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This document is a case study of a woman with acute kidney injury, likely caused by a reaction to penicillin. It includes detailed questions related to the possible causes, medical treatments, and dietary considerations for her condition.
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> 28-1 CASE Woman with Acute Kidney Injury STUDY Catherine Garber is a 42-year-old office manager admitted to the examples of other medical problems that can cause acute hospital’s in...
> 28-1 CASE Woman with Acute Kidney Injury STUDY Catherine Garber is a 42-year-old office manager admitted to the examples of other medical problems that can cause acute hospital’s intensive care unit. She was first seen in the emergency kidney injury. department with severe edema, headache, nausea and vomiting, 2. What medications may the physician prescribe to treat and a rapid heart rate. She reported an inability to pass more than Mrs. Garber’s edema and hyperkalemia? What recommenda- minimal amounts of urine for the past 2 days. Her son, who drove tion is likely regarding her continued use of penicillin? her to the emergency department, reported that she had missed work for several days and seemed confused and unusually tired. 3. What concerns should be kept in mind when determining Laboratory tests revealed elevated serum creatinine, BUN, and Mrs. Garber’s energy, protein, fluid, and electrolyte needs potassium levels. After learning from her medical history that Âduring acute kidney injury? How would dialysis treatment alter Mrs. Garber had begun taking penicillin in the previous week, the recommendations? physician diagnosed acute kidney injury, probably caused by a 4. After treatment begins, Mrs. Garber suddenly begins produc- reaction to the medication. Mrs. Garber is 5 feet 3 inches tall and ing copious amounts of urine. How may this development alter weighs 125 pounds. dietary treatment? 1. Describe the probable reason for Mrs. Garber’s inability to As you read through the discussion of chronic kidney disease, produce urine. Is her reaction to penicillin considered a pre- c onsider how Mrs. Garber’s diet would need to change if her kidney renal, intrarenal, or postrenal cause of kidney injury? Give problems became chronic. sodium.15 Patients undergoing dialysis may be allowed more liberal intakes. As mentioned previously, oliguric patients who experience diuresis at the beginning of the recovery period may need electrolyte replacement to compensate for uri- nary losses. Enteral and Parenteral Nutrition Many patients need nutrition support to obtain ad- equate energy and nutrients. Enteral support (tube feeding) is preferred over paren- teral nutrition because it is less likely to cause infection and sepsis. Although most patients can tolerate standard enteral formulas, some enteral formulas designed for patients with acute kidney injury are more calorically dense and have either higher or lower protein and electrolyte concentrations than standard formulas.16 Total par- enteral nutrition is necessary only if patients are severely malnourished or cannot consume food or tolerate tube feedings for an extended period. REVIEW IT Discuss the potential causes and effects of acute kidney injury and describe the approaches to treatment for this condition. Acute kidney injury is characterized by a rapid decline in kidney function, causing a buildup of fluid, electrolytes, and nitrogenous wastes in the blood. Causes of acute kidney injury may in- volve prerenal, intrarenal, or postrenal factors. Consequences may include fluid and electrolyte imbalances and uremia. If hyperkalemia develops, it can alter heart rhythm and lead to heart failure. Acute kidney injury is treated with medications, dialysis, and dietary modifications. Case Study 28-1 checks your understanding of acute kidney injury. 28.4 Chronic Kidney Disease LO 28.4 Describe the potential causes and consequences of chronic kidney disease, its medical treatment, and nutrition therapy for this condition. Unlike acute kidney injury, in which kidney function declines suddenly and rap- idly, chronic kidney disease is characterized by gradual, irreversible loss of kid- ney function that results from long-term disease or injury. Because the kidneys have a large functional reserve—they are able to increase their workload to meet demands—chronic kidney disease typically progresses over many years without chronic kidney disease: a condition characterized by the gradual, irreversible loss of kidney function resulting from causing symptoms. Patients are often diagnosed late in the course of illness, after long-term disease or injury; also called chronic renal failure. most kidney function has been lost. 800 Chapter 28 Kidney Diseases Copyright 2021 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. The most common causes of chronic kidney disease are diabetes mellitus and TABLE 28-3Clinical Effects of Chronic hypertension, which are estimated to cause 45 and 27 percent of cases, respec- Kidney Disease tively.17 Other conditions that lead to chronic kidney disease include inflamma- tory, immunological, and hereditary diseases that directly involve the kidneys. Early Stages Chronic kidney disease affects approximately 13 percent of the U.S. population.18 Anorexia Exercise intolerance Consequences of Chronic Kidney Disease In the early stages of Fatigue chronic kidney disease, the functional nephrons compensate for those that are Headache lost or damaged: they enlarge and filter blood more rapidly so that they are able Hypercoagulation to handle the extra workload. As more nephrons deteriorate, however, there is ad- Hypertension ditional work for the remaining nephrons. The overburdened nephrons continue Proteinuria, hematuria (blood in urine) to degenerate until eventually the kidneys are unable to function adequately, re- sulting in kidney failure. Once the extent of kidney damage necessitates active Advanced Stages treatment—either dialysis or a kidney transplant—the condition is classified as Anemia, bleeding tendency end-stage renal disease. Without intervention at this stage, an individual cannot Cardiovascular disease survive. The clinical effects of chronic kidney disease are often nonspecific (see Confusion, mental impairments Table 28-3), which may delay diagnosis of the condition. Electrolyte imbalances Chronic kidney disease is evaluated based on the glomerular filtration rate Fluid retention, edema (GFR), the rate at which the kidneys form filtrate, and the degree of albuminuria, the Hormonal abnormalities amount of albumin lost in urine daily.19 GFR is considered the best index of overall Itching kidney function, whereas albuminuria reflects the extent of kidney damage and cor- Metabolic acidosis relates well with disease progression and health risks. Table 28-4 shows how chronic Muscle wasting kidney disease is classified according to estimated GFR. Other laboratory measures Nausea and vomiting that help to assess kidney function include tests of urine quality, serum electrolyte Peripheral neuropathy and BUN levels, and the ratio of albumin to creatinine in a urine sample.20 Protein-energy malnutrition Reduced immunity Altered Electrolytes and Hormones As the GFR falls, the increased activity of the Renal osteodystrophy remaining nephrons is often sufficient for maintaining electrolyte excretion; thus, fluid and electrolyte imbalances may not develop until the fourth or fifth stage of chronic kidney disease. A number of hormonal adaptations also help to regulate electrolyte levels, but these changes may cause complications of their own. The increased secretion of aldosterone helps to prevent increases in serum potassium but contributes to fluid overload and the development of hypertension (in pa- tients who were not previously hypertensive). Increased secretion of parathyroid hormone helps to prevent elevations in serum phosphate but contributes to bone loss and the development of renal osteodystrophy, a bone disorder common in renal patients. Electrolyte imbalances are likely when the GFR is very low (below 5 milliliters per minute), when hormonal adaptations are inadequate, or when intakes of water or electrolytes are either very restricted or excessive. TABLE 28-4 Evaluation of Chronic Kidney Diseasea Stage of GFRb Disease Description (mL/min per 1.73 m 2) 1 Kidney damage with normal or high GFR $90 2 Mildly decreased GFR 60–89 3a Mildly to moderately decreased GFR 45–59 end-stage renal disease: an advanced stage of chronic 3b Moderately to severely decreased GFR 30–44 kidney disease in which dialysis or a kidney transplant is 4 Severely decreased GFR 15–29 necessary to sustain life. 5 Kidney failure ,15 (or undergoing dialysis) glomerular filtration rate (GFR): the rate at which filtrate is formed within the kidneys, normally about 125 mL/min in a A complete assessment of chronic kidney disease takes into account the likelihood of health risk, as indicated by the healthy young adults. degree of albuminuria and other markers of kidney damage. parathyroid hormone: a protein hormone secreted b Glomerular filtration rate, or GFR, is usually estimated using the Modification of Diet in Renal Disease study equation, by the parathyroid glands that helps to regulate serum which is based on serum creatinine levels, age, sex, body size, and ethnicity. Normal GFR averages 125 mL/min in young concentrations of calcium and phosphate. adults and declines with age. SOURCES: L. A. Inker and coauthors, KDOQI U.S. commentary on the 2012 KDIGO clinical practice guideline for the renal osteodystrophy: a bone disorder that develops in evaluation and management of CKD, American Journal of Kidney Diseases 63 (2014): 713–735; P.E. Stevens and A. Levin, patients with chronic kidney disease as a result of increased Evaluation and management of chronic kidney disease: Synopsis of the kidney disease: improving global outcomes 2012 secretion of parathyroid hormone, reduced serum calcium, clinical practice guideline, Annals of Internal Medicine 158 (2013): 825–830. acidosis, and impaired vitamin D activation in the kidneys. Chronic Kidney Disease 801 Copyright 2021 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Because the kidneys are responsible for maintaining acid–base balance, acido- sis often develops in chronic kidney disease. Although usually mild, the acidosis exacerbates renal bone disease because compounds in bone (for example, protein and phosphates) are released to buffer the acid in blood. Uremic Syndrome Uremia may develop during the final stages of chronic kid- ney disease, when the GFR falls below about 15 milliliters per minute.21 As men- tioned previously, the many complications that result from uremia are collectively known as the uremic syndrome. Clinical effects may include the following: Hormonal imbalances. Diseased kidneys are unable to produce erythropoi- etin, causing anemia. Reduced production of active vitamin D contributes to bone disease. Altered levels or activities of various other hormones may upset blood glucose regulation, growth, and reproductive function (includ- ing menstruation and sperm production). Altered heart function/increased heart disease risk. Fluid and electrolyte imbal- ances result in hypertension, arrhythmias, and eventual heart muscle en- largement. Excessive parathyroid hormone secretion leads to calcification of arteries and heart tissue. Patients with uremia are at increased risk of stroke, heart attack, and heart failure. Neuromuscular disturbances. Initial symptoms may be mild, and include mal- aise, irritability, and altered thought processes. Later effects include muscle cramping, restless leg syndrome, sensory deficits, tremor, and seizures. Other effects. Defects in platelet function and clotting factors prolong bleed- ing time and contribute to bruising, GI bleeding, and anemia. Skin changes include increased pigmentation and severe pruritus (itchiness). Many pa- tients have suppressed immune responses and are at high risk of developing infections. Malnutrition The metabolic derangements that occur in chronic kidney disease con- tribute to protein-energy wasting, a syndrome characterized by losses of muscle mass and energy reserves. The wasting occurs, in part, because the uremia-induced changes that accompany chronic kidney disease (such as chronic inflammation, metabolic acidosis, and hormonal disorders) lead to the breakdown of body pro- teins and negative nitrogen balance.22 In addition, patients with chronic kidney disease often eat poorly because of anorexia, dietary restrictions, depression, and the dietary challenges of other diseases. Nutrient losses contribute to malnutrition and may be a consequence of dialysis, frequent blood draws, or bleeding abnor- malities. A screening method sometimes used for assessing PEM risk is the Subjec- tive Global Assessment, described in Chapter 17 (Table 17-3 on p. 538). Treatment of Chronic Kidney Disease The goals of treatment for pa- tients with chronic kidney disease are to slow disease progression and prevent or alleviate complications. Depending on the stage of illness, potential problems in- clude fluid and electrolyte imbalances, acidosis, uremia, anemia, protein-energy wasting, and nutrient deficiencies. Once kidney disease reaches the final stages, dialysis or a kidney transplant is necessary to sustain life. Drug Therapy for Chronic Kidney Disease Medications help to control some of the complications associated with chronic kidney disease. Treatment of hyper- tension is critical for preventing disease progression and reducing cardiovascular disease risk; thus, antihypertensive drugs are usually prescribed (see Chapter 27). Some antihypertensive drugs (such as ACE inhibitors) can reduce proteinuria, helping to prevent additional kidney damage. Anemia is usually treated by in- jection or intravenous administration of erythropoietin (epoetin). Other drug treatments may include phosphate binders (taken with food) to reduce serum protein-energy wasting: a syndrome characterized by losses of muscle mass and energy reserves that result from phosphate levels, sodium bicarbonate to reverse acidosis, and c holesterol-lowering the complications of kidney disease. medications. 802 Chapter 28 Kidney Diseases Copyright 2021 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Dialysis Dialysis replaces kidney function by removing excess fluid and wastes from the blood. In hemodialysis, the blood is circulated through a dialyzer (arti- ficial kidney), where it is bathed by a dialysate, a solution that selectively removes fluid and wastes. In peritoneal dialysis, the dialysate is infused into a person’s peritoneal cavity, and the blood is filtered by the peritoneum (the membrane sur- rounding the abdominal cavity). After several hours, the dialysate is drained, re- moving unneeded fluid and wastes. Highlight 28 provides additional information about dialysis. Nutrition Therapy for Chronic Kidney Disease The patient’s diet strongly influences disease progression, the development of complications, and serum levels of nitrog- enous wastes and electrolytes. Because the dietary measures for chronic kidney disease are complex and nutrient needs change frequently during the course of ill- ness, a dietitian who specializes in renal disease is best suited to provide nutrition therapy. Table 28-5 summarizes the general dietary guidelines for patients in differ- ent stages of illness. As patients’ needs vary considerably, actual recommendations should be based on the results of a careful and complete nutrition assessment. Energy Because malnutrition is a common complication of chronic kidney dis- ease, patients are advised to consume enough energy to maintain a healthy body weight. Individuals at risk of protein-energy wasting should consume foods with hemodialysis (HE-moe-dye-AL-ih-sis): a treatment that high energy density; some malnourished patients may require oral supplements removes fluids and wastes from the blood by passing the blood through a dialyzer. or tube feedings to maintain an appropriate weight. Wasting is more prevalent dialyzer (DYE-ah-LYE-zer): a machine used in hemodialysis to during maintenance dialysis than in earlier stages of illness.23 Note that obesity filter the blood; also called an artificial kidney. has been associated with disease progression, and therefore some obese patients dialysate (dye-AL-ih-sate): the solution used in dialysis to may benefit from weight loss.24 draw fluids and wastes from the blood. Most dialysates used in peritoneal dialysis contain glucose in order to draw peritoneal (PEH-rih-toe-NEE-al) dialysis: a treatment that f luid from the blood to the peritoneal cavity by osmosis; on average, about removes fluids and wastes from the blood by using the body’s peritoneal membrane as a filter. 64 percent of this glucose is absorbed.25 The kcalories from glucose (as many as high energy density: a high number of kcalories per unit 600 kcalories daily) must be included in estimates of energy intake. Weight gain is weight of food; foods of high energy density are generally sometimes a problem when peritoneal dialysis continues for a long period. high in fat and low in water content. TABLE 28-5 Dietary Guidelines for Chronic Kidney Diseasea Nutrient Predialysis (stages 4–5) Hemodialysis Peritoneal Dialysis Energy 35 for ,60 years old 35 for ,60 years old 35 for ,60 years old (kcal/kg of body 30–35 for $60 years old 30–35 for $60 years old 30–35 for $60 years old weight) (or as necessary to maintain a (or as necessary to maintain a (or as necessary to maintain a healthy weight) healthy weight) healthy weight) Note: The energy intake includes kcalories absorbed from the dialysate. Protein 0.6–0.75 1.2 1.2–1.3 (g/kg of body weight) ($50% high-quality proteins) ($50% high-quality proteins) ($50% high-quality proteins) Fat As necessary to maintain a healthy As necessary to maintain a healthy As necessary to maintain a healthy lipid profile lipid profile lipid profile Fluid (mL/day) Unrestricted if urine output is Urine output plus 500–1000 mL 2000–3000; unrestricted in some cases normal Sodium (mg/day)