Upon completion of the CE activity, learners will be able to:
- Describe the key factors associated with the development of chronic kidney disease.
- Explain the pathophysiology and clinical manifestations for patients with chronic kidney disease.
- Differentiate between the different stages of chronic kidney disease.
- Understand the nursing and medical management of patients with chronic kidney disease.
This course is designed to help the nurse recognize and manage chronic kidney disease.
Terms related to Renal Alterations:
- Azotemia- increased nitrogenous waste products in blood
- Anuria- total urine output less than 50-100ml over 24hrs
- Anasarca- generalized edema
- Bacteriuria- bacteria in the urine, >100,000 colonies/ml
- Dysuria- discomfort with micturition
- Enuresis-involuntary voiding during sleep
- Frequency- the feeling of needing to void often
- Hematuria- red blood cells in the urine
- Hesitancy- difficulty initiating the flow of urine
- Micturition- voiding or urination
- Minimal urine output- 30ml/hr for adults
- Nocturia- awakening to void at night
- Oliguria- decreased urine output (less than 500ml over 24 hrs)
- Polyuria-increased urine output (>2000ml over 24 hr)
- Proteinuria- protein in the urine
- Renal glycosuria- excretion of glucose in the urine
- Uremia- increased urea levels in blood
- Urgency- sudden onset of immediate feeling to void
Kidney disease results when the kidneys cannot filter out the body’s metabolic waste or perform regulatory functions efficiently. Chronic kidney disease (CKD) is an umbrella term that consists of kidney damage or decreased glomerular filtration rate (GFR) lasting for three or more months. There are five stages of CKD, based on the patient’s GFR. A normal GFR is 125ml/min/1.73 m2. Untreated CKD can result in end-stage renal disease (ESRD), the retention of uremic waste products, and the need for renal replacement therapies such as dialysis or kidney transplantation (Hinkle & Cheever, 2018). The stages of CKD are:
Stage 1 (Kidney damage)
- GFR is 90 mL/min/1.73 m2 or above with minor kidney damage.
Stage 2 (Mild kidney damage)
- GFR is 60-89 mL/min/1.73 m2.
Stage 3 (Moderate kidney damage)
- GFR is 30-59 mL/min/1.73 m2 with a moderate decrease in renal function.
Stage 4 (Severe kidney damage)
- GFR is 15-29 mL/min/1.73 m2 with a severe decrease in renal function.
Stage 5 (ESRD, permanent kidney damage)
- Also known as chronic renal failure (CRF) or end-stage kidney disease (ESKD)
- GFR is < 15 mL/min/1.73 m2 (Hinkle & Cheever, 2018).
Recent research reports that 10% of the United States population over the age of 20 have CKD. Diabetes is the primary cause of CKD. More than 35% of American diabetics over the age of 20 have CKD. The second leading cause is hypertension, followed by glomerulonephritis, pyelonephritis, polycystic kidney disease, and renal cancers. More than 20% of the U.S. population aged 20 years and older with hypertension have CKD (Hinkle & Cheever, 2018).
1 in 3 American adults is at risk for kidney disease. Research clearly shows that diabetes and hypertension are the two leading risk factors for CKD. Further, recent research shows that a family history of kidney failure and advancing age (60 and older) increases patients’ risk for kidney disease. An albumin creatinine ratio (ACR) is a simple urine test that can help screen for kidney disease. The ACR measures the amount of protein (albumin) leaking out of the kidneys into the urine. Healthy kidneys should not excrete any protein, but when the amount gets higher than 25 mg/dL (called microalbuminuria), this indicates early kidney damage. Another screening test, the GFR, shows how effectively the kidneys are removing waste products from the blood (National Kidney Foundation, 2019a).
The nurse should educate patients about drinking two to three liters of water daily to keep healthy kidneys hydrated. Because diabetes and hypertension can both lead to kidney disease, patients need to make sure they are compliant with their diabetic and high blood pressure medications to prevent damage to their healthy kidneys (National Kidney Foundation, 2019a).
Anatomy and Physiology
To fully understand CKD, it is critical to remember the blood pathway through the kidneys (see Figure 1 below). Blood enters the kidney via the aorta to each renal artery→ arterial branches →afferent arterioles→ glomerulus →leaves through efferent arterioles →then divides into two networks: peritubular capillaries & vasa recta (which rejoin to form the venous branches)→exit via the renal vein →empties into the inferior vena cava. The kidneys receive 20% to 25% of the total cardiac output at a time. (Hinkle & Cheever, 2018).
Kidneys are bean-shaped, highly vascular, and brownish-red in color (see Figure 2 below). They are typically located bilaterally at the T12-L3 levels of the spine. The right kidney is located slightly lower than the left kidney in most people. Aside from urine formation, the kidneys are also responsible for specific functions such as:
- The regulation of electrolytes, specifically calcium and phosphorus balance.
- The regulation of fluid volume and blood pressure.
- The control of acid-base balance.
- The secretion of prostaglandins.
- Erythropoiesis (The production of red blood cells).
- The synthesis of vitamin D to an active form.
- The excretion of foreign substances (medications, poisons, food additives, etc.) (Hinkle & Cheever, 2018).
The ureters are responsible for the peristaltic contraction of smooth muscles. The bladder is a muscular sac, which holds about 400 to 500ml of urine at a time in most adults. The urethra arises from the base of the bladder and is also known as the urinary opening.
Each of the kidneys has about 1-3 million nephrons (see Figure 3 below). Nephrons are composed of the renal corpuscle (glomerulus & Bowman’s capsule) and tubular structures (proximal, loop of Henle, and distal tubules). They are the functional unit of the kidney and are responsible for urine formation. Usually, adult kidneys excrete 1500 to 2000ml of urine daily depending on the amount and type of fluid intake, the amount of perspiration, environmental effects, and the presence of vomiting or diarrhea (Hinkle & Cheever, 2018).
In the case of CKD, the function of the nephrons starts to decline, which reduces the filtration rate and urine output. Primary causes of CKD include:
- Diabetes mellitus
- Chronic glomerulonephritis
- Pyelonephritis or other infections
- Hereditary lesions such as polycystic kidney disease
- Obstruction of the urinary tract, such as renal cancers
- Vascular disorders
- Medications or toxic agents (non-steroidal anti-inflammatory drugs [NSAIDs], aminoglycosides [gentamicin], etc.) (Hinkle & Cheever, 2018).
In addition to the previously mentioned microalbuminuria, other urinary symptoms of early CKD include proteinuria, polyuria, and nocturia. As it progresses, CKD typically results in reduced urine output, which can lead to excess fluid, electrolyte imbalances, metabolic acidosis, and accumulation of urea and toxins in the body (Hinkle & Cheever, 2018). The most advanced form of CKD, ESRD affects the entire human body. Below are ESRD manifestations for each body system:
Neurological: lethargy & daytime drowsiness, inability to concentrate or short attention span, seizures, slurred speech, asterixis, tremors, twitching, or jerky movements, myoclonus, ataxia, paresthesias, and coma.
Cardiovascular: cardiomyopathy, hypertension, tachycardia, peripheral edema, heart failure, uremic pericarditis, pericardial effusion, and cardiac tamponade.
Respiratory: tachypnea, deep signing, yawning, Kussmaul’s respirations, shortness of breath, pulmonary edema, pleural effusion, depressed cough reflex, and crackles.
Hematological: anemia, abnormal bleeding, and bruising.
Gastrointestinal: anorexia, nausea and vomiting, metallic taste in the mouth, changes in taste acuity and sensation, uremic colitis (diarrhea), uremic gastritis with possible gastrointestinal bleeding, constipation, uremic fetor (urine-like odor on the breath), and stomatitis.
Urinary: oliguria, anuria, hematuria, and cloudy urine.
Integumentary: decreased skin turgor, yellow-gray pallor, dry skin, pruritus, ecchymosis, purpura, soft tissue calcifications, and uremic frost (development of tiny urea crystals on the skin).
Musculoskeletal: muscle weakness & cramping, bone pain, pathological fractures, and renal osteodystrophy (bone deformation).
Reproductive: decreased fertility, infrequent or absent menses, reduced libido, and impotence.
Psychological: emotional lability, depression, anxiety, suicidal behaviors, denial, dependence and independence conflict, and body image changes (Hinkle & Cheever, 2018).
Although there are many diagnostic tests to help identify kidney damage, a renal biopsy is the gold standard test to diagnose CKD. Other diagnostic tests include urinalysis with microscopic exam, urine microalbuminuria, serum renal function tests (blood urea nitrogen [BUN], creatinine [Cr], and GFR), serum electrolytes (sodium, potassium, magnesium, phosphorus, and calcium), creatinine clearance via 24-hr urine output, serum complete blood cell count (CBC), blood gases to detect metabolic acidosis, parathyroid hormone, and a renal ultrasound (Hinkle & Cheever, 2018).
Treatment and Nursing Considerations:
The treatment of chronic kidney disease includes monitoring weight, intake and output, and serum BUN, electrolytes, and Cr levels. Nutritional restrictions on sodium, potassium, and protein may be necessary, so the nurse must be prepared to spend time educating the patient about diet and nutrition. Patients must avoid potentially harmful medications and substances such as NSAIDs, contrast dyes, illegal drugs, and smoking. Much pharmacological management is aimed at control of the underlying disease processes such as diabetes mellitus and hypertension. Lipid management is usually a target of therapy to reduce morbidity from atherosclerosis disease, which may help prevent complications of kidney damage. Blood pressure medications such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) slow the progression of CKD in both diabetics and nondiabetics. Erythropoietin and calcitriol are two hormones produced by the kidneys, which often need to be replaced or augmented in CKD.
For patients with ESRD, it is critical that the nurse monitor for hypertension, tachycardia, dysrhythmias, and tachypnea. Daily weights are a good indicator of fluid loss or gain, so the nurse should educate the patient to weigh themselves at the same time and to use the same scale every day. If one kg (two to three pounds) of daily weight gain is noted, this indicates that the patient is retaining 1000ml of extra fluid. Fluid restrictions may be required with ESRD if the patient is in volume overload. Further, the nurse should expect to monitor for metabolic acidosis, proteinuria, hematuria, urinary casts, and urine specific gravity in patients with ESRD (Hinkle & Cheever, 2018).
Neurological assessment is critical, so the nurse should closely monitor the level of consciousness as uremia may alter this and lead to confusion or coma. ESRD clients are also at higher risk for developing infections, so the nurse will monitor CBC and vital signs for leukocytosis or fever. Furthermore, ESRD clients tend to be oliguric or anuric, so the nurse should monitor urine output and for fluid volume overload symptoms such as wheezing, rhonchi, edema, peripheral swelling, hypertension, tachycardia, and jugular venous distention. Frequent oral care will help to prevent stomatitis and decrease discomfort. A buildup of urea can lead to uremic frost and pruritus, so appropriate skincare with medicated creams and lotions may be required.
Further, ESRD patients are at risk for chronic anemia due to inadequate erythropoietin production by the kidneys, so hemoglobin and hematocrit should be monitored regularly. Exogenous growth factors such as epoetin alfa (Procrit, Epogen) can be administered to stimulate red blood cell production. Folic acid and ferrous sulfate (iron) may also increase healthy red blood cell production. Blood transfusions may be needed with acute blood loss or severe, symptomatic anemia (Hinkle & Cheever, 2018).
Many times, ESRD patients develop hyperkalemia, hypermagnesemia, or hyperphosphatemia as the kidneys are no longer able to excrete excess potassium, magnesium, and phosphorus. The nurse should expect to monitor serum potassium (reference range 3.5-5 mEq/L), magnesium (reference range 1.7-2.2 mg/dL), and phosphorus (reference range 2.5-4.5 mg/dL) in these patients regularly. Hyperkalemia above 6 mEq/L can cause peaked T waves, flat P waves, widened QRS complexes, and prolonged PR intervals, so continuous cardiac monitoring is advised. Hyperkalemia can be treated by administering Kayexalate, a combination of 50% dextrose, regular insulin, and calcium gluconate intravenously, or hemodialysis. For hypermagnesemia, the nurse should be prepared to administer loop diuretics and calcium to lower magnesium levels and address resulting cardiac problems. Patients should be encouraged to avoid magnesium in antacids, laxatives, or enemas. In severe cases, patients should avoid foods high in magnesium. Phosphate binders such as lanthanum carbonate (Fosrenol), sevelamer (Renagel), and calcium carbonate can be given with meals to eliminate excess phosphorus from the body. Patients can limit phosphorus in their diet by decreasing whole grains, dairy products, and poultry. Hypertension can be improved with adherence to fluid and sodium restrictions, as well as the administration of diuretics and antihypertensives regularly or as needed. Hypervolemia often occurs in ESRD, although it can be prevented by complying with the prescribed fluid restriction and avoiding excess intravenous fluids. The patient should be encouraged to consume a low sodium diet and avoid antacids or cold medications containing sodium bicarbonate. A diuretic such as furosemide (Lasix) may be necessary. The nurse should encourage frequent rest periods and advise the patient to avoid large crowds and sick people to reduce infection risk (Hinkle & Cheever, 2018).
Hemodialysis or peritoneal dialysis or renal transplantation is needed for ESRD patients (Hinkle & Cheever, 2018).
Diabetes is the leading cause of kidney damage. However, recent research highlights that only half of primary health care providers discuss CKD with their diabetic patients. It is critical to increase awareness amongst primary care providers and thus encourage early screening for CKD in diabetic patients. Therefore, future research is needed on the prevalence of CKD in adults with type 2 diabetes to optimize their care. To this end, the National Kidney Foundation has launched a multi-site cross-sectional study, Awareness, Detection, and Drug Therapy in Type 2 Diabetes Mellitus and Chronic Kidney Disease (ADD-CKD). The focus of this study is to assess how CKD is being identified and managed in type 2 diabetic patients, in the primary care setting, using a survey of 10,000 adult patients and their 500 primary care physicians (National Kidney Foundation, 2019b).
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