Helpful resources

How to remember nephritic vs. nephrotic syndrome

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One of the things I covered in our Renal Path lecture was nephritic and nephrotic syndromes. I thought it might help to review them a bit, since they can be maddeningly frustrating if you don’t understand the underlying principle in each one.

Here are the four main characteristics of each:

Nephrotic syndrome

  1. Massive proteinuria
  2. Hypoalbuminemia
  3. Edema
  4. Hyperlipidemia/hyperlipiduria

Nephritic syndrome:

  1. Hematuria
  2. Oliguria
  3. Azotemia
  4. Hypertension

How do you make these lists hang together in a way that you can remember?

First, let’s take nephrotic syndrome.

The thing to remember for this one is massive proteinuria. You might do this by remembering that nephrotic and protein both have an “o” in them. The massive proteinuria in these patients leads to hypoalbuminemia (they are peeing out albumin!), which results in edema (the oncotic pressure in the blood goes down, and fluid leaks out of the vasculature into the surrounding tissue).

So right there, you have three of the four features, just by remembering one. The hyperlipidemia/hyperlipiduria occurs because as the liver is trying to make more albumin (to make up for the albumin loss in the urine), it also ends up making more lipids.

As an aside, nephrotic syndrome is often more dangerous than nephritic syndrome, so you might want to think of this syndrome as the “oh sh*t” syndrome (again – nephrotic has an o in it, nephritic does not). Crude, but if it works, who cares?

How about nephritic syndrome?

In nephritic there is some proteinuria and edema, but it’s not nearly as severe as in nephrotic syndrome. The thing with nephritic syndrome is that the lesions causing it all have increased cellularity within the glomeruli, accompanied by a leukocytic infiltrate (hence the suffix “-itic”). The inflammation injures capillary walls, permitting escape of red cells into urine. Hemodynamic changes cause a decreased glomerular filtration rate (manifested clinically as oliguria and azotemia). The hypertension seen in nephritic syndrome is probably a result of fluid retention and increased renin released from ischemic kidneys.

Bottom line

If you really want to pare it down, just remember that nephrotic syndrome is characterized by massive proteinuria (the “o” in nephrotic), and nephritic syndrome is characterized by inflammation (the “-itic” in nephritic). Then at least you’ll have a shot at remembering the other features.

If you want to read more, you might want to take a look at “What causes nephritic and nephrotic syndrome” as a little review of the diseases we talked about in class.

A blueprint for studying diseases

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We’re going to be talking about a LOT of diseases in this course – everything from mild skin infections to deadly brain cancers – and each disease has its own unique features that you’ll need to learn and remember.

This is a lot of information.

If no one helps you organize all of this information, then all you can do is plow through it and try to memorize as much as possible. That becomes frustrating very quickly. Plus, it’s a crappy method for retaining information. Your brain only holds that type of stuff in short-term memory until exam day – after that, it’s gone.

In this course, we’ll take a different approach. We’ll limit brute force memorization to an absolute minimum, and focus more on understanding why things are the way they are. And because your brain is constantly searching for patterns and similarities, we’ll give it the structures and frameworks it wants, so it can relax and enjoy itself.

Here’s a blueprint.

Here’s the first structure we’ll give your brain – it’s a list of the four aspects we look for in every disease:

  1. Etiology: the cause of the disease.
  2. Pathogenesis: the underlying mechanism of the disease.
  3. Morphology: the tissue abnormalities you see in the disease.
  4. Clinical manifestations: the signs and symptoms of the disease.

You can use this as a blueprint for any disease, and it will help you keep all the information in a pattern that your brain can remember. Let’s see what it looks like for a few of the diseases in our first lecture.

Atherosclerosis

  • Etiology: numerous factors including hyperlipidemia, hypertension, smoking, genetics.
  • Pathogenesis: chronic endothelial injury makes the endothelium more permeable; macrophages and lipids accumulate, smooth muscle cells proliferate and lay down collagen, and you end up with a plaque in the wall of the vessel. Plaques can occlude the vessel, or sometimes a thrombus will form on top of a plaque, filling up and occluding the vessel.
  • Morphology: vessel walls show plaques consisting of a soft fatty core covered by a fibrous cap.
  • Clinical manifestations: range from nothing (if the plaque is small) to chest pain, shortness of breath, and death (if the plaque blocks a major artery feeding the heart).

Essential Hypertension

  • Etiology: unknown
  • Pathogenesis: unclear – but probably related to a decreased ability to excrete sodium, which would lead to high levels of sodium in the blood, which would pull water into the blood because osmosis – and then you have a high blood volume etc. etc. and high blood pressure.
  • Morphology: hyaline and hyperplastic arteriolosclerosis
  • Clinical manifestations: nothing, until you’ve had it for a while, then it can damage your vessels and lead to stroke, aortic dissection, etc.

Abdominal Aortic Aneurysm

  • Etiology: atherosclerosis, sometimes genetic defects
  • Pathogenesis: plaques damage the wall of the aorta, leading to bulging of the vessel.
  • Morphology: enlargement of the aorta below the renal arteries; lots of atherosclerotic plaques in the vessel wall.
  • Clinical manifestations: can rupture, leading to massive blood loss. High mortality rate.

Make sense? Let me know what you think!