{"id":433,"date":"2023-12-04T10:25:09","date_gmt":"2023-12-04T15:25:09","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/dcbiol2200\/chapter\/aki-chapter-summary\/"},"modified":"2023-12-04T10:49:03","modified_gmt":"2023-12-04T15:49:03","slug":"aki-chapter-summary","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/dcbiol2200\/chapter\/aki-chapter-summary\/","title":{"raw":"AKI Chapter Summary and Credits","rendered":"AKI Chapter Summary and Credits"},"content":{"raw":"\nAKI is a result of an insult to the kidneys - whether before (prerenal), within (intrarenal), or after the kidney (postrenal).  Regardless of the cause, nephrons are damaged or destroyed due to the insult - which is evident in both gross and microscopic examination of the nephrons.  The end result is impaired reabsorption of useful nutrients AND excretion of harmful wastes and excess fluid.  As a result, the body retains the wastes and fluid causing disturbances in multiple systems and signs of fluid overload.\n\n \n\nA common feature of AKI is high blood levels of nitrogenous wastes and creatinine at the same time as a reduction in urine output.  In addition to these common features, there will be additional features that suggest the cause as being pre-, intra-, or post-renal.   Diagnosis of AKI is usually by blood tests for creatinine and nitrogenous wastes in conjunction with urine output.  Imaging of the kidney through ultrasound will help give information as to the cause being pre-, intra-, or post-renal.\n\nTreatment of AKI is to address the underlying cause of the insult to the kidney.\n

Credits<\/h1>\nAuthors:  Lyz Boyd (UBC medical student) & Dr. Jennifer Kong (BCIT & UBC)\n\nAuthor of questions and exercises: Eva M. Su (UBC undergraduate student) & Dr. Jennifer Kong (BCIT & UBC)\n\nGross anatomy videos:  Eva M. Su (UBC undergraduate student ) & Dr. Jennifer Kong (BCIT & UBC)\n\nHistopathology video:  Lyz Boyd (UBC medical student) with supervision of Dr. Jonathan Bush (UBC, Director of DHPLC)\n\nSonographer:  Kenneth Marken (Diagnostic Sonography, BCIT)\n\nVideoproducer:  Ian Whittlesey (BCIT)\n\n \n","rendered":"

AKI is a result of an insult to the kidneys – whether before (prerenal), within (intrarenal), or after the kidney (postrenal).  Regardless of the cause, nephrons are damaged or destroyed due to the insult – which is evident in both gross and microscopic examination of the nephrons.  The end result is impaired reabsorption of useful nutrients AND excretion of harmful wastes and excess fluid.  As a result, the body retains the wastes and fluid causing disturbances in multiple systems and signs of fluid overload.<\/p>\n

 <\/p>\n

A common feature of AKI is high blood levels of nitrogenous wastes and creatinine at the same time as a reduction in urine output.  In addition to these common features, there will be additional features that suggest the cause as being pre-, intra-, or post-renal.   Diagnosis of AKI is usually by blood tests for creatinine and nitrogenous wastes in conjunction with urine output.  Imaging of the kidney through ultrasound will help give information as to the cause being pre-, intra-, or post-renal.<\/p>\n

Treatment of AKI is to address the underlying cause of the insult to the kidney.<\/p>\n

Credits<\/h1>\n

Authors:  Lyz Boyd (UBC medical student) & Dr. Jennifer Kong (BCIT & UBC)<\/p>\n

Author of questions and exercises: Eva M. Su (UBC undergraduate student) & Dr. Jennifer Kong (BCIT & UBC)<\/p>\n

Gross anatomy videos:  Eva M. Su (UBC undergraduate student ) & Dr. Jennifer Kong (BCIT & UBC)<\/p>\n

Histopathology video:  Lyz Boyd (UBC medical student) with supervision of Dr. Jonathan Bush (UBC, Director of DHPLC)<\/p>\n

Sonographer:  Kenneth Marken (Diagnostic Sonography, BCIT)<\/p>\n

Videoproducer:  Ian Whittlesey (BCIT)<\/p>\n

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