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1 ombined with aminoaciduria suggests proximal tubular dysfunction.
2 ring loss; pigmentary maculopathy; and renal tubular dysfunction.
3 ted with more advanced HF and glomerular and tubular dysfunction.
4 and necrosis of tubular cells, and abrogated tubular dysfunction.
5 ataracts, cognitive disability, and proximal tubular dysfunction.
6 elay, hypertrophic cardiomyopathy, and renal tubular dysfunction.
7 ensorineural deafness, enteropathy and renal tubular dysfunction.
8 aracterized by early onset of renal proximal tubular dysfunction.
9 retardation, congenital cataracts, and renal tubular dysfunction.
10 ntly associated with renal insufficiency and tubular dysfunction.
11 15 months, after they had developed proximal tubular dysfunction.
12 C, ACR, and KIM-1, indicating glomerular and tubular dysfunction.
13 bound uremic solutes and urine biomarkers of tubular dysfunction.
14 acute kidney injury, glomerulonephritis and tubular dysfunction.
15 ating a previously unknown role for PAI-1 in tubular dysfunction.
16 impairment, albuminuria, and proximal renal tubular dysfunction.
17 ion, HDL significantly reduced (1) renal and tubular dysfunction, (2) tubular and reperfusion-injury,
18 Clinical studies continue to show that mild tubular dysfunction and abnormalities in GFR are common
19 ic arthrogryposis multiplex congenita, renal tubular dysfunction and neonatal cholestasis with bile d
20 and cellular mechanisms underlying proximal tubular dysfunction and progressive renal failure in nep
21 tinosis, which exhibits generalized proximal tubular dysfunction and progressive renal failure, remai
22 int was to assess the prevalence of proximal tubular dysfunction and the correlation between elevated
23 To elucidate the relationship between renal tubular dysfunctions and urinary neonicotinoids concentr
24 injury progresses, the subsequent ischemia, tubular dysfunction, and glomerular scarring can result
26 = 5.8; 95% CI = 3.7-9.0), and proximal renal tubular dysfunction (aOR = 7.0; 95% CI = 4.9-10.2]).
27 ar disease and mortality, but focus on renal tubular dysfunction as a potential risk factor is growin
28 owing cystine accumulation and late signs of tubular dysfunction but lacking the glomerular phenotype
30 ram of renal fibrogenesis involving proximal tubular dysfunction, failed epithelial recovery and redi
31 dition characterized by generalized proximal tubular dysfunction from birth, slowly progressive chron
32 the relevance of microbial metabolism and/or tubular dysfunction in CKD, irrespective of protein bind
34 renal tubule exhibited generalized proximal tubular dysfunction indicative of Fanconi syndrome, char
36 dative stress and cardiomyocyte and proximal tubular dysfunction, leading to cardiomyopathy and kidne
37 ment, and signs of pronephric glomerular and tubular dysfunction mimicking the early phenotype of hum
38 initially affected with generalized proximal tubular dysfunction (renal Fanconi syndrome), then the d
39 nine ratio >/=3 mg/mmol), and proximal renal tubular dysfunction (retinol-binding protein/creatinine
41 l fumarate (TDF) is associated with proximal tubular dysfunction (tubulopathy) when used in the treat