Chronic Kidney Disease by M. Gooz PDF

By M. Gooz

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Sample text

The above events along with proteinuria eventually lead to tubulointerstitial fibrosis. Angiotensin II increases vascular tone (predominantly post-glomerular) and affects intraglomerular pressure. The increased pressure alters the structure of the pores in the glomerular basement membrane (GBM) and increases proteinuria. 1 Clinical manifestation and management What is the best way to manage these individuals? In the outpatient setting, achecklist for each patient ensures that each individual’s needs are met.

J Bone Miner Metab. 24(6): 434-8. Ganesh SK, Stack AG et al. (2001). ;12(10): 2131-8. Gao P, and D'Amour P (2005). ; 51(1-2): 21-9. Giachelli CM. (2004). ;15(12): 295964.

66(4): 1310-4. Felsenfeld AJ, Rodríguez M et al. (2007). ” CJASN; 2(6):1283-305. Floege J. (2008). ; 23(10):3050-2. Foley RN, Parfrey PS et al. (1998). “Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis; 32 (5 Suppl 3):S112-9. , Y. Hamada, et al. (2006). “The kidney and bone metabolism: Nephrologists' point of view”. J Bone Miner Metab. 24(6): 434-8. Ganesh SK, Stack AG et al. (2001). ;12(10): 2131-8. Gao P, and D'Amour P (2005). ; 51(1-2): 21-9. Giachelli CM.

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