Kidney Conditions Chapter 59 PDF

59 LEARNING OUTCOMES 1. Plan collaborative care with the interprofessional team to promote urinary elimination in patients with kidney conditions. 2. Teach adults how to decrease the risk for kidney conditions. 3. Teach the patient and caregiver(s) about common drugs and other management strategies used for kidney conditions. 4. Plan patient- and family-centered nursing interventions to decrease the psychosocial impact caused by living with kidney conditions. 5. Apply knowledge of anatomy, physiology, and pathophysiology to provide evidence-based care for patients KEY TERMS abscess A localized collection of pus caused by an inflammatory response to bacteria in tissues and organs. acute glomerulonephritis Inflammation of the glomerulus that develops suddenly from an excess immunity response within the kidney tissues. dysuria Painful urination. hydronephrosis Abnormal enlargement of the kidney. hydroureter Abnormal distention of the ureter. nephrectomy Surgical removal of the kidney. nephrosclerosis Degenerative kidney disorder resulting from changes in kidney blood vessels. nephrostomy The surgical creation of an opening directly into the kidney; performed to divert urine externally and prevent further damage to the kidney when a stricture PRIORITY AND INTERRELATED CONCEPTS The priority concept for this chapter is: Elimination The Elimination concept exemplar for this chapter is Pyelonephritis. The interrelated concepts for this chapter are: Fluid and Electrolyte Balance Acid-Base Balance Immunity Pain 1436 UNIT XIV Interprofessional Collaboration Intake of N Urine output substances of substances K N K N K K N K K N Normal intake balanced with appropriate urine output N = sodium K = potassium = protein/nitrogen = water FIG. 59.1 Unbalanced body water, vent adjustments in urinary elimination. can lead to life-threatening outcomes. This chapter describes a variety of infectious and noninfectious kidney disorders, kid- ney tumors, and kidney trauma. Acute kidney injury (AKI) and chronic kidney disease (CKD) are discussed in Chapter 60. ELIMINATION CONCEPT EXEMPLAR: PYELONEPHRITIS In the healthy adult, urine is normally sterile. Urinary infection (UTI) is an infection in any part of this normally sterile system. Pyelonephritis occurs as a complication ascending urinary tract infection that spreads from der to the kidneys (Belyayeva & Jeong, 2021). It can be acute or chronic. Pyelonephritis interferes with urinary elimination, which is the excretion of waste from the body by the urinary system (as urine). Chapter 3 provides a summary of the concept of elimination in more detail. Pathophysiology Review Acute pyelonephritis is an active bacterial infection, whereas chronic pyelonephritis results from repeated or continued upper urinary tract infections that occur almost exclusively in patients who have anatomic abnormalities of the urinary tract. Bacterial infection causes local (e.g., kidney) and systemic (e.g., fever, aches, and malaise) inflammatory symptoms. In pyelonephritis, organisms move up from the urinary tract into the kidney tissue. This is more likely to occur refluxes from the bladder into the ureters and then to the kid- ney. Reflux is the reverse or upward flow of urine toward the renal pelvis and kidney. Infection also can be transmitted by CHAPTER pyelonephritis usually occurs with structural deformities, uri- nary stasis, obstruction, or reflux. Conditions that lead to urinary stasis include prolonged bed rest and paralysis. Obstruction can be caused by stones, kidney cancer, scarring from pelvic radia- tion or surgery, recurrent infection, or injury. Reflux may occur from scarring or result from anatomic anomalies. Reflux also results from bladder tumors, prostate enlargement, or urinary stones. Reduced bladder tone from diabetic neuropathy, spinal cord injury, and neurodegenerative diseases (e.g., spina bifida, multiple sclerosis) contributes to stasis and reflux. Pyelonephritis from an ascending infection may follow manipulation of the urinary tract (e.g., placement of a urinary catheter), particularly in patients who have reduced immu- nity or diabetes. In patients with chronic kidney stone disease, stones may retain organisms, resulting in ongoing infection and kidney scarring. Drugs, such as high-dose or prolonged use of NSAIDs, can lead to papillary necrosis and reflux. The most common pyelonephritis-causing infecting organ- ism among community-dwelling adults is Escherichia coli. Enterococcus faecalis is common in hospitalized patients. Both organisms are in the intestinal tract. Other organisms that cause pyelonephritis in hospitalized patients include Proteus mirabilis, Klebsiella species, and Pseudomonas aeruginosa. When the infec- tion is bloodborne, common organisms include Staphylococcus aureus and Candida and Salmonella species. Other causes of kidney scarring contributing to increased risk for pyelonephritis are inflammatory responses resulting from immunity excesses with antibody reactions, cell-mediated immu- nity against the bacterial antigens, or autoimmune reactions. Incidence and Prevalence Young females who are sexually active are the most commonly affected by acute pyelonephritis (Belyayeva, & Jeong, 2021). Hormonal changes as well as obstruction caused by the fetus during pregnancy make acute pyelonephritis more common during the second trimester and beginning of the third trimes- ter. Pregnant females are at high risk for premature delivery from acute pyelonephritis (Belyayeva & Chronic pyelonephritis is rarely characterized by infection alone, so the incidence and prevalence are linked to the under- lying condition or conditions that lead to relapsing inflamma- tory damage of the kidney. These conditions include congenital structural abnormality, neurogenic bladder dysfunction, and primary vesicoureteral reflux (urine flows from the bladder to the kidneys) (Belyayeva & Jeong, 2021). Interprofessional Collaborative Care Depending on the severity of the disease, pyelonephritis may be managed in any care setting and in the community. Hospitalization becomes necessary in cases of bacteremia or hemodynamic instability and when oral medication cannot be tolerated. Bacteremia occurs in approximately 10% of cases. Bacteremia is more common in older adult females and females with diabetes (Ayatollahi et al., 2021). The focus of care for patients with chronic pyelonephritis requires continuing tion to managing the structural or functional abnormality that contributes to recurrent infection and inflammatory 1438 UNIT XIV Interprofessional Collaboration or practices, may be masked through delay in seeking treatment or through vague, nonspecific responses to specific or direct questions. Encourage patients to tell their own story in familiar, comfortable language. Laboratory Assessment. Urinalysis shows a positive leukocyte esterase and nitrite dipstick test and the presence of white blood cells (WBCs) and bacteria. Occasional red blood cells (RBCs) and protein may be present. The urine is cultured to determine the specific organisms causing the infection and the susceptibility or resistance of the specific organisms to various antibiotics. The urine sample for culture and sensitivity testing is usually obtained by the clean-catch method. In patients with recurrent pyelonephritis, more specific testing of bacterial antigens and antibodies may help determine whether the same organism is responsible for the recurrent infections. Blood cultures may be obtained to determine the source and spread of infectious organisms. Other blood tests include the WBC count and differential of the complete blood count, as well as C-reactive protein and erythrocyte sedimentation rate (ESR) to determine immunity responses and presence of inflamma- tion. Serum tests of kidney function, such as blood urea nitro- gen (BUN) and creatinine, are used as baseline and to trend recovery or deterioration. Estimate of glomerular filtration rate (GFR) also is used to trend kidney function. Imaging Assessment. An x-ray of the kidneys, ureters, and bladder (KUB) or CT is performed to visualize anatomy, inflammation, fluid accumulation, abscess formation, and defects in kidneys and the urinary tract. These tests also identify stones, kidney tumors or cysts, or prostate enlargement. Urine reflux caused by incompetent bladder-ureter valve closure can be seen with a cystourethrogram. (See Chapter 57 for more information on imaging assessment.) Other Diagnostic Assessment. Other diagnostic tests include examining antibody-coated bacteria in urine, testing for certain enzymes (e.g., lactate dehydrogenase isoenzyme 5), and performing radionuclide renal scans. Examining urine for antibody-coated bacteria helps identify patients who may need long-term antibiotic therapy. High-molecular- weight enzymes in urine, such as lactate dehydrogenase isoenzyme 5, are present with any kidney tissue deterioration problem and give trend data. The renal scan can identify active pyelonephritis or abscesses in or around the kidney. A kidney biopsy may be performed to rule out less obvious causes of inflammation. NCLEX Examination Challenge 59.1 Physiological Integrity The nurse is caring for a newly admitted client. Which ment data would cause the nurse to suspect acute pyelonephritis? that apply. A. Urinary frequency B. Dysuria C. Oliguria D. Heart rate 120 beats/min E. Costovertebral angle tenderness CHAPTER Nephrectomy is a last resort when all other measures to clear the infection have failed. For patients with poor ureter valve clo- sure or dilated ureters, ureteroplasty (ureter repair or revision) or ureteral reimplantation (through another site in wall) preserves kidney function and eliminates infections. Preventing Chronic Kidney Disease Planning: Expected Outcomes. The patient is expected to conserve existing kidney function. Underlying genitourinary abnormalities must be identified and appropriate interventions taken to manage a current infection and the risk for subsequent infections. The approach by the urologist or nephrologist depends on signs and symptoms, as well as on patient history. Interventions. Specific antibiotics are ordered to treat the infection. Stress the importance of completing the drug therapy as directed. Discuss with the patient and family the importance of regular follow-up examinations and completing the recommended diagnostic tests. Blood pressure control slows the progression of kidney dysfunction. Ensure that the patient is able to detect adverse changes in blood pressure using community resources, such as free blood pressure readings at community settings or retail pharmacies. When pyelonephritis causes or worsens CKD, ensure a referral to a nephrologist for additional assessment and management (see CKD in Chapter 60). Encourage the patient to drink sufficient fluid during waking hours to prevent dehy- dration because dehydration could further reduce kidney func- tion. When dietary protein is restricted, a registered dietitian nutritionist (RDN) can help the family select appropriate food and proportions. Collaborate with the RDN, and reinforce the prescribed interventions. Care Coordination and Transition Management Pyelonephritis may cause fear and anxiety in the patient and family. The severity of the acute process and its potential to develop into a chronic process are frightening. The patient and the family need reassurance that treatment and preventive mea- sures can be successful. If no surgery is performed, the patient may need self-care, nutrition, and drug management at home. If surgery is performed, the patient may need help with incision care, self- care, and transportation for follow-up appointments. Self-Management Education. After assessing the patient’s and family’s understanding of pyelonephritis and its therapy, explain: possible side effects) any limitations after surgery community resources Advise the patient to complete all prescribed antibiotic reg- imens and to report any side effects or unusual symptoms to the primary health care provider rather than stopping the drugs. 1440 UNIT XIV Interprofessional Collaboration BOX 59.4 Secondary Glomerular Diseases and Syndromes Systemic lupus erythematosus (SLE) Sustained liver disease (hepatitis B or C, autoimmune hepatitis, and cirrhosis) Amyloidosis Mesangiocapillary glomerulonephritis (MCGN) Alport syndrome Vasculitis IgA nephropathy Wegener granulomatosis HIV-associated nephropathy Diabetic glomerulopathy HIV, Human immunodeficiency virus. Data from Muthu, V.R. (2018, Jan-Feb). Clinicopathological of glomerular diseases in adolescents: A single-center experience over 4 years. Retrieved from U.S. National Library of Medicine, National Institutes of Health. https://www.ncbi.nlm.nih.gov/pmc/arti- cles/PMC5830804/; and Radhakrishnan, J. (2023). Glomerular Evaluation and differential diagnosis in adults. UpToDate. February 7, 2023, from https://www.uptodate.com/contents/glomeru- lar-disease-evaluation-and-differential-diagnosis-in-adults. same in both kidney and systemic disease, with both demon- strating altered immunity. Drugs and inherited disorders are also implicated in GN with an acute or chronic presentation. Interprofessional Collaborative Care Recognize Cues: Assessment History. Ask about recent infections, particularly of the skin or upper respiratory tract, and about recent travel or other possible exposures to viruses, bacteria, fungi, or parasites. Recent illnesses, surgery, or other invasive procedures may suggest infection. Ask about any systemic diseases that alter immunity, such as systemic lupus erythematosus (SLE), which could cause acute GN. Physical Assessment/Signs and Symptoms. Inspect the patient’s skin for lesions or recent incisions, including body piercings, because these may be the source of organisms causing GN. Assess the face, eyelids, hands, and other areas for edema because edema is present in most patients with acute GN. Assess for fluid overload and pulmonary edema that may result from fluid and sodium retention occurring with acute GN. Ask about any difficulty breathing or shortness of breath. Assess for crackles in the lung fields, an S3 heart sound (gallop rhythm), and neck vein distention. Ask about changes in urine elimination patterns and any change in urine color, volume, clarity, or odor. The patient may describe blood in the urine as smoky, reddish brown, rusty, or cola-colored. Ask about dysuria or oliguria. Weigh the patient to assess for fluid retention. Take the patient’s blood pressure and compare it with the baseline blood pressure. Mild to moderate hypertension occurs with acute GN as a result of impaired fluid and electrolyte bal- ance with fluid and sodium retention. The patient may have fatigue, a lack of energy, anorexia, nausea, and/or vomiting if uremia from severe kidney impairment is present. CHAPTER immunosuppressants need to take precautions to avoid expo- sure to new infections. Preventing complications is an important nursing interven- tion, especially when fluid and electrolyte balance For patients with fluid overload, hypertension, and edema, diuretics and sodium and water restrictions are prescribed. The usual fluid allowance is equal to the 24-hour urine out- put plus 500 to 600 mL. Patients with oliguria usually have increased serum levels of potassium and blood urea nitrogen (BUN). Potassium and protein intake may be restricted to pre- vent hyperkalemia and uremia as a result of the elevated BUN. Antihypertensive drugs may be needed to control hypertension (see Chapter 30). Nausea, vomiting, or anorexia indicates that uremia is pres- ent. Dialysis is necessary if uremic symptoms or fluid volume excess cannot be controlled with nutrition therapy and fluid management (see Chapter 60). Plasmapheresis (removal and fil- tering of the plasma to eliminate antibodies) also may be used (see Chapter 34). Coordinate care to conserve patient energy, and balance activity with rest to maintain function. Relaxation techniques and diversional activities can reduce emotional stress. Preparing for self-management includes teaching the patient and family members about the purpose of prescribed drugs, the dosage and schedule, and potential adverse effects. Ensure that they understand diet and fluid restrictions. Advise the patient to measure weight and blood pressure daily at the same time each day. Instruct the patient to notify the primary health care provider of any sudden increase in weight or blood pressure. If short-term dialysis is required to control fluid and electro- lyte balance or uremic symptoms, explain vascular access care and dialysis schedules and routines (see Chapter 60). Rapidly progressive glomerulonephritis (RPGN) is a pri- mary GN also called crescentic glomerulonephritis because of the presence of crescent-shaped cells in the Bowman capsule. RPGN develops acutely over several weeks or months. Patients become quite ill quickly and have symptoms of kidney impair- ment (fluid volume excess, hypertension, oliguria, electrolyte imbalances, and uremic symptoms). Regardless of treatment, RPGN often progresses to end-stage kidney disease (ESKD). CHRONIC GLOMERULONEPHRITIS Pathophysiology Review Chronic GN, or chronic nephritic syndrome, develops over years to decades. Mild proteinuria and hematuria, hypertension, fatigue, and occasional edema are often the only symptoms. Although the exact cause is not known, changes in kidney tissue result from infection, hypertension, inflammation from immunity excess, or poor kidney blood flow. Kidney tissue atrophies, and functional nephrons are greatly reduced. Biopsy in the late stages of atrophy may show glomerular changes, cell loss, protein and collagen deposits, and fibrosis of the kidney tissue. Microscopic examination shows deposits of immune complexes and inflammation. The loss of nephrons reduces glomerular filtration. Hypertension and renal arteriole sclerosis are often present. The 1442 UNIT XIV Interprofessional Collaboration level (less than 135 mEq/L [mmol/L]). When oliguria develops, potassium is not excreted, and hyperkalemia occurs exceed 5.4 mEq/L (mmol/L). Hyperphosphatemia develops with serum levels greater than 4.7 mg/dL (1.73 mmol/L). Serum calcium levels are usually low normal or are slightly below normal. Disturbances of acid-base balance with acidosis develop from hydrogen ion retention and loss of bicarbonate. However, there may be a decrease in serum carbon dioxide (CO2) levels as patients breathe more rapidly to compensate for the acidosis. If respiratory compensation is present, the pH of arterial is between 7.35 and 7.45. A pH of less than 7.35 means that the patient’s respiratory system is not completely compensating for the acidosis (see Chapter 14). The kidneys are abnormally small on x-ray or CT GN. Take Actions: Interventions Interventions focus on slowing the progression of the dis- ease and preventing complications. Management is systemic and consists of diet changes, fluid intake sufficient to prevent reduced blood flow to the kidneys, and drug therapy to con- trol the problems from uremia. Eventually elimination is so impaired that the patient requires dialysis or transplantation to prevent death. (Care for the patient requiring dialysis or trans- plantation is discussed in Chapter 60.) NEPHROTIC SYNDROME Pathophysiology Review Nephrotic syndrome (NS) is an immunologic kidney disorder in which glomerular permeability increases, so larger mole- cules pass through the membrane into the urine and are then excreted. This process causes massive loss of protein urine, edema formation, and decreased plasma albumin levels. Minimal change disease is the most common cause of NS and accounts for 90% of NS in children and 20% in adults. Minimal change disease can be detected using light microscopy and transmission electron microscopy utilizing standard procedures (Yan et al., 2020). The most common cause of glomerular membrane changes is altered immunity with inflammation. Defects in glomerular filtration can also occur as a result of genetic defects of the glo- merular filtering system, such as Fabry disease. Altered liver function may occur with NS, resulting in increased lipid pro- duction and hyperlipidemia (Mitchell-Brown & Veisze, 2019). Interprofessional Collaborative Care The main feature of NS is increased protein elimination with severe proteinuria (with more than 3.5 g of protein in a 24-hour urine sample). Patients also have low serum albu- min levels of less than 3 g/dL (30 g/L), high serum lipid levels, fats in the urine, edema, and hypertension (Box 59.5). Renal vein thrombosis often occurs at the same time as NS, either as a cause of the problem or as an effect. NS may progress to end-stage kidney disease (ESKD), but treatment can prevent progression. patients with the APOL1 allele will develop kidney disease, sug- gesting that there may be environmental factors as well. See the Patient-Centered Care: Genetics/Genomics box. PATIENT-CENTERED CARE: GENETICS/ GENOMICS APOL1 Gene About 15% of the general population (37 million people) kidney disease (Centers for Disease Control and Prevention, cans, American Indians, and Hispanic Americans are kidney disease than White Americans (Deng & Zhang, Black Americans (over 5 million people) have the high-risk 2023). People with this genotype have a 15% to 30% ESKD in their lifetime. Patients with this gene should of kidney function and blood pressure. It is important patient, as well as the clarity that while the risk those patients who have the APOL1 gene will not develop Interprofessional Collaborative Care Management focuses on controlling high blood pressure and reducing albuminuria to preserve kidney function. Although many antihypertensive drugs may lower blood pressure, the patient’s response is important in ensuring long-term adher- ence to the prescribed therapy. Factors that promote adherence include once-a-day dosing, low cost, and minimal side effects. Lack of knowledge or misinformation about hypertension poses many challenges to health care professionals working with patients who have hypertension. When kidney disease occurs, adherence to therapy is even more important for pre- serving health. A FIG. 59.3 External surface (A) Fausto, N., & Aster, J.. Robbins ders.) 1444 UNIT XIV Interprofessional Collaboration raising blood pressure. Control of hypertension is a top priority because proper treatment can disrupt the process that leads to further kidney damage, as well as avoid complications such as stroke from hypertension. Cysts may also occur in the liver and blood vessels. The incidence of cerebral aneurysms (outpouching and thinning of an artery wall) is higher in patients with PKD. Aneurysms may rupture, causing bleeding and sudden death. For unknown reasons, kidney stones occur in many patients with PKD. Heart valve problems (e.g., mitral valve prolapse), left ventric- ular hypertrophy, and colonic diverticula also are common in patients with PKD. Etiology and Genetic Risk Kidney cysts are genetically and clinically related to many symptoms and problems. PKD can be inherited as either an autosomal dominant trait or, less often, an autosomal recessive trait. Autosomal dominant PKD is the most common inherited kidney disease, occurring in 1 to 1000 live births. Rarely, a new gene mutation can cause PKD in a patient with no family his- tory of the trait. However, the cases of gene mutation tend to be a milder form of PKD. Recent advances have made the genetic forms of cystic disorders of the kidney easier to understand. However, the number of genes influencing PKD is challenging and requires geneticists and genetic counselors to be a part of the interprofessional team caring for patients with or at risk for the disease. PATIENT-CENTERED CARE: GENETICS/ GENOMICS Autosomal Dominant PKD Polycystic kidney disease (PKD) is a genetic condition, form being autosomal dominant. Autosomal dominant PKD is the underlying cause of kidney failure in 5% of patients who begin United States (Torres & Bennett, 2023). There is no way to prevent PKD, although early detection and management of hypertension may slow the progression of kidney damage and impaired elimination. Genetic coun- seling may be useful for adults who have one parent with PKD. Family history analysis is used to help identify people at risk. Interprofessional Collaborative Care Recognize Cues: Assessment Because PKD is a chronic disease with periods of acute prob- lems, most management occurs in the community rather than in an acute care hospital. With acute problems or when surgery is needed, initial care is in a hospital setting, and continuing care can occur in any setting. History. Explore the family history of a patient with suspected or actual PKD and ask whether either parent was known to have PKD or whether there is any family history of kidney Assess the age at which the problem was diagnosed in the parent and any related complications. Ask about pain, abdominal CHAPTER quantitative data regarding tissue oxygenation, fibrosis, edema, inflammation, and perfusion (Rankin et al., 2021). Urinalysis may show proteinuria (protein in the urine), which indicates a decline in kidney function and impaired ination. Hematuria may be gross or microscopic. Bacteria in the urine indicate infection, usually in the cysts. sample for culture and sensitivity testing when there is evidence of infection. As kidney function declines, serum creatinine and blood urea nitrogen (BUN) levels rise. With further decline, creatinine clearance decreases, and the GFR is low. Changes in kidney handling of sodium may cause either sodium losses or sodium retention. Take Actions: Interventions Treatment goals are to slow the progression to kidney failure and treat the signs and symptoms supportively (Bennett et al., 2023). This includes management of hypertension and pain, dietary sodium restriction, increased fluid intake, and slowing disease progression. Blood pressure control and lifestyle and dietary modifi- cations are necessary to reduce cardiovascular complications and slow the progression of kidney dysfunction. Dietary sodium intake of less than 2 g/day is advised. In patients with preserved kidney function, 3 L of fluid daily is recom- mended to slow cyst growth. Care must be taken to moni- tor for hypervolemic hyponatremia with excess water intake (Bellos, 2021). Drug therapy with angiotensin-converting enzyme inhibi- tors (ACEIs) to reach a blood pressure below 130/80 mm Hg in all patients with PKD or 110/75 mm Hg in young adults with preserved kidney function is recommended (Nishio et al., 2021). Because PKD-related pain is often persistent and associ- ated with multiple factors, a multidisciplinary pain manage- ment approach is helpful. Drugs may include opioids along with acetaminophen. NSAIDs are used cautiously because they can reduce kidney blood flow. Aspirin-containing drugs are avoided to reduce bleeding risk. When pain is severe, be reduced by needle aspiration and drainage; however, they usually refill. When the quality or severity of pain increases, assess for infection. Fever, abdominal pain, and either leukocytosis or serum markers of inflammation (e.g., elevated erythrocyte tion rate [ESR] or C-reactive protein [CRP]) may be with cystic or systemic infection. Blood and urine or may not be positive with cyst infection. Early infection man- agement can prevent or reduce complications and acute kidney injury. As the disease progresses, protein intake may be limited to slow the development of ESKD. Help the patient and fam- ily understand the diet plan and why it was prescribed. Work closely with the registered dietitian nutritionist (RDN) to foster the patient’s understanding. Strategies for kidney protection include the use pressin-suppressing agent such as tolvaptan to improve blood flow, slow kidney volume growth, and sustain kidney func- tion. When the disease progresses and the kidneys no longer 1446 UNIT XIV Interprofessional Collaboration necrosis can occur. Nitrogen waste products (urea, creatinine, and uric acid) and electrolytes (sodium, potassium, chlo- ride, and phosphorus) are retained, and acid-base balance is impaired. The cause of hydronephrosis or hydroureter is an obstruc- tion, which can occur at any location between the collecting duct and the urethral meatus. Common causes of urinary obstruc- tion include kidney stones, tumors, fibrosis, structural abnor- malities, trauma, abscess, and cysts. With cancer, obstructed ureters may result from tumors pressing on the ureters, pelvic radiation, or surgical treatment. Early treatment of the causes can prevent ureteral problems and permanent kidney damage. The time needed to prevent permanent damage depends on the patient’s kidney health. Permanent damage can occur in less than 48 hours in some patients and after several weeks in other patients. Interprofessional Collaborative Care Recognize Cues: Assessment Obtain a history from the patient, focusing on known kidney or urologic disorders. A history of childhood urinary tract prob- lems may indicate previously undiagnosed structural defects. Ask about the usual pattern of urinary elimination, especially amount, frequency, color, clarity, and odor. Ask about recent flank or abdominal pain. Chills, fever, and malaise may be pres- ent with a urinary tract infection (UTI). Inspect each flank to identify asymmetry, which may occur with a kidney mass, and gently palpate the abdomen to locate areas of tenderness. Palpate the bladder to detect distention, or use a bedside bladder scanner (see Chapter 57). Gentle pressure on the abdomen may cause urine leakage, which reflects a full bladder and possible obstruction. Urinalysis may show bacteria or white blood cells if infec- tion is present. When urinary tract obstruction is prolonged, microscopic examination may show tubular epithelial cells. Blood chemistries are normal unless glomerular filtration has decreased and waste elimination is impaired. Blood creatinine and BUN levels increase with a reduced GFR. Serum electro- lyte levels may be altered with elevated blood levels of potas- sium, phosphorus, and calcium along with a metabolic acidosis (bicarbonate deficit). Urinary outflow obstruction can be seen with ultrasound (US) or CT. Take Actions: Interventions Urinary retention and potential for infection are the primary problems. Failure to treat the cause of obstruction leads to infection and acute kidney injury (AKI). Urologic Interventions. If obstruction is caused by a kidney stone (calculus), it can be located and removed using cystoscopic or retrograde urogram procedures. See Chapter 58 for more information about kidney stone management. After stone removal, a plastic stent is usually left in the ureter for a few weeks to improve urine flow in the area irritated the stone. The stent is later removed by another cystoscopic procedure. Radiologic Interventions. When an abnormal narrowing of the urinary tract (stricture) causes hydronephrosis and CHAPTER RENOVASCULAR DISEASE Pathophysiology Review Processes affecting the renal arteries may severely narrow the lumen and greatly reduce blood flow to the kidney tissues. Uncorrected renovascular disease, such as renal vein throm- bosis or renal artery stenosis (RAS), atherosclerosis, or throm- bosis, causes ischemia and atrophy of kidney tissue, leading to severe impairment of urinary elimination, fluid and electrolyte balance, and acid-base balance (Fig. 59.5). Patients with renovascular disease, particularly those older than 50 years, often have a sudden onset of hypertension. Patients with high blood pressure but no family history of hypertension also may potentially have RAS. RAS from atherosclerosis or blood vessel hyperplasia is the main cause of renovascular disease. Other causes include thrombosis and renal vessel aneurysms. Atherosclerotic changes in the renal artery often occur along with sclerosis in the aorta and in other major vessels. Renal artery changes are often located where the renal artery and aorta meet. Fibrotic changes of the blood vessel wall occur through- out the length of the renal artery. Interprofessional Collaborative Care Recognize Cues: Assessment Hypertension usually first occurs after age 40 to 50, and often the patient does not have a family history of hypertension (Box 59.7). Diagnosis of renovascular disease is made by mag- netic resonance angiography (MRA), renal ultrasound, radio- nuclide imaging, or renal arteriography. MRA provides an excellent image of the renal vasculature and kidney anatomy. Radionuclide imaging is a noninvasive way of evaluating kidney blood flow and excretory function. Combining radionuclide imaging with ingestion of an angiotensin-converting enzyme inhibitor (ACEI) such as lisinopril improves the accuracy of the test. A renal arteriogram makes the features of the renal blood vessels visible. Take Actions: Interventions Identifying the type of defect, extent of narrowing, and condi- tion of the surrounding blood vessels is critical for treatment Renal artery stenosis Adrenal gland Kidney FIG. 59.5 Renal artery stenosis. 1448 UNIT XIV Interprofessional Collaboration RENAL CELL CARCINOMA Pathophysiology Review Renal cell carcinoma (RCC) or adenocarcinoma of the kidney is the most common type of kidney cancer and occurs as a result of impaired cellular regulation. Healthy kidney tissue is dam- aged and replaced by cancer cells, which impairs urine elimina- tion for that kidney. Systemic effects occurring with this cancer type are called paraneoplastic syndromes and include anemia, erythrocyto- sis, hypercalcemia, and liver dysfunction with elevated liver enzymes, hormonal effects, increased sedimentation rate, and hypertension. Anemia and erythrocytosis may seem confusing; however, most patients with this cancer have either anemia or tosis, not both at the same time. There is some blood loss from hematuria, but the small amount lost does not cause anemia. The cause of the anemia and the erythrocytosis is related to kidney cell production of erythropoietin. At times, the tumor cells produce large amounts of erythropoietin, causing erythro- cytosis. At other times, the tumor cells destroy the erythropoie- tin-producing kidney cells and anemia results. Parathyroid hormone produced by tumor cells can cause hypercalcemia. Other hormonal changes include increased renin levels (causing hypertension) and increased human cho- rionic gonadotropin (hCG) levels, which decrease libido and change secondary sex features. RCC has five distinct carcinoma cell types: clear cell, pap- illary cell, chromophobe cell, collecting duct carcinoma, and unclassified type (Rogers, 2023). Kidney tumors are classified into four stages (Box 59.8). Complications include metastasis and urinary tract obstruction. The cancer usually spreads to the adrenal gland, liver, lungs, long bones, or the other kidney. When the cancer surrounds a ureter, hydroureter and obstruction may result. BOX 59.8 Staging Kidney Tumors Stage I Tumors ≤7 cm in largest dimension in the kidney. fat, and adjacent lymph nodes have no tumor. Stage II Tumors are >7 cm in largest dimension in the kidney. remains in the kidney with no lymph node involvement. Stage III Tumor has penetrated the major veins or perinephric Gerota fascia. Tumors extend into the lymph nodes tasis. Stage IV Tumors include invasion of adjacent organs beyond sis to distant tissues. Adapted from Gallardo, E.A. (2017, November 13). SEOM guideline for treatment of kidney cancer. Retrieved Library of Medicine, National Institutes of Health. https://www.nc- bi.nlm.nih.gov/pmc/articles/PMC5785618/. CHAPTER and blood urea nitrogen (BUN) levels indicate impaired kidney function. Kidney masses may be detected by CT scan or MRI. RCC is often identified incidentally, as a result of another imaging study (Pullen, 2021). This is often when the patient is asymptomatic and when the RCC is in the early stage. Ultrasound is also used to detect masses or for initial screening. Kidney biopsy may be considered to help target therapy. Take Actions: Interventions Treatment for kidney cancer focuses on preventing the spread of the cancer and managing complications. Chemotherapy is not as effective when treating advanced kidney cancers. Targeted therapies that block the growth of new blood vessels that nour- ish cancer and immunotherapies can be effective (ACS, 2021). Nonsurgical Management. Microwave ablation or cryoablation can slow tumor growth. It is a minimally invasive procedure carried out after MRI has precisely located the tumor. Microwave ablation is used most commonly for patients who have only one kidney or who are not surgical candidates. Traditional chemotherapy has limited effectiveness against this cancer type (Pullen, 2021). Immunotherapy, such as inter- leukin-2 and interferon (IFN), and immunomodulating drugs are often used for treatment (Pullen, 2021). See Chapter 18. Surgical Management. Renal cell carcinoma (RCC) is usually treated surgically by nephrectomy (kidney removal). Renal cell tumors are highly vascular, and blood loss during surgery is a major concern. Before surgery, the arteries supplying the kidney may be occluded (embolized) by the interventional radiologist to reduce bleeding during nephrectomy. Preoperative Care. Instruct the patient about surgical routines (see Chapter 9). Explain the probable site of incision and the presence of dressings, drains, or other equipment after surgery. Reassure the patient about pain relief. Care before surgery may include giving blood and fluids IV to prevent shock. Operative Procedures. The patient is placed on the nonoperative side, with the kidney to be removed uppermost. The trunk area is flexed to increase exposure of the kidney area. The eleventh or twelfth rib may need to be removed to provide better access to the kidney. The surgeon removes either part or all of the kidney and all visible tumor. The renal artery, renal vein, and fascia also may be removed. A drain may be placed in the wound before closure. The adrenal gland may be removed when the tumor is near this organ. When a radical nephrectomy is performed, local and regional Concepts of Care for Patients With Kidney Conditions Robyn Mitchell http://evolve.elsevier.com/Iggy/ with kidney conditions affecting elimination, fluid and electrolyte balance, and acid-base balance. 6. Analyze assessment and diagnostic findings to generate solutions and prioritize nursing care for patients with kidney conditions. 7. Organize care coordination and transition management for patients with kidney conditions. 8. Use clinical judgment to plan evidence-based nursing care to promote urinary elimination and prevent complications in patients with kidney conditions. 9. Incorporate factors that affect health equity into the plan of care for patients with kidney conditions. is causing hydronephrosis and cannot be corrected with urologic procedures. nephrotic syndrome (NS) Immunologic kidney disorder in which glomerular permeability increases so that larger molecules pass through the membrane into the urine and are then excreted; causes massive loss of protein into the urine and decreased plasma albumin levels. polycystic kidney disease (PKD) Genetic disorder in which fluid-filled cysts develop in the kidneys. pyelolithotomy Surgical removal of a stone from the kidney. pyelonephritis A bacterial infection in the kidney and renal pelvis. stricture Narrowing of the urinary tract. ureteroplasty Surgical repair of the ureter. Healthy kidneys are the major controllers of urinary elim- ination. They perform this function by filtering wastes from the blood and selectively determining which substances remain in the body and which are eliminated. Thus the kidneys main- tain homeostasis by contributing to fluid and electrolyte bal- ance and acid-base balance. Any problem that disrupts kidney function has the potential to impair general homeostasis and all aspects of urinary elimination (Fig. 59.1). Interaction with other organs and systems is necessary for the kidneys to func- tion effectively. In addition, when the kidneys are impaired, the buildup of toxic wastes affects all other body systems and 1435 for Patients With Renal/Urinary System Conditions Intake of N K Urine output substances of substances K N K K N N K N N N N K N Normal intake not balanced with appropriate urine output as a result of kidney impairment electrolytes, and waste products as a result of kidney problems that pre- Microbial invasion of renal pelvis Inflammatory response Resulting fibrosis (scar tissue) tract Decreased tubular reabsorption and secretion of an the blad- Impaired kidney function FIG. 59.2 Pathophysiology of pyelonephritis. organisms in the blood, but this cause of pyelonephritis is rare unless the patient has impaired immunity. Acute pyelonephritis involves acute tissue inflammation, local edema, tubular cell necrosis, and possible abscess for- mation. Abscesses, which are pockets of infection, can occur anywhere in the kidney. The infection is scattered within the kidney; healthy tissues can lie next to infected areas. Fibrosis and scar tissue develop from chronic inflammation in the kid- ney glomerular and tubular structures. As a result, filtration, reabsorption, and secretion are impaired, and kidney function is reduced (Fig. 59.2). when urine Etiology and Genetic Risk Single episodes of acute pyelonephritis result from bacte- rial infection, with or without obstruction or reflux. Chronic 59 Concepts of Care for Patients With Kidney Conditions 1437 Recognize Cues: Assessment History. Ask about recurrent urinary tract infections (UTIs), diabetes mellitus (DM), stone disease, and known defects of the genitourinary tract. Ask about disease or treatment that results in reduced immunity, which also increases the risk for pyelonephritis. Ask about kidney function; knowledgeable patients may be able to describe their stage of chronic kidney disease (CKD) if chronic pyelonephritis has led to permanent kidney damage. Ensure that a woman is not pregnant before radiographic imaging. Physical Assessment/Signs and Symptoms. Ask about specific symptoms of acute pyelonephritis. See Box 59.1 for key features of acute pyelonephritis. Chronic pyelonephritis has a less dramatic presentation but similar symptoms. Ask the patient to describe any urinary symptoms or abdominal discomfort. Inquire about any history of repeated low-grade fevers. Changes in urine color or odor may accompany bacteriuria. See Box 59.2 for key features of chronic pyelonephritis. The objective assessment includes inspecting the flanks and gently palpating the costovertebral angle (CVA). Inflammation can be indicated by enlargement, asymmetry, edema, or redness/ hyperpigmentation found during the inspection of both CVAs (Fukaguchi, et al., 2021). If there is no tenderness to light palpa- tion in either CVA, the primary health care provider may firmly percuss each area. Tenderness or discomfort may indicate infec- tion or inflammation. Psychosocial Assessment. Any infection in an older adult can lead to acute confusion. Assess the older adult who has new-onset confusion for signs and symptoms of urinary or renal infection. The patient with any problem in the genitourinary area may have feelings of anxiety, embarrassment, or guilt. Listen for signs of anxiety or specific fears and prevent embarrassment during assessment. Feelings of guilt, often associated with sexual habits BOX 59.1 Key Features labor and Acute Pyelonephritis Jeong, 2021). Fever Chills Tachycardia and tachypnea Flank, back, or loin pain Tenderness at the costovertebral angle (CVA) Abdominal, often colicky, discomfort Nausea and vomiting General malaise or fatigue Burning, urgency, or frequency of urination Nocturia Recent cystitis or treatment for urinary tract infection (UTI) BOX 59.2 Key Features Chronic Pyelonephritis Hypertension Inability to conserve sodium atten- Decreased urine-concentrating ability, resulting in nocturia Tendency to develop hyperkalemia and acidosis fibrosis. for Patients With Renal/Urinary System Conditions Analyze Cues and Prioritize Hypotheses: Analysis The priority collaborative problems for the patient with pyelo- nephritis are: 1. Pain (flank and abdominal) due to inflammation and infec- tion 2. Potential for chronic kidney disease (CKD) due to kidney tissue destruction Generate Solutions and Take Actions: Planning and Implementation Managing Pain Planning: Expected Outcomes. With proper intervention, the patient with pyelonephritis is expected to achieve an acceptable state of comfort. Interventions. Interventions may be nonsurgical or surgical. Interventional radiologic techniques may be used to relieve obstruction or repair a stricture of the urinary tract. Nonsurgical Management. Interventions include the use of drug therapy, nutrition and fluid therapy, and education to ensure that the patient understands the treatment. Drug therapy can reduce pain. Acetaminophen is preferred over NSAIDs because it does not interfere with kidney autoreg- ulation of blood flow. Reduction of fever will also reduce pain. Some patients may require the use of opioids in the short term for pain control. Drug therapy with antibiotics is ordered to treat the infec- tion. At first the antibiotics are broad spectrum. After urine and blood culture and sensitivity results are known, more specific antibiotics may be prescribed. Antibiotics are given (usually IV in hospitalized patients; orally in community-dwelling patients) to achieve adequate blood levels or sterile blood culture results. A prophylactic antibiotic is not recommended for patients with impaired voiding or chronic catheter use because it does not limit recurrence or severity of UTI (Belyayeva & Jeong, 2021) Catheter replacement is supportive for a patient requiring a urinary catheter for 2 or more weeks (e.g., for neurogenic blad- der or wound healing). This involves removal and replacement of the catheter and closed drainage system before starting anti- biotic therapy. This intervention reduces bioburden by remov- ing a device with a biofilm of concentrated organisms. Nutritional therapy involves ensuring that the patient’s dietary intake has adequate calories from all food groups for healing to occur. A registered dietitian nutritionist should be part of the interprofessional team. Fluid intake is recommended at 2 L/day, sufficient to result in dilute (pale yellow) urine, unless another health problem requires fluid restriction. Surgical Management. Surgical interventions can correct structural problems causing urine reflux or obstruction of urine outflow or can remove the source of infection. Teach the patient of the following assess- the nature and purpose of the proposed surgery, the expected Select all outcome, and how the patient can participate. The surgical procedures used may be one of the following: pyelolithotomy (stone removal from the kidney), nephrectomy (removal of the kidney), ureteral diversion, or reimplantation of ureter(s) to restore proper bladder drainage. A pyelolithotomy is needed for removal of a large stone in the kidney pelvis that blocks urine flow and causes infection. 59 Concepts of Care for Patients With Kidney Conditions 1439 Ensure that interprofessional care includes nutritional counsel- ing, because many patients have special nutritional require- ments, such as those for diabetes or pregnancy. the bladder Evaluate Outcomes: Evaluation Evaluate the care of the patient with pyelonephritis based on the identified priority patient problems. Expected outcomes may include that the patient will: pain is controlled - ventions to prevent or reduce CKD progression ACUTE GLOMERULONEPHRITIS Pathophysiology Review Glomerulonephritis (GN) is categorized into conditions that primarily involve the kidney (primary glomerular nephritis) and those in which kidney involvement is only part of a sys- temic disorder (secondary GN). It is a group of diseases that injure and inflame the glomerulus, the part of the kidney that filters blood. Inflamed glomeruli allow passage of protein and blood in the urine. GN is associated with high blood pressure, progressive kidney damage (leading to CKD), and edema. Anemia from reduced production of erythropoietin and high cholesterol often co-occur. GN can cause altered urinary elimination. Acute glomerulonephritis (GN) develops suddenly from an excessive immunity response within the kidney tissues. Usually an infection is noticed before kidney symptoms of acute GN are present. The onset of symptoms is about 10 days from the time of infection. Patients usually recover quickly and completely from acute GN. Many causes of primary GN are infectious (Box 59.3). Secondary GN can be caused by multisystem diseases (Box 59.4) and can manifest as acute or chronic disease. However, the division of primary and secondary GN is complex because diag- nostic findings, histologic changes, and other changes are the help with BOX 59.3 Infectious Agents Associated With Glomerulonephritis Group A beta-hemolytic Streptococcus Staphylococcal or gram-negative bacteremia or sepsis Pneumococcal, Mycoplasma, or Klebsiella pneumonia Syphilis Dengue Hantavirus Varicella Parvovirus Hepatitis B and C Cytomegalovirus Parvovirus Epstein-Barr virus Human immunodeficiency virus Adapted from Patel, N.P. (2018, November 28). Infection-induced kidney diseases. Retrieved from U.S. National Library of Medicine, National Institutes of Health. https://www.ncbi.nlm.nih.gov/pmc/arti- cles/PMC6282040/. for Patients With Renal/Urinary System Conditions PATIENT-CENTERED CARE: OLDER ADULT HEALTH Glomerulonephritis Glomerulonephritis can lead to chronic kidney disease (CKD), making it essen- tial to prevent and treat in the older adult who is at greater risk for CKD. In the older adult, symptoms of glomerulonephritis can easily be confused with an exacerbation of heart failure. Older adults with immunocompromised back- grounds, such as diabetes mellitus, malignancies, or alcoholism, are reported to be at higher risk for death from glomerulonephritis than younger adults and children, where most cases are resolved without specific treatments (Oda & Yoshizawa, 2021). Laboratory Assessment. Urinalysis shows red blood cells spectrum (hematuria) and protein (proteinuria). An early morning specimen of urine is preferred for urinalysis because the urine is concentrated, most acidic, and filled with more intact formed disease: Retrieved elements at that time. Microscopic examination often shows red blood cell casts, as well as casts from other substances. A 24-hour urine collection for total protein assay is obtained. The protein excretion rate for patients with acute GN may be increased from 500 mg/24 hr to 3 g/24 hr. Serum albumin levels are decreased because this protein is lost in the urine and fluid retention causes dilution. Serum creatinine and BUN provide information about kid- ney function and may be elevated, indicating impairment of elimination. The glomerular filtration rate (GFR), either esti- mated from a single serum and urine creatinine value or mea- sured by the 24-hour urine test for creatinine clearance, may be decreased to 50 mL/min. Recall that the older adult has a decline in GFR, which may make GFR results challenging to interpret. Other Diagnostic Assessment. A kidney biopsy provides a precise diagnosis of the condition, assists in determining the prognosis, and helps in outlining treatment (see Chapter 57). The specific tissue features are determined by light microscopy, immunofluorescent stains, and electron microscopy to identify cell type, the presence of immunoglobulins, or the type of tissue deposits. Take Actions: Interventions Interventions focus on managing infection, preventing compli- cations, and providing appropriate patient education. Managing infection as a cause of acute GN begins with appro- priate antibiotic therapy. Penicillin, erythromycin, or azithro- mycin is prescribed for GN caused by streptococcal infection. Check the patient’s known allergies before giving any drug. Stress personal hygiene and basic infection control principles (e.g., handwashing) to prevent spread of the organism. Teach patients the importance of completing the entire course of the prescribed antibiotic. Modifying immunity with drugs can also benefit patients with acute glomerulonephritis (GN) that is not due to acute infec- tion but is related to excessive inflammation. Corticosteroids and cytotoxic drugs (e.g., cyclosporine, cyclophosphamide) to suppress immunity responses may be used. Patients receiving 59 Concepts of Care for Patients With Kidney Conditions 1441 glomerular damage allows proteins to enter the urine. Chronic GN always leads to end-stage kidney disease (ESKD) (see Chapter 60). is disrupted. Interprofessional Collaborative Care Recognize Cues: Assessment History. Ask about other health problems, including systemic diseases, kidney or urologic disorders, infectious diseases (i.e., streptococcal infections), and recent exposures to infections. Ask about overall health status and whether increasing fatigue and lethargy have occurred. Identify the patient’s urine elimination pattern. Ask whether the frequency of voiding has increased or the quantity of urine has decreased. Ask about changes in urine color, odor, or clarity and whether dysuria or incontinence has occurred. Nocturia is a common symptom. Assess the patient’s general comfort, and ask whether new-onset dyspnea has occurred, because fluid overload can occur with decreased urine output. Ask about and observe for changes in cognition (i.e., irritability, an inability to read, or incapacity during job-related functions) or disturbed con- centration. Changes in memory and the ability to concentrate occur as waste products collect in the blood. Physical Assessment/Signs and Symptoms. Assess for systemic circulatory overload. Auscultate lung fields for crackles, observe the respiratory rate and depth, and measure blood pressure and weight. Assess the heart rate, rhythm, and presence of an S3 heart sound. Inspect the neck veins for venous engorgement and check for edema of the feet and ankles, on the shins, and over the sacrum. Assess for uremic symptoms, such as slurred speech, ataxia, tremors, or asterixis (flapping tremor of the fingers or the inability to maintain a fixed posture with the arms extended and wrists hyperextended). Inspect the skin for a yellowish color, texture changes, bruises, rashes, or eruptions. Ask about itching, and document areas of dryness or any excoriation from scratching. Psychosocial Assessment. A diagnosis of chronic GN is associated with psychosocial responses of uncertainty, loss, and fear of the need for lifestyle changes as the disease progresses. While obtaining the history, listen carefully for spoken and unspoken feelings of anger, resentment, sadness, or anxiety, all of which may need further exploration. Diagnostic Assessment. Urine output decreases and urinalysis shows protein, usually less than 2 g in a 24-hour collection. The specific gravity is fixed at a constant level of dilution (around 1.010) despite variable fluid intake. Red blood cells and casts may be in the urine. The glomerular filtration rate (GFR) is low. The serum cre- atinine level is elevated; usually it is greater than 6 mg/dL (500 mcmol/L) but may be as high as 30 mg/dL (2500 mcmol/L) or more because of poor waste elimination. The BUN is increased, often as high as 100 to 200 mg/dL (35 to 70 mmol/L). Decreased kidney function disturbs fluid and electrolyte balance. Sodium retention is common, but dilution of the plasma from excess fluid can result in a falsely normal serum sodium level (135 to 145 mEq/L [mmol/L]) or a low sodium for Patients With Renal/Urinary System Conditions BOX 59.5 Key Features when levels Nephrotic Syndrome Key features include sudden onset of these symptoms: Massive proteinuria Hypoalbuminemia Edema (especially facial and periorbital) Lipiduria Hyperlipidemia Delayed clotting or increased bleeding with higher-than-normal values for serum activated partial thromboplastin time (aPTT), coagulation, or interna- blood tional normalized ratio (INR) for prothrombin time (PT) Reduced kidney function with elevated blood urea nitrogen (BUN) and serum creatinine and decreased glomerular filtration rate (GFR) in chronic Management varies, depending on which process is caus- ing the disorder (identified by kidney biopsy). Excess immu- nity may improve with suppressive therapy using steroids and cytotoxic or immunosuppressive agents. Angiotensin- converting enzyme inhibitors (ACEIs) can decrease protein loss in the urine, and cholesterol-lowering drugs can improve blood lipid levels. Heparin may reduce vascular defects and improve kidney function. Diet changes are often prescribed. If the glomerular filtration rate (GFR) is normal, dietary intake of proteins is needed. If the GFR is decreased, protein intake must be decreased. Mild diuretics and sodium restriction may be needed to control edema and hypertension. Assess the patient’s hydration status because vascular dehydration is common. If plasma volume is depleted, kidney problems worsen. Acute kid- ney injury (AKI) may be avoided if adequate blood flow to the kidney is maintained. NEPHROSCLEROSIS into the Pathophysiology Review Nephrosclerosis is a degenerative disorder resulting from changes in kidney blood vessels. Nephron blood vessels thicken, resulting in narrowed lumens and decreased kidney blood flow. The tissue is chronically hypoxic, with ischemia and fibrosis developing over time. Nephrosclerosis occurs with all types of hypertension, ath- erosclerosis, and diabetes mellitus (DM). The more severe the hypertension, the greater the risk for severe kidney damage. Nephrosclerosis is rarely seen when blood pressure is consis- tently below 160/110 mm Hg. The changes caused by hyper- tension may be reversible or may progress to end-stage kidney disease (ESKD) within months or years. Hypertension is the second leading cause of ESKD, with many patients requiring kidney replacement therapy (e.g., dialysis or transplantation). More recent advances in genetic testing have revealed a complex pathogenesis in nephrosclerosis. Patients were often diagnosed with nephrosclerosis thought to be caused by hyper- tension. However, advanced genetic evidence indicated many as having genetic focal segmental glomerulosclerosis. The apolipo- protein L1 (APOL1) allele is a risk factor for glomerulosclerosis that presents with symptoms such as nephrosclerosis. People with the APOL1 allele are usually of African ancestry. Not all CHAPTER 59 Concepts of Care for Patients With Kidney Conditions 1443 Many drugs can control high blood pressure (see Chapter 30), and more than one agent may be needed for best control. Angiotensin-converting enzyme inhibitors (ACEIs) are very useful in reducing hypertension and preserving kidney func- tion. Diuretics can maintain fluid and electrolyte balance in the presence of kidney function insufficiency. Hyperkalemia needs to be prevented when potassium-sparing diuretics, alone or in combination with other diuretics, are used to treat hypertensive is affected by chronic patients with known kidney disease. 2021). Black Ameri- more likely to have chronic 2022). About 13% of POLYCYSTIC KIDNEY DISEASE APOL1 gene (Bleyer, Pathophysiology Review chance of developing Polycystic kidney disease (PKD) is a genetic disorder in which have routine monitoring fluid-filled cysts develop in the nephrons (Fig. 59.3). Relentless to provide support to the is increased, two-thirds of development and growth of cysts from loss of cellular regula- ESRD (Bleyer, 2023). tion and abnormal cell division result in progressive kidney enlargement. Patients with PKD often experience hypertension, abdominal and flank pain, ruptured cysts, and infections. These complications can lead to kidney failure and reduced quality of life (Ma & Lambert, 2021) The cysts look like clusters of grapes (see Fig. 59.3). Over time, growing cysts damage the glomerular and tubular membranes. Each cystic kidney enlarges, becoming the size of a football, and may weigh 10 lb or more each. As cysts fill with fluid and become larger, kidney function becomes less effective, and urine formation and waste elimination are impaired. Most patients with PKD have high blood pressure. The cause of hypertension is related to kidney ischemia from the enlarg- ing cysts. As the vessels are compressed and blood flow to the kidneys decreases, the renin-angiotensin system is activated, B and internal surface (B) of a polycystic kidney. (From Kumar, V., Abbas, A., and Cotran Pathologic basis of disease [8th ed.]. Philadelphia: Saun- for Patients With Renal/Urinary System Conditions discomfort, constipation, changes in urine color or frequency, hypertension, headaches, and a family history of stroke or sudden death. Physical Assessment/Signs and Symptoms. Pain is often the first symptom. Inspect the abdomen. A distended abdomen is common as the cystic kidneys swell and push the abdominal contents forward. Polycystic kidneys are easily palpated because of their increased size. Use gentle abdominal palpation because the cystic kidneys and nearby tissues may be tender and palpation is uncomfortable. The patient also may have flank pain as a dull ache or as a sharp and intermittent discomfort. Dull, aching pain is caused by increased kidney size with distention, abnormal stimulation of sensory neurons in the kidney, or infection within the cyst. Sharp, intermittent pain occurs when a cyst ruptures or a stone is present. When a cyst ruptures, the patient may have bright red or cola-colored urine. Infection is suspected if the urine is cloudy or foul smelling or if there is dysuria (pain on urination). See Box 59.6. Nocturia (the need to urinate excessively at night) is an early symptom and occurs because of decreased urine concentrat- ing ability. Patients with early PKD often have hyperfiltration leading to wasting of sodium and water, which disrupts fluid and electrolyte balance. Later, as kidney function declines (i.e., reduced glomerular filtration rate [GFR]), the patient retains water and sodium, which causes hypertension, edema, and ure- mic symptoms such as anorexia, nausea, vomiting, pruritus, and fatigue (see Chapter 60). Because intracranial aneurysms occur in patients with PKD, a severe headache with or without neuro- logic or vision changes requires attention. Psychosocial Assessment. A PKD diagnosis is associated with psychosocial responses of uncertainty, loss, and fear due with the most common to the life-threatening complications that can occur (Ma & Lambert, 2021). The patient may have had a parent who died dialysis annually in the or relatives who required dialysis or transplantation. Listen for spoken and unspoken feelings of anger, resentment, futility, sadness, or anxiety. Such feelings may need further exploration. Feelings of guilt and concern for the patient’s children may also complicate the issue. Diagnostic Assessment. Ultrasound is the primary method for diagnosing PKD. The size of the kidney is measured by ultrasound, as well as cysts within the kidney. MRI or CT may be used in order to confirm ultrasound findings and provide BOX 59.6 Key Features Polycystic Kidney Disease Abdominal or flank pain Hypertension Nocturia Frequent urinary tract infections Increased abdominal girth Constipation Hematuria (bloody urine) disease. Sodium wasting and inability to concentrate urine in early stage Progression to kidney failure with anuria (Nishio et al., 2021) 59 Concepts of Care for Patients With Kidney Conditions 1445 function for waste elimination, care becomes similar to that needed for the patient with end-stage kidney disease (see Chapter 60). elim- HYDRONEPHROSIS AND HYDROURETER Obtain a urine Pathophysiology Review Hydronephrosis and hydroureter are problems of urinary elimination with outflow obstruction. Urethral strictures obstruct urine outflow and may contribute to bladder disten- tion, hydroureter, and hydronephrosis. Prompt recognition and treatment are crucial to preventing permanent kidney damage. In hydronephrosis, the kidney enlarges as urine collects in the renal pelvis and kidney tissue. Because the capacity of the renal pelvis is normally 5 to 8 mL, obstruction in the renal pelvis or at the point where the ureter joins the renal pelvis quickly distends the renal pelvis. Kidney pressure increases as the vol- ume of urine increases. Over time, sometimes in only a matter of hours, the blood vessels and kidney tubules can be damaged extensively (Fig. 59.4). In patients with hydroureter (enlargement of the ureter), the effects are similar, but the obstruction is in the ureter rather than in the kidney. The ureter is most easily obstructed where the iliac vessels cross or where the ureters enter the bladder. Ureter dilation occurs above the obstruction and enlarges as urine collects (see Fig. 59.4). Urinary obstruction causes damage when pressure builds up directly on kidney tissue. Tubular filtrate pressure also increases in the nephron as drainage through the collecting system is impaired and glomerular filtration decreases or ceases. Kidney Hydronephrosis Hydroureter cysts can abruptly Stone sedimenta- associated cultures may Stone Urinary Urinary bladder bladder of a vaso- FIG. 59.4 Hydronephrosis is caused by obstruction in the upper part of the ureter. Hydroureter is caused by obstruction in the lower part of the ureter. for Patients With Renal/Urinary System Conditions cannot be corrected with urologic procedures, a nephrostomy is performed. Most nephrostomy drains provide only external drainage (diversion). Other styles of nephrostomy drains enter the kidney and extend to the bladder, draining urine out to a bag or past a ureteral obstruction and into the bladder. With these, there are both internal and external parts to the nephrostomy tubing. Externally, a fully external or an internal/ external diversion drain appears the same. The urine output will fluctuate more if all urine goes to the bladder before external drainage. Patient Preparation. If possible, the patient is kept NPO for 4 to 6 hours before the procedure. Clotting studies (e.g., international normalized ratio [INR], prothrombin time [PT], and partial thromboplastin time [PTT]) should be normal or corrected. Drugs are used to reduce hypertension. The patient receives moderate sedation for the procedure. Procedure. The patient is placed in the prone position. The kidney is located under ultrasound or fluoroscopic guidance, and a local anesthetic is given. A needle is placed into the kidney, a soft-tipped guidewire is placed through the needle, and then a catheter is placed over the wire. The catheter tip remains in the renal pelvis, and the external end is connected to a drainage bag. The procedure immediately relieves the pressure and prevents further damage. The nephrostomy tube remains in place until the obstruction is resolved. Follow-up Care. Assess the amount of drainage in the collection bag. The amount of drainage depends on whether a ureteral catheter is also being used (with a separate drainage bag). Patients with ureteral tubes may have all urine pass through to the bladder or may have it drain into the collection bags. The type of urine drainage system placed must be clearly communicated in the chart. If urine is expected to drain into the collection bag, assess the amount of drainage hourly for the first 24 hours. If the amount of drainage decreases and the patient has back pain, the tube may be clogged or dislodged. Monitor the nephrostomy site for leaking urine or blood. Urine drainage may be bloody for the first 12 to 24 hours after the procedure and should gradually clear. If prescribed, the nephrostomy tube can be irrigated with 5 mL sterile saline to check patency and dislodge clots. It is common for diuresis to occur when a nephrostomy is placed for obstruction. Monitor intake and output hourly for the first several hours, and inform the surgeon if the patient begins to have symptoms of dehy- dration (i.e., hypotension, poor skin turgor, dry mucous mem- branes, increased thirst). Assess for indications of infection (i.e., fever, change in urine character). NURSING SAFETY PRIORITY Critical Rescue by After nephrostomy, monitor the patient for indications of complications (i.e., decreased or absent drainage, cloudy or foul-smelling drainage, leakage of blood or urine from the nephrostomy site, back pain) (Martin & Baker, 2019). If any indications are present, respond by notifying the surgeon immediately. 59 Concepts of Care for Patients With Kidney Conditions 1447 choice, as is the patient’s overall health. Many patients with renovascular disease also have cardiovascular disease, and both conditions require treatment. RAS may be managed by drugs to control high blood pressure and by procedures to restore the blood supply to the kidney. Drugs may control high blood pressure but may not lead to long-term preservation of kidney function. In younger adults, a lifetime of treatment with many drugs for high blood pressure makes treatment difficult and outcomes uncertain. Endovascular techniques are nonsurgical approaches to repair RAS. Stent placement with or without balloon angio- plasty is an example of an endovascular intervention (see Chapter 30). These techniques are less risky and require less time for recovery than does renal artery bypass sur- gery. After the procedure, the patient usually remains under close observation for 24 hours to monitor for sudden blood pressure fluctuations as the kidneys adjust to increased blood flow. Renal artery bypass surgery is a major procedure and requires 2 or more months for recovery. A bypass may be per- formed for either one or both renal arteries. A synthetic blood vessel graft is inserted to redirect blood flow from the abdom- inal aorta into the renal artery, beyond the area of narrowing. A splenorenal bypass can also restore blood flow to the kidney. The process is similar to other arterial bypass procedures (see Chapter 30). DIABETIC NEPHROPATHY Diabetic nephropathy is a vascular complication of diabe- tes mellitus (DM) and the leading cause of chronic kidney disease in the world. Approximately 40% of patients who are diabetic will develop diabetic kidney disease (Du et al., 2021). It occurs with either type 1 or type 2 DM. Severity of diabetic kidney disease is related to the degree of hypergly- cemia the patient generally experiences. With poor control of hyperglycemia, the complicating problems of atheroscle- rosis, hypertension, and neuropathy (which promotes loss of bladder tone, urinary stasis, and urinary tract infection) are more severe and more likely to cause kidney damage. Chapter 56 discusses diabetic nephropathy. Management of diabetic nephropathy is the same as for chronic kidney dis- ease (see Chapter 60). Adrenal gland BOX 59.7 Key Features Kidney Renovascular Disease Significant, difficult-to-control high blood pressure Poorly controlled diabetes or sustained hyperglycemia Elevated serum creatinine Decreased glomerular filtration rate (GFR) for Patients With Renal/Urinary System Conditions The causes of nonhereditary RCC are unknown, but the risk is slightly higher for adults who use tobacco or are exposed to cadmium and other heavy metals, asbestos, benzene, and tri- chloroethylene. Males are twice as likely to have kidney cancer as females, and this cancer is more common in Black Americans and American Indians and Alaska Native people (American Cancer Society [ACS], 2022). There are 79,000 new cases of kidney cancer in the United States each year (American Cancer Society, 2022). About 13,920 people die annually from kidney cancer in the United States. Kidney cancer is among the top 10 most common cancers in men and women, with the average age at diagnosis of 64 years. Kidney cancer is not common in people younger than 45 (ACS, 2022). erythrocy- Interprofessional Collaborative Care The most common treatment for RCC is a nephrectomy. When the cancer is local (i.e., only in the kidney), a nephrectomy can provide a cure. For patients with metastasis, nephrectomy is fol- lowed by targeted chemotherapy combined with cytokine treat- ment. Patients with RCC are at risk for CKD and cardiovascular complications. Patients need ongoing, interprofessional care with surveillance for best outcomes. Follow-up therapy is man- aged on an outpatient basis. Recognize Cues: Assessment History. Ask the patient about known risk factors (e.g., smoking or chemical exposures), weight loss, changes in urine color, abdominal or flank discomfort, and fever. Also ask whether any other family member has ever been diagnosed with cancer of the kidney, bladder, ureter, prostate gland, uterus, or ovary. Physical Assessment/Signs and Symptoms. Some patients with RCC have flank pain, obvious blood in the urine, and a kidney mass that can be palpated. Ask about the nature of the flank or abdominal discomfort. Patients often describe the pain as dull and aching. Pain may be more intense if bleeding into the tumor or kidney occurs. Inspect the flank area, checking for asymmetry or an obvious bulge. An abdominal mass may The renal vein, perinephric be felt with gentle palpation. A renal bruit may be heard on auscultation. Bloody urine is a late common sign. Blood may be visible as However, the tumor bright red flecks or clots, or the urine may appear smoky or cola colored. Without gross hematuria, microscopic examination may or may not reveal red blood cells (RBCs). Inspect the skin for pallor/ash gray appearance, darkening tissues, yet not beyond of the nipples, and, in men, breast enlargement (gynecomas- but do have distant metas- tia) caused by changing hormonal levels. Other findings may include muscle wasting, weakness, and weight loss. All tend to occur late in the disease. Gerota fascia or metasta- Diagnostic Assessment. Urinalysis may show RBCs. Hematologic studies show decreased hemoglobin and hematocrit values, hypercalcemia, increased erythrocyte clinical from U.S. National sedimentation rate, and increased levels of adrenocorticotropic hormone, human chorionic gonadotropin (hCG), cortisol, renin, and parathyroid hormone. Elevated serum creatinine 59 Concepts of Care for Patients With Kidney Conditions 1449 hypotension, decreased urine output, and an altered level of consciousness. A decrease in blood pressure is an early sign of both hemor- rhage and adrenal insufficiency. With hypotension, urine output also decreases immediately. Large water and sodium losses in the urine occur in patients with adrenal insufficiency, leading to impaired fluid and electrolyte balance. As a result, a large urine output is followed by hypotension and oliguria (less than 400 mL/24 hr or less than 25 mL/hr). IV replacement of fluids and packed RBCs may be needed. The second kidney is expected to provide adequate function, but this may take days or weeks. Assess urine output hourly for the first 24 hours after surgery (urine output of 0.5 mL/kg/hr or about 30 to 50 mL/hr is acceptable). A low urine output of less than 25 to 30 mL/hr suggests decreased blood flow to the remaining kidney and potential for acute kidney injury (AKI). The hemoglobin level, hematocrit values, and white blood cell count may be measured every 6 to 12 hours for the first day or two after surgery. Monitor the patient’s temperature, pulse rate, and respiratory rate at least every 4 hours. Accurately measure and record fluid intake and output. Weigh the patient daily. The patient may be in a special care unit for 24 to 48 hours after surgery for monitoring of bleeding and adrenal insuffi- ciency. A drain placed near the site of incision removes residual fluid. Because of the discomfort of deep breathing, the patient is at risk for atelectasis. Fever, chills, thick sputum, or decreased breath sounds suggest pneumonia. Managing pain after surgery usually requires opioid anal- gesics given IV. The incision was made through major muscle groups used with breathing and movement. Liberal use of anal- gesics is needed for 3 to 5 days after surgery to manage pain. Oral agents may be tried when the patient can eat and drink. The prevention of complications focuses on infection and management of adrenal insufficiency. Antibiotics may be pre- scribed during and after surgery to prevent infection. The need for additional antibiotics is based on evidence of infection. Assess the patient at least every 8 hours for indications of sys- temic infection or local wound infection. Adrenal insufficiency is possible as a complication of kidney and adrenal gland removal. Although only one adrenal gland may be affected, the remaining gland may not be able to secrete sufficient glucocorticoids immediately after surgery. Steroid replacements may be needed in some patients. Chapter 54 dis-

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