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  • W.B.C.S. Main 2018 Question Answer – Medical Science – Acute Kidney Injury.
    Posted on January 5th, 2019 in Medical Science
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    W.B.C.S. Main 2018 Question Answer – Medical Science – Acute Kidney Injury.

    WBCS মেইনস ২০১৮ প্রশ্ন উত্তর – চিকিৎসা বিজ্ঞান – তীব্র কিডনি আঘাত ।

    Acute kidney injury in a clinical diagnosis guided by standard criteria based on changes in serum creatinine, urine output or both. Severity of acute kidney injury is determined by the magnitude of increase in serum creatinine or decrease in urine output. Patients manifesting both oliguria and azotemia and those in which these impairments are persistent are more likely to have worse disease and worse outcomes. Both short- and long-term outcomes are worse when patients have some stage of AKI by both criteria. Duration of AKI was also a significant predictor of long-term outcomes irrespective of severity. New biomarkers for AKI may substantially aid in the risk assessment and evaluation of patients at risk for AKI.Continue Reading W.B.C.S. Main 2018 Question Answer – Medical Science – Acute Kidney Injury.

    Acute kidney injury (AKI) is a clinical diagnosis. Already in ancient times it was noted that the failure to pass urine was lethal if untreated and might be due to either “an empty bladder” or an obstruction. Indeed, urinary catheters were used as early as 3000 BC. It was Galen who first established the kidneys as the source of urine and as organs that “filtered the blood”.1 Prior to this, it was generally believed that urine was made in the bladder from food and drink. Progress in the clinical assessment of renal function was quite limited from the time of Galen until the 18th century when urea was discovered—however, it would be more than a century later before increases is blood urea and serum creatinine would be used to quantify azotemia (“azote” is a very old name for nitrogen). Azotemia results from reductions in glomerular filtration rate (GFR) and together with oliguria (“small” urine) or anuria (no urine) form the cardinal features of kidney failure.

    However, azotemia and oliguria represent not only disease but a normal response of the kidney to extracellular volume depletion or a decreased renal blood flow. Conversely, a “normal” urine output and GFR in the face of volume depletion could only be viewed as renal dysfunction. Thus, changes in urine output and GFR are neither necessary nor sufficient for the diagnosis of renal pathology.2 Still, they serve as the backbone for our existing diagnostic criteria.

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