Reply to the following 2 posts.  In your reply posts, include how the information you learned from your peer’s initial post will help you to provide care to a patient. 

Reply to the following 2 posts.  In your reply posts, include how the information you learned from your peer’s initial post will help you to provide care to a patient.



Glomerulonephritis (acute poststreptococcal glomerulonephritis, APSGN), is a representative form of nephritic disease, that occurs following an infection of streptococcal with strains of group A beta-hemolytic streptococcus. According to the National kidney foundation (2020), there are two types, acute and chronic. (NKF, 2020). I will be focusing this discussion on the acute type APSGN. This occurs following an infection in the upper respiratory tract, middle ear infections or strep throat. Whenever there are infections with strains of streptococcus, the immune response is usually initiated in the kidney. This condition develops 10 days up to two weeks following exposure to the strep strain and occurs in children between the ages of 3-7 years, mostly affecting boys. (Hubert & VanMeter, 2018).


When persons become infected with the streptococcal strain, subsequent infections causes the body to form antistreptococcal antibodies, thus creating an antigen-antibody complex (type 3 hypersensitivity reaction). When this occurs, the complement systemin becomes activated, which causes the glomeruli of both kidneys to develop an inflammatory response. The inflammatory responses further leads to increase permeability and cell proliferation, where protein and erythrocytes infiltrates and leak into the system. Immunoglobulin G and C3 becomes present in the glomerular tissue and reduction of the serum C3 is noted. If the inflammatory response is severe, and causes reduction in the filtration of the kidney, the glomerular filtration rate (GFR) will decrease and a build up of waste and fluids will occur in the body. If there is impairment in the blood flow, then acute renal failure can occur, increased renin secretion occurs which cause edema and high blood pressure. When these changes are over a prolonged period, scarring of the kidneys can occur. (Hubert et al, (2018).

Signs and symptoms

Edema of the face and periorbital region, generalized edema, due to the retention of fluid and sodium, and the fall in the osmotic pressure, blood pressure elevated, urine color is dark and cloudy, flank or back pain, oliguria results from the decrease in the GFR, and generalized signs of inflammation such as headache, malaise, anorexia and nausea. (Hubert et al, 2018).

Diagnostic testing

The diagnostic tests are blood test (serum urea, creatinine) these will be elevated. GFR will decrease. Blood levels to measure anti-DNase B, streptococcal antibodies. ASO (antistreptolysin O) and ASK (antistreptokinase) will be elevated. Urinalysis will be done to confirm the presence of protein, hematuria and erythrocyte casts. Serum bicarbonate levels and pH will be done same will be decreased, and metabolic acidosis will be present. The patients complement level will be decreased due to the inflammatory response in the kidneys. (Hubert & VanMeter, 2018).


The treatment modality of this condition includes dietary changes, drug intervention, follow up management of this condition. The plan is to reduce the edema, restrict sodium, fluid and protein intake. The patient will be placed on prophylactic antibiotics to prevent future occurrence. Drugs such as glucocorticoids are given to reduce the inflammation and antihypertensives are given to reduce the blood pressure. The patients are tested post recovery to ensure that chronic inflammation is not present. (Hubert & VanMeter, 2018).


The prognosis is good as recovery takes place with minimal residual damage. Children with edema usually see a resolve within 5-10 days and the hypertension decreases in 2-3 weeks. The proteinuria and hematuria can persist for some time. In adult patients, there are a few cases that does not completely resolved, and this can lead to acute renal failure (2%) of cases, chronic glomerulonephritis occurs in 10% of cases, and some patient end up with end stage renal disease and uremia. The aim of having a good prognosis is to prevent future exposure to streptococcal infections that can trigger another inflammatory response and hypersensitivity reaction. (Hubert & VanMeter, 2018).

Impact on NP plan of care (PMHNP)

As a future PMHNP, it would be a great idea to understand the pathophysiological changes that occurs in this condition and the treatment modalities, so that when patients are entrusted in my care, I will be able to maintain effective and efficient treatment of their condition. Understanding the signs and symptoms that the patients present with and being able to perform head to toe assessment so that a baseline can be established to measure intervention and outcomes. Caring for patients with this diagnosis may not be prevalent, however when the NP has a general knowledge of the treatment modalities and the diagnostic testing available, the patient will be able to receive the best care with a positive outcome.
As a PMHNP I must be knowledgeable about this condition, so that the patients in my care can be educated on lifestyle changes and encourage a healthy nutrition. Patient will be encouraged to eat smaller frequent meals, restrict fluids, limit sodium intake, exercise and maintain a healthy weight. Patients will be encouraged to complete medications and to take measures to prevent future exposure to the bacteria responsible. As a PMHNP I would need to be cognizant of the drug reaction that could possible occur and the renal dysfunction on the medication absorption, hence continued monitoring of the kidneys would need to be done. In an article by Fanton et al (2011), the author recommends that since several patients have compromised renal function, psychiatrist will need to collaborate with primary care providers and nephrologist when prescribing psychotropic medications. (Fanton, et al, 2011)

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Acute Renal Failure

The purpose of this paper is to define Acute Renal Failure. In defining Acute Renal failure, this paper will outline the pathophysiology of the disease, diagnostics, treatment plans, and prognosis. Additionally, this paper will look at the impact this diagnosis on the APRNs plan of care for the patient. Generalizations will be used, where appropriate, as this paper is intended to be an overview.


The kidneys play a crucial role in homeostasis. The body contains two kidneys, each about the size of a fist and are located on the posterior abdominal wall on each side of the spine. Normal kidney function removes metabolic wastes, hormones, drugs, and foreign materials from the body. The kidneys are also responsible for the regulation of water, electrolytes, and the acid-base balance. Other important functions of the kidney include the production of erythropoietin for red blood cell production, activation of Vitamin D, and the stabilization of the blood pressure cardiovascular system through renin-angiotensin-aldosterone system (Hurbert & VanMeter, 2018).

Multiple significant functional responsibilities leave multiple avenues in which something may go wrong. Acute renal failure (ARF), also known most recently as Acute Kidney Injury (AKI), is an abrupt decline in the function of the kidney reducing the ability of the kidney to filter out toxins. This inability to filter greatly reduces the kidneys glomerular filtration rate (GFR) and results in elevated metabolic waste, creatinine, and serum blood urea nitrogen (BUN) (Okusa & Rosner, 2019). Causes of adult AKI include prolonged exposure to nephrotoxins such as drugs, chemicals, or other toxins that cause tubule necrosis and obstruction, mechanical obstruction such as blood clots, renal calculi, or tumors, heart failure or circulatory shock. The cause of AKI in shock differs depending on the type of shock experienced. Lastly, kidney disease exacerbation causing significant decline in the GFR (Hurbert & VanMeter, 2018).

An infant, or neonate, is more vulnerable to AKI than an adult due to their developmental and functional immaturity of the kidney. This immaturity effects the tubular function, glomerular filtration, hemodynamic changes at delivery, and the risk of hypovolemia due to large insensible water losses. Eighty-five percent of neonatal AKI cases arise from inadequate perfusion, 11% from intrarenal pathology, and 3% from obstruction (Mattoo, 2019).

Diagnostic Testing

Diagnostic testing differs as well when diagnosis AKI in an adult versus a neonate. In a neonate, differential factors include gestational age and postnatal age. Because of this the gold standard for measuring the GFR in a neonate is through the creatinine clearance measurements of serum creatinine (SCr) (Mattoo, 2019). Other diagnostic assessment tools include measurement of blood pressure and hydration status assessment for hyper/hypovolemia. Hydration assessments include weight monitoring and signs of heart failure such as edema and tachypnea (Mattoo, 2019).

A urinalysis would be inconclusive for a neonate when assessing renal failure, however, is a beneficial tool for assessment of an adult. In conjunction with patient history, physical exam, and serum chemistries, a urinalysis will play a significant role in identifying AKI (Wald, 2020). A urine protein level is one aspect in which the urine identifies kidney injury. When kidneys are damaged protein leaks into urine and can be an early sign indicator. A urinalysis will also identify the specific gravity which measures the ability of the tubules to concentrate urine. Assuming a patient is properly hydrated, the specific gravity will be very low in the presence of renal failure (Hubert & VanMeter, 2018).

Serum chemistries include serum Creatinine, blood urea nitrogen (BUN), and GFR. Creatinine is a muscle metabolism waste product excreted by the kidneys. The increase in creatinine is a sign the kidneys are not functioning properly. Blood urea nitrogen is a waste production in blood that comes from protein breakdown of ingested food and body metabolism. The BUN level will rise in AKI. The GFR marks kidney function and is estimated from the SCr. A level below 15 is indicative of AKI (National Kidney Foundation, 2020).


Treatment includes identifying and rectifying root cause of injury. This may take place in an emergency setting or in primary care depending on the patient’s clinical presentation and root cause. It is important to reverse the cause of ARI as quickly as possible to avoid necrosis and permanent damage to the kidneys (Hubert & VanMeter, 2018). In both the adult and neonate general management would include fluid management, electrolyte management, nutritional support, and adjustments to drug therapy as the directed therapy should be based on the etiology of the AKI (Mattoo, 2019). Dialysis may be one method of treatment that can be used acutely until the kidneys are able to return to normal function (Hubert & VanMeter, 2018).


In neonates, AKI increases the risk for morbidity and mortality, especially in infants with low birth weight or other underlying conditions that may tax the kidneys such as cardiac complications. Prevention is key but also challenging. Preventative measures would involve adjusting medications to avoid medications excreted though the kidneys. Additionally, avoid medications that are toxic to the kidneys. Avoid hypovolemia by making sure the neonate is properly hydrated with balanced electrolytes, reduce fluid intake when appropriate and monitor serum levels, such as SCr, routinely (Mattoo, 2019). Any intervention towards correction and intervention are beneficial for a more positive prognosis.

Kidney health outcome is determined by the cumulation of many factors. The duration of the AKI directly impacts the prognosis as the increased length and severity of the AKI may cause irreversible damage. The degree to which the kidneys recover from initial attack plays as role in prognosis, more so if recurrent attacks present. Recurrent AKI, which is noted to occur within 12 months of prior injury, decreases the kidneys ability to fully recover to the established baseline prior to attack. Recurrent attacks increase risk of chronic kidney disease and death. A variety of other factors play a role in patient prognosis. These factors include sex, age, and other comorbidities such as heart failure, diabetes, or chronic hypertension (Liangos & Bertrand, 2020).

Impact on NP Plan of Care

In any plan of care for a patient, the goal is to prevent injury and illness. Predetermining risk factors for AKI such as HTN, cardiac disease, and diabetes need to be taken into consideration when treating a patient. Knowing these conditions increase risk the APRN may decide a different course of medications to reduce kidney exposure. Additionally, educating the patient on the disease processes and how they may affect other systems in the body will also be a critical part of the plan of care for prevention.

Once AKI has occurred, it will be imperative that the APRN identifies the causative factor and rectifies this as to prevention or reduce likelihood of recurrent AKI and also to expedite recovery and reduce kidney injury. This is true in both the adult and neonatal patient. Early intervention leads to reduced long-term effects and could prevent recurrent injury. It is also important for the APRN to modify a plan of care once an AKI has occurred as patients who recovery form AKI may not return to their initial baseline of function. This is likely in patients over the age of 65. If a patient has an AKI and is hospitalized, the APRN in the primary setting will need to be reevaluated within three months to determine resolution (Liangos & Bertrand, 2020).

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