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1. Glomerular filtration rate did not vary.

2. Patients with impaired glomerular filtration rate are particularly susceptible to hypermagnesemia when given a magnesium load.

3. The efferent glomerular capillaries form a capillary plexus surrounding the proximal tubules.

4. Changes in glomerular filtration rate and filtered load of sodium are regularly and continuously paralleled by comparable alterations in tubular fluid reabsorption.

5. The fractional excretion of magnesium rises as glomerular filtration rate falls.

6. Glomerular changes are both frequent and severe.

7. The glomerular filtration rate remains relatively constant.

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8. The branches reach to glomerular basal membrane.

9. DNA fragmentation localized to glomerular cells.

10. Furthermore, glomerular damaged showed a significant correlation with tubular DNA damage in proliferatie GN.

11. An increased glomerular staining with Peanut agglutinin lectin, indicate of removal of neuraminic acid, was noted.

12. It is mainly inhibited as glomerular sclerosis, renal interstitial fibrosis and intrarenal vascular sclerosis.

13. Methods Changes relating to glomerular function, structure and glomerular basement membrane ultrastructure were observed.

14. NO was related to both the glomerular hyperfiltration and changes of renal morphology in the early diabetes.

15. Objective To evaluate the value differentiating glomerular hematuria from non-glomerular hematuria with multiple urine acanthocyte(G1 cell)counts.

16. CICs were determined in 92 children with glomerular diseases by PEG precipitation - complement consumption ( PEG - CC ) test.

17. An increased glomerular staining with Peanut agglutinin lectin , indicative of removal of neuraminic acid, was noted.

18. Angiotensin I converting enzyme inhibitors may act in reducing glomerular basement membrane pore size.

19. Data on experimental animals show that it may be the long term consequence of glomerular haemodynamic abnormalities induced by long term hyperglycaemia.

20. This caution can not be overstated in light of the decreased glomerular filtration often present in chronic liver failure.

21. Dynamic renal imaging studies were performed in 132 patients using 99m Tc DTPA and 131 I OIH. Effective renal plasma flow(ERPF) and glomerular filtration rate(GFR) was obtained.

22. Conclusion: Fas and its ligand could play a an role in the injury of human glomerular cell.

23. Conclusions There is early abnormality of renal function in CHF patients without primary renal disorder and the abnormality was featured by impaired glomerular filtration function.

24. Objective To study the expression of lipoprotein lipase(LPL) in human glomerular mesangial cells and the effect of very low-density lipoprotein(VLDL) on the expression of LPL.

25. Results Positive correlations were found between the degree of FN in glomerular mesangium or basement membranes and glomerular lesion grading or tubulointerstitial lesion grading.

26. Results In normal kidney tissues, ILK was mainly located in the glomerular visceral epithelialcells.

27. The primary end point was a change in the fraction of glomerular volume occupied by mesangium in kidney-biopsy specimens.

28. Results consistently demonstrated that DNA colocalized with autoantibodies in glomerular membrane associated EDS.

29. This is a normal glomerulus by light microscopy . The glomerular capillary loops are thin and delicate.

30. Objective : To investigate the mechanism inducing apptosis of human glomerular mesangial cells ( Mcs ) by anti Fas antibody.