نتایج جستجو برای: polycystic kidney diseases pkd

تعداد نتایج: 1000149  

2016
Timothy L. Kline Maria V. Irazabal Behzad Ebrahimi Katharina Hopp Kelly N. Udoji Joshua D. Warner Panagiotis Korfiatis Prasanna K. Mishra Slobodan I. Macura Sudhakar K. Venkatesh Lilach O. Lerman Peter C. Harris Vicente E. Torres Bernard F. King Bradley J. Erickson

PURPOSE Noninvasive imaging techniques that quantify renal tissue composition are needed to more accurately ascertain prognosis and monitor disease progression in polycystic kidney disease (PKD). Given the success of magnetization transfer (MT) imaging to characterize various tissue remodeling pathologies, it was tested on a murine model of autosomal dominant PKD. METHODS C57Bl/6 Pkd1 R3277C ...

Journal: :American journal of physiology. Renal physiology 2015
Kelli M Sas Hong Yin Wayne R Fitzgibbon Catalin F Baicu Michael R Zile Stacy L Steele May Amria Takamitsu Saigusa Jason Funk Marlene A Bunni Gene P Siegal Brian J Siroky John J Bissler P Darwin Bell

In polycystic kidney disease (PKD), the rate of cyst formation and disease progression is highly variable. The lack of predictability in disease progression may be due to additional environmental factors or pathophysiological processes called "third hits." Diabetes is a growing epidemic, and recent studies suggest that PKD patients may be at an increased risk for this disease. We sought to dete...

Journal: :Human Mutation 2023

Biallelic PKD1 variants, including hypomorphic can cause very early onset polycystic kidney disease (VEO-PKD). A family with unexplained recurrent VEO-PKD and neonatal demise in one dizygotic twin was referred for clinical testing. Further individuals the putative variant, p.(Ile3167Phe), were identified from UK 100,000 genomes project (100 K), Biobank (UKBB), a review of literature. We likely ...

Journal: :Kidney diseases 2016
Ming Wu Shengqiang Yu

BACKGROUND Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the PKD1, PKD2 or PKHD1 gene, which encodes polycystin-1, polycystin-2 or fibrocystin, respectively. Embryonic and postnatal mutation studies show that transport or channel function is dysregulated before the initiation of cystogenesis, suggesting that the abnormality of transport...

2017
Masanori Kugita Kazuhiro Nishii Tamio Yamaguchi Atsushi Suzuki Yukio Yuzawa Shigeo Horie Eiji Higashihara Shizuko Nagao

Increased intracellular cyclic AMP (cAMP) in renal tubular epithelia accelerates the progression of polycystic kidney disease (PKD). Thus, decreasing cAMP levels by an adenylyl cyclase inhibitory G protein activator is considered to be an effective approach in ameliorating PKD. In fact, pasireotide (PAS) was effective in reducing disease progression in animal models of PKD. However, hyperglycem...

1997

We report the clinical and morphological features of an unusual hepatorenal disorder in 2 patients. The main clinical features were early onset of cholestatic liver disease and progressive tubulointerstitial nephritis, leading to renal death in early childhood. Renal histology showed interstitial fibrosis, tubular atrophy and dilatation, glomerular cysts in the cortex and periglomerular fibrosi...

1997

We report the clinical and morphological features of an unusual hepatorenal disorder in 2 patients. The main clinical features were early onset of cholestatic liver disease and progressive tubulointerstitial nephritis, leading to renal death in early childhood. Renal histology showed interstitial fibrosis, tubular atrophy and dilatation, glomerular cysts in the cortex and periglomerular fibrosi...

1997

We report the clinical and morphological features of an unusual hepatorenal disorder in 2 patients. The main clinical features were early onset of cholestatic liver disease and progressive tubulointerstitial nephritis, leading to renal death in early childhood. Renal histology showed interstitial fibrosis, tubular atrophy and dilatation, glomerular cysts in the cortex and periglomerular fibrosi...

1997

We report the clinical and morphological features of an unusual hepatorenal disorder in 2 patients. The main clinical features were early onset of cholestatic liver disease and progressive tubulointerstitial nephritis, leading to renal death in early childhood. Renal histology showed interstitial fibrosis, tubular atrophy and dilatation, glomerular cysts in the cortex and periglomerular fibrosi...

1997

We report the clinical and morphological features of an unusual hepatorenal disorder in 2 patients. The main clinical features were early onset of cholestatic liver disease and progressive tubulointerstitial nephritis, leading to renal death in early childhood. Renal histology showed interstitial fibrosis, tubular atrophy and dilatation, glomerular cysts in the cortex and periglomerular fibrosi...

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