Additional file 7: Table S2. of Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis

Urine biochemistry test in Wnt11 -/- and WT mice. Creatinine clearance (ml/min) was calculated from the formula UV/P ×1/1440. U; urinary concentration of the substance (mmol/l), V; urinary volume (ml), P; plasma creatinine concentration (μmol), 1440: minutes in 24 h. Creatinine clearance and urine volume were scaled to body weight. (DOCX 18 kb

Additional file 5: Figure S4. of Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis

OPT-based kidney morphometric. Wnt11 knockout (C, C´) alters the volumetric measures such as the relative volumes of the kidney and pelvis relative to WT (B, B´). (A) OPT volumetry data (n = 6-8). Drishti reconstruction of the pelvis (B, C) and highlighted regions depicted as B´ and C´ (boxed areas in B, C) revealing the sagittal/rostro-caudal tubular view. Note that the Wnt11 deficiency led to considerable changes in the overall 3D arrangement of the tubules as well as the degree of their convolution when compared to control (compare C to B and C’ to B´). Bars: B, C 800 μm; B’, C’ 300 μm. (JPG 379 kb

Additional file 6: Figure S5. of Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis

Wnt11 deficiency influences kidney function. Creatinine clearance (A) is significantly reduced in the Wnt11 -/- mice when compared to WT, indicating reduced glomerular filtration rate (GFR). This situation corresponds to a diagnosis of mild to moderate renal failure in a human and is in line with the observed increase in blood urea nitrogen (BUN) (B) and reduced daily urine excretion (C). n = 8-10, p < 0.05. (JPG 146 kb

Additional file 2: Figure S1. of Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis

Formation of glomerular cysts and anomalies of papillary duct due to Wnt11 deficiency. A and D) Note discrete glomerular changes in E16.5 as the Bowman’s capsule of the glomerulus is enlarged and contains parietal podocytes (compare D to A, red arrows). B and E) Advanced cystic formation is found in NB, the glomerular tuft has an abnormal architecture when compared to the WT (arrow) and it is microcystic (star). C and F) Typical findings in all adult Wnt11 -/- are cortical glomerular microcysts that contain rudiments of the tuft (F, G stars) and hypertrophied glomeruli (compare F to C, black arrows). In the severe kidney tubular anomalies of Wnt11 deficient mice interstitial fibrosis is noted (F, empty arrow). G) High magnification of a cortical glomerular cyst (star) with dysmorphic tuft (arrow) in the kidney of Wnt11 -/- mouse. H, I) TEM shows normal structure of non-cystic glomeruli in Wnt11 -/- mice (RBC: red blood cell; US: urinary space; M: mesangial cell; GBM: glomerular basement membrane). J-M) Immunohistochemistry with AQP2 in kidney indicates that AQP2 staining is more intense in Wnt11 deficient papillary ducts compared to controls (arrows). In contrast, the cell morphology of the cortical collecting duct was normal and expression of AQP2 is not different from controls (arrows). Bars: J, L 200 μm, A, D, C-G 100 μm, B, E, K, M 50 μm, H, I 2 μm. (JPG 1128 kb