Orderly Function of the Urinary System

The urinary system is responsible for producing, storing, and excreting urine; these processes prevent the body from becoming toxic. The kidneys facilitate reabsorption of necessary nutrients, water, and electrolytes. Cleansing the blood of the waste products of metabolism and regulating the water, salts, and acids in the body fluids ensure the body’s homeostasis. Regulation of volume of water in the body is an essential function of the urinary system. E11-1 The urinary system includes the kidneys, which manufacture urine and play a role in the regulation of systemic blood pressure and the accessory structures. The ureters transport urine and the bladder stores urine until it is excreted voluntarily through the urethra. The organs and accessory structures of the urinary system consist of two kidneys, two ureters, the urinary bladder, and the urethra (Figure 11-1).

Each kidney (Figure 11-2) is composed of about 1 million microstructures called nephrons (Figure 11-3). The nephrons, the units of function in the kidney, are responsible for filtration, reabsorption, and secretion of urine. Figure 11-4 depicts the formation of urine. The urine is transported from the nephron to the renal pelvis and then to the ureters. The kidney has many other functions, including the secretion of rennin, a hormone that raises blood pressure, and erythropoietin, which acts as a stimulus for red blood cell (RBC) production. It also has a role in the activation of vitamin D.

Nephrons are composed of the glomerulus, Bowman’s capsule, the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule and the collecting duct. The nephrons, the units of function in the kidney, are responsible for filtration, reabsorption, and secretion of urine.

Each kidney, (see Figure 11-2) as a primary organ of the urinary system, processes blood to form urine that contains waste products to be eliminated from the body. The bean-shaped organs, about the size of a human fist, are located in the back retroperitoneally to the abdominal cavity and lateral to the spinal column. Each kidney is separated into three areas or regions: the cortex, the medulla, and the renal pelvis.

Blood enters the kidneys by way of the renal arteries through the hilum. Refer to Figures 11-1 and 11-2 for blood supply to and from the kidneys. The arteries divide and divide again and again into smaller arteries that ultimately enter the nephrons. Blood leaves the kidneys by way of the renal veins.

Urine leaves the kidneys by way of two long, slender tubes, the ureters that enter the lower part of the urinary bladder. Peristalsis in the muscular walls of the ureters moves the urine into the urinary bladder where it is temporarily stored until it is passed from the body by way of the urethra. Urine is voluntarily excreted from the bladder by way of the urethra in a process called urination or micturition. The urethra is a tubular structure that extends from the base of the urinary bladder to the urinary meatus (urethral orifice) on the external surface of the body. Refer to Figure 11-1.

Infection, scarring, toxic necrosis, or trauma of the urinary tract can result in disturbances of renal function that allow urea (the nitrogenous waste of metabolism in urine) or extracellular fluid and electrolytes to accumulate in the blood. Congenital or acquired structural defects and tumors cause obstructive diseases of the urinary system. Other important diseases of the urinary tract are immunologic disorders, circulatory disturbances, cystic disease, and metabolic disorders (e.g., diabetes mellitus).

The function of the urinary system often is evaluated by urinalysis (Table 11-1) and blood tests (Table 11-2). Normal results demonstrate proper filtration, absorption, and elimination of metabolic waste, as well as precise fluid and electrolyte balance. Other tests for urinary tract disorders include culture and sensitivity tests to determine appropriate antibiotic therapy, radiologic tests that visualize structural and functional abnormalities, cystoscopy (see Figure 11-4), and biopsy of lesions.

Usually symptoms of urinary diseases reflect an accumulation of waste products in the blood and cause electrolyte imbalances in the body. Common symptoms include the following:

Acute Glomerulonephritis

Description

Acute glomerulonephritis is an inflammation and swelling of the glomeruli (see Figure 11-3) of the kidneys. It can be a primary disease of the kidney or may develop secondary to a systemic disease. This condition usually follows a streptococcal bacterial infection of the throat or skin.

 ICD-9-CM Code 580 (Requires 4th digit)

 ICD-10-CM Code N00.3 (Acute nephritic syndrome with diffuse mesangial proliferative glomerulonephritis)

(N00.0-N00.5 = 6 codes of specificity)

Acute glomerulonephritis is coded according to sites and types of lesions. Refer to the physician’s diagnosis for site and type of lesion and to the current editions of the ICD-9-CM and ICD-10-CM coding manuals.

Symptoms and Signs

Acute glomerulonephritis is marked by proteinuria (protein in the urine), edema, and decreased urine volume. Hematuria can range from insignificant to a sudden onset of urine that is grossly bloody (gross hematuria). The urine may appear dark or may be described as coffee colored. Occurring most often in children and adolescents, this disease process usually follows a streptococcal infection by 1 to 2 weeks (poststreptococcal glomerulonephritis). Hypertension related to altered renal function and fluid retention is possible, accompanied by headaches, visual disturbances, malaise, anorexia, and a low-grade fever. Flank or back pain develops as a result of swelling of the kidney tissue.

Patient Screening

Patients complaining of bloody urine accompanied by edema, headache, and flank or pelvic pain require prompt medical attention.

Etiology

This condition usually follows an infection caused by group A β-hemolytic streptococcus. E11-2 It also can be idiopathic or may result from an immune reaction that causes circulating antigen-antibody complexes to become trapped within the network of capillaries of a glomerulus. In some cases, the antigen is endogenous (arising from within) as an accompaniment of tumors. The injury to the glomeruli results in a decrease in the rate of filtration of the blood, and consequently retention of water and salts in the body. Figure 11-5 is a schematic representation of changes occurring in the nephron with acute poststreptococcal glomerulonephritis.

Diagnosis

The diagnosis is made by the clinical findings, clinical history, and urinalysis. The urine shows gross blood and the presence of RBCs, white blood cells (WBCs), renal tubular cells, and casts. Proteinuria may be present because of increased permeability of the glomerular membrane. Blood tests show elevated blood urea nitrogen (BUN), hypoalbuminemia, and an elevated erythrocyte sedimentation rate (ESR). Kidney-ureter-bladder (KUB) radiographic films and ultrasonography may reveal bilateral enlargement of the kidneys. Renal biopsy may confirm the diagnosis (Figure 11-6).

Treatment

No specialized therapy is available for the poststreptococcal type of glomerulonephritis other than antibiotic therapy, if infection is still present, and rest. Diuretics help control edema and hypertension. Sodium intake is restricted to prevent circulatory overload and convulsions. Occasionally, corticosteroids are used if an immune reaction is the suspected cause.

Prognosis

Most cases resolve within 2 weeks, and the patient experiences a spontaneous recovery.

Prevention

Prevention depends on the cause of the condition. Streptococcus type of infections require medical intervention with antibiotics.

Patient Teaching

Explain the underlying cause to patients and their families. Patients are instructed to take medications as prescribed, especially antibiotics, until all are gone. During the acute stage, bed rest should be instituted along with sodium intake restriction. It is helpful to review the symptoms being reported to the physician. These symptoms include weight gain, decreased urinary output, changes in urine color, and an increase in blood pressure. Pregnant women with a history of acute glomerulonephritis require frequent medical evaluation. Provide the patient visual aids depicting the urinary system and its functions.

Chronic Glomerulonephritis

Description

Chronic glomerulonephritis (CGN) is a slowly progressive, noninfectious disease that can lead to irreversible renal damage and renal failure. As an advanced stage of many kidney disorders, CGN results in inflammation followed by progressive destruction of the glomeruli. This progressive destruction causes a reduction in glomerular filtration with resulting retention of uremic poisons.

 ICD-9-CM Code 582 (Requires 4th digit)

 ICD-10-CM Code N03.2 (Chronic nephritic syndrome with diffuse membranous glomerulonephritis)

(N03.0-N03.5 = 6 codes of specificity)

Chronic glomerulonephritis is coded according to sites and types of lesions. Refer to the physician’s diagnosis for site and type of lesion and to the current editions of the ICD-9-CM and ICD-10-CM coding manuals.

Symptoms and Signs

At first, chronic glomerulonephritis is asymptomatic; then subclinical progression of the disease leads to hypertension, hematuria, proteinuria, oliguria, and edema. In the later stages with increasing renal failure, the hypertension becomes severe and azotemia develops. When the kidneys fail to remove urea from the blood (the condition of azotemia), the body compensates by attempting to excrete urea through the sweat glands. Tiny crystals of urea appear on the skin; this condition is termed uremic frost. The patient experiences fatigue, malaise, nausea, vomiting, pruritus, and dyspnea.

Patient Screening

Patients with CGN probably will already have been diagnosed and scheduled for routine follow-up visits. New patients may be referrals and will require scheduling as soon as possible. Any patient complaining of hematuria should be scheduled for an appointment as soon as possible. Often, hypertension symptoms along with malaise and edema are the reported symptoms that indicate the need for prompt attention.

Etiology

Immune mechanisms are suspected to be a major cause of chronic glomerulonephritis; antigen-antibody complexes lodge in the glomerular capsular membrane, triggering an inflammatory response and glomerular injury. Primary renal disorders and multisystem diseases, such as systemic lupus erythematosus are other possible causes.

Diagnosis

The diagnostic studies used to detect CGN are the same as those used for acute glomerulonephritis: urinalysis, blood tests, radiographic studies, ultrasonography, and renal biopsy. The findings include signs of advanced renal insufficiency, rising BUN and serum creatinine levels, and grossly abnormal findings on urinalysis. Renal biopsy and the use of sophisticated tools, such as electron microscopy and immunofluorescence, are valuable in determining the optimal treatment and the prognosis.

Treatment

The goals of treatment are to control edema, treat the hypertension, and prevent congestive heart failure and uremia. The patient is given supportive measures for comfort. Medical treatment includes the administration of antihypertensives, diuretics, and antibiotics if urinary tract infection (UTI) develops. Protein, salt (Na⁺ and phosphate), and fluid intake may be limited in the diet. ACE inhibitors are often used to aid in the reduction of excess protein in the urine. The patient may require dialysis (see Figure 11-8) or may be a candidate for kidney transplantation.

Prognosis

Prognosis is variable according to the extent of the destruction to the kidney and the patient’s response to therapy. Eventually chronic glomerulonephritis will lead to end-stage renal disease (Figure 11-7). Dialysis may help the patient until a kidney transplant can be performed.

Prevention

Prompt treatment of acute glomerulonephritis, diabetes, and hypertension can help in the prevention of CGN.

Patient Teaching

Compliance with treatment regimens to reduce hypertension should be stressed to the patient. Prompt attention to infections is an important factor also to be stressed. When dialysis is necessary, encourage the patient and family to seek out support groups as well as available community resources. Advise patients to take diuretics in the morning to avoid disruption of sleep at night. Offer visual aids, including videos when available, that explain the anatomy and function of the urinary system.

 Enrichment

Dialysis and Kidney Transplantation

In the United States, end-stage renal disease (ESRD) develops in an average of 1.3 in 10,000 people each year. In renal failure, the kidneys no longer can process blood and form urine. Therapy should begin before the development of ultimately fatal uremic symptoms. Dialysis or kidney transplantation, if successful, offers rehabilitation and extended life to patients with ESRD.

Dialysis

Dialysis filters out unwanted elements from the blood by diffusion across a semipermeable membrane; the healthy kidneys usually remove these wastes. Thus the proper fluid, electrolyte, and acid-base balances are maintained in the body. Two methods used to perform blood dialysis are hemodialysis and peritoneal dialysis

Even though these procedures do not cure renal failure, many patients are stabilized after 10 to 15 years of treatment.

Hemodialysis. Hemodialysis can take place in the home or at a hospital. It removes impurities or wastes from the patient’s blood by using an artificial kidney (hemodialyzer). Access to the bloodstream is created surgically in the arm, leg, or subclavian vein with an internal fistula, which allows the blood to pass from the patient’s body to the semipermeable membrane in the machine. The cleaned blood then returns to the patient in a procedure that takes 3 to 4 hours. The patient usually receives two or three sessions a week.

Peritoneal dialysis. Peritoneal dialysis is carried out in the patient’s own body by using a dialysate solution and the peritoneal membrane to filter out the harmful toxins and excessive fluid. The clean dialyzing fluid passes into the peritoneal cavity through a permanent indwelling peritoneal catheter, and wastes diffuse across the peritoneal membrane into the fluid. The contaminated fluid then is drained and replaced with fresh fluid.

• Continuous ambulatory peritoneal dialysis (CAPD) takes place without a machine by allowing the solution to drain by gravity into a dialysis bag worn around the waist. This procedure takes about 15 minutes and is repeated 3 to 4 times a day and once at night.

• Continuous cycling peritoneal dialysis (CCPD) takes place while the patient sleeps, using a cycling machine.

• Intermittent peritoneal dialysis (IPD) takes several hours, 3 to 5 times a week, and usually is done in a clinic.

Kidney Transplantation

Kidney transplantation is the surgical placement of a donor kidney into a patient with irreversible renal failure. Used synergistically with clinical dialysis, kidney transplantation is one of medicine’s success stories. Kidney transplantation leads the field of organ replacement, with many patients being on waiting lists. Immunosuppressive agents are used to prevent or treat rejection syndrome. Sophisticated evaluation of the donor and the recipient to find a good human leukocyte antigen (HLA) match offers the best chance for a good prognosis.

Of the 10,000 kidney transplants done annually in the United States, 75% are performed on patients with diabetes, adrenal failure, hypertensive renal disease, and glomerulonephritis.

Nephrotic Syndrome (Nephrosis)

Description

Nephrotic syndrome, a disease of the basement membrane of the glomerulus, is secondary to a number of renal diseases and a variety of systemic disorders. Nephrotic syndrome encompasses a group of symptoms sometimes referred to as the protein-losing kidney.

 ICD-9-CM Code 581 (Requires 4th digit)

 ICD-10-CM Code N04.4 (Nephrotic syndrome with diffuse endocapillary proliferative glomerulonephritis)

(N04.0-N04.5 = 6 codes of specificity)

Nephrotic syndrome is coded according to sites and types of lesions. Refer to the physician’s diagnosis for site and type of lesion and to the current editions of the ICD-9-CM and ICD-10-CM coding manuals.

Symptoms and Signs

The patient with nephrotic syndrome loses excessive amounts of protein, mainly albumin, in the urine (proteinuria). The excessive loss of protein in the urine results in depressed plasma protein levels (hypoalbuminemia). Glomerular filtration becomes diminished and water and sodium are retained, resulting in edema and hypertension. The syndrome includes microscopic or gross hematuria. Plasma lipid levels are elevated, but the reason for this is not understood. Sloughed-off fat bodies can be found in the urine. The patients are especially susceptible to infections.

The syndrome causes the patient to feel lethargic and depressed, with loss of appetite. He or she appears pale and puffy around the eyes, has swollen ankles (pitting edema), and gains weight. Skin irritation related to edema may be present.

Patient Screening

As previously mentioned, patients complaining of bloody urine accompanied by edema, headache, and flank or pelvic pain require prompt medical attention. The additional complaints of lethargy and sudden weight gain indicate the need for prompt attention as well.

Etiology

Nephrotic syndrome is caused by increased permeability of the glomerulus, indicating renal damage. This condition may follow an attack of glomerulonephritis or it may be the result of exposure to certain toxins or drugs (Box 11-1), pregnancy, or kidney transplants. Metabolic diseases, such as diabetes mellitus, certain infections, and allergic reactions are conditions that may lead to nephrotic syndrome.

Box 11-1

Nephrotoxic Agents

SOLVENTS

Carbon tetrachloride

Methanol

Ethylene glycol

HEAVY METALS

Lead

Arsenic

Mercury

PESTICIDES

ANTIBIOTICS

Kanamycin

Gentamicin

Polymyxin B

Amphotericin B

Colistin

Neomycin

Phenazopyridine

NONSTEROIDAL ANTIINFLAMMATORY DRUGS

IODINATED RADIOGRAPHIC CONTRAST MEDIA

ANTINEOPLASTIC AGENTS

MISCELLANEOUS COMPOUNDS

Acetaminophen

Amphetamines

Heroin

Silicon

Cyclosporine

POISONOUS MUSHROOMS

Modified from Monahan F et al: Phipps’ medical-surgical nursing, health and illness perspectives, ed 8, St Louis, 2007, Mosby.

Diagnosis

The diagnosis is based on the clinical findings and the presence of gross proteinuria and lipiduria (the presence of fatty casts) in a 24-hour urine specimen. Abnormal blood study serum values, including hypoalbuminemia and hyperlipidemia, support the diagnosis. If a renal tumor is suspected, a renal biopsy with histologic study is indicated.

Treatment

Effective treatment begins by addressing the underlying cause. Dietary intake of protein is adjusted to the glomerular filtration rate (GFR). Diuretics and decreased sodium intake help to control edema. The use of ACE inhibitors is helpful for treating hypertension and usually reduces protein loss. A course of corticosteroids, such as prednisone, may have the positive effect of controlling the proteinuria for some patients. Urine output must be monitored. If the condition does not improve with treatment, the syndrome can progress to end-stage renal disease.

Prognosis

Prognosis is variable according to the extent of the destruction and patient response to therapy. Eventually nephrotic syndrome that is nonresponsive to treatment leads to end-stage renal disease.

Prevention

Prompt treatment of glomerulonephritis is important in prevention of this condition. Avoiding exposure to certain toxins or drugs (see Box 11-1) helps prevent the syndrome, as does prompt treatment after exposure to these toxins. Monitoring the kidney function of women during pregnancy and of any patients with metabolic diseases, such as diabetes mellitus, certain infections, and allergic reactions may assist the physician in detecting malfunction early on, and therefore treatment can be instituted early on.

Patient Teaching

Advise patients and families to contact the physician immediately if any exacerbation of symptoms is noted. Encourage patients to remain active, to exercise, and to practice good skin care. Additionally, encourage them to seek out support groups and resource agencies in the community. Refer patients to a dietitian for instruction on planning a high-protein, low-sodium diet as prescribed. Offer visual aids, including videos when available, that explain the anatomy and function of the urinary system.

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