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Each peer reply should be at least a paragraph in length and contain substantive addition to the discussion

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Each peer reply should be at least a paragraph in length and contain substantive addition to the discussion.

Peer 1: AKI is a sudden decline in kidney function and can occur in less than a day. Azotemia is one of the most common indicators of AKI. This is a buildup of nitrogenous wastes of urea nitrogen, uric acid, and creatinine in the blood (Makris, 2016). The glomerular filtration rate of the kidney is reduced causes this buildup of wastes therefore fluid and electrolyte balances cannot be maintained. The causes of AKI can be broken down into three categories: prerenal, intrarenal, and postrenal. Prerenal AKI can be caused by hypovolemia, decreased vascular filling, heart failure, and decreased renal function (due to sepsis, drugs, diagnostic agents, or vasoactive mediators). Intrarenal AKI can be caused by acute tubular necrosis which occurs from ischemia, sepsis, nephrotoxic effects of drugs, or massive infections. Obstruction of the bladder or ureters can cause postrenal AKI (Norris, 2020, p.891).

Ms. S is suffering from dry mucus membrane and dry skin which is a sign of dehydration and fluid imbalance. Ms. S urine analysis tested positive for protein, RBC, WBC, and nitrites which should not be present in the urine. This is an indication that she could have intrarenal AKI from acute tubular injury, which causes hematuria, proteinuria, decreased GFR, azotemia, and oliguria (Norris, 2020, p. 883).  

The top priorities for Ms. S currently are fluid resuscitation and antibiotic. Fluid resuscitation with an isotonic is necessary to increase her blood pressure and help draw sodium back onto the cells, since her sodium levels are elevated (Kher et al., 2017). Increasing Ms. S cardiac output will make sure the kidneys are perfused and hopefully increase the GFR. Antibiotics are also recommended to treat sepsis, which Ms. S is suspected to be in the early stages of sepsis due to her elevated WBC, decreased BP, increased pulse, tenting skin, and elevated temperature. Treating the cause of AKI quickly is necessary to prevent any further damage to the kidneys. 

Additional assessments include continuing lab work to monitor electrolyte levels, WBC, and RBC count. Strict intake and output are vital for Ms. S at this point to assess kidney function. Performing s CT scan can prove beneficial to assess the kidneys further. Ultimately a consult to a nephrologist is needed and should be made as soon as she is admitted to the hospital. 

peer 2: Ms. S is exhibiting several common signs of dehydration, which include dry and cracked mucous membranes, dry skin with tenting, tachycardia, hypotension, acute urinary retention, and more. This hypovolemic dehydration from excessive vomiting has caused Ms. S to have an acute kidney injury (AKI). Acute kidney injuries are very rapid, happening in a matter of hours to a day (Norris, 2020, pp. 891).

            There are three types of acute kidney injuries: prerenal, intrarenal, and postrenal. Some causes of prerenal AKI include hypovolemia, shock, heart failure, sepsis, and more. Intrarenal AKIs are caused by acute injuries and tubular necrosis. Finally, postrenal AKIs are caused by obstructions to either the ureters or bladder outlets (Norris, 2020, pp. 891-892). In Ms. S’s case, she is experiencing a prerenal AKI due to hypovolemia from the excessive vomiting from what is probably food poisoning from ingestion of tainted spinach.

            A reduction in blood flow to the kidneys is how a prerenal AKI begins. When there is a reduction in the renal blood flow, GFR will increase, filtration of electrolytes and other substances will decrease, urine output will decrease, and the BUN to creatinine ratio will elevate (Norris, 2020, pp. 894). We see several of these examples in Ms. S’s case. A normal BUN ranges from 8.0-20.0 mg/dL, however we see that Ms. S has a BUN of 35 mg/dL. Creatinine ranges from 0.6- 1.2 mg/dL and this patient has a 3.5 mg/dL result. Along with both of these numbers being elevated, her sodium is also elevated. This is because the kidneys are no longer able to effectively filter some electrolytes out at present due to the AKI. Another lab value to mention is her GFR, currently reading at 65 mL/minute instead of the normal 115-125 mL/minute. This is showing that the filtration rate is low in her kidneys due to the AKI (Norris, 2020, pp. 857-858).

            Top priorities for Ms. S include fluid resuscitation (with isotonic crystalloid), discontinuing any current medications that could cause further damage to the kidneys, and potentially using vasopressors to increase her blood pressure depending on how she responds to the fluid resuscitation. It will be important to continue to monitor her volume status, kidney function, and electrolyte levels. It appears that Ms. S also has a UTI, so treatment of this with antibiotics that are dose adjusted to take her AKI into consideration will also be important (Mercado et al., 2019).

            We will continue to assess Ms. S’s urine output and anticipate that it will increase. If after fluid resuscitation and treatment of the AKI the urine output does not increase significantly, renal replacement therapy may be needed. Other ways to assess Ms. S’s volume deficit and her response to treatment would be to monitor her heart rate, blood pressure, serum lactate, and other electrolyte levels (Taylor & Jones, 2022).