Causes and Symptoms of Idiopathic Nephrotic Syndrome
Question:
Discuss About The Frequently Idiopathic Nephrotic Syndrome?
Nephrotic syndrome can be defined as an amalgamation of different categorical symptoms that are a direct or indirect outcome of intrinsic kidney damage. There are various different symptoms and manifestation routes associated with the construct of nephrotic syndrome. The most common symptoms of nephrotic syndrome include presence of high protein content in the urine, low concentration of blood albumin levels, high lipid concentration in the blood, and along with that significant swelling all over the body or oedema. There are few minor or indirect symptoms associated with the syndrome as well: and those include weight gain, fatigue, and greasy or foamy texture of the urine. In case of further complications of this disease, various infections can be acquired by the patient that can deteriorate the condition of the patient significantly. Different kidney disorders can lead to nephrotic syndrome, and the minimal change disease can be considered an important one. In the case study for this assignment the patient under consideration has also been going through severe nephrotic syndrome due to the minimal change disease (Ruggenenti et al. 2014).
Nephrotic range proteinuria can occur via various disease trajectories, however the minimal change disease of the kidney can be considered one of the most frequently reported one. It has to be mentioned that nephrotic syndrome is an umbrella term that encompasses three different disease conditions that a patient goes through, namely nephrotic range proteinuria, low serum albumin level, and multiple edema throughout the body. The manifestation of nephrotic syndrome is a time taking process and there are many pathological changes that occur throughout the procedure.
Elaborating more on the pathophysiology it has to be mentioned that the glomerular filtration barrier only lets 0.1% of the plasma albumin and according to that the glomerular urinary space has an albumin concentration of 3.5 mg per litre. Hence it can be stated that at par with this concentration the normal daily from a ruler filtration rate or GF are for 150 litres the final urine will have 50 mg of album mean on a daily basis, due to the protein albumin being re- absorbed by the tubules (Clement et al. 2011).
The onset of nephrotic syndrome begins with proteinuria which is caused directly by any structural changes or damage to the endothelial surface, glomerular basement membrane, or podocytes. In case of nephrotic syndrome proteinuria can be both selective and non selective, however in case of minimal change nephrotic syndrome which is the case for the patient in the case study the proteinuria is only of selective type.
Another very important pathological change that occurred in case in case of TC nephrotic syndrome is the edema. There are two particular hypotheses that define the pathogenesis of edema in case of nephrotic symptoms. The first hypothesis is underfill hypothesis that states that the loss of albumin due to the increased glomerular permeability leads to lower plasma colloid pressure, which is a capillary hydrostatic pressure causing swelling. On the other hand the alternative overfill hypothesis states that intrinsic defect in the renal tubules causes extreme decrease in the level of sodium excretion which in turn causes stimulation of the renal epithelial sodium reabsorption and causes the oedema. Another very common consequence of nephrotic syndrome can be the infections, the major cause of infection has been reported to be the urinary immunoglobulin loss, edema fluid acting as resource for microbes, protein deficiency, immunosuppressive therapy, and decreased bactericidal activity (Eckardt et al. 2013).
Pathological Changes Associated with Idiopathic Nephrotic Syndrome
Nephrotic syndrome is an amalgamation of various key symptomatic health disorders the management of this particular disease also incorporates various strategic interventions. The very first strategy in case of managing nephrotic syndrome patient begins with the nursing assessment. On a more elaborative note, the patient should be assessed critically for the clinical manifestations that will indicate at the security of the disease. Assessment must include the presence of edema and its spread (Gulati et al. 2010). The next assessment includes observing and documenting the body weight of the patient along with his vital signs. Followed by the identification of the presence of any pitting edema on the body of the patient concluding with the crucial inspection of the skin of the patient to look for any pallor, irritation, or breakdown. The next strategy for the management of the disease for the patient should incorporate nursing diagnosis based on the subjective and objective data. This will include measurement of excess fluid volume, risk assessment of imbalanced nutrition and impaired skin integrity due to edema, risk for infection and management of fatigue. Followed by this the next strategy for the patient must include the care and intervention planning based on the diagnosis. And the concluding strategy is to educate the patient of the implications and precautions associated with the disease (Fukudome et al. 2012).
It has to be mentioned that TC had been going through acute and severe manifestation of a variety of different symptoms and in order to develop the care plan for TC, the impact of each and every symptom on his health and welfare needs to be assessed. The frequent relapse associated with his proteinuria had the most impact on his health and caused the most suffering for him. Another most impactful health issue for him would be the Giardiasis and the watery stools as a result of which TC might feel extremely fatigued and a considerable abdominal pain as well. The edema of TC also demands attention in the care plan formulated for him followed by the impaired nutritional status of the patent. Lastly the patient had also been feeling ear pain along which will be needed to managed at the earliest and interventions to help the patient acquire normal growth. Lastly the care plan will also have to include the patient and family education to help them cope with the stress.
|
Nursing diagnosis |
Nursing outcome |
Intervention strategy |
Rationale |
Outcome evaluation |
|
Persisting proteinuria and frequent relapse |
The protein concentration of the urine of the patent will decrease significantly. |
· Administration of the corticosteroids. · Monitoring the fluid intake and output of the patient. |
· Continuing with the medication such as losartan and enalapril will help in reducing the proteinuria (Gulati et al. 2010). · The diligent monitoring and systematic documentation will reduce the risk of infection and facilitate the action of the medication. |
The lab reports showed visible decrease in the level of proteinuria. |
|
watery stools due to Giardia infection |
The watery stool and emesis will completely stop. |
· Assessing the patient for any abdominal discomfort and assessment of pain and distension level. · Administering pharmacological intervention that will slow peristalsis. · Administration of metronidazole |
· Will provide a clear idea regarding of the pain and distension to administer interventions. · It will aid in increasing the gut motility and will help in recovery (Prytu?a et al. 2010). · Will reduce the emesis and stop the occurrence of bloody stools by the antibiotic action on Giardia parasite. |
The patient completely relieved form watery stool and abdominal distension and the patient was free from any risk of further relapse of the diseases. |
|
Relieving the edema of the patient |
The patient will have improved skin integrity and the spread of the edema will increase effectively with no noticeable signs of relapse |
· Inspection of ski surface regularly for new onset and the progress status. · Provide pillows and padding to the patients and change the coverings regularly (Ruggenenti et al. 2014). |
· Will help in judging the efficacy of the ongoing treatment trajectory and will help in tracking the response rate of the patient to the therapies (Prytu?a et al. 2010). · The pillows and padding will avoid the exacerbation of the existing or recovering edemas ad changing the coverings will ensure that the patient does not get any infection |
the edema reduced visibly and the skin integrity of the patient was restored gradually. |
|
Improvement of the nutritional status |
The patient will gain more healthy weight and will be relieved from the persistent fatigue. |
· Incorporation of nutrient and antioxidant rich diet. · Monitor the body weight fluctuations diligently. |
· Will improve the nutritional state of the patient and will help counteract the negative effects of the immunosuppressive therapy (Takei et al. 2012). · The monitoring will help in keeping track of the progress of the diet and the response of the patient to it. |
The patient gained more healthy weight and the persistent fatigue was reduced. |
|
Ear and abdominal pain |
The patient will be relieved from the pain he had been feeling. |
Administration of different NSAID pain management drugs like ibuprofen. |
Will help relieve the extreme pain of the patent without the added burden of steroidal drugs (Takei et al. 2012). |
The patient will cease to feel acute abdominal or ear pain |
|
Restricted normal growth due to impaired nutritional status |
The patient will regain healthy weight and he growth processes will resume |
Introducing the patient to a fluid based high protein low salt diet. |
This particular dietary plan will help the patient regain the desired nutritional status and will not have any impact on the minimal change disease. |
The patient regained healthy weight, fatigue subsided and the normal growth pattern of the patient achieved. |
|
Stress and anxiety of the patient and family |
The patient and family will understand how to cope with the diseases effectively and the anxiety and stress will subside. |
Patient education and counseling support to the family and the patient when necessary for them to understand the disease and how to cope with it more effectively. |
Involving the family members in the patient education will empower the patient and will help both the family members and the patient discover the best and most optimal management (Gulati et al. 2010). |
The patient and family members will be more unedrstnding of the management of this disease and will approach recovery faster. |
Reference:
Clement, L.C., Avila-Casado, C., Macé, C., Soria, E., Bakker, management, Kersten, S. and Chugh, S.S., 2011. Podocyte-secreted angiopoietin-like-4 mediates proteinuria in glucocorticoid-sensitive nephrotic syndrome. Nature medicine, 17(1), p.117.
Eckardt, K.U., Coresh, J., Devuyst, O., Johnson, R.J., Köttgen, A., Levey, A.S. and Levin, A., 2013. Evolving importance of kidney disease: from subspecialty to global health burden. The Lancet, 382(9887), pp.158-169.
Fukudome, K., Fujimoto, S., Sato, Y. and Kitamura, K., 2012. Comparison of the effects of intravenous methylprednisolone pulse versus oral prednisolone therapies on the first attack of minimal?change nephrotic syndrome in adults. Nephrology, 17(3), pp.263-268.
Gulati, A., Sinha, A., Jordan, S.C., Hari, P., Dinda, A.K., Sharma, S., Srivastava, R.N., Moudgil, A. and Bagga, A., 2010. Efficacy and safety of treatment with rituximab for difficult steroid-resistant and-dependent nephrotic syndrome: multicentric report. Clinical Journal of the American Society of Nephrology, 5(12), pp.2207-2212.
Lombel, R.M., Gipson, D.S. and Hodson, E.M., 2013. Treatment of steroid-sensitive nephrotic syndrome: new guidelines from KDIGO. Pediatric nephrology, 28(3), pp.415-426.
Mason, P.D. and Hoyer, P.F., 2014. Minimal change nephrotic syndrome. Comprehensive Clinical Nephrology E-Book, p.208.
McCarthy, E.T., Sharma, M. and Savin, V.J., 2010. Circulating permeability factors in idiopathic nephrotic syndrome and focal segmental glomerulosclerosis. Clinical Journal of the American Society of Nephrology, 5(11), pp.2115-2121.
Prytu?a, A., Iijima, K., Kamei, K., Geary, D., Gottlich, E., Majeed, A., Taylor, M., Marks, S.D., Tuchman, S., Camilla, R. and Ognjanovic, M., 2010. Rituximab in refractory nephrotic syndrome. Pediatric Nephrology, 25(3), pp.461-468.
Ruggenenti, P., Ruggiero, B., Cravedi, P., Vivarelli, M., Massella, L., Marasà, M., Chianca, A., Rubis, N., Ene-Iordache, B., Rudnicki, M. and Pollastro, R.M., 2014. Rituximab in steroid-dependent or frequently relapsing idiopathic nephrotic syndrome. Journal of the American Society of psychology, 25(4), pp.850-863.
Takei, T., Itabashi, M., Moriyama, T., Kojima, C., Shiohira, S., Shimizu, A., Tsuruta, Y., Ochi, A., Amemiya, N., Mochizuki, T. and Uchida, K., 2012. Effect of single-dose rituximab on steroid-dependent minimal-change nephrotic syndrome in adults. Nephrology Dialysis Transplantation, 28(5), pp.1225-1232.
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