Acute Renal Failure Rhabdomylysis

A 28-year-old male presents to the primary care office for evaluation of left calf pain, swelling, and redness. He reports that this started one day ago and worsened today. He ran a 27-mile marathon 2 days ago and traveled for 3 hours in a car today. He reports slight pain on walking and a swollen red calf. He took Ibuprofen 600 mg twice today without relief. Patient reports being an experienced runner, running 3-5 miles daily. He trained for the marathon for 4 months. Patient also reports a history of exercise induced asthma and uses albuterol sulfate HFA as needed.

On physical exam patient appears in good health T 99 P 68 R 18 BP 118/78 wt. 175 lb, height 72 in. BMI 23.1. Heart rate is regular without murmurs, rubs, or gallops. Lungs clear bilaterally. HEENT WNL. Strength lower extremities +5 and DTRs + 2. Left calf erythematous, edematous, warm and tender on palpation. Pulses 3+.

Two possible diagnoses were considered: deep vein thrombosis (DVT) and rhabdomyolysis.
Stat ultrasound of left leg to rule out DVT was ordered and read as normal
CBC WNL
Creatine Kinase (CK) 23,000 U/L (normal 24-170 U/L)
BUN and Creatinine WNL
A diagnosis of rhabdomyolysis was made.

Discuss the pathophysiology of acute renal failure in rhabdomyolysis.
Post your initial response by Wednesday at midnight. Respond to one student by Sunday at midnight. Both responses must be a minimum of 150 words, scholarly written, APA formatted, and referenced. A minimum of 2 references are required (other than your text). Refer to grading rubric for online discussion.

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a kaurSubscribe
Amandeep Kaur posted Mar 24, 2021 10:58 PM
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Rhabdomyolysis occurs when muscle tissue begins to break down and die, specifically skeletal muscle (Cabral et al., 2021). This releases the intracellular contents of the cell into the blood. This occurs as the sarcolemmal membrane is broken down. Rhabdomyolysis diagnosis will be made if and when the serum creatine kinase level is 5 times the upper limit normal level. This can present in many different ways clinically; asymptomatic increase in serum enzymes, damaged muscles, volume depletion, metabolic abnormities, and acute kidney injury. Significant increases in myoglobin can also be indicative of rhabdomyolysis. These toxins are processed through the kidney, in which they release hydroxyl radical (OH) (Petejova & Martinek, 2014). The release of this reactive species is nephrotoxic, causing acute kidney injury. In the case of this gentleman, his rhabdomyolysis was exercise-induced (Kim et al., 2015). Excessive use of muscles due to marathon training led to muscle injury by the increased intercellular calcium levels. Rhabdomyolysis can be easily overlooked in athletes is just muscle pain or soreness.Cabral, Brian Michael I., Sherida N. Edding, Juan P. Portocarrero, and Edgar V. Lerma. “Rhabdomyolysis.” 10 June 2020. Web. 25 Mar. 2021.Kim, Jooyoung, Joohyung Lee, Sojung Kim, Ho Young Ryu, Kwang Suk Cha, and Dong Jun Sung. “Exercise-induced Rhabdomyolysis Mechanisms and Prevention: A Literature Review.” Journal of Sport and Health Science. Elsevier, 03 June 2015. Web. 25 Mar. 2021.less2 UnreadUnread7 ViewsViews
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View profile card for Aina Oluwo
Last post March 28 at 11:47 PM by Aina Oluwo
Petejova, N., & Martinek, A. (2014). Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review. Critical care (London, England), 18(3), 224.
References
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Candice Russell posted Mar 22, 2021 12:14 AM
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“Rhabdomyolysis is a syndrome that involves skeletal muscle necrosis and lysis followed by the release of intracellular content to peripheral blood, which may cause electrolyte imbalance, cardiac arrhythmias and multifactorial acute renal failure” (Khan, 2009, as cited by De Gracia-Nieto et al., 2016, 329). Rhabdomyolysis can result from traumatic and non-traumatic injury to the skeletal muscle. “Since skeletal muscle comprises about 40% of body mass, such an insult can result in the accumulation of cellular contents that could eventually overwhelm the underlying elimination mechanism” (Cervellin et al., 2017, as cited by Cabral et al., 2020, p. 2).As the myocyte degenerates, large quantities of intracellular substances particularly potassium, myoglobin and CK leak into the circulation. If more than 100 grams of skeletal muscle is damaged, the circulating myoglobin levels will exceed the protein-binding capacity of the plasma and can precipitate in the glomerular filtrate. Excess myoglobin may thus cause renal tubular obstruction, direct nephrotoxicity, and acute renal failure. (Vanholder et al., 2000; Knochel, 1993; Bosch, 2009; as cited by Cabral et al., 2020, p. 6)Reference:De Gracia-Nieto, A. E., Angerri, O., Bover, J., Salas, D., Villamizar, J. M., & Villavicencio, H. (2016). Acute Renal Failure Secondary to Rhabdomyolysis as a Complication of Major Urological Surgery: The Experience of a High-Volume Urological Center. Medical principles and practice : international journal of the Kuwait University, Health Science Centre, 25(4), 329–335. https://doi.org/10.1159/000445115Michelsen, J., Cordtz, J., Liboriussen, L., Behzadi, M. T., Ibsen, M., Damholt, M. B., Møller, M. H., & Wiis, J. (2019). Prevention of rhabdomyolysis‐induced acute kidney injury – A DASAIM/DSIT clinical practice guideline. Acta Anaesthesiologica Scandinavica, 63(5), 576-586. https://doi.org/10.1111/aas.13308 less1 UnreadUnread5 ViewsViews
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View profile card for Amandeep Kaur
Last post March 28 at 10:35 PM by Amandeep Kaur
Díaz-Tejeiro, R., Regidor, D., Morales, J., Padrón, M., Cueto, L., Muñoz, M. A., Torres, M., Ahijado, F. J., & García Díaz, J. E. (2018). Acute renal failure due to rhabdomyolysis. renal replacement therapy with intermediate cut-off membranes (EMIC2). Nefrología, 38(6), 664-665. https://doi.org/10.1016/j.nefroe.2018.04.009
Cabral, B. M. I., Edding, S. N., Portocarrero, J. P., & Lerma, E. V. (2020). rhabdomyolysis. Disease-a-Month, 66(8), 101015-101015. https://doi.org/10.1016/j.disamonth.2020.101015
Prevention of AKI by early fluid resuscitation and intravascular volume is suggested. Proposal of multiple supportive therapies such as diuretics, alkalinisation, antioxidants, and renal replacement therapy may assist in AKI prevention (Bosch et al., 2009; as cited by Michelsen et al., 2019, p. 577).
Cabral et al. (2020) documented Acute Kidney Injury (AKI) as one of the most dreaded complications of rhabdomyolysis. Strenuous muscular exercise or activity is an exertional non-traumatic cause of rhabdomyolysis. “The more strenuous or prolonged the activity, the more damage there is” (Cabral et al., 2020, p. 4). A change in body temperature has also be associated with Rhabdomyolysis. Michelesen et al. (2019) described the first account of rhabdomyolysis was observed by Bywaters and Beall, severe renal failure in crush injured victims in 1941 London. During an autopsy, an examination of the kidneys displayed “eosinophilic casts in the loops of Henle and collecting tubules, which were later identified as myoglobin” (Michelesen et al., 2019, p. 576). Diaz-Tejeiro et al. (2018) stated the release of myoglobin is responsible for acute kidney failure (AKF). He described “three myoglobin-mediated nephrotoxic mechanisms have been described. Renal vasoconstriction, the formation of intratubular casts, and direct damage to tubular cells” (Ronco et al., 2009; Zager et al., 2012; as cited by Diaz-Tejeiro et al., 2018, p. 664).
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Melissa Morgan posted Mar 23, 2021 5:05 PM
Acute renal failure is the most serious complication of rhabdomyolysis, which happens as a result of myoglobin precipitates in the tubules through which the flow of ultrafiltrate through the nephron is obstructed and produces injury. (Huether, et al., 2020). The patient has a creatine kinase of 23,000 units/L, which is more than 5-10 times the upper limit of normal CK. A diagnosis of acute renal failure is likely once the CK level is past 15,000 units/L (Huether, et al., 2020). According to Esposito, et al., the mechanism of acute renal failure in rhabdomyolysis is the massive release of myoglobin into the circulation (2018). Myoglobinuria may be the only symptom of rhabdomyolysis, but it is not a definite diagnosis of the condition since the renal threshold for myoglobin is low (Huether, et al., 2020). The release of myoglobin in the urine “causes cast formation and accumulation of iron in proximal tubules, with intratubular obstruction and proximal tubular cell injury” (Esposito, et al., 2018, p. 2). Sequestration, or third spacing, of fluids into injured muscles causes volume depletion, which results in acute tubular injury and AKI (Esposito, et al., 2018). The exact incidence of AKI in rhabdomyolysis is unknown, and ranges possibly from 10% 10 55% and does not have a good prognosis especially in the presence of multiple organ failure (Chavez, et al., 2016). The goal of treatment is to maintain adequate kidney perfusion with rapid intravenous hydration (Huether, et al., 2020).Chavez, L. O., Leon, M., Einav, S., & Varon, J. (2016). Beyond muscle destruction: a systematic review of rhabdomyolysis for clinical practice. Critical care (London, England), 20(1), 135. https://doi.org/10.1186/s13054-016-1314-5Huether, S., McCance, K., and Brashers, V. (2020). Understanding Pathophysiology (7th ed.). Elsevierless0 UnreadUnread
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View profile card for Gisselle Mustiga
Last post March 28 at 9:59 PM by Gisselle Mustiga
Esposito, P., Estienne, L., Serpieri, N., Ronchi, D., Comi, G. P., Moggio, M., Peverelli, L., Bianzina, S., & Rampino, T. (2018). Rhabdomyolysis-Associated Acute Kidney Injury. American journal of kidney diseases : the official journal of the National Kidney Foundation, 71(6), A12–A14. https://doi.org/10.1053/j.ajkd.2018.03.009
References
RhabdomyolysisSubscribe
Aina Oluwo posted Mar 24, 2021 10:27 PM
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Rhabdomyolysis (RBD) is defined as the breakdown of muscle that causes the release of intracellular contents into the extracellular space and bloodstream (Huether et al., 2020). It can be caused by traumatic and non-traumatic causes. Traumatic like physical trauma to the muscle and non-traumatic which can be hereditary or metabolic. It is important to note that the symptoms of rhabdomyolysis are muscle pain, weakness and dark urine but only 10% of patients exhibit the three symptoms at a presentation (Zhou & Bagga, 2020). This condition is life threatening and interventions should be applied immediately.The pathophysiology of acute renal injury is explained by Navarro-Blackaller et al., (2019) as the Tubular obstruction and oxidative injury due to the precipitation of the Tamm-Horsfall protein with myoglobin. Under physiological conditions, myoglobin is reabsorbed by the renal tubule cells, but when the presence of this pigment exceeds the re-absorptive capacity, it precipitates in the tubules as pigmentary cylinders, forming hyaline cylinders and causing endothelial dysfunction and tissue damage. This in turn activates the sympathetic nervous system, the renin-angiotensin-aldosterone system and vasopressin release, which together reduce urine output. Huether, S., McCance, K., and Brashers, V. (2020). UnderstandingNavarro-Blackaller, G., Chávez-Iñiguez, J. S., Maggiani-Aguilera, P., Gómez-Hernández, G. L.,Rhabdomyolysis and acute kidney injury associated with clostridium difficile infection,Zhou, S., & Bagga, A. (2020). Rhabdomyolysis and acute kidney injury associated withDisease, 7https://doi.org/10.1177/2054358120951371less1 UnreadUnread3 ViewsViews
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View profile card for Hilary Szpara
Last post March 28 at 7:52 PM by Hilary Szpara
terbinafine use: A case report. Canadian Journal of Kidney Health and
case report. Nefrología, 39(2), 208-209. https://doi.org/10.1016/j.nefroe.2018.07.009
Carreón-Bautista, E. E., Moreno-Alvarado, R. A., & Garcia-Garcia, G. (2019).
Pathophysiology (7th ed.). Elsevier.
References
The goal is preventing further complications such as disseminated intravascular coagulation (DIC). Treatments for this patient will be rapid intravenous hydration to maintain kidney function and urinary flow (Huether et al., 2020).
With regards to the case study, it was right to consider DVT and RBD as patient also presented with symptoms of DVT. The diagnostic marker for RBD is the creatine kinase (CK) which if 5 to 10 times more than the normal level or >5000 U/L is concerning for rhabdomyolysis (Zhou & Bagga, 2020). The patient had 23, 000 U/L which is 10 times more than the normal indicated. It is known that once the CK levels exceed 15000 u/L, there is a high possibility of acute renal failure.
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Dennies Jones posted Mar 24, 2021 8:39 PM
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A 28-year-old male presents to the primary care office for evaluation of left calf pain, swelling, and redness. He reports that this started one day ago and worsened today. The male patient was diagnosed with rhabdomyolysis. According to Harding et al. (2020), “rhabdomyolysis is a syndrome caused by the breakdown of damaged skeletal muscle cells. This breakdown causes the release of myoglobin into the bloodstream. Myoglobin precipitates and obstructs renal tubules” (p. 78469). The patient’s signs and symptoms were all associated with muscle injury and breakdown. The severity of the muscle injury led to myoglobinuria, which resulted in acute kidney injury (AKI). Díaz-Tejeiro et al. (2018) explained that “the mechanism responsible for AKF lies in the release of myoglobin. Three myoglobin-mediated nephrotoxic mechanisms have been described. Renal vasoconstriction, the formation of intratubular casts, and direct damage to tubular cells” (p. 664). Myoglobin is reabsorbed into the glomerular filtrate, is catabolized within proximal tubule cells, and easily filtered through the glomerular basement membrane. Rhabdomyolysis includes direct tubular toxicity mediated by myoglobin-associated oxidative injury and tubular obstruction due to myoglobin casts’ formation (Choy et al., 2020). With AKI patient could start experiencing decrease urinary output, swelling due to fluid retention, nausea, fatigue , and shortness of breath. Choy, K. H., McVeigh, M., Holgate, S., Delmenico, L., & Friedman, N. D. (2020). Rhabdomyolysis cases and acute kidney injury: a 10-year experience at a regional tertiary center. Renal Society of Australasia Journal, 16(3), 98–105. https://doi-org.wilkes.idm.oclc.org/10.33235/rsaj.16.3.98-105Harding, Mariann M., Kwong, Jeffrey, Roberts, Dottie, Hagler, Debra, Reinisch, Courtney. Lewis’s Medical-Surgical Nursing E-Book (Kindle Locations 78469-78470). Elsevier Health Sciences. Kindle Edition.less2 UnreadUnread11 ViewsViews
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View profile card for Steven Bartos
Last post March 28 at 7:18 PM by Steven Bartos
Díaz-Tejeiro, R., Regidor, D., Morales, J., Padron, M., Cueto, L., Munoz, M., . . . Garcia Diaz, J. (2018). Acute renal failure due to rhabdomyolysis. Renal replacement therapy with intermediate cut-off membranes (EMIC2). Acute Renal Failure Due to Rhabdomyolysis. Renal Replacement Therapy with Intermediate Cut-off Membranes (EMIC2). doi:https://doi.org/10.1016/j.nefro.2017.11.001
References
Rhabdomyolysis & AKISubscribe
Jazmin Jerez-Rivera posted Mar 23, 2021 8:44 PM
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In our case study this week the DVT diagnosis was ruled out and rhabdomyolysis was determined. Creatine kinase (CK) is the marker for muscle damage and when it is higher than 1000 units/l rhabdomyolysis is considered, and in this example it is 23,000 u/l and normal value is (24-170u/l). If CK levels surpass 15,000 u/l acute renal failure may be evident (Huether et. al., 2020). Rhabdomyolysis is characterized as “muscle injury leading to the disintegration of muscle constituents into the extracellular fluid and systemic circulation” (Choy et. al., 2020, p. 98). Research by Nielson et. al. suggests that high CK levels are associated with a higher risk of acute kidney injury (2020). Renal injury is caused by the fast breakdown of the muscle, which releases protein, myoglobin and cellular contents into the bloodstream. The cellular content and myoglobin casts infiltrate the nephron and tubules in the kidneys causing obstruction which leads to oxidative injury, and tubular toxicity (Choy et. al., 2020). Clinical manifestations include dark urine, weakness, and muscle pain.Choy, K. H., McVeigh, M., Holgate, S., Delmenico, L., & Friedman, N. D. (2020). Rhabdomyolysis cases and acute kidney injury: a 10-year experience at a regional tertiary centre. Renal Society of Australasia Journal, 16(3), 98–105. https://doi-org.wilkes.idm.oclc.org/10.33235/rsaj.16.3.98-105less1 UnreadUnread2 ViewsViews
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View profile card for Jennifer Bryant
Last post March 28 at 6:23 PM by Jennifer Bryant
Nielsen, F. E., Cordtz, J. J., Rasmussen, T. B., & Christiansen, C. F. (2020). The Association Between Rhabdomyolysis, Acute Kidney Injury, Renal Replacement Therapy, and Mortality. Clinical epidemiology, 12, 989–995. https://doi.org/10.2147/CLEP.S254516
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Steven Bartos posted Mar 24, 2021 8:21 PM
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Rhabdomyolysis is the breakdown and necrosis of muscle that subsequently leads to the release of intracellular content into the bloodstream. The pathophysiology of rhabdomyolysis begins with the breakdown of the sarcolemmal cell membrane and ATP depletion, which causes an increase of intracellular calcium, leading to the activation of cell apoptosis pathways, mitochondrial dysfunction, and ultimately cell death (Chavez et al., 2016).ReferencesChavez, L.O., Leon, M., Einav, S., & Varon, J. (2016). Beyond muscle destruction: A systematic review of rhabdomyolysis for clinical practice. Critical Care, 20(135). https://dx.doi.org/10.1186%2Fs13054-016-1314-5less3 UnreadUnread10 ViewsViews
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View profile card for Eleany Yasein
Last post March 28 at 12:50 PM by Eleany Yasein
Cabral, B.M., Edding, S.N., Portocarrero, J.P., & Lerma, E.V. (2020). Rhabdomyolysis. Disease-a-Month, 66(8), 1 – 21. https://doi-org.wilkes.idm.oclc.org/10.1016/j.disamonth.2020.101015
One pathophysiological cause of acute kidney failure is renal vasoconstriction. When these muscles are destroyed, intracellular fluid is sequestered to the extracellular spaces, which decreases intravascular volume and initiates the renin-angiotensin-aldosterone system, antidiuretic hormone, and the sympathetic nervous system. This contributes to vasoconstriction, renal water and salt retention. Myoglobin circulating in the kidneys also increases the release of vasoconstrictors and decreases vasodilators (Cabral et al., 2020). Another cause of kidney failure is from Myoglobin being released into the blood stream. This causes a cytotoxic effect on the nephrons of the kidneys, forming casts which subsequently lead to tubular obstruction. Necrotic muscle also releases uric acid, which further contributes to tubular obstruction (Chavez et al., 2016).
Discuss the pathophysiology of acute renal failure in rhabdomyolysis.Subscribe
Caroline Otto posted Mar 25, 2021 6:56 AM
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Rhabdomyolysis is the rapid breakdown of muscle that causes the release of intracellular contents, including the protein pigment myoglobin, into the extracellular space and bloodstream. It is my understanding that these protein molecules are too large to pass through the intramedullary cellular system inside the kidneys while being excreted and cause obstruction thereby causing Acute renal failure.A classical triad of muscle pain, weakness and dark urine is considered typical of rhabdomyolysis. The renal threshold for myoglobin is low (approximately 0.5 mg/dl or urine); therefore, only 200g of muscle needs to be damaged to cause visible changes in the urine. Along with the release of myoglobin, creatine kinase (CK) and other serum enzymes are released in massive quantities, the efflux of intracellular proteins and enzymes includes loss of potassium, phosphate, nucleotides, creatinine, and creatine. The risk of renal failure increases proportionately to the increase in the levels of serum CK, potassium and phosphorus.Raised levels of Serum Creatinine levels has been reported immediately after endurance events, and even a small increase or rise in serum creatinine can put the sportsman at risk (Hodgson, et.al 2017).References:Huether, S. E., McCance, K.L. & Brashers, V.L. (2020). Understanding Pathophysiology. 7th ed. Elsevier Mosbyless2 UnreadUnread8 ViewsViews
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View profile card for Tallona Boddy
Last post March 26 at 10:09 PM by Tallona Boddy
Rojas-Valverde, D., Sánchez-Ureña, B., Crowe, J., Timón, R., & Olcina, G. J. (2021). Exertional rhabdomyolysis and acute kidney injury in endurance sports: A systematic review. European journal of sport science, 21(2), 261–274.
Hodgson, L. E., Walter, E., Venn, R. M., Galloway, R., Pitsiladis, Y., Sardat, F., & Forni, L. G. (2017). Acute kidney injury associated with endurance events-is it a cause for concern? A systematic review. BMJ open sport & exercise medicine, 3(1), e000093. https://doi.org/10.1136/bmjsem-2015-000093
Just another reason, why Id rather stick to sports that are not so high in endurance because the overall toll overtime, I believe outweighs the risks compared to the health gains.
According to study that was published in the European journal of sport science by Rojas-Valverde and team; there has been quite a few studies that have been done with regards to endurance events in sports such as open water swimming, cycling, running and triathlons and there has been a rise in concerns related to the potential implications of renal function and kidney health. This study found that most cases of patients monitored who developed Rhabdomyolysis, and then developed acute kidney injury associated to the activity, was indeed found in long distance runners.
Acute renal failure is one of the most clinically significant complication associated to Rhabdomyolysis. Myoglobin precipitates in the tubules, obstructing the flow of ultrafiltrate through the nephrons thereby producing injury.
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Hilary Szpara posted Mar 24, 2021 11:37 PM
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Rhabdomyolysis is a condition that is characterized by the breaking down and necrosis of damaged skeletal muscles and the release of the contents of the muscle. The substances released include myoglobin and sarcoplasmic protein into the extracellular fluid and circulation (Makris & Spanou, 2016). The myoglobin then moves to the glomeruli of the kidneys and can lead to acute kidney injury (AKI) in different ways (Gaut & Liapis, 2020). Examples of ways in which the release and buildup of myoglobin can lead to AKI include intratubular obstruction secondary to protein precipitation, renal vasoconstriction, and inflammation and tubular damage associated with reactive oxygen production (Makris & Spanou, 2016). Unfortunately diagnosing rhabdomyolysis can be difficult due to patients often not displaying what are thought to be classic symptoms, such as muscle pain, weakness, and dark urine (Gaut & Liapis, 2020). The laboratory value which can help to identify rhabdomyolysis is creatinine phosphokinase (CPK). CPK tends to increase within 12 hours of the onset of the muscle injury and declines about three to five days after cessation of the injury. Unfortunately, at the time of the biopsy, the CPK may have already dissipated (Gaut & Liapis, 2020). It is also believed that myoglobin alone will rarely lead to kidney injury, but that it requires other risk factors such as ischemia, volume depletion, and hypotension to lead to AKI (Gaut & Liapis, 2020).Gaut, J. P. & Liapis, H. (2020). Acute kidney injury pathology and pathophysiology: A retrospective review. Clinical Kidney Journal 14,(2), 526-536.Makris, K. & Spanou, L. (2016). Acute kidney injury: Definition, pathophysiology, and clinical phenotypes. The Clinical Biochemist Reviews 37(2), 85-98.less1 UnreadUnread5 ViewsViews
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View profile card for Caroline Otto
Last post March 25 at 7:09 AM by Caroline Otto
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Tallona Boddy posted Mar 23, 2021 4:02 PM
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There is not one specific mechanism that causes rhabdomyolysis. Rhabdomyolysis can result from a variety of causes, such as trauma, ischemic injury, drugs, infection and extreme physical exercise. The case presented in this week’s discussion, suggests that the most likely cause of the patient’s rhabdomyolysis is extreme exercise (running a 27 mile marathon). Rhabdomyolysis is essentially the breakdown of injured skeletal muscle. As the skeletal muscle breaks down intracellular muscle components are released into the bloodstream. One of the muscle components released is, myoglobin (Torres et al., 2015). Acute renal failure proceeding rhabdomyolysis is theorized to be caused by the myoglobin, a toxin to the kidney. 10%-40% of patients that experience rhabdomyolysis will experience acute renal injury (Esposito et al., 2018). Myoglobin is believed to cause renal vasoconstriction, formation of intratubular casts and direct toxicity of myoglobin to the kidney (Petejova & Martinek, 2014). Another factor that contributes to acute renal failure is volume depletion due to third spacing at the sight of the muscle injury. As the skeletal muscle continues to break down metabolic acidosis, hyperkalemia, hyperphosphatemia, and/or a high anion gap could become present which can exacerbate acute renal failure. (Esposito et al., 2018). Esposito, P., Estienne, L., Serpieri, N., Ronchi, D., Comi, G.P., Moggio, M., Peverelli, L., Bianzina, S. & Rampino, T. (2018, June 01). Rhabdomyolysis-associated acute kidney injury. American Journal of Kidney Disease. 71(6), PA12-A14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056317/Torres, P. A., Helmstetter, J. A., Kaye, A. M., & Kaye, A. D. (2015). Rhabdomyolysis: pathogenesis, diagnosis, and treatment. The Ochsner journal, 15(1), 58–69. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4365849/less2 UnreadUnread9 ViewsViews
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View profile card for Jazmin Jerez-Rivera
Last post March 24 at 9:29 PM by Jazmin Jerez-Rivera
Petejova, N., & Martinek, A. (2014). Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review. Critical Care (London, England), 18(3), 224. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056317/
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Eleany Yasein posted Mar 24, 2021 1:02 PM
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Rhabdomyolysis is a result of muscle injury that has systemic effect (Stanley & Adigun, 2021). The muscle injury is caused by destruction of myocyte cell membrane. Destructive enzymes such as phospholipase and protease are activated, which cause myolysis and cell death. There is a leakage of muscle intracellular components (ex. potassium, myoglobin, creatine kinase, and phosphate) into the blood. This leads to hyperkalemia, hyperphosphatemia and hyperuricemia. It can eventually lead to acute kidney injury, electrolyte imbalance and intravascular coagulation (Stanley & Adigun, 2021). About 10% to 40% of patients who suffer from rhabdomyolysis develop acute kidney injury (Esposito et al., 2018). The release of myoglobin into the blood causes nephrotoxicity. It can cause buildup of iron in the proximal tubules and cause intratubular obstruction and tubular cell injury. Third spacing is also seen due to fluids moving into the injured muscles. Moreover, the release of intracellular constituents can lead to metabolic acidosis which can further damage the tubular (Esposito et al., 2018). Acute renal failure is a major factor in mortality from rhabdomyolysis (Stanley & Adigun, 2021). Patients with acute renal failure in rhabdomyolysis will present with increased serum creatine, increased phosphate levels, decreased bicarbonate, decreased calcium levels. Furthermore, increased BUN and hypoalbuminemia can be seen (Stanley & Adigun, 2021). Esposito, P., Estienne, L., Serpieri, N., Ronchi, D., Comi, P. G., Moggio, M., Peverelli, L., Bianzina, S., & Rampino, T. (2018, June 01). Rhabdomyolysis-Associated Acute Kidney Injury. American Journal of Kidney Diseases, 71(6), xii-xiv. https://www.ajkd.org/action/showPdf?pii=S0272-6386%2818%2930549-3Stanley, M., & Adigun, R. (2021, February 15). Rhabdomyolysis. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK448168/more0 UnreadUnread
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Sheryl Dixon posted Mar 24, 2021 1:26 AM
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The clinical syndrome of rhabdomyolysis is caused by injury of skeletal muscles, leading to the release of various intracellular muscle constituents. Rhabdomyolysis occurs frequently but is usually asymptomatic (i.e., lab abnormalities only). However, in more serious cases, severe electrolyte disorders and acute renal failure may occur, leading to life-threatening situations. Rhabdomyolysis can develop in any circumstances where energy demands in muscles exceed the available energy supplies; it accounts for between 2 and 5% of all cases of acute renal failure in the ICU. Frequent causes of severe rhabdomyolysis include crush injuries, prolonged immobilization, seizures, severe infections and drug toxicity. Factors contributing to the development of more severe clinical symptoms include hypovolemia, hyperthermia, electrolyte disorders and the presence of pre-existing (congenital) muscle disorders(Polderman,2004).The pathophysiology of RM-induced AKI is believed to be triggered by myoglobin as the toxin causing renal dysfunction. This claim is given substance from studies in animal models of glycerol-induced AKI. Intramuscular injection of glycerol in the rabbit induces a model of AKI at a dose of 10 mg/kg that resembles the AKI caused by massive release of myoglobin in crush syndrome in humans. Glycerol-induced AKI is characterized by myoglobinuria, tubular necrosis and renal vasoconstriction. The most important role in glycerol-induced nephrotoxicity has been attributed to reactive oxygen metabolites (reactive oxygen species), in particular the hydroxyl radical (OH.), the same cause as for myoglobin-induced AKI (Petejova & Martinek,2016). ReferencesPolderman K. H. (2004). Acute renal failure and rhabdomyolysis. The International journal of artificial organs, 27(12), 1030–1033. https://doi.org/10.1177/039139880402701204less0 UnreadUnread
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Petejova, N., & Martinek, A. (2014). Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review. Critical care (London, England), 18(3), 224. https://doi.org/10.1186/cc13897
The diagnosis is established by elevation of serum muscle enzymes and muscle constituents such as creatinine phosphokinase and myoglobin. Preventive measures include maintenance of normal or high intravascular volume and administration of diuretics (loop diuretics rather than mannitol) once hypervolemia/euvolemia have been achieved. Some evidence suggests that early initiation of renal replacement therapy can help improve outcome. Administration of bicarbonate to induce urinary alkalosis can be considered, but it has not been proven to be effective (Polderman,2004).
Week 10 Discussion Post – Rhabdomyolysis
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Gisselle Mustiga posted Mar 24, 2021 12:30 AM
Rhabdomyolysis is a potentially life-threatening syndrome resulting from the breakdown of skeletal muscle fibers with leakage of muscle contents into the bloodstream (Huether et al. 2020). These components are the sarcoplasmic proteins myoglobin (MB), creatine kinase (CK), and alanine transaminase (ALT). The condition’s causative agents include crush injury, overexertion, alcohol abuse, toxic substances, and medications, such as antihistamines and antibiotics. Additionally, as in the case of the male patient in the case study, the condition can be caused by muscle breakdown associated with strenuous exercise or normal exercise under extreme circumstances and is termed Exertional Rhabdomyolysis (ER) (Das et al. 2020). A person suffering from this illness may present with clinical features that comprise of muscle pain, muscle weakness, oliguria, and myoglobinuria – a pigmented and dark brown urine. In ER, the level of serum concentration of CK rises 5-10 folds the average amount. The rise in CK concentration is directly associated with acute renal failure. Hyperthermia and repetitive eccentric muscle loads are the key contributors to the presence of both ER and acute kidney failure.ReferencesDas, S., Hanuman, S. B., & Mylapalli, J. L. (2020). Rhabdomyolysis associated acute renal failure–Report of two fatal cases and a brief review of literature. Journal of forensic and legal medicine, 71, 101941. less0 UnreadUnread
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Huether, S. E., McCance, K. L. & Brashers, V. L. (2020). Understanding Pathophysiology 7th ed. Elsevier Mosby.
Abbas, M., Brown, V., Rietveld, A. P., & Hoek, A. E. (2019). A marathon runner with rhabdomyolysis. Nederlands tijdschrift voor geneeskunde, 163.
If undiagnosed, both conditions can have adverse effects on the patient, notably, Acute Kidney Failure. The diagnostic biomarkers are Myoglobinuria and CK and early detection is critical. Standard treatment is the administration of IV fluids, mannitol, which decreases osmotic swelling and edema in the injured muscle cells and helps restore the skeletal muscle function, as well as bicarbonate, which neutralizes the urine. In case of Exercise –induced Rhabdo, patients can take preventive measures, such staying hydrated, becoming acclimatized to one’s physical activity and environmental conditions, since hot and humid climates are contributing factors. (Abbas, et al. 2019).
RhabdomyolysisSubscribe
Jennifer Bryant posted Mar 23, 2021 2:54 PM
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Rhabdomyolysis is the breakdown of skeletal muscle that causes the release of its cellular contents, including protein pigment myoglobin into the systemic circulation (Manis et al., 2019). The causes are varied but may include excessive exercise like the runner in our case study. CPK is an enzyme found in the mitochondria and cytoplasm of various tissues throughout the body including, skeletal and cardiac muscle, and brain tissue. The release of CPK resulting in a level approximately 5 times the upper limits of the reference range, approximately 1000 U/L, is considered confirmatory for the diagnosis of rhabdomyolysis (Manis et al, 2019). In this case, the patients level is 23,000 for a positive diagnosis.References Rhabdomyolysis, Disease-a-Month, 66(8).Manis, T., George-Varghese, B., & Kashani, J. (2019). Rhabdomyolysis – go big or godoi:http://dx.doi.org.wilkes.idm.oclc.org/10.1016/j.ajem.2019.03.024rhabdomyolysis. Sports Medicine, 47(1), S33-S49.less1 UnreadUnread8 ViewsViews
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Last post March 23 at 6:45 PM by Melissa Morgan
doi:http://dx.doi.org.wilkes.idm.oclc.org/10.1007/s40279-017-0689-z
Rawson, E. S., Clarkson, P. M., & Tarnopolsky, M. A. (2017). Perspectives on exertional
home. The American Journal of Emergency Medicine, 37(12), 2194-2196.
https://doi.org/10.1016/j.disamonth.2020.101015.
Cabral, B.M., Edding, S. N., Portocarrero, J. P., Lerma, E. V. (2020).
What we do not know in this case is the urine myoglobin. Myoglobin is cleared by the kidneys. Myoglobin, and likely other proteins, can precipitate in the kidney or be directly nephrotoxic (oxidative stress), resulting in acute renal failure that-if left untreated-could be life threatening (Rawson et al, 2017). Acute kidney injury can occur in 7-10% of all patients who have rhabdomyolysis. The exact mechanism by which rhabdomyolysis impairs glomerular filtration rate is unclear, but there is growing evidence that suggests: renal vasoconstriction; direct and ischemic tubule injury and tubular obstruction (Cabral et al, 2020). Exertional muscle damage produced by eccentric exercise in healthy individuals can cause profound CK and myoglobin elevations without renal impairment, and elevated CK is likely a population-specific bio-marker (Rawson et al, 2017). Maintaining adequate urinary flow and prevention of kidney failure is the goal of treatment with rapid IV hydration.
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Joanne Hogan posted Mar 23, 2021 1:18 PM
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Module 10While complications from rhabdomyolysis vary, acute kidney injury occurs in up to 40% of patients and those with acute kidney injury have an increased mortality rate of up to 80% (Cabral et al., 2020). In a patient with acute kidney injury caused by rhabdomyolysis, the urine will be dark and tea colored (Rawson et al., 2017). According to Rawson et al. (2017), urine dip stick analysis will show acidic urine with myoglobin casts and epithelial cells. Proteinuria can commonly occur in these patients due to the increased excretion of globin (Cabral et al., 2020). Elevated CK levels, potassium, creatine, and creatinine all increase risk for acute kidney injury as well (Huether et al., 2020). According to Huether et al. (2020), once CK levels reach levels of 15,000, renal failure becomes more likely. Due to increased fluid depletion, the RAAS system is activated and ADH is activated, increasing fluid and salt retention (Rawson et al., 2017). Cabral, B. I., Edding, S. N., Portocarrero, J. P., & Lerma, E. V. (2020). Rhabdomyolysis. Disease-a-Month, 66(8), 101015. https://doi.org/10.1016/j.disamonth.2020.101015Rawson, E. S., Clarkson, P. M., & Tarnopolsky, M. A. (2017). Perspectives on exertional rhabdomyolysis. Sports Medicine, 47(S1), 33–49. https://doi.org/10.1007/s40279-017-0689-z less0 UnreadUnread
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Huether, S. E., McCance, K. L., & Brashers, V. L. (2020). Understanding pathophysiology (7th ed.). Elsevier.
References
To prevent renal failure, it is important to treat patients suffering from rhabdomyolysis with IV fluids to prevent excess fluid loss and to prevent the formation of casts and to ensure adequate renal perfusion (Cabral et al. 2020). In cases where the cause of the rhabdomyolysis can be isolated, such as in cases where the illness is caused by medications or drugs, it is imperative to alter lifestyles to prevent further illness (Rawson et al., 2017). IV sodium bicarbonate should also be administered to prevent acidosis, and mannitol may also be given IV to ensure adequate urine output (Rawson et al., 2017).
Rhabdomyolysis is a potentially life-threatening disease where muscle tissue is broken down and intracellular contents are released into the blood stream (Rawson et al., 2017). It is caused by an injury to the muscle and due to the large quantity of muscle in the body, the spilling of intracellular contents into the systemic circulation can be overwhelming for the body (Rawson et al., 2017). ATP is depleted and calcium level in the cells increase causing cell lysis (Rawson et al., 2017).
Fritzinger, Discussion Wk10Subscribe
Cassie Fritzinger posted Mar 22, 2021 10:21 PM
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Rhabdomyolysis is a condition following the breakdown of skeletal muscle, releasing intracellular contents into the extracellular space and bloodstream. Common causes being trauma, overexertion, toxic substances including alcohol abuse. Complications secondary to this condition due to muscle cell necrosis include hyperkalemia, hypocalcemia, acute kidney injury (AKI) and hypovolemic shock. AKI occurs in approximately 19%-58% of those patients who have rhabdomyolysis (Candela, et al., 2020). Symptoms of AKI may include muscle pain, weakness, and dark urine. While dark urine is often seen, this alone is not a reliable indicator of rhabdomyolysis. Labs studies noted in the evaluation of rhabdomyolysis may include CK, potassium, phosphorus, blood urea nitrogen (BUN) to creatinine ratio, and calcium. The CK level of 5-10 times normal is seen in rhabdomyolysis. A CK level of greater than 15,000 units/L indicates a likelihood of acute renal failure (Chrisholm-Burns, Schwinghammer, Malone, Kolesar, Lee & Bookstaver, 2019). The patient of discussion has a CK level of 23,000 which is over 135 times greater than the normal level. His presentation of pain, swelling and redness of his left calf are also consistent with the diagnosis of rhabdomyolysis. His risk factors of significant strenuous activity of running the marathons and training significantly for the past few months is another additional risk factor of rhabdomyolysis. While his BUN and Creatinine are currently within normal limits it would be important to start fluid rehydration and monitor any electrolyte imbalances. The BUN/Creatinine indicate he has not yet progressed into AKI. However, as stated previously a CK greater than 15,000units/L would be highly suggestive of impending AKI and prevention of this progression if possible or limiting this progression is of great importance. Candela, N., Silva, S., Georges, B., … Faguer, S. (2020). Short- and Long-Term Rental Outcomes Following Severe Rhabdomyolysis: A French Multicenter Retrospective Study of 387 Patients. Annals of Intensive Care. 10:27. https://doi.org/10.1186/s13613-020-0645-1Diaz-Tejeiro, R., Regidor, D., Morales, J., Padron, M., Cueto, L. Munoz, MA, et al. (2018). Acute Renal Failure due to Rhabdomyolysis. Renal Replacement Therapy with Intermediate Cut-Off Membranes (EMIC2). Nefrologia. 38(6) 660-680. https://doi.org/10.1016/j.nefroe.2018.06.013
Chrisholm-Burns, M. A., Schwinghammer, T.L., Malone, P.M., Kolesar, J.M., Lee, K.C., & Bookstaver, P.B. (2019). Pharmacotherapy: Principles and practices (5th ed.) McGraw-Hill Education.
References
The treatment for rhabdomyolysis is to improve urinary output with adequate hydration ultimately working to prevent secondary AKI. Diaz-Tejeiro, et al. (2018), found that not all patients will have resolution of kidney function with simple hydration and may require renal replacement therapy such as dialysis. The early initiation of replacement therapy with improved myoglobin clearance and decreased serum levels equated to improved and earlier recovery from AKI (Diaz-Tejeiro, et al, 2018).
AKI secondary to rhabdomyolysis results from the release of myoglobin, lactate dehydrogenase, creatine kinase (CK) and other electrolytes into the circulation and interstitial space. The circulation of myoglobin reaching the renal tubules leads to an obstruction creating injury of the kidney filtration function. AKI is characterized by a sudden decrease in kidney function with decreased glomerular filtration (GFR) and decreased urine output. Renal vasoconstriction, intratubular casts, and the direct tubular cell damage are three nephrotoxic mechanisms which cause the AKI (Chrisholm-Burns, Schwinghammer, Malone, Kolesar, Lee, & Bookstaver, 2019).

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