ASKEP CRF PDF

Lp Dan Askep CKD. pembahasan tentang ckd atau gagal ginjal Askep Ckd. Asuhan keperawatan CKD askep CKD+ANEMIA revisi 2. askep CKD+ANEMIA . H. pe] askep FH. vs] faire vs F; you Cr Loked] He looked CrF. and] whan he F. Metabolic acidosis is associated with many of the complications of chronic kidney disease (CKD), including bone disease, muscle protein catabolism, and.

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Metabolic acidosis is a common complication of chronic kidney disease and believed to contribute to a number of sequelae, including bone disease, altered protein metabolism, skeletal muscle wasting, and progressive GFR loss. Small trials in animal models and humans suggest a role for alkali therapy to lessen these complications.

Recent studies support this notion, although more definitive evidence is needed on the long-term benefits of alkali therapy and the optimal serum bicarbonate level. The role of dietary modification should also be given greater consideration. In addition, potential adverse effects of alkali treatment must be taken into consideration, including sodium retention and the theoretical concern of promoting vascular calcification.

This teaching case summarizes the rationale for and the benefits and complications of base therapy in patients with chronic kidney disease. Metabolic acidosis is associated with many of the complications of chronic kidney disease CKDincluding bone disease, muscle protein catabolism, and progressive glomerular filtration rate GFR loss. However, a definitive randomized clinical trial zskep not yet been performed. A year-old man with a history of sickle cell disease, hepatitis B, hypertension, and CKD stage 4 asmep seen in renal clinic.

He had a progressive decline in kidney function over 13 years with a urine protein-to-creatinine ratio of 1. His kidney function had been stable for the past 2 ctf. Medications included nifedipine 60 mg daily, calcitriol 0. Relevant laboratory data from one month prior and the day of the asep appear in Table 1. Conversion factors for units: Earlier urinalyses revealed a urine pH consistently above 6. Chronic metabolic acidosis presumed given the lack sskep confirmatory pH and pCO 2 and hyperkalemia in the setting of CKD, sickle cell disease, and distal nephron dysfunction.

The patient was started on oral sodium bicarbonate mg three times daily and returned to the clinic one month later. Nifedipine was crg to 90 mg daily. A basic metabolic panel revealed improvement in the serum bicarbonate Table 1. Calcitriol was increased to 1 mg daily due to the persistently elevated parathyroid hormone PTH level. A year later the patient was found to have decreasing kidney function thought to be secondary to progression of CKD and hypercalcemia.

After cessation of calcitriol and normalization of the serum calcium, kidney function improved. Crff was a slight increase in serum albumin, but no change in body weight 77 to 79 kg. Low serum bicarbonate has been associated with increased mortality in patients with moderate and advanced CKD, as well as among patients receiving both peritoneal dialysis PD and hemodialysis. Chronic acidosis results in negative calcium balance from bone buffering, which cf ameliorated by treatment with alkali.

However, in children askpe renal tubular acidosis, sustained alkali therapy attained and maintained normal stature. Selected adverse effects of chronic metabolic acidosis in chronic kidney disease, and evidence for alkali therapy. A large body of evidence drf that metabolic acidosis is an important contributor to muscle wasting in patients with CKD.

Treatment of Metabolic Acidosis in Patients With CKD

Acidosis impairs insulin and insulin-like growth factor IGF -1 signaling, leading to skeletal muscle protein breakdown via activation of caspase-3 and the ubiquitin-proteasome system. In patients with CKD stage 4, oral sodium bicarbonate increased albumin levels and mid-arm muscle circumference after 12 months. Metabolic acidosis may also contribute to the progression of CKD by promoting tubulointerstitial injury via ammonia-induced complement activation and endothelin and aldosterone activation.

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After 24 months, urine endothelin-1 excretion was significantly lower in the treatment group, as was the rate of eGFR decline. Even large doses of alkali appear to be well-tolerated in individuals without edema who have preserved urine output.

Given the variability of serum bicarbonate measurements, the presence of acidosis should be verified with a second measurement. In addition, in most cases the serum bicarbonate alone should not be the basis for starting treatment.

A blood gas should be obtained to verify the acid-base disturbance, especially if there is suspicion of a respiratory disorder.

A venous blood gas is sufficient for these purposes. In our patient with advanced CKD, treatment was appropriately begun after a second low serum bicarbonate measurement, although without a confirmatory blood gas. The initial prescribed dose was higher than we would generally recommend, but was tolerated in this patient with well-controlled hypertension askrp no edema.

The need for a high dose might have been predicted based on the inappropriately high urine pH indicative of a defect in urine acidification from sickle cell disease. The serum potassium normalized after starting alkali, which may have been partly been due to the kaliuretic effect of sodium bicarbonate.

Fortunately, the patient did not experience gastrointestinal side effects and was able to continue treatment with long-term maintenance of a normal to low-normal serum bicarbonate. Also consider sodium citrate if the patient does not tolerate sodium bicarbonate. We suggest using sodium bicarbonate to treat the chronic acidosis of CKD, usually starting with mg twice daily In a short-term intervention, each 0.

If a poor response is observed and medication adherence is confirmed, renal bicarbonate wasting should be evaluated by measuring the urine pH. The most common side effect of sodium bicarbonate is bloating because of generation of carbon dioxide in the gastrointestinal tract. Sodium citrate is an alternative as citrate is aske metabolized to bicarbonate without produce bloating.

However, it should be avoided in patients taking aluminum-containing antacids since citrate enhances intestinal aluminum absorption and increases the risk of aluminum toxicity.

Phosphorus binders, such as calcium acetate or carbonate and sevelamer carbonate, also contribute small quantities of exogenous base. In contrast, sevelamer hydrochloride may exacerbate acidosis; the base form is therefore most commonly used. Medications that impair net acid excretion, such as potassium-sparing diuretics and non-steroidal anti-inflammatory agents, should be avoided whenever possible. The importance of diet should also be considered. The typical Western diet, high in animal protein, has a large dietary acid load.

Conversely, a diet rich in fruits and vegetables contains greater quantities of base precursors. Increased fruit and vegetable consumption increased serum bicarbonate After 1 year, eGFR was not different between the 2 groups.

Therefore, in patients at low-risk for hyperkalemia, increased fruit and vegetable intake should be routinely considered, with careful monitoring of the serum potassium early in the intervention. The target serum bicarbonate with alkali therapy remains unclear. The goal set by KDOQI was opinion-based, and there are now intriguing data that a higher target may be preferable. The acid-inducing Western diet may increase tissue acidity without an observable change in plasma acid-base parameters.

Thirty days of oral sodium bicarbonate in patients with mildly reduced eGFR reduced plasma endothelin-1 and aldosterone without a change in blood acid-base parameters. However, increased fruit and vegetable intake seems a reasonable intervention given its numerous potential health benefits. Clearly, further studies are needed to better define the long-term effects of alkali therapy and to determine the efficacy of treating mild metabolic acidosis. Base administration in the form of sodium salts is not without potential complications, including worsened hypertension, volume overload, and congestive heart failure.

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However, less sodium retention occurs with sodium bicarbonate compared to equimolar sodium chloride. Thus, in certain patients the addition of a diuretic or the increase in diuretic dose may be needed to avoid volume overload. There is also the possibility of increased vascular calcification from systemic alkalinization.

This potentially serious complication has not been well studied. In animal and in vitro studies, metabolic acidosis inhibited extraskeletal calcification. Finally, it is important to consider the pill burden and lesser side effects associated with alkali.

Significant bloating or nausea may reduce appetite and food intake, which should be steadfastly avoided. The problems of high pill burden and polypharmacy have been well documented in the CKD population, and the impact of these additional pills should be considered on an individual basis. In summary, chronic metabolic acidosis is associated with increased morbidity and mortality in patients with CKD.

Existing evidence suggests alkali therapy might improve long-term outcomes in bone disease, muscle mass, and progression to ESRD. However, more data is needed to optimally guide treatment decisions.

The key teaching points are listed in Box 1. The authors declare that they have no relevant financial interests. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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See other articles in PMC that cite the published article. Abstract Metabolic acidosis is a common complication of chronic kidney disease and believed to contribute to a number of sequelae, including bone disease, altered protein metabolism, asksp muscle wasting, and progressive GFR loss. Table 1 Laboratory Data. Open in a separate window.

Treatment of Metabolic Acidosis in Patients With CKD

Diagnosis Chronic metabolic acidosis presumed given the lack of confirmatory pH and pCO 2 and hyperkalemia in the setting of CKD, sickle cell disease, and distal nephron dysfunction. Clinical Follow-up The patient was started on oral sodium bicarbonate mg three times daily and returned to the clinic one month later.

Table 2 Selected adverse effects of chronic metabolic acidosis in chronic kidney disease, and evidence for alkali therapy. Adverse effect Evidence for alkali therapy Bone disease Enhances bone resorption and impairs bone formation 48 Reduces calcium losses in pre-dialysis CKD; has benefit in children with RTA 20postmenopausal women with normal kidney function 21 and dialysis patients 22 Protein metabolism Decreases albumin synthesis, increases muscle proteolysis, and causes negative nitrogen balance 26 Decreases protein degradation and may increase albumin concentration.

Box 1 Key Teaching Points.

In patients with CKD, alkali therapy may decrease bone loss and protein degradation, increase muscle mass, and slow the progression of kidney disease. However, the optimal goal serum bicarbonate has not been defined. It is important to verify metabolic acidosis by a second measurement of serum bicarbonate and a venous blood gas before initiation of alkali therapy.