Month: January 2021

Renal Disorders and How Dialysis Can Help Your Kidneys ‘Let It Go’

Renal Disorders and How Dialysis Can Help Your Kidneys ‘Let It Go’

Kidneys are a good example of the saying, “you don’t know what you’ve got ‘till it’s gone”. This is primarily because most people genuinely do not know they have reached an irreversible loss of kidney function until it is too late. You may be wondering how such a drastic decline in kidney function can silently progress under the radar, and in what ways we can help patients with renal dysfunction to still lead highly active and fulfilling lives. Well, to answer why and how renal dysfunction typically goes undetected, it is important to first understand what makes the kidneys unique to other aspects of the body.

Your vital organs are all special with their own unique abilities and superpowers. For example, the liver is the only organ in your body with the capacity to regenerate itself. The key quality to remember when it comes to kidneys is they like to both work together as a team. Now working together may not seem as much of a superpower, but it’s incredibly useful because one kidney can compensate for the impaired function of the other kidney. Even alone, a single kidney’s working nephrons can also compensate for the loss or degeneration of other nephrons within the organ itself4. In fact, the kidneys are so highly adaptable they do a stellar job of making a sinking ship look like it is sailing, but this also means trying to identify declining renal function early to prevent progression of disease can be very challenging… because a ship that is sailing does not look like it is sinking. Many patients will find themselves in this position and although we can screen for risk factors, a decline in renal function remains silent and unrecoverable.

The above figure outlines the differences between acute kidney injury (AKI) and chronic kidney disease (CKD). Since kidney damage is irreversible, prevention of AKI and CKD is paramount. For renal disorders, there is no real cure as therapy is typically supportive and dependent on the etiology1. With this in mind, you may be wondering how we can go about being more proactive towards kidney disease. Clinical surveillance is an example of an effort that serves this very cause. If we take a look at an implementation of the Nephrotoxic Injury Negated by Just-in-time Action (NINJA) project, we can see a 38% decrease in AKI exposure (estimated 633 cases avoided) and a 64% decrease in AKI (398 cases avoided) due to surveillance providing a timelier approach in identifying AKI2. Again, there is no cure for kidney disease so prevention is paramount and clinical surveillance can be an invaluable asset in this area. Likewise, although we have medications in place to treat the secondary complications and further progression of CKD, patients who do progress to end stage renal disease will find themselves dependent on dialysis in the absence of a kidney transplant1.

So, what happens to patients who officially progress to end stage renal disease and require dialysis? Well, the good news is there are some options. Patients can decide between hemodialysis (HD) or peritoneal dialysis (PD)1. HD requires several visits a week to a HD center and may cause a further decline in residual renal function as compared to PD, which may be conveniently performed at home but has a higher risk of peritonitis1. Dialysis works by helping your kidneys ‘Let It Go’. Yes, the title of this post references Frozen because that’s exactly how dialysis works: by letting all the toxins in your body go. You see, a decline in kidney function is essentially a decline in the glomerular filtration rate (GFR)1. When your kidneys are damaged, they cannot filter out all the toxins in your body as well so waste products and fluid can accumulate to a fatal degree3. Dialysis helps prevent this accumulation by allowing toxins to essentially move from the blood to the dialysate (thereby filtering the blood and acting in place of the kidneys)1. I hope our brief overview of renal dysfunction has been helpful and all the best for your studies!

Sincerely,

Jean Hanna

References

  1. DiPiro, J. T. (2020). Pharmacotherapy: A pathophysiologic approach. New York: McGraw Hill.
  2. Goldstein, S., Mottes, T., Simpson, K., Barclay, C., Muething, S., Haslam, D., & Kirkendall, E. (2016). A sustained quality improvement program reduces nephrotoxic medication-associated acute kidney injury. Kidney International, 90(1), 212-221. doi: 10.1016/j.kint.2016.03.031.
  3. Dialysis. (n.d.). Retrieved from https://www.nhs.uk/conditions/dialysis/
  4. Fattah, H., Layton, A., & Vallon, V. (2019). How Do Kidneys Adapt to a Deficit or Loss in Nephron Number? Physiology, 34(3), 189-197. doi:10.1152/physiol.00052.2018

Thyroid Disorders and What Happens When Your Glands Go to the Dark Side

Thyroid Disorders and What Happens When Your Glands Go to the Dark Side

If you are familiar with the Star Wars franchise, you know there is a “light side” and a “dark side” of the force. These sides represent either the selfless or the selfish and essentially act to hold the galaxy together. If you consider our galactic friends and their adventures for a second, you may be able to see there is a large parallel between the galaxy and the human body. After all, the goal for all Jedi is to keep the force within balance, or in the context of the human body and for our purposes, within homeostasis. So then, what happens when your body or the galaxy is no longer in homeostasis? Well, if you go back to our simplified analogy, you’ll find it suggests some aspect within our complex body has pulled a ‘Darth Vader’ and gone to the dark side… which can predictably have devastating consequences. This Star Wars analogy is also a stellar example for the pathogenesis of cancer: a cancerous cell is in essence simply a “Darth Vader cell”, but we will dive further into cancer a couple weeks from now (so stay tuned).

The thyroid gland is situated at the base of the neck and plays an important role in metabolism and development within the human body1. The thyroid is glandular in nature (meaning it secretes hormones) and therefore can be categorized under dysfunctions of the endocrine system. Specifically, we can identify the type of dysfunction or disease by looking a little closer at where exactly regulation goes haywire. Regulation of the thyroid occurs through the hypothalamic-pituitary-thyroid (HPT) axis1. It is important to understand the HPT axis encompasses the hypothalamus, anterior pituitary and thyroid gland which also stores the thyroid hormones T3 (triiodothyronine) and T4 (thyroxine)1. An appropriate feedback loop for the HPT axis is illustrated below:

As annotated in the figure, the hypothalamus releases thyrotropin-releasing hormone (TRH) allowing for positive feedback to the pituitary gland. The pituitary gland then produces thyroid-stimulating hormone (TSH) allowing for positive feedback to thyroid gland. Lastly, the thyroid gland produces T3 and T4 allowing for negative feedback on hypothalamus and pituitary gland to decrease levels of TRH + TSH (homeostasis and balance is now upheld within the body). Notice how TRH and TSH are regulated through the negative feedback loop? In the context of a thyroid gland, an appropriate regulation of homeostasis like the example above would be referred to as “euthyroid”, meaning everything is working as it should and the force is in balance. When the force is unbalanced, we hit situations of “hypothyroidism” and “hyperthyroidism” where your glands officially go to the dark side. The good thing about thyroid dysfunction is these processes are entirely predictable if you understand what goes wrong in what part of the loop.

HYPOTHYROIDISM

In hypothyroidism, you have low levels of T3 and T41. We can predict decreased levels of both T3 and T4 leads to an increase in both TSH and TRH to ‘amp’ up the loop. However, Hashimoto’s disease is an example of an autoimmune condition where antibodies essentially destroy the thyroid gland (Hashimoto’s is typical of primary hypothyroidism)1. Destruction of the thyroid gland will cause decreased levels of both T3 and T4 leading to increased levels of TSH and TRH but because the gland is destroyed, an increase in TSH and TRH does not work, and thyroid hormones remain low. In this case, patients are typically exogenously supplemented with medications such as levothyroxine since their endogenous production is impaired.

HYPERTHYROIDISM

In hyperthyroidism, you have high levels of T3 and T41. Again, we can predict that an increase in both T3 and T4 will lead to a decrease in both TSH and TRH in an attempt to slow down the loop. However, Graves’ disease is another example of an autoimmune condition where antibodies stimulate the gland to produce more hormones (Grave’s disease is typical of primary hyperthyroidism)1. Stimulation of the thyroid gland causes increased levels of both T3 and T4 leading to decreased levels of both TSH and TRH to try and slow down hormone production. However, since the gland is being stimulated by the antibodies regardless, T3 and T4 levels remain elevated. 

Notice how in both cases of primary hyperthyroidism and primary hypothyroidism, the negative feedback loop is still trying to work, it just does not matter because there is an autoimmune issue with the gland itself. So, although the negative feedback loop is still there, the process fails due to either the destruction or dysfunction of the gland itself. In other words, if we go back to our analogy the light side is still there and trying to restore balance to the force, but it does not matter because the glands themselves have gone to the dark side. I hope our little galactic journey through primary thyroid disorders has been informative and helpful for your studies. All the best!

Sincerely,

Jean Hanna

References

  1. Kane M.P., & Bakst G (2020). Thyroid disorders. DiPiro J.T., & Yee G.C., & Posey L, & Haines S.T., & Nolin T.D., & Ellingrod V(Eds.), Pharmacotherapy: A Pathophysiologic Approach, 11e. McGraw-Hill. https://accesspharmacy.mhmedical.com/content.aspx?bookid=2577&sectionid=223397495

Risk Factors of Hypertension and Why You Shouldn’t Take Your Stress with a Grain of Salt

It would not be an understatement to say almost all cases of high blood pressure are likely to be classified under the term “primary” or “essential” hypertension. Even so, primary hypertension can be a real head scratcher as we have a very poor understanding of the etiology despite an estimated 90% of patients fitting the bill. As such, primary hypertension is often labeled as “idiopathic”, which is medical terminology for “no identifiable cause” that we are aware of at this time. We do, however, have an inkling for several risk factors which are associated with the development of hypertension. In this post, we will break them down using a mnemonic that helps tie everything together and provides a system to recall these characteristics moving forward. Can you think of what might be a good mnemonic for this cause? That is right: stress!

We’ve all experienced stress at some point in our lives. Imagine yourself in peak rush hour traffic, the time is now 7:45 AM and your final starts at 8:00 AM. You are moving 5 miles per hour bumper to bumper with at least a 40-minute estimated delay. Can you feel your heart racing? Maybe not, but the point stands that stress can exacerbate blood pressure and it is an excellent way to outline the following known risk factors:

“S” is for SODIUM
Excessive sodium consumption can increase risk for hypertension and even blunt antihypertensive medications. It is generally recommended patients limit their intake to less than 1,500 milligrams a day which can further help in reducing systolic blood pressure by ~5-6 mmHg2
“T” is for TIMESPAN
Time refers to patients greater than 65 years of age as they are more likely to acquire hypertension and are therefore at a further increased risk of cardiovascular disease1
“R” is for RAZZAMATAZZ  Did you know razzamatazz is a type of alcoholic beverage? Neither did we, but the name has a ring to it and highlights the fact that excessive alcohol consumption should be avoided! Men who lower consumption to 2 drinks a day and women who lower consumption to 1 drink a day can expect systolic blood pressure to decrease by ~4 mmHg1
“E” is for ETHNICITY
A family history of hypertension is a significant factor to keep in mind alongside the disproportionate degree of African American cases for this disease state: here is a study entitled, “Differences in Stroke Mortality Among Adults Aged 45 and Over: United States, 2010–2013” from the CDC. It details the implications of the “stroke belt” in the United States
“S” is for SUNDAES
Yes, we all love sundaes, but it would be wise to lay off the ice cream occasionally as Obesity and Diabetes Mellitus are commonly associated with hypertension. Exercise and a healthy well-balanced diet like the “Dietary Approaches to Stop Hypertension” (DASH) diet is crucial for hypertensive individuals as a 1-kilogram reduction in weight generally equals 1 mmHg reduction in blood pressure2
“S” is for SMOKING
Smoking is classified as a risk factor for hypertension alongside obstructive sleep apnea and should be avoided prior to blood pressure measurements1

As you soak in all these risk factors and suggested lifestyle changes, if there is only one thing you remember from this blog post it is the following: hypertension tends to be a disease state where adherence to therapy can be particularly troublesome. This is understandable as hypertensive patients generally feel no different but may still be expected to take several classes of medications, follow up routinely, and tolerate various adverse effects of medications that can interfere with their overall quality of life. Therefore hypertension is known as a “silent killer” and as with any disease state, a solid line of communication is vital to ensuring appropriate therapy and patient satisfaction.

Sincerely,

Jean Hanna

References

  1. Hypertension.  (n.d.).  In Micromedex.  Retrieved December 26, 2020, from https://www.micromedexsolutions.com
  2. Whelton, P. K., Carey, R. M., Aronow, W. S., Casey, D. E., Jr, Collins, K. J., Dennison Himmelfarb, C., DePalma, S. M., Gidding, S., Jamerson, K. A., Jones, D. W., MacLaughlin, E. J., Muntner, P., Ovbiagele, B., Smith, S. C., Jr, Spencer, C. C., Stafford, R. S., Taler, S. J., Thomas, R. J., Williams, K. A., Sr, Williamson, J. D., … Wright, J. T., Jr (2018). 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension (Dallas, Tex. : 1979), 71(6), 1269–1324. https://doi.org/10.1161/HYP.0000000000000066
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