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Troponin I is not entirely specific for myocardial damage secondary to infarction. Other causes of raised troponin I include chronic kidney failure, heart failure, subarachnoid haemorrhage and pulmonary embolus. [9] [10] In veterinary medicine, increased cTnI has been noted from myocardial damage after ionophore toxicity in cattle. [11]
Other conditions that directly or indirectly lead to heart muscle damage and death can also increase troponin levels, such as kidney failure. [ 18 ] [ 19 ] Severe tachycardia (for example due to supraventricular tachycardia ) in an individual with normal coronary arteries can also lead to increased troponins for example, it is presumed due to ...
Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in heart failure patients. Several studies have shown that as a result of this increased intra-abdominal pressure there is increased central venous pressure and congestion of the kidneys' veins, which can lead to ...
Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis. Troponins can also calculate infarct size but the peak must be measured in the 3rd day. After myocyte injury, troponin is released in 2–4 hours and persists for up to 7 days.
Other conditions that have symptoms similar to heart failure include obesity, kidney failure, liver disease, anemia, and thyroid disease. [7] Common causes of heart failure include coronary artery disease, heart attack, high blood pressure, atrial fibrillation, valvular heart disease, excessive alcohol consumption, infection, and cardiomyopathy.
In short, renal angina is a clinical guide that identifies patients at high-risk for AKI by integrating baseline, contextual, and clinical evidence of kidney injury. When criteria for fulfilling renal angina are met, an AKI biomarker (a renal troponin) is optimally used (Figure 1 - Renal Angina Thresholds).
Acute kidney injuries can be present on top of chronic kidney disease, a condition called acute-on-chronic kidney failure (AoCRF). The acute part of AoCRF may be reversible, and the goal of treatment, as with AKI, is to return the person to baseline kidney function, typically measured by serum creatinine .
Renal azotemia (acute kidney failure) typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of kidney parenchymal damage. Causes include kidney failure, glomerulonephritis, acute tubular necrosis, or other kidney disease. [3] The BUN:Cr in renal azotemia is less than 15.
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