- Paperback: 378 pages
- Publisher: Lippincott Williams and Wilkins; 3rd Revised edition edition (1 Sept. 2009)
- Language: English
- ISBN-10: 0781799953
- ISBN-13: 978-0781799959
- Product Dimensions: 22.6 x 15 x 1.5 cm
- Amazon Bestsellers Rank: 632,537 in Books (See Top 100 in Books)
- See Complete Table of Contents
Renal Pathophysiology: The Essentials Paperback – 1 Sep 2009
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Most Helpful Customer Reviews on Amazon.com (beta)
EXCELLENT book, I would think it's pretty close to a "Lily Pathophysiology of the Heart" for renal pathophys. and when I make that comparison, if you haven't read the Lily pathophys book, you're also seriously missing out.
For example, from the glomerular disease section, there was a great explanation on the significance of immune complex deposits. In classic Nephritic Syndromes ICs deposit characteristically subendothelially or mesangially and b/c of this close location to systemic circulation they are able to attract WBCs when they activate complement and induce inflammation, as opposed to classic nephrotic syndrome where the IC is deposited subepithelially, which is unable to contact WBC in systemic circulation.
Anyways, you get the idea. GET THIS BOOK if you want to learn renal!!!!
For example, one of the other reviewers states that this book attempts to differentiate the clinical manifestations of nephrotic versus nephritic syndrome on the basis of sub-epithelial versus sub-endothelial deposits. The authors claim that one of the reasons why diseases that cause sub-epithelial deposits manifest as nephrotic syndrome is because circulating inflammatory cells are not able to access the sub-epithelial space and thus there is no inflammation. Similarly, the book posits that diseases with sub-endothelial deposits tend to manifest as nephritic, because the circulating inflammatory cells are able to access the deposited antigen/antibody/complement.
But this does not really explain why post-streptococcal glomerulonephritis, which is classified in First Aid, Robbins, and Goljan as primarily nephritic, has sub-epithelial deposits (in which case, according to this theory, you would expect a primarily nephrotic presentation). In addition, it does not explain why membranoproliferative glomerulonephritis, which has sub-endothelial deposits, tends to present as a nephrotic syndrome.
I encountered other parts of the book in which I noticed a similar phenomena: I found the explanations to sort of make sense, but they were at odds with what I'd read from many other sources. I think this book may be helpful for persons with a background in renal pathophysiology who are interested in attempting to understand the mechanistic basis of renal disease, but it can be confusing and contradictory for students (and others) who are learning the basics.
I think this book would more aptly be named Renal Pathophysiology: The Extras.
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