Endothelin Antagonism and Reversal of Proteinuric Renal Disease in Humans

2011 ◽  
pp. 210-222 ◽  
Author(s):  
Matthias Barton
Keyword(s):  
Renal Disease ◽  
Proteinuric Renal Disease

Increased plasma acylation-stimulating protein in pediatric proteinuric renal disease

2008 ◽  
Vol 23 (6) ◽  
pp. 959-964 ◽  
Author(s):  
Jin Hui Tang ◽  
Yu Wen ◽  
Fei Wu ◽  
Xiao Y. Zhao ◽  
Mei X. Zhang ◽  
...  
Keyword(s):  
Renal Disease ◽  
Acylation Stimulating Protein ◽  
Proteinuric Renal Disease

A case of pheochromocytoma presenting as secondary hyperaldosteronism, hyperparathyroidism, diabetes and proteinuric renal disease

2011 ◽  
Vol 26 (3) ◽  
pp. 1104-1107 ◽  
Author(s):  
M. Bernini ◽  
A. Bacca ◽  
G. Casto ◽  
V. Carli ◽  
A. Cupisti ◽  
...  
Keyword(s):  
Renal Disease ◽  
Secondary Hyperaldosteronism ◽  
Proteinuric Renal Disease

MYH9 and renal disease

2018 ◽  
Author(s):  
Neil Turner ◽  
Bertrand Knebelmann
Keyword(s):  
Renal Disease ◽  
Alport Syndrome ◽  
Autosomal Dominant ◽  
Cell Structure ◽  
Myosin Ii ◽  
Giant Platelets ◽  
The Past ◽  
Sensorineural Hearing Impairment ◽  
Muscle Myosin ◽  
Proteinuric Renal Disease

MYH9 encodes one of three heavy chain isoforms for the non-muscle myosin II (NM II) molecule. NM II is involved in cell structure and shape and motility. Myosin II is very widely expressed but MYH9 is highly expressed in podocytes. MYH9 diseases are characterized by various combinations of autosomal dominant progressive, proteinuric renal disease, giant platelets with low platelet counts, progressive sensorineural hearing impairment, granulocyte inclusions, and in some patients also cataracts. Although the eponyms Epstein and Fechtner have been given to MYH9 renal syndromes, there is a spectrum of manifestations of MYH9 diseases that do not correlate perfectly with genotype. They are best described as MYH9-associated renal disease. The occurrence of progressive deafness and renal failure led to this condition being considered an Alport syndrome variant in the past, but phenotype as well as molecular genetics clearly separate the disorders.

scholarly journals Patients with Epstein–Fechtner syndromes owing to MYH9 R702 mutations develop progressive proteinuric renal disease

2010 ◽  
Vol 78 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Takashi Sekine ◽  
Mutsuko Konno ◽  
Satoshi Sasaki ◽  
Suzuko Moritani ◽  
Takuma Miura ◽  
...  
Keyword(s):  
Renal Disease ◽  
Proteinuric Renal Disease

scholarly journals Endothelial function in proteinuric renal disease

1999 ◽  
Vol 56 ◽  
pp. S57-S61 ◽  
Author(s):  
Jaap A. Joles ◽  
Erik S.G. Stroes ◽  
Ton J. Rabelink
Keyword(s):  
Renal Disease ◽  
Endothelial Function ◽  
Proteinuric Renal Disease

scholarly journals Familial partial lipodystrophy and proteinuric renal disease due to a missense c.1045C > T LMNA mutation

2017 ◽  
Vol 2017 ◽  
Author(s):  
Athanasios Fountas ◽  
Zoe Giotaki ◽  
Evangelia Dounousi ◽  
George Liapis ◽  
Alexandra Bargiota ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Renal Disease ◽  
Subcutaneous Adipose Tissue ◽  
Lower Limbs ◽  
List Type ◽  
Partial Loss ◽  
Partial Lipodystrophy ◽  
Familial Partial Lipodystrophy ◽  
Subcutaneous Adipose ◽  
Proteinuric Renal Disease

Summary Proteinuric renal disease is prevalent in congenital or acquired forms of generalized lipodystrophy. In contrast, an association between familial partial lipodystrophy (FPLD) and renal disease has been documented in very few cases. A 22-year-old female patient presented with impaired glucose tolerance, hyperinsulinemia, hirsutism and oligomenorrhea. On examination, there was partial loss of subcutaneous adipose tissue in the face, upper and lower limbs, bird-like facies with micrognathia and low set ears and mild acanthosis nigricans. Laboratory investigations revealed hyperandrogenism, hyperlipidemia, elevated serum creatine kinase and mild proteinuria. A clinical diagnosis of FPLD of the non-Dunnigan variety was made; genetic testing revealed a heterozygous c.1045C > T mutation in exon 6 of the LMNA gene, predicted to result in an abnormal LMNA protein (p.R349W). Electromyography and muscle biopsy were suggestive of non-specific myopathy. Treatment with metformin and later with pioglitazone was initiated. Due to worsening proteinuria, a renal biopsy was performed; histological findings were consistent with mild focal glomerular mesangioproliferative changes, and the patient was started on angiotensin-converting enzyme inhibitor therapy. This is the fourth report of FPLD associated with the c.1045C > T missense LMNA mutation and the second with co-existent proteinuric renal disease. Patients carrying this specific mutation may exhibit a phenotype that includes partial lipodystrophy, proteinuric nephropathy, cardiomyopathy and atypical myopathy. Learning points: Lipodystrophy is a rare disorder characterized by the complete or partial loss of subcutaneous adipose tissue, insulin resistance, diabetes mellitus and hyperlipidemia. Proteinuric renal disease is a prevalent feature of generalized lipodystrophy but rare in familial partial lipodystrophy. Patients carrying the c.1045C > T missense LMNA mutation (p.R349W) may present with familial partial lipodystrophy, proteinuric nephropathy, cardiomyopathy and atypical myopathy.

scholarly journals Supramaximal Dose of Candesartan in Proteinuric Renal Disease

2009 ◽  
Vol 20 (4) ◽  
pp. 893-900 ◽  
Author(s):  
Ellen Burgess ◽  
Norman Muirhead ◽  
Paul Rene de Cotret ◽  
Anthony Chiu ◽  
Vincent Pichette ◽  
...  
Keyword(s):  
Renal Disease ◽  
Proteinuric Renal Disease
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