Physical Examination in a patient with post-renal AKI may reveal a distended bladder and abdominal pain.
The BUN:Cr ratio in the initial stages of post-renal AKI is typically at or above 20:1. This is similar to pre-renal acute kidney injury and can be a source of confusion. As such, the BUN:Cr ratio cannot be used alone to establish a diagnosis of either pre-renal or post-renal AKI. Further diagnostic studies are needed to differentiate between these 2 diseases.
The BUN:Cr ratio in the late stages of post-renal AKI is typically at or above 10:1. This ratio is similar to that which is seen in intrinsic AKI and can be a source of confusion.
As the obstruction persists for a prolonged period of time and the kidney undergoes permanent damage, more tubular cells die. The increased tubular cell death is similar to that which is seen in acute tubular necrosis, a subtype of intrinsic AKI. Hence, the BUN:Cr creatinine ratio in the late stages of post-renal AKI is similar to that of intrinsic AKI.
The BUN:Cr ratio cannot be used alone to establish a diagnosis of either intrinsic or post-renal AKI. Further diagnostic studies are needed to differentiate between these 2 diseases.
The Urine Osmolality in post renal AKI is typically below 350 mOsm/kg.
The FENA is variable and cannot be used to distinguish post-renal AKI from pre-renal or intrinsic AKI.
Ultrasound can be used to evaluate the degree of hydronephrosis present in patients with post-renal acute kidney injury.
CT scan can be used to diagnose the cause of the post-renal acute kidney injury as well as the degree of hydronephrosis.
There are multiple etiologies of post-renal acute kidney injury including: benign prostatic hyperplasia, neoplasms, incomplete bladder emptying due to autoimmune diseases such as multiple sclerosis, and other causes of bilateral kidney outflow obstruction. Severe acute obstructions can cause permanent damage to the kidney. Complete recovery is possible if the obstruction is relieved within 14 days of onset.
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