Renal and Urologic Disorders

INTRODUCTION

The kidneys are located retroperitoneally in the lumbar area, with the right kidney a little lower than the left because of the liver mass above it. The left kidney is slightly longer than the right and closer to the midline. The kidneys move as body position changes. They’re covered by the fibrous capsule, perirenal fat, renal fascia, and pararenal fat. (See Structure of the kidneys, page 340.)

Renal arteries branch into five segmental arteries that supply different areas of the kidneys. The segmental arteries then branch into several divisions from which the afferent arterioles and vasa recta arise. Renal veins follow a similar branching pattern, characterized by stellate vessels and segmental branches, and empty into the inferior vena cava. The tubular system receives its blood supply from a peritubular capillary network of vessels.

The gross structure of each kidney includes the lateral and medial margins, the hilus, the renal sinus, and renal parenchyma. The hilus, located at the medial margin, is the indentation where the blood and lymph vessels enter the kidney and the ureter emerges. The hilus leads to the renal sinus, which is a spacious cavity filled with adipose tissue, branches of the renal vessels, calyces, the renal pelvis, and the ureter. The renal sinus is surrounded by parenchyma, which consists of a cortex and a medulla.

The cortex (outermost layer of the kidney) contains glomeruli (parts of the nephron), cortical arches (areas that separate the medullary pyramids from the renal surface), columns of Bertin (areas that separate the pyramids from one another), and medullary rays of Ferrein (long, delicate processes from the bases of the pyramids that mix with the cortex). The medulla contains pyramids (cone-shaped structures of parenchymal tissue), papillae (apical ends of the pyramids through which urine oozes into the minor calyces), and papillary ducts of Bellini (collecting ducts in the pyramids that empty into the papillae).

URETERS

The ureters are a pair of retroperitoneally located, mucosa-lined, fibromuscular tubes that transport urine from the renal pelvis to the urinary bladder. Although the ureters have no sphincters, their oblique entrance into the bladder creates a mucosal fold that may produce a sphincterlike action.

The adult urinary bladder is a spherical, hollow muscular sac, with a normal capacity of 300 to 600 ml. It’s located anterior and inferior to the peritoneal cavity, and posterior to the pubic bones. The gross structure of the bladder includes the fundus (large central, posterosuperior portion of the bladder), the apex (anterosuperior region), the body (posteroinferior region containing the ureteral orifices), and the urethral orifice, or neck (most inferior portion of the bladder). The three orifices comprise a triangular area called the trigone.

NEPHRONS

The functional units of each kidney are its 1 to 3 million nephrons. Each nephron is composed of the renal corpuscle and the tubular system. The renal corpuscle includes the glomerulus (a network of minute blood vessels) and Bowman’s capsule (an epithelial sac surrounding the glomerulus that’s part of the tubular system). The renal corpuscle has a vascular pole, where the afferent arteriole enters and the efferent arteriole emerges, and a urinary pole that narrows to form the beginning of the tubular system. The tubular system includes the proximal convoluted tubule, the loop of Henle, and the distal convoluted tubule. The last portion of the nephron consists of the collecting duct.

INNERVATION AND VASCULATURE

The kidneys are innervated by sympathetic branches from the celiac plexus, upper lumbar splanchnic and thoracic nerves, and the intermesenteric and superior hypogastric plexuses, which form a plexus around the kidneys. Similar numbers of sympathetic and parasympathetic nerves from the renal plexus, superior hypogastric plexus, and intermesenteric plexus innervate the ureters. Nerves that arise from the inferior hypogastric plexuses innervate the bladder. The parasympathetic nerve supply to the bladder controls micturition.

The ureters receive their blood supply from the renal, vesical, gonadal, and iliac arteries, and the abdominal aorta. The ureteral veins follow the arteries and drain into the renal vein. The bladder receives blood through vesical arteries. Vesical veins unite to form the pudendal plexus, which empties into the iliac veins. A rich lymphatic system drains the renal cortex, the kidneys, the ureters, and the bladder.

HOMEOSTASIS

Through the production and elimination of urine, the kidneys maintain homeostasis. These vital organs regulate the volume, electrolyte concentration, and acid-base balance of body fluids; detoxify the blood and eliminate wastes; regulate blood pressure; and aid in erythropoiesis. The kidneys eliminate wastes
from the body through urine formation (by glomerular filtration, tubular reabsorption, and tubular secretion) and excretion. Glomerular filtration, the process of filtering the blood flowing through the kidneys, depends on the permeability of the capillary walls, vascular pressure, and filtration pressure. The normal glomerular filtration rate (GFR) is about 120 ml/minute.

CLEARANCE MEASURES FUNCTION

Clearance is the volume of plasma that can be cleared of a given substance per unit of time, and depends on how renal tubular cells handle the substance that has been filtered by the glomerulus:

If the tubules don’t reabsorb or secrete the substance, clearance equals the GFR.
If the tubules reabsorb it, clearance is less than the GFR.
If the tubules secrete it, clearance is greater than the GFR.
If the tubules reabsorb and secrete it, clearance is less than, equal to, or greater than the GFR.

The most accurate measure of glomerular function is creatinine clearance, because this substance is filtered only by the glomerulus and isn’t reabsorbed by the tubules.

The transport of filtered substances in tubular reabsorption or secretion may be active (requiring the expenditure of energy) or passive (requiring none). For example, energy is required to move sodium across tubular cells (active transport), but none is required to move urea (passive transport). The amount of reabsorption or secretion of a substance depends on the maximum tubular transport capacity for that substance; that is, the greatest amount of a substance that can be reabsorbed or secreted per minute without saturating the system.

WATER REGULATION

Hormones partially control water regulation by the kidneys. Hormonal control depends on the response of osmoreceptors to changes in osmolality. The two hormones involved are antidiuretic hormone (ADH), produced by the pituitary gland, and aldosterone, produced by
the adrenal cortex. ADH alters the collecting tubules’ permeability to water. When plasma concentration of ADH is high, the tubules are very permeable to water, so a greater amount of water is reabsorbed, creating a high concentration but small volume of urine. The reverse is true if ADH concentration is low.

Aldosterone regulates sodium and water reabsorption from the distal tubules. High plasma aldosterone concentration promotes sodium and water reabsorption from the tubules and decreases sodium and water excretion in the urine; low plasma aldosterone concentration promotes sodium and water excretion. Aldosterone also helps control the distal tubular secretion of potassium. Other factors that determine potassium secretion include the amount of potassium ingested, number of hydrogen ions secreted, level of intracellular potassium, amount of sodium in the distal tubule, and the GFR.

The countercurrent mechanism — composed of a multiplication system and an exchange system that occur in the renal medulla via the limbs of the loop of Henle and the vasa recta — is the method by which the kidneys concentrate urine. It achieves active transport of sodium and chloride between the loop of Henle and the medullary interstitial fluid. Failure of the countercurrent mechanism produces polyuria and nocturia.

To regulate acid-base balance, the kidneys secrete hydrogen ions, reabsorb sodium and bicarbonate ions, acidify phosphate salts, and synthesize ammonia — which keep the blood at its normal pH of 7.37 to 7.43.

The kidneys assist in regulating blood pressure by synthesizing and secreting renin in response to an actual, or perceived, decrease in the volume of extracellular fluid. Renin, in turn, acts on a substrate to form angiotensin I, which is converted to angiotensin II. Angiotensin II increases arterial blood pressure by peripheral vasoconstriction and stimulation of aldosterone secretion. The resulting increase in the aldosterone level promotes the reabsorption of sodium and water to correct the fluid deficit and renal ischemia.

The kidneys secrete erythropoietin in response to decreased oxygen tension in the renal blood supply. Erythropoietin then acts on the bone marrow to increase the production of red blood cells (RBCs).

Renal tubular cells synthesize active vitamin D and help regulate calcium balance and bone metabolism.

CLINICAL ASSESSMENT

Assessment of the renal and urologic systems begins with an accurate patient history and requires a thorough physical examination and certain laboratory data and test results from invasive and noninvasive procedures. When obtaining a patient history, ask about symptoms that pertain specifically to the pathology of the renal and urologic systems, such as frequency or urgency, and about the presence of any systemic diseases that can produce renal or urologic dysfunction, such as hypertension, diabetes mellitus, or bladder infections. Family history may also suggest a genetic predisposition to certain renal diseases, such as glomerulonephritis or polycystic kidney disease. Also, ask what medications the patient has been taking; abuse of analgesics or antibiotics may cause nephrotoxicity.

PHYSICAL EXAMINATION FOR RENAL DISEASE

The first step in physical examination is careful observation of the patient’s overall appearance, because renal disease affects all body systems. Examine the patient’s skin for color, turgor, intactness, and texture; mucous membranes for color, secretions, odor, and intactness; eyes for periorbital edema and vision; general activity for motion, gait, and posture; muscle movement for motor function and general strength; and mental status for level of consciousness, orientation, and response to stimuli. (See Common renal symptoms, page 342.)

Renal disease causes distinctive changes in vital signs: hypertension due to fluid and electrolyte imbalances and hyperactivity of the renin-angiotensin system; a strong, fast, irregular pulse due to fluid and electrolyte imbalances; hyperventilation to compensate for metabolic acidosis; and an increased susceptibility to infection due to overall decreased resistance. Palpation and percussion may reveal little because the kidneys and bladder are difficult to palpate unless they are enlarged or distended.

NONINVASIVE TESTS AND MONITORING

Laboratory tests analyze serum levels of chemical substances such as uric acid, creatinine, and blood urea nitrogen; tests also determine urine characteristics, including the presence of RBCs, white blood cells, casts, or bacteria; specific gravity and pH; and physical properties, such as clarity, color, and odor. (See Serum and urine values in renal disease, page 343.)

Intake and output assessment: Fluid intake and output measurement helps determine the patient’s hydration status but isn’t a reliable
method of evaluating renal function because urine output varies with different types of renal disorders. To provide the most useful and accurate information, use calibrated containers, establish baseline values for each patient, compare measurement patterns, and validate intake and output measurements by checking the patient’s weight daily. Monitor all fluid losses — including blood, vomitus, and diarrhea. Also assess wound and stoma drainage daily.
Specimen collection: Meticulous specimen collection is vital for valid laboratory data. If the patient is collecting the specimen, explain the importance of cleaning the meatal area thoroughly. The culture specimen should be caught midstream, in a sterile container; a specimen for urinalysis, in a clean container, preferably at the first voiding of the day. Begin a 24-hour specimen collection after discarding the first voiding; such specimens often necessitate special handling or preservatives. When obtaining a urine specimen from a catheterized patient, remember to avoid taking the specimen from the collection bag; instead, aspirate a sample through the collection port in the catheter, with a sterile needle and a syringe.
Kidney-ureter-bladder radiography: This test assesses size, shape, position, and areas of calcification of these organs.
Ultrasonography: This safe, painless procedure allows for visualization of the renal parenchyma, calyces, pelvis, ureters, and bladder. Because the test doesn’t depend on renal function, it’s useful in patients with renal failure and in detecting complications after kidney transplantation.
Invasive tests: See Invasive diagnostic tests for assessing the renal and urologic systems, pages 344 and 345.

Common renal symptoms

Symptom	Possible cause
Dribbling	Prostatic enlargement, strictures
Dysuria	Infection, inflammation of bladder or urethra
Edema	Nephrotic syndrome, failure
Frequency	Infection, diabetes, bladder tumors, medications
Hematuria	Glomerular diseases, trauma, neoplasms, renal calculi
Hesitancy	Neurogenic bladder, infection
Incontinence	Infection, neoplasms, prolapsed uterus
Nocturia	Infection, nephrotic syndrome, diabetes, medications
Oliguria	Failure, insufficiency, neoplasms
Proteinuria	Glomerular diseases, infection
Pyuria	Infection
Renal colic	Calculi
Urgency	Infection, prostatic disease, medications

TREATMENT METHODS

Treatment of intractable renal or urinary system dysfunction may require urinary diversion, dialysis, or kidney transplantation. Urinary diversion is the surgical creation of an outlet for excreting urine. The types of urinary diversion include ileal conduit, cutaneous ureterostomy, ureterosigmoidostomy, and creation of a rectal bladder.

In dialysis, a semipermeable membrane, osmosis, and diffusion imitate normal renal function by eliminating excess body fluids, maintaining or restoring plasma electrolyte and acid-base balance, and removing waste products and dialyzable poisons from the blood. Dialysis is most often used for patients with acute or chronic renal failure. The two most common types of dialysis are peritoneal dialysis and hemodialysis.

In peritoneal dialysis, a dialysate solution is infused into the peritoneal cavity. Substances then diffuse through the peritoneal membrane. Waste products remain in the dialysate solution and are removed.

Hemodialysis separates solutes by differential diffusion through a cellophane membrane placed between the blood and the dialysate solution, in an external receptacle. Because the blood must actually pass out of the body into a dialysis machine, hemodialysis requires an access route to the blood supply by an arteriovenous fistula or cannula or by a bovine or synthetic graft. When caring for a patient with such an access route, monitor the patency of the access route, prevent infection, and promote safety and adequate function. After dialysis, watch for such complications as headache, vomiting, agitation, and twitching.

Serum and urine values in renal disease

	Normal serum value	Deviation	Normal urine value	Deviation
Sodium	135 to 145 mEq/L	↑ or N	30 to 280 mEq/L	V
Potassium	3.8 to 5.5 mEq/L	↑	25 to 100 mEq/L	↓
Chloride	100 to 108 mEq/L	↑	110 to 250 mEq/24hr	↓
Calcium	8.9 to 10.1 mg/dl	↓	Female: < 250 mg/24 hr	↓
			Male: < 275 mg/24 hr
Phosphorus	2.5 to 4.5 mg/dl	↑or N	1 g/24 hr	V
Magnesium	1.7 to 2.1 mEq/L	↑	< 150 mg/24 hr	↓
Carbon dioxide combining power	22 to 34 mEq/L	↓
Specific gravity			1.005 to 1.035	↓
pH			4.5 to 8	↑
Blood urea nitrogen	8 to 20 mg/dl	↑	10 to 20 g/L	↓
Creatinine	Female: 0.6 to 0.9 mg/dl	↑	Female: 0 to 80 mg/24 hr	↓
	Male: 0.8 to 1.2 mg/dl		Male: 0 to 40 mg/24 hr
Osmolality	280 to 295 mOsm/kg	V	500 to 1,400 mOsm/kg	↓
Uric acid	Female: 2.3 to 6 mg/dl	↑
	Male: 4.3 to 8 mg/dl
Glucose	70 to 100 mg/dl	N	0	N
Protein	6.9 to 7.9 g/dl	↓ or N	0	V
Hematocrit	Female: 38% to 46%	↓
	Male: 42% to 54%
Hemoglobin	Female: 12 to 16 g/dl	↓
	Male: 14 to 18 g/dl
White blood cells	4,000 to 10,000/l		None	V
Red blood cells			None	V
Casts			None	V
Bacteria			None	V
Alkaline phosphatase	Female age 24 to 65: 82 to 282 U/L	↑
	Male age 19 or older: 98 to 251 U/L
KEY: ↑ = increased; ↓ = decreased; N = normal; V = varies

Invasive diagnostic tests for assessing the renal and urologic systems

Several invasive tests are available to assist in diagnosis of renal and urologic problems. The most serious complication, which occurs with many of these procedures, is hypersensitivity to the contrast media. Symptoms may include increased pulse rate, itching, hives, chills, fever, dyspnea, and shock.

Procedure	Purpose	Special considerations
Computed tomography scan (CT) or magnetic resonance imaging (MRI)	Although CT scan and MRI can be noninvasive, I.V. contrast material is often given to enhance the views obtained. These tests are especially helpful in evaluating renal or bladder mass lesions.	Before: Check for prior history of contrast sensitivity. After: After using I.V. contrast medium, observe for hypersensitivity reaction and hematoma at injection site.
Cystoscopy	A fiber-optic scope is used to visualize the inside of the bladder in cystoscopy.	Before: Give sedatives as ordered. After: Offer increased fluids; administer analgesics; watch for hematuria and signs of perforation, hemorrhage, and infection (chills, fever, increased pulse rate, shock).
Cystourethrography	In cystourethrography, X-rays and I.V. contrast material are used to determine size and shape of the bladder and urethra.	Before: Check for prior history of contrast sensitivity. During: Catheterize the patient. After: Offer increased fluids; observe for hypersensitivity reaction.
Cystometry	Cystometry is used to evaluate bladder pressure, sensation, and capacity. A catheter is introduced into the bladder, and saline solution is instilled. Results are shown on a computer at the time of testing.	Before: Observe voiding; catheterize for residual urine. After: Remove catheter; watch for stress incontinence when patient coughs; watch voiding; catheterize for residual urine.
Excretory urography	Excretory urography uses X-rays and I.V. contrast material to allow visualization of renal parenchyma, calyces, pelves, ureters, bladder, and stones.	Before: Check for prior history of contrast sensitivity. After: Observe for hypersensitivity reaction; watch for hematomas at injection site.
Nephrotomography	In nephrotomography, I.V. contrast material and tomography are used to visualize parenchymia, calyces, and pelves in layers.	Before: Check for prior history of contrast sensitivity. After: Observe for hypersensitivity reaction.
*Renal angiography*	Renal angiography uses contrast material injected into a catheter in the femoral artery or vein to allow visualization of the arterial tree and capillaries as well as venous drainage of the kidney.	Before: Check for prior history of contrast sensitivity. After: Observe for hypersensitivity reaction, hematomas and hemorrhage at injection site, and nephrotoxicity. Offer increased fluids.
*Renal scan*	In renal scan, radioisotopes are administered I.V., and images of the kidney are taken at intervals to determine renal function.	Before: Check for prior history of sensitivity. After: Observe for hypersensitivity reaction.
*Renal biopsy*	The specimen obtained in renal biopsy is used to develop histologic diagnosis and determine therapy and prognosis.	Before: Make sure the patient’s clotting times, prothrombin times, and platelet count are recorded on his chart. After: Apply gentle pressure to the bandage site. Watch for hemorrhage and hematoma at the biopsy site, and look for hematuria.

Patients with end-stage renal disease may benefit from kidney transplantation, despite its limitations: a shortage of donor kidneys, the chance of transplant rejection, and the need for lifelong medications and follow-up care. After kidney transplantation, maintain fluid and electrolyte balance, prevent infection, monitor for rejection, and promote psychological wellbeing.

CONGENITAL ANOMALIES

Medullary sponge kidney

In medullary sponge kidney, the collecting ducts in the renal pyramids dilate, and cavities, clefts, and cysts form in the medulla. This disease may affect only a single pyramid in one kidney or all pyramids in both kidneys. The kidneys are usually somewhat enlarged but may be of normal size; they appear spongy.

Because this disorder is usually asymptomatic and benign, it’s often overlooked until the patient reaches adulthood. The prognosis is generally very good. Medullary sponge kidney is unrelated to medullary cystic disease; these conditions are similar only in the presence and location of the cysts.

CAUSES AND INCIDENCE

Medullary sponge kidney may be transmitted as an autosomal dominant trait, but this remains unproven. Most nephrologists consider it a congenital abnormality.

Although medullary sponge kidney may be found in both sexes and in all age-groups, it primarily affects males ages 40 to 70. It occurs in about 1 in every 5,000 to 20,000 persons.

SIGNS AND SYMPTOMS

Symptoms usually appear only as a result of complications and are seldom present before adulthood. Complications include formation
of calcium oxalate stones, which lodge in the dilated cystic collecting ducts or pass through a ureter, and infection secondary to dilation of the ducts. These complications, which occur in about 30% of patients, are likely to produce severe colic, hematuria, lower urinary tract infection ([UTI]; burning on urination, urgency, frequency), and pyelonephritis. Secondary impairment of renal function from obstruction and infection occurs in only about 10% of patients.

SPECIAL CONSIDERATIONS

Patient care includes explaining the disease to the patient and his family and reassuring them that the condition is benign and the prognosis good.

To prevent infection, instruct the patient to bathe often and use proper toilet hygiene; this is especially important for a female patient because the proximity of the urinary meatus and the anus increases the risk of infection.
If infection occurs, stress the importance of completing the prescribed course of antibiotic therapy.
Emphasize the need for adequate fluid intake.
Explain all diagnostic procedures, and provide emotional support. Teach the patient how to collect a clean-catch urine specimen for culture. Check for allergy to excretory urography dye.
When the patient is hospitalized for a stone, strain all urine, administer analgesics as ordered, and force fluids. Before discharge, tell the patient to watch for and report any signs of stone passage and UTI.

Polycystic kidney disease

Polycystic kidney disease is an inherited disorder characterized by multiple, bilateral, grapelike clusters of fluid-filled cysts that grossly enlarge the kidneys, compressing and eventually replacing functioning renal tissue. (See Polycystic kidney.) The disease appears in two distinct forms: The infantile form typically causes stillbirth or early neonatal death, although some infants may survive for 2 years, then develop fatal renal, cardiac, or respiratory failure. The adult form begins insidiously but usually becomes obvious between ages 30 and 50; rarely, it causes no symptoms until the patient is in his 70s. In the adult form, renal deterioration is more gradual but, as in the infantile form, progresses relentlessly to fatal uremia.

The prognosis in adults is extremely variable. Progression may be slow, even after symptoms of renal insufficiency appear. However, after uremic symptoms develop, polycystic kidney disease is usually fatal within 4 years, unless the patient receives treatment with dialysis, kidney transplantation, or both.

CAUSES AND INCIDENCE

Although both types of polycystic kidney disease are genetically transmitted, the incidence in two distinct age-groups and different inheritance patterns suggest two unrelated disorders. The infantile type appears to be inherited as an autosomal recessive trait, whereas the adult type seems to be an autosomal dominant trait. The gene has been located on chromosome 6, supporting the premise that this is a single genetic disease with variable phenotype presentation.

Polycystic kidney disease reportedly affects 1 in every 1,000 Americans; that number may be even higher because some cases from patients who aren’t symptomatic go unreported. Both types of polycystic kidney disease affect males and females equally.

SIGNS AND SYMPTOMS

PEDIATRIC TIP

The neonate with infantile polycystic disease often has pronounced epicanthal folds, a pointed nose, a small chin, and floppy, low-set ears (Potter facies). At birth, he has huge bilateral masses on the flanks that are symmetrical, tense, and can’t be transilluminated. He characteristically shows signs of respiratory distress and heart failure. Eventually, he develops uremia and renal failure. Accompanying hepatic fibrosis may cause portal hypertension and bleeding varices to develop, requiring sclerotherapy or portacaval shunting.

Adult polycystic kidney disease is commonly asymptomatic through the patient’s 40s, but may induce nonspecific symptoms, such as hypertension, polyuria, and recurrent UTIs. Later, the patient develops overt symptoms related to the enlarging kidney mass, such as lumbar pain, widening girth, and swollen or tender abdomen. Abdominal pain is usually worsened by exertion and relieved by lying down. In advanced stages, this disease may cause recurrent hematuria, life-threatening retroperitoneal bleeding resulting from cyst rupture, proteinuria, and colicky abdominal pain from the ureteral passage of clots or calculi. Generally, about 10 years after symptoms appear, progressive compression of kidney structures by the enlarging mass produces renal failure and uremia. Hypertension is found in about 20% to 30% of children and up to 75% of adults due to intrarenal ischemia, which activates the reninangiotensin system.

DIAGNOSIS

A family history and a physical examination revealing large bilateral, irregular masses in the flanks strongly suggest polycystic kidney disease. In advanced stages, grossly enlarged and palpable kidneys make the diagnosis obvious. In patients with these findings, the following laboratory results are typical:

Excretory urography reveals enlarged kidneys, with elongation of pelvis, flattening of the calyces, and indentations caused by cysts. Excretory urography of the neonate shows poor excretion of contrast medium.
Ultrasound and computed tomography scan show kidney enlargement and the presence of cysts; tomography demonstrates multiple areas of cystic damage. Ultrasonography is the preferred imaging technique because it’s less expensive, doesn’t require contrast or radiation exposure, and is easily and safely performed on children and pregnant females.
Urinalysis and creatinine clearance tests are nonspecific tests that evaluate renal function and reveal urine protein or blood in the urine.

Diagnosis must rule out the presence of renal tumors.

TREATMENT

Polycystic kidney disease can’t be cured. The primary goal of treatment is preserving renal parenchyma and preventing infectious complications. Management of secondary hypertension will also help prevent rapid deterioration in function. Progressive renal failure requires treatment similar to that for other types of renal disease, including dialysis or, rarely, kidney transplantation.

When adult polycystic kidney disease is discovered in the asymptomatic stage, careful monitoring is required, including urine cultures and creatinine clearance tests every 6 months. Prompt and vigorous antibiotic treatment is needed when a urine culture reveals infection — even when the patient is asymptomatic. As
renal impairment progresses, selected patients may undergo dialysis, transplantation, or both. Cystic abscess or retroperitoneal bleeding may require surgical drainage; intractable pain (a rare symptom) may also require surgery. However, because this disease affects both kidneys, nephrectomy usually isn’t recommended because it increases the risk of infection in the remaining kidney.

SPECIAL CONSIDERATIONS

Because polycystic kidney disease is usually relentlessly progressive, comprehensive patient teaching and emotional support are essential.

Refer the young adult patient or the parents of infants with polycystic kidney disease for genetic counseling. Parents will probably have many questions about the risk to other offspring.
Provide supportive care to minimize any associated symptoms. Carefully assess the patient’s lifestyle and his physical and mental status; determine how rapidly the disease is progressing. Use this information to plan individualized patient care.
Acquaint yourself with all aspects of endstage renal disease, including dialysis and transplantation, so you can provide appropriate care and patient teaching as the disease progresses.
Explain all diagnostic procedures to the patient or to his family if the patient is an infant. Before beginning excretory urography or other procedures that use an iodine-based contrast medium, determine whether the patient has ever had an allergic reaction to iodine or shellfish. Even if the patient has no history of allergy, watch for an allergic reaction after performing the procedures.
Administer antibiotics as ordered for UTI. Stress to the patient the need to take the medication exactly as prescribed, even if symptoms are minimal or absent.

ACUTE RENAL DISORDERS

Acute kidney injury

Acute kidney injury (AKI) is the sudden interruption of kidney function due to obstruction, reduced circulation, or renal parenchymal disease. It’s usually reversible with medical treatment; otherwise, it may progress to end-stage renal disease, uremic syndrome, and death.

CAUSES AND INCIDENCE

The causes of AKI are classified as prerenal, intrinsic (or parenchymal), and postrenal. Prerenal failure is associated with diminished blood flow to the kidneys, possibly resulting from hypovolemia, shock, severe anaphylaxis, embolism, blood loss, sepsis, pooling of fluid in ascites or burns, or from cardiovascular disorders, such as heart failure, arrhythmias, and tamponade.

Intrinsic renal failure results from damage to the kidneys themselves, usually due to acute tubular necrosis, but possibly due to acute poststreptococcal glomerulonephritis, systemic lupus erythematosus, periarteritis nodosa, vasculitis, sickle-cell disease, bilateral renal vein thrombosis, nephrotoxins, chronic misuse of nonsteroidal anti-inflammatory drugs, radiopaque contrast agents, ischemia, renal myeloma, acute pyelonephritis, and exposure to heavy metals, such as lead or mercury.

Postrenal failure results from bilateral obstruction of urinary outflow. Its multiple causes include kidney stones, blood clots, papillae from papillary necrosis, tumors, benign prostatic hyperplasia, strictures, and urethral edema from catheterization.

In the United States, the annual incidence of AKI is 100 cases for every million people. It’s diagnosed in 1% of hospital admissions. Hospital-acquired AKI occurs in 4% of all admitted patients and 20% of patients who are admitted to critical care units.

SIGNS AND SYMPTOMS

AKI is a critical illness. Its early signs are oliguria, azotemia and, rarely, anuria. Electrolyte imbalance, metabolic acidosis, and other severe effects follow, as the patient becomes increasingly uremic and renal dysfunction disrupts other body systems:

GI: anorexia, nausea, vomiting, diarrhea or constipation, stomatitis, bleeding, hematemesis, dry mucous membranes, uremic breath
Central nervous system (CNS): headache, drowsiness, irritability, confusion, peripheral neuropathy, seizures, coma
Cutaneous: dryness, pruritus, pallor, purpura and, rarely, uremic frost
Cardiovascular: early in the disease, hypotension; later, hypertension, arrhythmias, fluid
overload, heart failure, systemic edema, anemia, altered clotting mechanisms
Respiratory: pulmonary edema, Kussmaul’s respirations.

Fever and chills indicate infection, a common complication.

DIAGNOSIS

The patient’s history may include a disorder that can cause renal failure. Blood test results indicating intrinsic renal failure include elevated blood urea nitrogen, serum creatinine, and potassium levels and low blood pH, bicarbonate, hematocrit (HCT), and hemoglobin (Hb) level. Urine specimens show casts, cellular debris, decreased specific gravity and, in glomerular diseases, proteinuria and urine osmolality close to serum osmolality. Urine sodium level is less than 20 mEq/L if oliguria is due to decreased perfusion; more than 40 mEq/L if due to an intrinsic problem. Other studies include renal ultrasonography, kidney-ureter-bladder X-rays, cautious use of excretory urography, renal scan, and nephrotomography.

TREATMENT

The goal of treatment is to correct or eliminate any reversible causes of kidney failure, such as obstructive uropathy, volume depletion, or the use of kidney-toxic medications. Supportive measures include a diet high in calories and low in protein, sodium, and potassium, with supplemental vitamins and restricted fluids. Meticulous electrolyte monitoring is essential to detect hyperkalemia. If hyperkalemia occurs, acute therapy may include dialysis, I.V. administration of hypertonic glucose, insulin infusion, and sodium bicarbonate, and administration of a potassium exchange resin (orally by enema) to remove potassium from the body.

If measures fail to control uremic symptoms, hemodialysis or peritoneal dialysis may be necessary. Continuous arteriovenous hemodiafiltration and continuous venovenous hemodiafiltration are alternative hemodialysis techniques for the treatment of AKI. They’re generally reserved for when intermittent dialysis fails to control hypervolemia or uremia, or for patients for whom peritoneal dialysis isn’t possible.

SPECIAL CONSIDERATIONS

Patient care includes careful monitoring and dietary education.

Measure and record intake and output, including all body fluids, such as wound drainage, nasogastric tube output, and diarrhea. Weigh the patient daily.
Assess Hb levels and HCT and replace blood components, as indicated. Don’t use whole blood if the patient is prone to heart failure and can’t tolerate extra fluid volume. Packed red blood cells deliver the necessary blood components without added volume.
Monitor vital signs. Watch for and report any signs of pericarditis (pleuritic chest pain, tachycardia, pericardial friction rub), inadequate renal perfusion (hypotension), and acidosis.
Maintain proper electrolyte balance. Strictly monitor potassium levels. Watch for symptoms of hyperkalemia (malaise, anorexia, paresthesia, or muscle weakness) and electrocardiogram changes (tall, peaked T waves, widening QRS segment, and disappearing P waves), and report them immediately. Avoid administering medications containing potassium.

Maintain nutritional status. Provide a highcalorie, low-protein, low-sodium, and lowpotassium diet, with vitamin supplements. Give the anorectic patient small, frequent meals.
Use sterile technique, because the patient with AKI is highly susceptible to infection. Personnel with upper respiratory tract infections shouldn’t provide care for the patient.
Prevent complications of immobility by encouraging frequent coughing and deep breathing and by performing passive range-of-motion exercises. Help the patient walk as soon as possible.
Provide good mouth care frequently because mucous membranes are dry. If stomatitis occurs, an antibiotic solution may be ordered. Have the patient swish the solution around in his mouth before swallowing.
Monitor for GI bleeding by guaiac testing all stools for blood. Administer medications carefully, especially antacids and stool softeners. Use aluminum-hydroxide-based antacids; magnesium-based antacids can cause serum magnesium levels to rise to critical levels.
Use appropriate safety measures, such as side rails and restraints, because the patient with CNS involvement may be dizzy or confused.
Provide emotional support to the patient and his family. Reassure them by clearly explaining all procedures.
If the patient requires hemodialysis, check the blood access site (arteriovenous fistula, subclavian or femoral catheter) as per facility protocol or every 2 hours for patency and signs of clotting. Don’t use the arm with the shunt or fistula for taking blood pressures or drawing blood. Weigh the patient before beginning dialysis. During dialysis, monitor vital signs, clotting times, blood flow, the function of the vascular access site, and arterial and venous pressures. Watch for complications, such as septicemia, embolism, hepatitis, and rapid fluid and electrolyte loss. After dialysis, monitor vital signs and the vascular access site; weigh the patient; watch for signs of fluid and electrolyte imbalances.
During peritoneal dialysis, position the patient carefully. Elevate the head of the bed to reduce pressure on the diaphragm and aid respiration. Be alert for signs of infection (cloudy drainage, elevated temperature) and, rarely, bleeding. If pain occurs, reduce the amount of dialysate. Monitor the diabetic patient’s blood glucose periodically, and administer insulin as ordered. Watch for complications, such as peritonitis, atelectasis, hypokalemia, pneumonia, and shock.
Use standard precautions when handling all blood and body fluids.

Acute pyelonephritis

Acute pyelonephritis (also known as acute infective tubulointerstitial nephritis) is a sudden inflammation caused by bacteria that primarily affects the interstitial area and the renal pelvis or, less often, the renal tubules. It’s one of the most common renal diseases. With treatment and continued follow-up care, the prognosis is good, and extensive permanent damage is rare. (See Chronic pylenonephritis.)

CAUSES AND INCIDENCE

Acute pyelonephritis results from bacterial infection of the kidneys. Infecting bacteria usually are normal intestinal and fecal flora that grow readily in urine. The most common causative organism is Escherichia coli, but Proteus, Pseudomonas, Staphylococcus aureus, and Enterococcus faecalis (formerly Streptococcus faecalis) may also cause this infection.

Typically, the infection spreads from the bladder to the ureters, then to the kidneys, as in vesicoureteral reflux due to congenital weakness at the junction of the ureter and the bladder. Bacteria refluxed to intrarenal tissues may create colonies of infection within 24 to 48 hours. Infection may also result from instrumentation (such as catheterization, cystoscopy, or urologic surgery), from a hematogenic infection (as in septicemia or endocarditis), or possibly from lymphatic infection.

Pyelonephritis may also result from an inability to empty the bladder (for example, in patients with neurogenic bladder), urinary stasis, or urinary obstruction due to tumors, strictures, or benign prostatic hyperplasia.

Pyelonephritis occurs more commonly in women, probably because of a shorter urethra and the proximity of the urinary meatus to the vagina and the rectum — both of which allow bacteria to reach the bladder more easily — and a lack of the antibacterial prostatic secretions produced by men. Incidence increases with age and is higher in the following groups:

Sexually active women: Intercourse increases the risk of bacterial contamination.
Pregnant women: About 5% develop asymptomatic bacteriuria; if untreated, about 40% develop pyelonephritis.
Diabetics: Neurogenic bladder causes incomplete emptying and urinary stasis; glycosuria may support bacterial growth in the urine.
Persons with other renal diseases: Compromised renal function aggravates susceptibility.

SIGNS AND SYMPTOMS

Typical clinical features include urgency, frequency, burning during urination, dysuria, nocturia, and hematuria (usually microscopic but may be gross). Urine may appear cloudy and have an ammonia-like or fishy odor. Other common symptoms include a temperature of 102° F (38.9° C) or higher, shaking chills, flank pain, anorexia, and general fatigue.

These symptoms characteristically develop rapidly over a few hours or a few days. Although these symptoms may disappear within days, even without treatment, residual bacterial
infection is likely and may cause symptoms to recur later.

DIAGNOSIS

Diagnosis requires urinalysis and culture. Typical findings include:

Pyuria (pus in urine): Urine sediment reveals the presence of leukocytes singly, in clumps, and in casts; and, possibly, a few red blood cells.
Significant bacteriuria: Urine culture reveals more than 100,000 organisms/µl of urine.
Low specific gravity and osmolality: These findings result from a temporarily decreased ability to concentrate urine.
Slightly alkaline urine pH.
Proteinuria, glycosuria, and ketonuria: These conditions are less common.
Costovertebral angle tenderness Excretory urography or computed tomography scan of the kidneys, ureters, and bladder also help in the evaluation of acute pyelonephritis by revealing calculi, tumors, or cysts in the kidneys and the urinary tract. In addition, excretory urography may show asymmetrical kidneys.

TREATMENT

Treatment centers on antibiotic therapy appropriate to the specific infecting organism after identification by urine culture and sensitivity studies. When the infecting organism can’t be identified, therapy usually consists of a broadspectrum antibiotic. Urinary analgesics are also appropriate.

Symptoms may disappear after several days of antibiotic therapy. Although urine usually becomes sterile within 48 to 72 hours, the course of such therapy is 10 to 14 days. Follow-up treatment may include reculturing urine 1 week after drug therapy stops, then periodically for the next year to detect residual or recurring infection. Most patients with uncomplicated infections respond well to therapy and don’t suffer reinfection.

In infection from obstruction or vesicoureteral reflux, antibiotics may be less effective; treatment may then necessitate surgery to relieve the obstruction or correct the anomaly. Patients at high risk of recurring urinary tract and kidney infections, such as those with prolonged use of an indwelling catheter or maintenance antibiotic therapy, require long-term follow-up. Recurrent episodes of acute pyelonephritis can eventually result in chronic pyelonephritis.

Chronic pyelonephritis

Chronic pyelonephritis is a persistent kidney inflammation that can scar the kidneys and may lead to chronic renal failure. Its etiology may be bacterial, metastatic, or urogenous. This disease is most common in patients who are predisposed to recurrent acute pyelonephritis, such as those with urinary obstructions or vesicoureteral reflux.

Patients with chronic pyelonephritis may have a childhood history of unexplained fevers or bedwetting. Clinical effects may include flank pain, anemia, low urine specific gravity, proteinuria, waxy casts, leukocytes in urine and, especially in late stages, hypertension. Uremia rarely develops from chronic pyelonephritis unless structural abnormalities exist in the excretory system. Bacteriuria may be intermittent. When no bacteria are found in the urine, diagnosis depends on excretory urography (renal pelvis may appear small and flattened) and renal biopsy.

Effective treatment of chronic pyelonephritis requires control of hypertension, elimination of the existing obstruction (when possible), and long-term antimicrobial therapy.

SPECIAL CONSIDERATIONS

Patient care is supportive during antibiotic treatment of the underlying infection.

Administer antipyretics for fever.
Encourage fluids to achieve urine output of more than 2,000 ml/day. This helps to empty the bladder of contaminated urine. Don’t encourage intake of more than 2 to 3 qt (2 to 3 L) because this may decrease the effectiveness of the antibiotics.
Provide an acid-ash diet to prevent stone formation.
Teach proper technique for collecting a clean-catch urine specimen. Be sure to refrigerate or culture a urine specimen within 30 minutes of collection to prevent overgrowth of bacteria.
Stress the need to complete prescribed antibiotic therapy, even after symptoms subside. Encourage long-term follow-up care for highrisk patients.

To prevent acute pyelonephritis:

Acute poststreptococcal glomerulonephritis

Acute poststreptococcal glomerulonephritis (APSGN), also known as acute glomerulonephritis, is a relatively common bilateral inflammation of the glomeruli. It usually follows a streptococcal infection of the respiratory tract or, less often, a skin infection such as impetigo.

CAUSES AND INCIDENCE

APSGN results from the entrapment and collection of antigen-antibody complexes (produced as an immunologic mechanism in response to streptococcus) in the glomerular capillary membranes, inducing inflammatory damage and impeding glomerular function. Sometimes, the immune complement further damages the glomerular membrane. The damaged and inflamed glomerulus loses the ability to be selectively permeable, and allows red blood cells (RBCs) and proteins to filter through as the glomerular filtration rate (GFR) falls. Uremic poisoning may result.

APSGN is most common in boys ages 3 to 7, but it can occur at any age. Incidence is rising in the United States and Europe, with epidemics occurring in developing countries in Africa, the West Indies, and the Middle East.

Up to 95% of children and up to 70% of adults with APSGN recover fully; the rest may progress to chronic renal failure within months.

SIGNS AND SYMPTOMS

APSGN begins within 1 to 3 weeks after pharyngitis. Symptoms include mild to moderate edema, oliguria (less than 400 ml/24 hours), proteinuria, azotemia, hematuria, and fatigue. Mild to severe hypertension may result from either sodium or water retention (due to decreased GFR) or inappropriate renin release. Heart failure from hypervolemia leads to pulmonary edema.

DIAGNOSIS

Diagnosis requires a detailed patient history and assessment of clinical symptoms and laboratory tests.

Urinalysis typically reveals proteinuria and hematuria. RBCs, white blood cells, and mixed cell casts are common in urinary sediment. Elevated serum creatinine levels and low creatinine clearance accompany impaired glomerular filtration. Elevated antistreptolysin-O titers (in 80% of patients), elevated streptozyme and anti-DNase B titers, and low serum complement levels verify recent streptococcal infection. A throat culture may also show group A betahemolytic streptococcus. Renal ultrasound may show a normal or slightly enlarged kidney. A renal biopsy may confirm the diagnosis or assess renal tissue status.

TREATMENT

The goals of treatment are relief of symptoms and prevention of complications. Vigorous supportive care includes bed rest, fluid and dietary sodium restrictions, and correction of electrolyte imbalances (possibly with dialysis, although this is rarely necessary). Therapy may include diuretics to reduce extracellular fluid overload and an antihypertensive. The use of antibiotics is recommended for 7 to 10 days if staphylococcal infection is documented. Otherwise, antibiotic use is controversial.

SPECIAL CONSIDERATIONS

APSGN usually resolves within 2 weeks, so patient care is primarily supportive.

Check vital signs and electrolyte values. Monitor intake and output and daily weight. Assess renal function daily through serum creatinine, blood urea nitrogen, and urine creatinine clearance levels. Watch for and immediately
report signs of acute renal failure (oliguria, azotemia, and acidosis).
Consult the dietitian to provide a diet high in calories and low in protein, sodium, potassium, and fluids.
Protect the debilitated patient against secondary infection by providing good nutrition, using good hygienic technique, and preventing contact with infected persons.
Bed rest is necessary during the acute phase. Allow the patient to gradually resume normal activities as symptoms subside.
Provide emotional support for the patient and his family. If the patient is on dialysis, explain the procedure fully.
Advise the patient with a history of chronic upper respiratory tract infections to immediately report signs of infection (fever, sore throat).
Tell the patient that follow-up examinations are necessary to detect chronic renal failure. Stress the need for regular blood pressure, urinary protein, and renal function assessments during the convalescent months to detect recurrence. After APSGN, gross hematuria may recur during nonspecific viral infections; abnormal urinary findings may persist for years.
Encourage pregnant women with a history of APSGN to have frequent medical evaluations because pregnancy further stresses the kidneys and increases the risk of chronic renal failure.

Acute tubular necrosis

Acute tubular necrosis (ATN), also known as acute tubulointerstitial nephritis, accounts for about 75% of all cases of acute kidney injury and is the most common cause of acute kidney injury in critically ill patients. ATN injures the tubular segment of the nephron, causing renal failure and uremic syndrome. Mortality ranges from 40% to 70%, depending on complications from underlying diseases. Nonoliguric forms of ATN have a better prognosis.

CAUSES AND INCIDENCE

ATN results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill or those who have undergone extensive surgery. In ischemic injury, disruption of blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or reactions to transfusions. Nephrotoxic injury may follow ingestion of certain chemical agents or result from a hypersensitive reaction of the kidneys. (See Rise in nephrotoxic injury.) Because nephrotoxic ATN doesn’t damage the basement membrane of the nephron, it’s potentially reversible. However, ischemic ATN can damage the epithelial and basement membranes and can cause lesions in the renal interstitium. ATN may result from:

Rise in nephrotoxic injury

Incidence of acute tubular necrosis (ATN) due to ingestion or inhalation of toxic substances is rising. ATN may occur in hospitalized patients following exposure to toxic agents, such as antibiotics, chemotherapeutic agents, or contrast material. Other nephrotoxic agents include pesticides, fungicides, heavy metals (for example, mercury, arsenic, lead, bismuth, uranium), and organic solvents containing carbon tetrachloride or ethylene glycol, such as cleaning fluids or industrial solvents. Ingestion of these substances may be accidental or intentional.

diseased tubular epithelium that allows leakage of glomerular filtrate across the membranes and reabsorption of filtrate into the blood
obstruction of urine flow by the collection of damaged cells, casts, red blood cells (RBCs), and other cellular debris within the tubular walls
ischemic injury to glomerular epithelial cells, resulting in cellular collapse and decreased glomerular capillary permeability
ischemic injury to vascular endothelium, eventually resulting in cellular swelling and obstruction.

SIGNS AND SYMPTOMS

Nephrotoxic injury causes multiple symptoms similar to those of renal failure, particularly azotemia, anemia, acidosis, overhydration, and hypertension. Some patients may also experience fever, rash, and eosinophilia. However, ATN is usually difficult to recognize in its early stages because effects of the critically ill patient’s primary disease may mask the symptoms
of ATN. (See A close look at acute tubular necrosis.) The first recognizable effect may be decreased urine output. Generally, hyperkalemia and the characteristic uremic syndrome soon follow, with oliguria (or, rarely, anuria) and confusion, which may progress to uremic coma. Other possible complications may include heart failure, uremic pericarditis, pulmonary edema, uremic lung, anemia, anorexia, intractable vomiting, and poor wound healing due to debilitation.

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Tags: Professional Guide to Diseases

Aug 27, 2016 | Posted by drzezo in PATHOLOGY & LABORATORY MEDICINE | Comments Off

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