Renal toxicity is one of the most important side effects of MTX at high dose(Muhsin & Latif, 2012).
Studies report that oxidative stress plays an important role in MTX-induced renal toxicity(Ibrahim et al., 2014). MTX produces active oxygen species (ROS), resulting in lipid peroxidation and resulted in mitochondrial dysfunction. Neutrophil infiltration and oxidative stress have been proposed for MTX induced renal toxicity(Bozkurt et al., 2014). Garlic has been selected due to its antioxidant and antiradical properties(Santhosha, Jamuna, & Prabhavathi, 2013) and its potential protective role in MTXinduced renal toxicity has been addressed.
The results of this study show that administration of MTX to rats increased the serum BUN and serum
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The damaged kidney tubular cells interfere with tubular cell renewal and cause renal dysfunction and reduce GFR and thus increase serum BUN and creatinine amount. In addition, these cells can be poured into lumen tubules, thereby reducing the flow of tubule fluids and exacerbating the precipitation of methotrexate in tubules. MTX is actively reabsorbed in the proximal tubule, so
MTX accumulation in the tubules causes damage to the region and impaired renal circulation, resulting in a decrease in the amount of glomerular filtration and the concentration of creatinine and
BUN Plasma increases(Ahmed et al., 2015).
Histopathologic results confirm MTX-induced renal toxicity. Outstanding histopathologic findings in kidney tissue of the methotrexate group include injuries such as congestion, Bowman capsule dilatation, mononuclear infiltration of cells in the interstitial tissue around the urinary tubules and connective tissue surrounding the glomeruli, swelling of the wall of the ureter tubules And fusion of their lumen and in general, interstitial nephritis, and tubular necrosis were observed (Fig. 3).
Histopathological evidence is consistent with previous findings that have addressed methotrexateinduced renal damage(Armagan et al., 2015; Asvadi et al., 2011; El-Twab, Hozayen, Hussein, &
Mahmoud, 2016; Uzkesera et al., 2012; Yuksel et al., 2017)
It has been
As suggested by Seagull et al. (1980), while the rate of cytoplasmic streaming does not vary with the size of the motile particle (organelle, cargo molecule, etc.) or the size of the cell itself, larger cells with increased surface area may absorb these mechanism-inhibitory substances more readily and may therefore have slower rates of cytoplasmic streaming as less F-actin is available to the myosin complex at any one time.
Consequently, the efferent arteriole, which filters blood away from the glomerulus, is tinier in diameter than the afferent arteriole, which carries blood into each glomerulus. This puts blood under high pressure in the glomerulus; thus it forces tiny molecules and liquid out of the capillary and into the Bowman’s capsule. Soon afterwards, the tiny and liquid molecules cross the epithelium of the Bowman’s capsule, the basement membrane and capillary wall in order to get into the Bowman’s capsule and to arrive in the nephron tubules. The consequence of this is that the filtrate (the tiny and liquid molecules) pass along the remainder of the nephron and helpful substances are reabsorbed along the route. Last of all, “the filtrate flows through the collecting duct and passes out of the kidney along the ureter” as mentioned by (Parson’s, R: p128).
b. Explain the urea recycling process. The constant transfer of urea between the renal tubule and interstitial fluid of the medulla.
Low GFR indicated by serum creatinine > 1.5 mg/dL or creatinine clearance < 40 mL/min in 24 hour.
Every day, 180 liters of filtrate is passing through nephron tubule, and not all of them are excreted. Instead, reabsorption occurs, which is the process of water and dissolved substances transporting back into the blood. Kidney usually throws everything and takes back only what body needs, and this is how kidney removes drugs and toxic compounds. Loop of Hele conserves water and minimizes the volume of the filtrate. It is part of the nephron tubule. Finally the last step, urine goes through collecting duct, ready to be removed by urethra.
Digoxin toxicity. Digoxin has a narrow therapeutic index and chronic toxicity is more likely in the elderly and those with renal impairment. Since Mr Buchanan is 75 years old, he may already have some form of renal impairment and therefore is at a higher risk of developing toxic serums levels if continually taking Digoxin (Australian Medicines Handbook, 2016 and Nickson, 2014). Digoxin toxicity can be caused by prolonged use, an overdose or a general increase in the current dose (Australian Medicines Handbook, 2016). If Mr Buchanan is taking digoxin for an extended amount of time, he may build up a tolerance to its effects due to being consistently exposed to the drug (Australian Medicines Handbook, 2016). This is significant risk
Acute kidney injury (AKI) is rapid renal function decline with a decrease in glomerular filtration and consequently the build up of nitrogenous waste products in the body. AKI is reversible, but is it also more likely to progress into chronic kidney disease. Acute kidney injury incidence is common in the United States and it’s growing. According to research, acute kidney injury accounts for ten to twenty percent of hospitalized adults (Levey, 2015). Since it is fairly common there is a need to diagnose earlier with increased meticulousness in order to prevent total kidney failure. Acute kidney injury can be categorized as prerenal, intrinsic, and postrenal (Yaklin, 2011) Prerenal injury prevalence is the most common and will be discussed further.
leads to the decrease in blood glucose due to the increase in renal glucose excretion. The
Methotrexate is a phase-specific substance the main action of which is directed to the S-phase of cell mitosis. It acts generally most effectively on actively increasing tissues, such as malignant cells, bone marrow, foetal cells, oral and intestinal mucosa as well as urinary bladder cells. As the production of malignant cells is higher than that of most normal cells, methotrexate can slow down the production of malignant cells without causing, however, irreversible damage to normal tissue.
Two different mouse models were used to test (in vitro) the effects of the drug. Cell lines [in vitro, n=6] were given either the metformin drug, or phosphate-buffered saline solution and cellular proliferation and metabolic alterations (adenosine monophosphate-activated protein kinase activity, glycolysis, and lipid synthesis)]. Each of which
Rhabdomyolysis is defined as: “a clinical and biochemical syndrome that occurs when skeletal muscle cells disrupt and release creatinine phosphokinase (CK), lactate dehydrogenase (LDH), and myoglobin in the interstitial space and plasma.” (Althay, Bezerra, Loborio & Daher, 2008. p. 721). The breakdown of muscle will set forth the release of the guts, per say, of the cell which will also pertains to myoglobin. It is this myoglobin that will occlude the tubules, this occlusion will lead to injury of the kidney’s nephron. (Huether & McCane, 2017. p. 997). It is stipulated by Althayd et al. that when the patient is not hypovolemic that myoglobin is less caustic to the
Increase in serum creatinine (SCr) by > 0.3 mg/dl (> 26.5 µmol/l) within 48 hours. OR
Acute renal failure is the sudden loss of the kidneys ability to function; affecting more than 100,000 people in the United States alone each year (NIDDK, 2008). This paper will discuss the basic pathophysiology of acute renal failure, including its cause, disease mechanisms, symptoms, some of the treatments and pharmacological therapies.
The A0 urine sample comes from a 30-year-old adult who is also an extreme athlete.