Books on the topic 'Renal dysplasia'
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1
Schreuder, Michiel F. Renal dysplasia. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0347.
Full textAbstract:
Renal dysplasia refers to abnormal and incomplete development of the kidney, which may be segmental, for instance, in the upper part of a duplex kidney, or affect the entire kidney. Dysplasia is by definition a histological diagnosis, but in most patients diagnosis is made on the basis of evaluation with ultrasound and renography. This typically shows cysts and/or a small kidney with decreased corticomedullary differentiation and a reduced split renal function. The latter can also be found in other conditions, such as hypoplasia, vascular insults, renal post-infectious damage, or polycystic kidney disease, making it difficult to establish the diagnosis and thereby estimate the incidence of renal dysplasia. The clinical consequences of renal dysplasia depend upon the residual renal function and may range from hypertension to chronic kidney disease.
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Schreuder, Michiel F. Renal hypoplasia. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0348.
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In true renal hypoplasia, normal nephrons are formed but with a deficit in total numbers. As nephron number estimation is not possible in vivo, renal size is used as a marker. A widely used definition of renal hypoplasia is kidneys with a normal appearance on ultrasound but with a size less than two standard deviations below the mean for gender, age, and body size. A distinct and severe form of renal hypoplasia is called (congenital) oligomeganephronia, which is characterized by small but normal-shaped kidneys with a marked reduction in nephron numbers (to as low as 10–20% of normal), a distinct enlargement of glomeruli, and a reduced renal function. In many cases, the small kidney also shows signs of dysplasia on ultrasound, leading to the diagnosis of renal hypodysplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal hypoplasia is desirable.
3
Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Renal vascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0171.
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Renal vascular disease typically occurs with progressive narrowing of the main renal artery or smaller arterial vessels. Often, both patterns of disease coexist and result in ‘ischaemic nephropathy’ with damage to renal tissue. Much less commonly, inflammatory vasculitis can affect small or medium vessels. Ninety per cent of renal vascular disease is caused by atherosclerosis. Patients with renal vascular disease have an increased risk of cardiovascular death from associated cerebrovascular and coronary heart disease. Less than 10% of renal vascular disease is caused by fibromuscular dysplasia. The cause is unknown, but smoking is a risk factor. The disease is often bilateral and multifocal. It tends to affect the mid-portion of the renal artery, while atherosclerosis tends to occur at points of stress, especially at the junction of renal arteries with the aorta. This chapter reviews the diagnosis and management of renal vascular disease.
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Vester, Udo, and Stefanie Weber. Townes–Brocks syndrome. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0359.
Full textAbstract:
Townes–Brocks syndrome (TBS) is an autosomal dominant disease with variable expression. Classical features are imperforate anus, dysplastic ears with congenital hearing deficit, and triphalangeal thumbs in most cases. A variety of other malformations (renal, genitourinary, heart, central nervous system, eyes) or hypothyroidism has been described. Mutations in SALL1 have been identified in patients with TBS and genetic testing allows confirmation of the diagnosis. Familiar and sporadic forms (caused by de novo mutations) seem to be equally distributed. Renal involvement in TBS is not uncommon and includes renal agenesis, hypo-/dysplasia, and renal cysts and may eventually lead to chronic renal failure. As renal function may not deteriorate before adulthood, renal function should be monitored in all patients. As cases with TBS can be oligosymptomatic, TBS should be suspected in every case with unexplained renal failure, minor abnormalities, or indicative family history. Genetic counselling is mandatory in identified cases.
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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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Goodyer, Paul. Kidney/ear syndromes. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0170.
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Malformations of the external ear may signal renal disease, but it is actually the disorders of the inner ear which reflect molecular pathways that are also crucial for kidney development. In a number of monogenic renal diseases, renal dysplasia is associated with deafness. Disorders of the kidney and inner ear are also linked in complex syndromes such as the human ciliopathies. In some cases, the loss of specific genes affects shared transport physiology, basement membrane assembly, or energy metabolism.The kidney and cochlea have a common susceptibility to toxins that are selectively concentrated by comparable uptake mechanisms in the two tissues.This chapter provides an overview of the many ways in which pathologies of the two organs are linked.
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Thomas, David F. M. Vesicoureteric reflux. Edited by David F. M. Thomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0115.
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The term vesicoureteric reflux (VUR) describes the retrograde flow of urine from the bladder into the upper urinary tract. VUR is not a disease entity in its own right. Nevertheless, it has the potential to cause significant morbidity by preventing effective emptying of the urinary tract and by facilitating the transport of bacteria into the upper tract and renal parenchyma. Mechanisms of renal damage associated with VUR include pyelonephritic scarring and congenital dysplasia or hypoplasia. The long-term complications of pyelonephritic scarring may include hypertension, renal failure, and an increased risk of complications during pregnancy. VUR of mild or moderate severity is best managed conservatively and surgical intervention is generally reserved for failed medical management and high grade or complex VUR. Although the introduction of endoscopic correction has revolutionized surgical management, there remains a role for open surgery for the correction of higher grades of reflux.
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Schreuder, Michiel F. Posterior urethral valves. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0354.
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Posterior urethral valves is the most common congenital cause of lower urinary tract obstruction in males, and a common cause (15–17%) for end-stage renal disease in childhood. Most commonly, posterior urethral valves is suspected on basis of a screening antenatal ultrasound. Ultrasound will not detect posterior urethral valves itself, but recognizes the consequences of lower urinary tract obstruction with a dilated thick-walled bladder and dilation of the prostatic portion of the urethra. After birth, urine drainage has to be secured by placement of a bladder catheter, and imaging is needed to confirm the presence of the urethral valves and estimate the degree of damage to the kidney. Consequences of posterior urethral valves depend on the degree of renal dysplasia and bladder dysfunction. Prevention or minimization of such consequences by intrauterine urine drainage has not definitively shown a benefit of early vesico-amniotic shunting.
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Schreuder, Michiel F. Renal agenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0346.
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In renal agenesis, the kidney never forms due to an absence of interaction in the developing embryo between the ureteric bud and the metanephric mesenchyme. Most cases of renal agenesis are unilateral, for which the reported incidence is around 1 in 3000. The prenatal diagnosis of unilateral renal agenesis is based on the absence of a recognizable kidney, either at the normal or an ectopic site. However, such cases of an empty renal fossa can also be explained by an involuted multicystic dysplastic kidney, or by renal aplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal agenesis is desirable.
10
Lambert, Heather. Primary vesicoureteric reflux and reflux nephropathy. Edited by Adrian Woolf. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0355_update_001.
Full textAbstract:
Vesicoureteric reflux (VUR) describes the flow of urine from the bladder into the upper urinary tract when the ureterovesical junction fails to perform as a one-way valve. Most commonly, VUR is primary, though it can be secondary to bladder outflow obstruction and can occur in several multiorgan congenital disorders. There is good evidence of a genetic basis with a greatly increased risk of VUR in children with a family history of VUR. VUR is a congenital disorder, which largely shows improvement or complete resolution with age. Fetal VUR may be associated with parenchymal developmental defects (dysplasia). Postnatally non-infected, non-obstructed VUR does not appear to have a detrimental effect on the kidneys. However there is an association of VUR with urinary tract infection and acquired renal parenchymal defects (scarring). The parenchymal abnormalities detected on imaging, often termed reflux nephropathy, may be as a result of reflux-associated dysplasia or acquired renal scarring or both. It is difficult to distinguish between the two on routine imaging. Higher grades of VUR are associated with more severe reflux nephropathy. The precise role of VUR in pyelonephritis and scarring is not clear and it may be that VUR simply increases the risk of acute pyelonephritis. Whilst most VUR resolves during childhood, it is associated with an increased risk of urinary tract infection and burden of acute disease. Investigation strategies vary considerably, related to uncertainties about the natural history of the condition and the effectiveness of various interventions. The long-term prognosis is chiefly related to the morbidity of reflux nephropathy leading in some cases to impairment of glomerular filtration rate, hypertension, proteinuria, and pregnancy-related conditions including hypertension, pre-eclampsia, and recurrent urinary tract infection. Management is controversial and ranges from simple observation with or without provision of rapid access to diagnosis and treatment of urinary tract infections; to long-term prophylactic antibiotics or various antireflux surgical procedures.
11
Thomas, David F. M. Prenatal diagnosis and perinatal urology. Edited by David F. M. Thomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0113.
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The kidney is formed by the interaction of the ureteric bud and metanephros during the fifth week of gestation and urine is excreted into the amniotic cavity from the ninth week onwards. The introduction of routine antenatal ultrasonography into obstetric practice has had a profound impact on the specialty of paediatric urology and the majority of urological abnormalities which pose a serious threat of morbidity are now detected prenatally. The results of foetal intervention to treat severe lower tract obstruction have been disappointing because renal damage (notably dysplasia) is largely irreversible by the time the anomaly is first identified. Indications for urgent postnatal evaluation include bilateral upper tract dilatation, thick-walled bladder, and impaired bladder emptying. A selective approach to the postnatal investigation of unilateral pelvic dilatation is required to avoid submitting healthy infants to unnecessary investigations.
12
Chenault, Kristin. Pediatric Renal Transplantation. 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/9780190685157.003.0043.
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Approximately 700 pediatric kidney transplants were performed in 2014, with roughly one-third of those being living-related kidney transplantations. There are distinct differences between renal disease and transplantation in children compared to adults. Overall, end-stage renal disease (ESRD) is less common in the pediatric population than in adults. While the most common etiology for ESRD in adults is diabetes mellitus, the most common etiologies of ESRD in the pediatric population are congenital, such as dysplastic kidney or obstructive uropathy. Surgical technique can also vary depending on the age and size of the recipient, as well as the donor kidney size.
13
Bergmann, Carsten, Nadina Ortiz-Brüchle, Valeska Frank, and Klaus Zerres. The child with renal cysts. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0305.
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Renal cysts of different aetiology are a common diagnosis in paediatric nephrology. The classification is usually based on the clinical picture, morphology, and family history. In syndromic forms, additional features have to be evaluated. Most common are cystic dysplastic kidneys with a broad phenotypic spectrum ranging from asymptomatic clinical courses in unilateral cases to severe, lethal manifestations in patients with considerable bilateral involvement. Simple cysts are rare. Polycystic kidneys are usually subdivided according to the mode of inheritance into autosomal recessive and autosomal dominant polycystic kidney disease. The most useful investigation in order to distinguish between these two types is the family history with parental ultrasound and demonstration of polycystic kidneys in one parent in the majority of cases with dominant polycystic kidney disease. Finally, cystic kidneys are associated with a variety of hereditary, usually recessive syndromes affecting cilia.
14
Sybert, Virginia P. Tumors/Hamartomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190276478.003.0010.
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Chapter 10 covers Basal Cell Nevus Syndrome, Cowden Syndrome, Cylindromatosis, Dysplastic Nevus Syndrome, Epidermal Nevus, Gardner Syndrome, Giant congenital nevocytic nevus, Hereditary Keratoacanthomas, Hereditary Leiomyomatosis and renal cell cancer, Infantile Myofibromatosis, Multiple Endocrine Neoplasia Types 1, 2A, and 2B/3, Pilomatricoma, Proteus Syndrome, Sebaceous Nevus Syndrome, and Tumoral Calcinosis. Each condition is discussed in detail, including dermatologic features, associated anomalies, histopathology, basic defect, treatment, mode of inheritance, prenatal diagnosis, and differential diagnosis.
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Sayer, John A., and Roslyn J. Simms. Nephronophthisis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0317_update_001.
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Nephronophthisis (NPHP) is a clinically heterogeneous autosomal recessive cystic kidney disease and the leading genetic cause of end-stage renal failure in children and young adults. Whilst enlarged dysplastic cystic kidneys are associated with infantile NPHP, more typically renal ultrasound reveals normal kidney size and corticomedullary cysts in a child with polyuria and secondary enuresis. Extrarenal manifestations occur in 10–15% including retinal degeneration, cerebellar vermis hypoplasia and liver fibrosis, requiring referral to other specialists. Mutations in 18 genes have been identified to cause NPHP, but a genetic diagnosis still cannot be found in many patients. NPHP is classified as a ciliopathy because of the localization of the protein products of the associated genes. Currently there is no specific therapy for NPHP.
16
Hutton, Kim. Disorders of the kidney and upper urinary tract in children. Edited by David F. M. Thomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0116.
Full textAbstract:
The majority of clinically significant congenital disorders of the upper urinary tract are now detected prenatally. Commonly identified abnormalities include pelviureteric junction obstruction (PUJO), vesicoureteric junction obstruction (VUJO), duplication anomalies, multicystic dysplastic kidney (MCDK), high grade vesicoureteric reflux (VUR) and anomalies of renal migration and/or fusion. Most affected infants are asymptomatic at birth and further investigation can usually be undertaken on a non-urgent basis in the first few weeks or months of life. Long-term natural history studies have shown that many of these conditions can be managed non-operatively. In most cases, standardized procedures such as pyeloplasty and ureteric reimplantation give predictably satisfactory results. Long-term outcome data for surgical and conservative management of upper tract disorders in children is sparse and research in this area is still required.