Ascites and Renal Dysfunction in Liver Disease: by Pere Gines

April 3, 2017 | Digestive Organs | By admin | 0 Comments

By Pere Gines

There was little or no written at the interplay of the liver and kidney. This booklet addresses the expanding prevalence and value of ailments, corresponding to ascites, renal disorder, cirrhosis and high blood pressure the place either organs are concerned. This textbook is vital, even for proven practitioners and includes present information about remedy and treatment for sufferers with cirrhosis and ascites, sincerely and successfully offered by way of the head overseas specialists inside this box. the second one variation is totally revised and up to date and locations better emphasis on treatment.

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Semin Nephrol 1995; 15:214–27. 133 Swan SK, Rudy DW, Lasseter KC et al. Effect of cyclooxygenase-2 inhibition on renal function in elderly persons receiving a low salt diet. A randomized, controlled trial. Ann Intern Med 2000; 133:1–9. 134 Dunn MJ. Are COX-2 selective inhibitors nephrotoxic? Am J Kidney Dis 2000; 35:976. 135 Whorton AR, Lazar JD, Smigel MD, Dates JA. Prostaglandin mediated renin release from renal cortical slices. Adv Prostaglandin Thromboxane Res 1980; 7:1123–6. 136 Franco-Saenz R, Suzuki S, Tan SY, Mulrow PJ.

Physiologic adaptations of the tubuloglomerular feedback system. Kidney Int 1990; 38:577–83. 26 Braam B, Mitchell KD, Koomans HA, Navar LG. Relevance of the tubuloglomerular feedback mechanism in pathophysiology. J Am Soc Nephrol 1993; 4:1257–74. 27 Blantz RC, Peterson OW, Gushwa L, Tucker BJ. The effect of modest hyperglycemia upon tubuloglomerular feedback activity. Kidney Int 1982; 22:S206–S212. 28 Vallon V, Blantz RC, Thomson SC. Homeostatic efficiency Physiology of the Renal Circulation 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 of tubuloglomerular feedback is reduced in established diabetes mellitus in rats.

This interaction is further complicated by the fact that certain types of cyclooxygenasederived prostaglandins stimulate renin as does NO (48), generating a rather consistent pattern in which certain hormones antagonize AII at effector cells, yet stimulate the generation of the AII via effects on the enzyme, renin. Acute inhibition of NO synthase (49) and of cyclooxygenase (50) magnifies the effects of AII. However, chronic inhibition of these systems exerts more complex effects 20 Chapter 2 because of their capacity to decrease renin activity, and therefore AII generation (51).

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