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Renal disease is a well-recognized cause of ill health and death in rheumatoid arthritis. Three broad categories of renal disease occur. The first—and by far the most common—arises from the nephrotoxicity of the drugs used in the treatment of arthritis, particularly with non-steroidal anti-inflammatory drugs. Disease-modifying antirheumatic drugs such as gold and D-penicillamine may lead to proteinuria and a glomerulonephritis in 10–30% of patients. Ciclosporin is associated with significant nephrotoxicity and hypertension. A second major but diminishing cause of renal disease in rheumatoid arthritis is amyloidosis. Thirdly, rheumatoid arthritis may be associated with the development of glomerulonephritis. The main types described are a mesangial proliferative glomerulonephritis with or without immunoglobulin A deposits, a membranous nephropathy, and a focal segmental necrotizing glomerulonephritis of the vasculitic type.Renal disease in mixed connective tissue disease and polymyositis is infrequent, but the former can be associated with a membranous and mesangial proliferative glomerulonephritis.Sjögren syndrome is rarely associated with clinically significant renal disease, but patients can present with proteinuria, acidosis, or hyperchloraemia. Interstitial nephritis and immune complex glomerulonephritis reflect the exocrinopathy and circulating immune complex disease pathognomonic of Sjögren syndrome. Evidence for effective treatment of the renal complications is lacking. Corticosteroids and cyclophosphamide are most commonly used, with newer biological drugs, such as rituximab, showing promise.
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46

Bramham, Kate, and Catherine Nelson-Piercy. Specific renal conditions in pregnancy. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0298.

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Pre-pregnancy glomerular filtration rate, proteinuria, and blood pressure are usually more important in determining the risk of pregnancy in patients with chronic kidney disease, but some diseases may be exacerbated in pregnancy, or appear more liable to complications. This chapter considers immunoglobulin A nephropathy, systemic lupus erythematosus (which may also be associated with some manifestations in the infant), diabetic nephropathy, polycystic kidney disease, reflux nephropathy, single kidney, urological disorders, and angiomyolipomata. Distinguishing underlying renal disease exacerbation from pre-eclampsia and other complications of pregnancy can be challenging. Renal biopsy is sometimes indicated.
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47

Phipps, Lisa M., Titi Chen, and David C. H. Harris. Radiation nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0091_update_001.

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Radiation nephropathy usually arises after inadvertent exposure of kidneys to radiotherapy. It may manifest as acute nephropathy as early as 6 months after exposure, or later as chronic nephropathy, hypertension, or asymptomatic proteinuria. Glomerular and peritubular endothelium and renal tubular cells are especially radiosensitive. There are no pathognomonic histological features, but renal pathology may be similar to that of haemolytic uraemic syndrome. Radiation nephropathy may be prevented by renal shielding and mitigated by radiation dose fractionation. Control of hypertension is important and angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists appear to have protective effects beyond those of blood pressure control.
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48

Bianchi, Claudio, Velio Bocci, Italy) International Symposium of Nephrology 1989 (Montecatini Terme, F. A. Carone, and Ralph Rabkin. Kidney, Proteins and Drugs: 6th International Symposium of Nephrology at Montecatini, Montecatini Terme, June 1-3, 1989 (Contribution to Nephrology). S Karger Pub, 1991.

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49

Schreuder, Michiel F. Congenital solitary functioning kidney. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0351.

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The main cause for unilateral non-formation or non-functioning of a kidney can be found in renal agenesis/aplasia and multicystic dysplastic kidney. Even though kidney donation at adult age is considered safe, studies in recent years have shown that this may be different in congenital solitary functioning kidneys. Whether this is based on dysplasia in the remaining kidney or based on glomerular hyperfiltration damage, follow-up has shown renal injury, defined as hypertension and/or proteinuria, in up to 32% of children with a congenital solitary functioning kidney. Therefore, long-term infrequent follow-up of all patients with a congenital solitary functioning kidney seems to be indicated.
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50

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Renal medicine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0017.

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Chapter 17 covers the basic science and clinical topics relating to ophthalmology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers renal basic science, pathophysiology of renal disease, the kidney as an 'endocrine' organ, renal investigations, acute kidney injury, chronic kidney disease/renal failure, renal replacement therapy, renal transplantation, haemodialysis, peritoneal dialysis, nephrotic syndrome, primary glomerular causes of nephrotic syndrome/proteinuria, rapidly progressive glomerulonephritis, IgA nephropathy, mesangiocapillary glomerulonephritis, tubulointerstitial nephritis, renal tubular disorders, urinary tract obstruction, renal stone disease, urinary tract infection in adults, renovascular disease, renal tumours, inherited renal disease, and renal disease and pregnancy.
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