I’ve had quite a few questions about renal pathology lately. Some of you want to know how to differentiate renal diseases clinically (is it glomerular? or tubulointerstitial?), and some of you are more concerned about how to tell apart the different causes of glomerulonephritis. I thought we might address the clinical question first, and then get into the different kinds of glomerulonephritis in another post.
First, before we talk specifics, a couple points about kidney disease in general. We divide kidney diseases into three main groups: glomerular diseases, tubulointerstitial diseases, and vascular diseases. This works because there are some basic clinical differences in the way these groups present (as we’ll see in a minute). Also, the causes of each group tend to be different (glomerular diseases tend to be caused by immune problems, and tubulointerstitial diseases tend to be caused by toxic or infectious agents).
However, this separation into three groups is somewhat artificial because eventually, destruction of one component tends to affect the other components. If things go on long enough, the patient will end up with end-stage kidneys, no matter what the initial cause was. It’s really important to be able to detect kidney disease as soon as possible – because by the time you get to end-stage kidney disease, most of the kidney has already been damaged.
So let’s take a quick look at some of the clinical differences between the three main types of kidney disease.
Glomerular diseases tend to present with nephritic or nephrotic syndrome (both of which we’ve talked about previously, here and here ). Nephritic syndrome is characterized by hematuria, mild to moderate proteinuria and hypertension. Nephrotic syndrome is characterized by big-time proteinuria, hypoalbuminemia, edema, and hyperlipidemia/lipiduria.
Other ways that glomerular diseases can present include:
Asymptomatic hematuria and/or proteinuria (this is typical of mild glomerular disease).
Acute renal failure (ARF). Patients with ARF generally have decreased urine flow (oliguria) or no urine flow (anuria), and they may also have an elevation of BUN and creatinine.
Tubular and interstitial diseases are usually lumped together because diseases that affect one component tend to affect the other. There are two main groups of tubulointerstitial diseases: those that are caused by ischemic or toxic injury to the tubules, and those that are characterized by inflammation of the tubules/interstitium.
The first group (ischemic/toxic tubular injury) used to be called acute tubular necrosis. A more common term now is acute kidney injury (AKI). We could go on forever about the different causes of AKI, and maybe someday if I’m in the right mood (masochistic? sadistic?), I’ll write about those. The clinical course of AKI is variable – but classically, there are three phases:
Initiation: dominated by whatever medical event caused the AKI. Slight oliguria and rise in BUN
Maintenance: oliguria, salt and water overload, rising BUN, hyperkalemia, metabolic acidosis
Recovery: increase in urinary output (up to 3L/day), hypokalemia, BUN returns to normal.
That being said, about half of patients with AKI don’t have oliguria – they have increased urine output (polyuria). This happens more with toxic agents, and tends to indicate a more mild kind of AKI.
The second group (inflammatory disorders of the tubules and interstitium) can be caused by tons of things, from infectious agents to toxins to metabolic diseases. In general, patients with these disorders may present initially with an inability to concentrate urine (resulting in polyuria), salt wasting, and metabolic acidosis. Later on, it can be hard to tell these disorders apart from other renal disorders, at least from a clinical standpoint. Patients with renal infections usually present with dysuria, urgency and frequency (if the infection is limited to the bladder) or sudden costovertebral pain, fever and pain (if the infection has ascended to the kidney).
There are a bunch of different vascular diseases that can affect the kidney. Benign nephrosclerosis (hardening of the arterioles and arteries in the kidney) can cut down on blood flow to the kidney, leading to focal ischemia of the kidney. Usually, though, there is ample normal kidney remaining, and the patient doesn’t develop renal insufficiency. Sometimes there’s a slight drop in the glomerular filtration rate, and a little bit of proteinuria – but unless the patient also has hypertension (which increases the risk of renal failure), there aren’t a ton of symptoms.
Malignant nephrosclerosis is a different story. It’s associated with malignant hypertension, and is characterized clinically by a rapidly increasing blood pressure, increased intracranial pressure (with headaches, vomiting, and scotomas or spots before the eyes), and a bunch of other symptoms including papilledema, retinal hemorrhages, cardiovascular problems, and renal failure. Yikes.