Congestive Heart Failure’s Effects on the Kidneys in Patients with Type Two Diabetes
Authors: David Busch, Holly Clark, Matt Gleason, Jennifer Nickol
Key Words: Heart Failure, Kidney Disease, thiazide diuretics, NSAID, renin-angiotensin mechanism, hyponatremia, hypokalemia
The effects that congestive heart failure (CHF) has on the cardiovascular system can cause serious consequences for the rest of the body. When blood flow is reduced to major organ systems, their functions can be altered. Specifically, when the kidneys experience hypoperfusion, it is more difficult to maintain internal environment fluid balance and to successfully filter waste products and toxins. Renal dysfunction is a common side effect of CHF and can lead to imbalances such as hyponatremia. In this case, the renal and cardiovascular systems greatly affect one another because of their correlation. In this case report, a 64-year old woman presented with shortness of breath, fatigue, edema, and a patient history of coronary artery disease, creating a correlation between CHF and renal disease. While her body attempted to compensate for low fluid volume and pressure because of the decrease in blood flow, her kidneys were attempting to overcome a decrease in glomerular filtration rate (GFR). The patient was also taking medications such as a thiazide diuretic and a cardiac glycoside that altered her serum sodium and potassium levels. Overall, advised treatment includes the discontinuation of the thiazide diuretic while implementing an ACE inhibitor and potassium-sparing diuretics.
Each year in the United States, there is an estimated 400,000 new cases of congestive heart failure. Congestive heart failure occurs when the heart is unable to pump an efficient amount of blood flow throughout the body because of a decrease in contractility of the heart. This causes the body to be oxygen deprived because of a decrease in circulating blood. Because of this deficiency in pumping action, blood and fluid backup can occur in various areas of the body, such as in the lungs, arms, and legs. The main symptoms of congestive heart failure include shortness of breath (dyspnea), fatigue, coughing, jugular vein distention, and edema (Chen & Zieve, 2012).
Since the kidneys are the main center for homeostasis of the internal environment, their function is detrimentally affected by an imbalance in blood flow. Reduced perfusion to the kidneys will stimulate multiple homeostatic mechanisms -such as the renin-angiotensin mechanism- in order to maintain fluid balance in the body. Hormones such as anti-diuretic hormone (ADH) will signal the body to retain fluid in response to the body’s hypotensive and hypovolemic state that accompanies congestive heart failure. This increases water reabsorption in the renal collecting ducts of the kidney, which in turn will increase blood volume but can decrease certain solute concentrations (Chen & Zieve, 2012). Blood flow is also critical to maintain the glomerular filtration rate (GFR), which is an important assessment for kidney function and kidney disease. A low GFR is a result of low blood perfusion and creates difficulties for the kidneys to filter out toxins and waste products from the blood. Serum creatinine levels can be directly linked to the GFR, as long as the individual has no metabolic disorders (Levey, et al., 2003).
This case involves a 64-year old woman complaining of shortness of breath and fatigue. Her symptoms and history indicate CHF. In turn, this is leading to kidney dysfunction, which can be determined by evaluating her plasma laboratory results that show she faces multiple instances of electrolyte imbalance. When addressing this case report, her medications, past family history, and laboratory results will be key in establishing a connection between her CHF and the kidney complications resulting from it.
This case presents a 64-year old woman whose chief complaint is shortness of breath (“I wake up short of breath”) and fatigue. She is unable to walk to her mailbox without feeling extremely exhausted. She has gained 14 pounds in the last few weeks, and her extremities are experiencing edema. Her family history includes hypertension and the death of her father by myocardial infarction. She smoked 40 packs a year until 10 years ago when she quit, and she occasionally drinks alcohol. She was diagnosed with osteoarthritis two months ago and gave up exercising. She also has hypertension, coronary artery disease (diagnosed at 54), and Type 2 Diabetes (diagnosed at 62). She is positive for cardiomegaly. Her plasma solute concentrations show hyponatremia, hypokalemia, high serum creatinine levels, low CO2 levels, and both high plasma BUN and BNP levels (Figure 2).
Starting with the patient’s symptoms of dyspnea, fatigue, and edema, a red flag immediately flew up signaling a heart problem. Upon physical examination, jugular distention and an S3 gallop were found, classic signs of heart failure. To explain the low levels of CO2 and HCO3- we look toward the respiration rate, which is high. The Henderson-Hasselbach equation can be applied to get blood pH (7.4). Even though the pH is at the normal range, metabolic acidosis can be reasoned because of the low CO2 levels (9). The plasma electrolyte levels indicate a renal insufficiency. High levels of creatinine, BUN, and BNP are all indicative of a filtration problem (Figure Three).
Relative to normal, it is expected that the patient would have an elevated capillary wedge pressure. Capillary wedge pressure can be used to estimate the pressure in the left atrium. This patient’s elevated capillary wedge pressure can be inferred from the rales and crackles heard in the bilateral lower lobes of the chest. The combination of low heart rate and CAD results in low cardiac output, as well as a decreased effective circulation volume (1), and results in increased left atrial pressure (LAP); increasing right atrial pressure (RAP) and causing edema and distended neck veins. To access the cardiovascular system of the patient, the human serum albumin technique could be used instead of cardiac catheterization. (Walker, Hurst, & W., 1990) (2) The distended jugular veins, caused by increased RAP, along with bilateral extremity edema indicate that Ms. Smith’s extracellular fluid volume was above normal. As the blood begins to back up, the jugular veins become distended and fluid accumulates in the tissues, causing edema (1).
Ms. Smith presented with low blood pressure. To increase blood pressure, Ms. Smith’s kidneys would conserve Na+ that would increase plasma volume via water retention. Fluid retention by the kidneys can be indicated by the patient’s edema. Na+ plasma levels are roughly half of the plasma osmolarity leading to an estimate of 260 mOsm/kg (290-310mOsm/kg average) (Widmaier, Raff, & Strang, 2011). (3)
The patient was prescribed thiazide diuretics and digoxin to treat hypertension. The diuretics can account for the hyponatremia because they work directly on the NaCl pumps in the Distal Convoluted Tubule by inhibiting the reabsorption of sodium (Hanna & Starling, 2008). The release of ADH is initiated by the angiotensin II and is responsible for reabsorbing water without sodium. This results in the dilution of plasma sodium and hyponatremia. Hypokalemia is also cause by the diuretic because it causes the secretion of potassium.
The patient’s blood sample results indicated both hyponatremia and hypokalemia. When the patient’s congestive heart failure caused a drop in both circulating blood volume and blood pressure, the renin-angiotensin mechanism was activated in response. Aldosterone was released, stimulating sodium reabsorption and potassium excretion. Angiotensin II also signals the release of anti-diuretic hormone (ADH), which caused free-water reabsorption in the renal collecting ducts, diluting plasma sodium concentrations. At the same time, aldosterone is causing overexcretion of potassium, causing the patient to be hypokalemic (Oren, 2005). The patient was also taking a thiaziade diuretic, which causes excretion of both sodium and potassium in the urine (Hanna & Starling, 2008). (4, 5)
Based on the serum creatinine levels of the patient (2.4 mg/dL), the GFR can be estimated based on a standardization curve. This value can also be used to evaluate the progression of the patient’s current kidney function. Even the small increase that was seen in this patient’s creatinine levels from normal (1.2 mg/dL) decreased her GFR by approximately 75%. Her GFR can be estimated to be around 30 mL/min (Figure 4). The estimated GFR places this patient in between the third and fourth stages of chronic kidney disease. Her CHF caused her kidney function to dramatically decrease (Simon, Amde, & Poggio, 2011). ( 6).
With her persistent headaches the patient was taking a daily regimen of Ibuprofen. Ibuprofen is a Non Steroidal Anti-Inflammatory Drug (NSAID), which are known to reduce GFR in those people with pre-renal disorders. Since this patient has CHF and diabetes, which is affecting her renal function already, the NSAIDs are only lowering her GFR and renal blood flow by inhibiting the production of prostaglandin. The NSAIDs lower the ability of the glomerulus to process and filter the blood plasma properly. (7)
Ms. Smith’s treatment options should start with the removal of the thiazide diuretic, which is causing her kidney damage and potassium depletion. A potassium-sparing diuretic should be administered in place of the thiazide, because it will decrease the amount of work-load for the heart without causing hypokalemia. An ACE inhibitor would also be a good treatment option for Ms. Smith because it would promote vasodilation and water reabsorption. Also, a special exercise program/ physical therapy should be implemented not only to maintain heart and kidney health, but also to improve the pain associated with her osteoarthritis (NIH, 2012).
Chen, M., & Zieve, D. (2012, July 22). Heart Failure. Retrieved March 27, 2012, from PubMed Health: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001211/
Hanna, M., & Starling, R. (2008). Diuretics. In D. Walsh, A. Caraceni, R. Fainsinger, K. Foley, P. Glare, C. Goh, et al., Palliative Medicine, 1st ed. Philladelphia: Saunders Elsevier.
Levey, A., Coresh, J., Balk, E., Kausz, A., Levin, A., Steffers, M., et al. (2003). National Kidney Foundation Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification. Annals of Internal Medicine , 139 (2), 137-150.
NIH. (2012, February). Exercise: Benefits of Exercise. Retrieved March 27, 2012, from NIH Senior Health : http://nihseniorhealth.gov/exerciseforolderadults/healthbenefits/01.html
Oren, R. (2005). Hyponatremia in Congestive Heart Failure. American Journal of Cardiology , 95 (9A), 2B-7B.
Renin-angiotensin-aldosterone system. (n.d.). Retrieved March 27, 2012, from Wikipedia: http://www.google.com/imgres?imgurl=http://upload.wikimedia.org/wikipedia/commons/thumb/a/a2/Renin-angiotensin-aldosterone_system.png/550px-Renin-angiotensin-aldosterone_system.png&imgrefurl=http://en.wikipedia.org/wiki/Renin-angiotensin_system&h=306&w=55
Simon, J., Amde, M., & Poggio, E. (2011). Interpreting the Estimated Glomerular Filtration Rate in Primary Care: Benefits and Pitfalls. Cleveland Clinic Journal of Medicine , 78 (3), 189-196.
(1990). In H. Walker, J. Hurst, & H. W., Clinical Methods: History, Physical, and Laboratory Examinations. Boston: Butterworth Heinemann.
Widmaier, E., Raff, H., & Strang, K. (2011). Vander's Human Physiology The Mechanisms of Body and Function. New York: McGraw-Hill.
Figure 1: Renin-angiotensin mechanism in the kidneys (Renin-angiotensin-aldosterone system).
Figure 2: Patients blood plasma lab results showing low electrolytes, and high creatinine.
Figure 3: Differential diagnosis, reasonings leading towards the diagnosis of heart failure.
Figure 4: Creatinine levels in relation to GFR and stages of kidney disorders (Levey, et al., 2003).