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Angiotensin Blockade Beyond Hypertension in Autosomal Dominant Polycystic Kidney Disease
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Autosomal Dominant Polycystic Kidney Disease
Primary Care: Clinics in Office Practice, 2020Autosomal Dominant Polycystic Kidney Disease is an inherited multisystemic disorder of the renal tubules with subsequent formation of multiple cysts and enlargement of the kidney, affecting various organs. Diagnosis is initially suspected in those with family history and/or individuals who develop hypertension early on (secondary hypertension) or ...
Parvathi, Perumareddi, Darin P, Trelka
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Autosomal dominant polycystic kidney disease
Disease-a-Month, 2015Autosomal dominant polycystic kidney disease (ADPKD) is an inherited disease of the kidneys that can cause an irreversible decline in kidney function leading to end-stage renal disease. It is one of the most common hereditary disorders. It is 10 times more common than sickle cell disease and 20 times more common than Huntington's disease.
Jonathan, Silverman +2 more
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Autosomal dominant polycystic kidney disease
The Lancet, 2019Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and one of the most common causes of end-stage kidney disease. Multiple clinical manifestations, such as enlarged kidneys filled with growing cysts, hypertension, and multiple extrarenal complications, including liver cysts, intracranial aneurysms, and ...
Emilie, Cornec-Le Gall +2 more
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Autosomal dominant polycystic kidney disease in the fetus
American Journal of Medical Genetics, 1994AbstractWe report on 3 cases with a fetal presentation of autosomal dominant polycystic kidney disease (ADPKD), which illustrate the variable expression of ADPKD during fetal life. Fetus 1 was diagnosed at 20 weeks of gestation by ultrasonography; a molecular prenatal diagnosis was performed at 10 weeks on fetus 2, a sib of fetus 1; and ADPKD was an ...
J, Michaud +7 more
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Diagnosis of autosomal dominant polycystic kidney disease
Expert Opinion on Medical Diagnostics, 2008Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and accounts for 5 - 10% of end stage renal disease. Mutations of two genes, PKD1 and PKD2, account for ∼ 85 and ∼ 15% of cases, respectively.This paper reviews the clinical features of ADPKD, highlights the current roles for image- and molecular-based ...
York, Pei, Xiao, Zhao
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Pregnancy in Autosomal Dominant Polycystic Kidney Disease
Advances in Kidney Disease and Health, 2023Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disorder occurring in approximately 1:1000 individuals. ADPKD is characterized by gradual cyst expansion and kidney enlargement and is a slowly progressive disorder where patients typically initiate renal replacement therapy in the sixth decade of life.
Mina, Al Sayyab, Arlene, Chapman
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Autosomal Dominant Polycystic Kidney Disease
New England Journal of Medicine, 1990Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease occurring in 1 in 200 to 1 in 1,000 individuals. ADPKD is characterized by cystic lesions in the kidneys and often by structural abnormalities in the gastrointestinal tract and cardiovascular system.
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Autosomal dominant polycystic kidney disease
BMJ, 2016#### What you need to know Polycystic kidney disease (PKD) is an inherited condition defined by the pathological development of fluid-filled cysts throughout the kidneys leading to organ enlargement (fig 1⇓) and chronic kidney disease. Autosomal dominant polycystic kidney disease (ADPKD) is the commonest inherited kidney disease1 and is the fourth ...
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Nephrolithiasis in Autosomal Dominant Polycystic Kidney Disease
Journal of Endourology, 2010Autosomal dominant polycystic kidney disease (ADPKD) manifests with renal and extrarenal abnormalities and is inherited in an autosomal dominant fashion. In addition to multiple renal cysts, abnormalities such as liver cysts (80%), pancreatic cysts, splenic cysts, pulmonary cysts, berry aneurysms in the distribution of arterial circle of Willis (8 ...
Uwais B, Mufti, Sarath K, Nalagatla
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