Complex Test Map (Exam 1)
Acute Renal Failure: rapid loss of renal function with progressive azotemia (accumulation of nitrogenous waste products
such as urea nitrogen and creatinine in the blood).
 Uremia is the condition in which renal function declines to the point that symptoms develop in multiple body
systems.
 oliguria, urinary output of less than 400 ml/day.
 develops over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium
with or without oliguria.
 Most commonly follows severe, prolonged hypotension or Hypovolemia or nephrotoxic agent exposure.
Types:
 Prerenal: due to factors external to the kidneys that reduce renal blood flow & lead to decreased glomerular
perfusion & filtration. These include hypovolemia, decreased cardiac output, decreased peripheral vascular
resistance, vascular obstruction, myocardial infarction, and burns.
- Oliguria occurs as the kidneys respond to the decreased blood flow by activating the RAAS , which results in
sodium and water conservation. Decreased renal perfusion also decreases clearance of wastes (azotemia). As
decreased perfusion continues, the kidneys lose their ability to engage in compensatory mechanisms &
intrarenal damage to renal tissue occurs.
- The result is low urine output, a rise in BUN & serum creatinine proportionate to each other (ratio > 10:1), and
the inability of the kidneys to conserve sodium.
 Intrarenal: conditions that cause direct damage to the renal tissue, resulting in impaired nephron function. This is
usually caused by prolonged ischemia, nephrotoxins (antibiotics, contrast media, aminoglycoside), hemoglobin from
hemolyzed RBCs, or myoglobin from necrotic muscle cells. Nephrotoxins can cause obstruction of intrarenal
structures by crystallization or actual damage to the epithelial cells of the tubules. Primary renal diseases such as
acute glomerulonephritis and systemic lupus erythematosus may also cause ARF. Hemoglobin and myoglobin block
the tubules and cause renal vasoconstriction.
- Acute Tubular Necrosis: an intrarenal condition caused by ischemia, nephrotoxins, or pigments. Severe renal
ischemia causes a disruption in the basement membrane and patchy destruction of the tubular epithelium. ATN
is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates.
Nephrotoxic agents=necrosis of tubular epithelial cells which slough off and plug tubules.
 Postrenal: involve mechanical obstruction of urinary outflow. As the flow of urine is obstructed, urine reflexes into
the renal pelvis, impairing kidney function. The most common causes are benign prostate hyperplasia, prostate
cancer, calculi, trauma, and extrarenal tumors.
- Azotemia can be reversed if the outflow obstruction is relieved before kidney damage occurs.
- Outflow obstructions that are not corrected will damage renal parenchyma and cause ARF.
Lab values:
 Prerenal
- Specific gravity >1.025
- Low sodium concentration <10-20 meq/l
- Rise to BUN and creatinine proportionate to each other
 Intrarenal
- Presence of urine sediment
- Urine sodium >40 mEq/L
- Specific gravity 1.010 (fixed)
- ATN is characterized by the presence of tubular, RBC, and white blood cell casts in the urine
 Postrenal
- Normal urine sodium levels to 40meq/l
- Specific gravity 1.000-1.010
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Phases:
 Initiating phase: from time of insult until S&S become apparent.
 Oliguric Phase: causes by a reduction in the GFR and usually occurs within 1 to 7 days of the causative event. If
caused by ischemia, could be within 24 hrs. Oliguria of intrarenal failure caused by ATN=tubular, RBC, and WBC
casts in the urine.
- Urinary changes: UO less than 400 ml/24 hr; a urinalysis may show casts, RBCs, WBCs, a specific gravity fixed at
around 1.010, and a urine osmolality at about 300 mOsm/kg, reflecting tubular damage with a loss of
concentrating ability by the kidney. Proteinuria may be present if the renal failure is related to glomerular
membrane dysfunction.
- Fluid volume excess: neck vein distention with a bounding pulse, edema, hypertension; fluid overload can
eventually lead to HF, pulmonary edema, and pericardial and pleural effusions.
- Metabolic acidosis: kidneys cannot synthesize ammonia needed for hydrogen ion excretion or excrete acid
products. Serum bicarb is decreased b/c used up to buffer hydrogen=kussmaul respirations to increase
excretion of carbon dioxide=lethargy and stupor.
- Sodium balance: damaged tubules cannot conserve Na+. Urinary excretion of Na+ may increase. Uncontrolled
hyponatremia or H2O excess=cerebral edema.
- Potassium excess: acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of
the cells & into the ECF. When K+ levels exceed 6 mEq/L or dysrhythmias are identified, treatment must be
initiated immediately. Before clinical signs of hyperkalemia are apparent, the ECG with show tall, peaked T
waves; widening of the QRS complex, and ST segment depression.
- Hematologic disorders: anemia occurs because renal failure results in impaired erythropoietin production.
Anemia may be compounded by platelet abnormalities that can lead to bleeding from multiple sources. WBCs
are also altered causing immunodeficiency.
- Calcium deficit and phosphate excess: there is decreased absorption from the GI tract because of a decreased
amount of activated vitamin D, which can only be activated by the kidneys. PTH is secreted which causes the
bone to demineralize, releasing Ca to the blood as well as phosphate, raising the phosphate levels. A low ionized
Ca level can lead to tetany.
- Waste product accumulation: The best serum indicator of renal failure is creatinine because it is not significantly
altered by other factors. Kidney failure = increased BUN and serum creatinine b/c no excretion.
- Neurologic disorders: can occur as the nitrogenous waste products accumulate in the brain. The symptoms can
be as mild as fatigue and difficulty concentrating, then escalate to seizures, stupor, and coma.
 Diagnostic Studies
- Urine sediment containing abundant cells, cast, or proteins suggests intrarenal.
- Urine osmolality, sodium content, specific gravity
- Hematuria, pyuria, and crystals=postrenal
- Renal ultrasound-eval for poss renan disease and obstruction of the urinary collection system.
- Renal scan-renal blood flow, tubular function, and collecting system integrity.
- CT and MRI-lesions, masses, obstructions, vascular anomalies.
- Renal biopsy-diagnosis of intrarenal causes of ARF.
 Collaborative Care
- Tx of precipitating cause
- Fluid restriction (600ml + previous 24 hr/loss)
- Phosphate restriction, Na+ restriction, CA+ supplement or phosphate binding agents
 Diuretic phase: begins with a gradual increase in daily UO of 1 to 3 L/day, but may reach 3 to 5 L/day. In this phase
the kidneys have recovered their ability to excrete wastes, but not to concentrate the urine. Hypovolemia and
hypotension can occur from massive fluid losses. The patient must be monitored for hyponatremia, hypokalemia,
and dehydration because of large losses of fluids & electrolytes.
 Recovery phase: begins when the GFR increases, allowing the BUN and serum creatinine levels to plateau and then
decrease.
Nursing
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 Intervention: the nurse has an important role in managing fluid & electrolyte balance during the oliguric and diuretic
phases. Observing and recording intake & output are essential.
- Daily weights (1 kg = 1000ml of fluid)
- Hyperkalemia is typically manifested by dysrhythmias & impairment of neuromuscular function, including
muscle weakness, abdominal cramps, flaccid paralysis, and absence of deep tendon reflexes. Cardiac conduction
abnormalities to watch for include a prolonged PR interval; prolonged QRS internal; tall, peaked T wave; and
depressed ST segment.
- Aseptic technique is critical; the nurse should be alert for local manifestations of infection (swelling, redness,
pain), as well as systemic manifestations (malaise, leukocytosis) because an elevated temp may not be present.
- Respiratory complications, especially pneumonitis, can be prevented. Humidified oxygen, incentive spirometry;
coughing, turning, & deep breathing; and ambulation
- Skin care because of edema; mouth care to prevent stomatatis
- Diet: high in calories; protein & potassium should be regulated according to renal function
- Teach: S & S of recurrent kidney disease.
Medical Treatment
- Diuretic therapy is often administered along with volume expanders to prevent fluid overload. If ARF is already
established, forcing fluids & diuretics will not be effective and may be harmful.
- Fluid intake must be closely monitored in the oliguric phase. The general rule for calculating the fluid restriction is to
add all losses for the previous 24 hours plus 600 ml for insensible losses.
- Hyperkalemia is one of the most serious & life threatening complications of ARF.
- Regular Insulin IV: causes potassium to move into cells, glucose is given concurrently to prevent hypoglycemia;
when the effects of insulin diminish, K+ shifts back out of cells.
- Sodium Bicarbonate: can correct acidosis and causes shift of K+ into cells
- Calcium Gluconate IV: used in advance cardiac toxicity; raises the threshold for excitation resulting in
dysrhythmias.
- Dialysis: can bring K+ levels to normal within 30 mins to 2 hrs.
- Sodium Polystyrene Sulfonate (Kayexalate): administered PO or by enema; causes K+ to be exchanged for Na; it
is mixed with water with sorbitol to produce osmotic diarrhea, allowing for evacuation of K+ rich stool from
body. ***listen to bowel sounds, must never be given to patient with paralytic ileus because bowel necrosis may
occur.***
- Nutritional therapy: adequate calories, low protein, low K+, low Na
- Eval of treatment for ARF pt
- Regain and maintain normal fluid/lyte balance
- Comply w treatment regimen
- Experience no infections
- Have complete recovery
Hemolytic Uremic Syndrome
Pathophysiology: most frequent cause of ARF in children.
 Nearly all cases are the result of an antecedent infection by Shiga’s toxin-producing strains of E. coli.
 First, the bacteria attaches itself to the intestinal mucosa, its clearance through the intestines decrease, and it is
allowed to grow and multiple.
 Second, the bacteria produce a toxin that damages the endothelial cells of capillary walls and the subsequent
inflammatory response results in occlusion of capillaries. This is especially significant in the renal glomeruli. The
occlusion of the glomerular vessels decreases filtration & results in ARF
Manifestations
 It is an acute disorder characterized by anemia, thrombocytopenia, and ARF. Children with HUS become infection by
E. coli in improperly cooked meat or contaminated dairy products.
 Most affected children have an associated prodrome of GI symptoms, including bloody diarrhea. As well as,
abdominal pain, fever, and vomiting. Dehydration can result.
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 Anemia results from fragmentation of RBCs, which are damaged as they try to pass through the occluded vessels
and are removed from circulation by the spleen.
 Thrombocytopenia occurs because platelets get trapped within the small vessels.
Medical Treatment
 Peritoneal dialysis and corticosteroids
Nutrition
 Low sodium and potassium
 Maximum calories and moderate restriction of protein
Chronic Renal Failure
 Progressive, irreversible loss of kidney function; defined as either the presence of kidney damage or GFR <60ml/min
for 3 months or longer.
 ESRD occurs when the GFR is less than 15ml/min; at this point dialysis or transplant is required.
Risk factors
 The leading causes of ESRD are diabetes mellitus and hypertension
 The rate of chronic kidney disease is 6 times higher among Native Americans with diabetes than other ethnic groups
with diabetes.
 The risk of chronic kidney disease as a complication of hypertension is significantly increased in African Americans.
Categories
Clinical Manifestations
 Urinary system: in the early stage polyuria develops from the inability of the kidneys to concentrate urine, also
causing nocturia. Because of this decreased concentrating ability, the specific gravity of urine becomes fixed around
1.010. As CKD worsens, oliguria develops & eventually anuria (<100 ml/24hr).
 Metabolic disturbances
 Waste product accumulation: Decrease in GFR, increase in creatinine and BUN. As the BUN increases, nausea,
vomiting, lethargy, fatigue, impaired thought process, and headaches become more common.
 Altered carbohydrate Metabolism: Moderate hyperglycemia, hyperinsulinemia and abnormal glucose tolerance
tests may be seen. Patients with diabetes who become uremic may require less insulin than before the onset of
CKD, this is because insulin, which is dependent on the kidneys for excretion, remains in circulation longer.
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 Elevated triglycerides: hyperinsulinemia stimulates hepatic production of triglycerides. Hyperlipidemia b/c
decreased lipoprotein lipase which breaks down lipoproteins. Hyperlipidemia=risk factor for atherosclerosis.
Increased glucose=increased insulin production=stimulation of liver to produce more triglycerides.
Electrolyte & acid-base imbalances
- Potassium: Increased b/c decreased sxcretion, breakdown of cellular protein, bleeding, metabolic acidosis. Fatal
dysrhythmias can occur when the serum K+ level reaches 7 to 8 mEq/L.
- Sodium: Decreased secretion=Na+/H2O retention. If large quantities of body water are retained, dilutional
hyponatremia occurs. Sodium retention can contribute to edema, hypertension, and heart failure.
- Magnesium: hypermagnesemia is generally not a problem unless the patient is ingesting magnesium(milk of
mag, mag citrate, antacids). Clinical manifestations of hypermagnesemia can include absence of reflexes,
decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure.
- Metabolic acidosis: Decreased excretion of acid and defective reabsorption and regeneration of bi-carb.
Decreased bi-carb=decreased acid buffer=kussmaul’s to decreased acidosis by increasing carbon dioxide
excretion.
Hematologic system
- Anemia: due to decreased production of erythropoietin by the kidneys.
- Bleeding tendencies: defect in platelet function.
- Infection: immune system is depressed resulting in diminished inflammatory response
- Increase incidence of cancer: there is a significant increase in the incidence of neoplasms in the patient with
renal failure who has not had a transplant compared with the general population. Lung, breast, uterus, colon,
prostate, and skin malignancies are most commonly found.
Cardiovascular system
- Hypertension is aggravated by sodium retention and increased extracellular volume
- Vascular changes from long-standing hypertension and accelerated atherosclerosis from triglyceride levels are
responsible for many cardio complications (MI, stroke).
- Uremic pericarditis can develop & occasionally progress to pericardial effusion and cardiac tamponade.
Pericarditis is manifested by a friction rub, chest pain, & low-grade fever.
- Left Ventrical Hypertrophy-b/c long standing hypertension, ECF overload (pulmonary, peripheral edema)
Respiratory system
- Kussmaul breathing from metabolic acidosis, dyspnea from fluid overload, pulmonary edema, uremic pleuritis,
pleural effusion, and “uremic lung” or uremic pneumonitis which usually responds to vigorous fluid removal
during dialysis treatments.
- Sputum=thick and tenacious
- Decreased cough reflex
GI system
- Mucosal ulcerations, found throughout the GI tract, are caused by the increase ammonia produced by bacterial
breakdown of urea.
- Stomatitis with exudates & ulcerations, a metallic taste in the mouth, and uremic fetor (urine breath odor) are
commonly found.
- Anorexia, nausea, & vomiting
- Diarrhea because of hyperkalemia & altered Ca+ metabolism
- Constipation due to ingestion of iron salts and/or Ca+ containing phosphate binders.
Neurologic system
- In renal failure a general depression of the CNS results in lethargy, apathy, decreased ability to concentrate,
fatigue, irritability, and altered mental ability. Seizures & coma may result from a rapidly increasing BUN and
hypertensive encephalopathy.
- Peripheral neuropathy is initially manifested as “restless leg syndrome” and a burning sensation in the legs &
feet. Motor involvement may later be involved manifesting as bilateral foot drop, muscular weakness & atrophy,
muscular twitching, jerking, asterixis (hand flapping tremor), nocturnal leg cramps, and loss of DTR.
- Altered mental status is often the signal that dialysis must be initiated.
Musculoskeletal system
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- Renal osteodystrophy is a syndrome of skeletal changes found in CKD that is a result of alterations in Ca+ and
phosphate metabolism. PTH causes Ca+ and phosphate resorption from the bone. The excess phosphate binds
with calcium, leading to the formation of metastatic calcifications that are deposited throughout the body.
Common sites are the muscles, lungs, skin & SQ tissue, GI tract, and eyes(uremic red eye). Two types of
osteodystrophy are associated with ESRD.
 Osteomalacia: condition of demineralization results from slow bone turnover & defective mineralization of
newly formed bone. Result of PTH suppression from high Ca+ diet, high vit D dosage, and DM.
 Osteitis fibrosa cystic: condition results from decalcification of bone & replacement of bone tissue with
fibrous tissue. Primarily a result of markedly elevated levels of PTH
Integumentary system
- Yellow-gray discoloration of the skin; pale skin from anemia; dry scaly skin because of decreased oil & sweat
gland activity
- Pruritus from the dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy. The itching may
be so intense that it leads to bleeding or infection.
- Uremic frost is a rare condition in which urea crystallizes on the skin & is usually seen only when BUN levels are
extremely high. Occurs when patient refuses dialysis or is withdrawn from dialysis.
- Hair is dry & brittle and may fall out; nails are then, brittle, & ridged; petechiae & ecchymoses may be present
from platelet abnormalities.
 Reproductive system: infertility & decreased libido; menstrual changes & anovulation (return after dialysis starts);
men have decreased testosterone and low sperm counts; peripheral neuropathy=impotence in men, anorgasmy in
women.
 Endocrine system: many CKD patients exhibit symptoms of hypothyroidism
 Psychologic changes: personality & behavioral changes, emotional lability, withdrawal, and depression are common.
Fatigue & lethargy also exhibited.
Diagnostic
 Because persistent proteinuria is usually the 1st indication of kidney damage, screening for CKD involves a dipstick
evaluation of protein in the urine. A person with persistent proteinuria (1+ protein on standard dipstick testing two
or more times over a 3 month period) should have further assessment of risk factors and a diagnostic work up with
blood and urine tests.
 A urine test for albumin-to-creatinine ratio provides an accurate estimate of the protein & albumin excretion rate. A
ratio greater than 300 mg albumin per 1 g creatinine signals CKD.
 Serum creatinine values, rather than urine creatinine clearance tests, are used to estimate GFR and stage CKD.
 Ultrasound to exclude obstruction and note size of kidneys
 Renal biopsy
 Protein-to-creat in 1st morning urine
 Hct/Hgb
Medical
 Drug therapy
- Hyperkalemia: restrict high K+ foods; IV glucose & insulin; Kayexalate (expect diarrhea); if life threatening
dysrhythmias a present, dialysis may be required to remove excess potassium.
- Hypertension: treatment includes (1) with loss if obese, (2) therapeutic lifestyle changes including exercise,
smoking cessation, alcohol cessation, (3) diet recommendations such as DASH diet, (4) administration of
antihypertensive drugs
 Most commonly used antihypertensive drugs are diuretics (Lasix), B-blockers (metoprolol), calcium channel
blockers (nifedipine), ACE inhibitors (catopril). Prescribed meds are dependent on whether the patient with
CKD is diabetic or non-diabetic.
 NONDIABETICS: diuretics and B-adrenergic blockers are the recommended initial therapy.
 DIABETICS: ACE inhibitors and ARBs are used because the decrease proteinuria and delay the progression of
CKD.
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- Renal osteodystrophy: limit dietary phosphorus, administering phosphate binders, supplement vit D, and control
hyperparathyroidism.
 Phosphate binders should be administered with each meal to be effective because most phosphate is
absorbed within 1 hour after eating. Constipation is a frequent side effect of phosphate binders and may
necessitate the use of stool softeners.
 Hypocalcemia is often a problem. If hypocalcemia persists in the setting of controlled serum phosphate
levels and supplemental calcium, the active form of vit D should be given. It is important that the serum
phosphate level is lowered before administering calcium or vit D because these drugs may contribute to soft
tissue calcification if both calcium & phosphate levels are elevated.
- Anemia: erythropoietin is available for the treatment of anemia & can be administered IV or SQ. A common
adverse effect of exogenous erythropoietin is the development or acceleration of hypertension (because of
increased blood viscosity). Oral iron supplements may also be needed.
- Dyslipidemia: statins are the most effective drugs for lowering LDL cholesterol levels. Fibrates are the most
effective drugs available for lowering triglyceride levels & can also increase HDLs. .
- Complications of drug therapy: delayed & decreased elimination lead to an accumulation of drugs & the
potential for drug toxicity. Drugs of particular concern include digitalis, antibiotics, and pain medication.
 Hypokalemia can potentiate the action of digitalis.
 Demerol should NEVER be administered to a patient with CKD because the liver metabolizes it to
normeperidine, which is dependent on the kidneys for excretion. If Demerol accumulates, seizures can
result.
 Vancomycin (vancocin) and gentamicin (Garamycin) depend on kidneys for excretion
 Avoid NSAIDS!
- Nutritional therapy:
 Protein restriction: 0.6 to 0.8 g/kg body weight/day
 Water restriction: Intake depends on daily urine output
 Sodium restriction
o Diets vary from 2 to 4 g depending on
degree of edema and hypertension
o Sodium and salt should not be equated
o Patient should be instructed to avoid
high-sodium foods
o Salt substitutes should not be used because they contain potassium chloride
 Potassium restriction
o 2 to 4 g
o High-potassium foods should be avoided: Oranges, Bananas, Tomatoes, Green vegetables
 Phosphate restriction
 1000 mg/day
 Foods high in phosphate (Dairy products)
 Most foods high in phosphate are also high in calcium
 Pt/Fam Teaching
o Ways to reduce thirst (suck on ice, lemon, hard candy)
o Explain rationale for drugs and side effects: phosphate binders (including Ca+=supplements) should be taken
with meals. Ca+ supplements to treat hypocalcemia should be taken on empty stomach separate from iron
supplements.
o Iron supplements should be taken in between meals.
Nursing
 Assessment
- Current & past use of prescription and OTC drugs & herbal preparations must be reviewed
- Manifestations of CKD are apparent in multiple body systems. Early symptoms are often fatigue, lethargy, and
pruritus. First signs are often hypertension & proteinuria.
 Intervention
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- Teach pt and family about the diet, drugs, and follow up responsibilities of the patient.
- The patient should check daily wt; learn to take daily BPs; and be able to identify S & S of fluid overload,
hyperkalemia, and other electrolyte imbalances.
- The patient should also be aware that meperidine and ACE inhibitors may be harmful because of renal
insufficiency.
 Renal Biopsy
- Renal biopsy is done to obtain renal tissue for examination to determine type of renal disease or to follow
progress of renal disease. Technique is usually done as a skin (percutaneous) biopsy through needle
insertion into lower lobe of kidney. Can be performed with CT or ultrasound guidance. Absolute
contraindications are bleeding disorders, single kidney, and uncontrolled hypertension. Relative
contraindications include suspected renal infection, hydronephrosis, and possible vascular lesions.
- Type and crossmatch patient for blood. Ensure consent form is signed.
- Before: Ascertain coagulation status through patient history, medication history, CBC, hematocrit,
prothrombin time, and bleeding and clotting time. Patient should not be taking aspirin or warfarin
(Coumadin).
- After: Apply pressure dressing, and keep on affected side for 30-60 min; bed rest for 24 hr. Vital signs every
5-10 min, first hour. Assess for flank pain, hypotension, ↓ hematocrit, ↑ temperature, chills, urinary
frequency, dysuria, and serial urine specimens (gross/microscopic hematuria). Urine dipstick can be used to
test for bleeding in urine. Inspect biopsy site for bleeding. Instruct patient to avoid lifting heavy objects for
5-7 days and not to take anticoagulant drugs until allowed by physician.
Polycystic Kidney Disease
Pathophysiology
 The childhood form of PKD is a rare autosomal recessive disorder that is often rapidly progressive.
 The adult form of PKD is an autosomal dominant disorder. It is latent for many years and is usually manifested
between 30 and 40 yrs old. It involves both kidneys.
 The cortex & medulla are filled with large, thin-walled cysts that are several millimeters to several centimeters in
diameter. The cysts enlarge & destroy surrounding tissue by compression. They are filled with fluid and may contain
blood or pus.
Clinical Manifestations
 Early in the disease there are generally no symptoms. Symptoms appear when the cysts begin to enlarge.
 Often the 1st manifestations are hypertension, hematuria (from ruptured cysts), or a feeling of heaviness in the back,
side, or abdomen.
 Sometimes the 1st manifestations are UTI and/or urinary calculi.
 Chronic pain is one of the most common problems for people with PKD. The pain can be constant and severe. Flank
pain-dull, intermittent, sharp.
 Physical exam – palpable bilateral enlarged kidneys are often found.
 Other organs can be affected, including the liver, heart, & intestines. This results in liver cysts, abnormal heart
valves, aneurysms, and diverticulosis.
Treatment
 Restrict Na+
 Ace inhibitors=DOC
 Possible nephrectomy if pain, bleeding, and infection becomes a chronic, serious problem.
 Transplant remains only cure
Glomerulonephritis: inflammation of the glomeruli
Pathophysiology: two types of antibody-induced injury can initiate glomerular damage
 First type – antibodies have a specificity for antigens within the glomerular basement membrane. Immunoglobulins
are deposited along the basement membranes. Production of these autoantibodies (antibodies to one’s own tissue)
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may be stimulated by a structural alteration in the basement membrane or by a reaction of the basement
membrane with an exogenous agent (virus, hydrocarbon).
 Second type – the antibodies react with NON-glomerular antigens and are randomly deposited as immune
complexes along the basement membrane. In this process, the antigens do not come from the glomeruli but rather
from endogenous circulating native DNA or exogenous sources (bacteria, viruses, chemicals). Bacterial products
appear to be important in poststreptococcal glomerulonephritis.
 All forms of immune complex disease are characterized by an accumulation of antigen, antibody, and complement in
the glomeruli, which can result in tissue injury. The immune complexes activate complement; complement
activation results in the release of chemotactic factors that attract leukocytes, histamine, and other inflammatory
mediators. The end result of these processes is glomerular injury.
Manifestations
 Hematuria (from microscopic to gross) and urinary excretion of various elements including RBCs, WBCs, and casts.
 Proteinuria and elevated BUN and serum creatinine
 In most cases, recovery from the acute illness is complete. However, if progressive involvement occurs, the result is
destruction of renal tissue and marked renal insufficiency.
 History – assess exposure to drugs, immunizations, microbial infections, and viral infections (hep). Also evaluate
immune disorders such as systemic lupus erythematosus and systemic sclerosis.
Nephrotic Syndrome: glomerulus excessively permeable to plasma protein, causing proteinuria that leads to low plasma
albumin and tissue edema
Pathophysiology & Clinical Manifestations
 In adults, about 1/3 of patients with nephrotic syndrome will have a systemic disease such as diabetes or systemic
lupus erythematosus. The remaining have idiopathic nephrotic syndrome.
 The characteristic manifestations include peripheral edema, massive proteinuria, hypertension, hyperlipidemia, &
hypoalbuminemia.
 The characteristic blood chemistries include decreased serum albumin, decreased total serum protein, and elevated
serum cholesterol.
 The increased glomerular membrane permeability is responsible for the massive excretion of protein in the urine.
This results in decreased serum protein and subsequent edema formation. Ascities and anasarca (massive
generalized edema) develop if there is severe hypoalbuminemia.
 The diminished plasma oncotic pressure from the decreased serum proteins stimulates hepatic lipoprotein
synthesis, which results in hyperlipidemia. Fat bodies (fatty casts) commonly appear in the urine)
 Immune responses are altered in nephrotic syndrome and as a result infection is an important cause of morbidity.
 Calcium & skeletal abnormalities may occur, including hypocalcemia, blunted calcemic response to parathyroid
hormone, hyperparathyroidism, and osteomalacia.
 With nephrotic proteinuria, loss of clotting factors can result in a hypercoagulable state. Hypercoagulability with
thromboembolism is a serious complication. The renal vein is the most common site for thrombus formation.
Collaborative Care
 Goals=relieve edema and cure or control the primary disease.
 Management of edema=cautious use of ACE Inhibitors, NSAIDS, and a low-sodium, low-to-moderate-protein diet.
 Dietary salt restrictions
 Thiazide or loop diuretics
 Severe cases of nephritic syndrome=corticosteroids and cyclophosphamide (Cytoxan).
Nursing Management
 Daily weight, I&O, measure abdominal girth or extremity size.
 Clean edematous skin carefully
 Monitor effectiveness of diuretic therapy
 Serve small, frequent meals in a pleasant setting
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
Avoid exposure to persons with known infections
Nephrosclerosis: sclerosis of the smaller arteries & arterioles of the kidney; there is decreased blood flow which results
in patchy necrosis of the renal tissue.
Pathophysiology
 Benign nephrosclerosis usually occurs in adults 30-50 yrs. It is caused by the vascular changes resulting from
hypertension & the atherosclerosis process. There is a direct relationship between the degree of nephrosclerosis
and the severity of hypertension. The patient with benign nephrosclerosis may have normal renal function in the
early stages. The only detectable abnormality may be hypertension.
 Accelerated or Malignant nephrosclerosis is associated with malignant hypertension, which is characterized by a
sharp increase in BP with a diastolic pressure greater than 130 mm Hg. Renal insufficiency progresses rapidly.
Nursing Intervention
 Treatment for benign nephrosclerosis is the same as that for essential hypertension (lifestyle modifications, drug
therapy)
 Malignant nephrosclerosis is treated with aggressive antihypertension therapy (hospitalization, IV antihypertensive
drugs, and intensive care monitoring).
 Renal dysfunction and renal failure constitute two of the major complications of hypertension.
 Educate on the importance of managing hypertension
Hemodialysis
Complications
 Hypotension: results from rapid removal of vascular volume (hypovolemia), decreased cardiac output, and
decreased systemic intravascular resistance. The drop in BP during dialysis may precipitate light headedness,
nausea, vomiting, seizures, vision changes, & chest pain (from cardiac ischemia). Treatment – decreasing volume of
fluid being removed and infusion of 0.9% saline solution (100-300 ml). BP drugs should be held before dialysis if
there are frequent episodes of hypotension.
 Muscle cramps: result from rapid removal of Na and water or from neuromuscular hypersensitivity. Treatment –
reducing ultrafiltration rate & infusing hypertonic saline or a NS bolus.
 Loss of blood: may result from blood not being completely rinsed from the dialyzer, accidental separation of blood
tubing, dialysis membrane rupture, or bleeding after the removal of needles at the end of dialysis. It is essential to
rinse back all blood, closely monitor heparinization to avoid excess anticoagulation, & to hold firm but not occlusive
pressure on access site until bleeding risk has passed.
 Hepatitis: cause includes blood transfusions or the lack of adherence to precautions used to prevent the spread of
infection.
 Sepsis: most often related to infections of vascular access sites. Aseptic technique is essential to prevent this
problem. Nurses must monitor patients for S&S of sepsis such as fever, hypotension, and an elevated WBC.
 Disequilibrium syndrome: develops as a result of very rapid changes in the composition of the extracellular fluid.
Urea, sodium, and other solutes are removed more rapidly from the blood than from the cerebrospinal fluid & the
brain. This creates a high osmotic gradient in the brain resulting in the shift of fluid into the brain, causing cerebral
edema. Manifestations – N&V, confusion, restlessness, headaches, twitching, jerking, & seizures. It may also cause
muscle cramps & worsen hypotension. Treatment – slowing or stopping dialysis; and infusing hypertonic saline
solution, albumin, or mannitol to draw fluid from the brain cells back into systemic circulation. It is more commonly
observed in the initial treatment of the patient when the BUN level is high.
Assessment
 Before beginning the treatment, the nurse must complete an assessment that includes fluid status (weight, BP,
peripheral edema, lung & heart sounds), condition of vascular access, temperature, and general skin condition.
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 The difference between the last postdialysis weight and the present predialysis weight determines the ultrafiltration
or the amount of weight to be removed. Ideally, no more than 1 to 1.5 kg should be gained between treatments to
avoid causing hypotension with the removal of large volumes of fluid.
 While the patient is on dialysis, vital signs should be taken at least every 30 to 60 minutes because rapid changes
may occur in the BP.
 After dialysis, vital signs & weight are taken.
Venous Access Devices
 Shunts: external devices that are rarely used except with CRRT because of the numerous complications (infection,
thrombosis) associated with them.
 Internal arteriovenous fistulas: is created most commonly in the forearm with an anastomosis between an artery
and vein. The fistula provides for an arterial blood flow through the vein. The increase pressure of the arterial blood
flow through the vein makes the vein dilate & become tough, making it amenable to repeated venipuncture in 4-6
wks, although its recommended that the AVF be place atleast 3 months prior to initiating HD. Native fistulas have
the best overall patency rates & least number of complications (thrombosis, infection) of all vascular accesses, yet
are not frequently used.
 Arteriovenous grafts: are made of synthetic materials and form a bridge between the arterial and venous blood
supplies. An interval of 2-4 wks is usually necessary to allow the graft to heal, but some centers may use it earlier.
Because grafts are made of artificial materials, they are easily infected and are thrombogenic.
 Normally a thrill can be felt by palpating the area of anastomosis, and a bruit can be heard with a stethoscope.
 Blood pressure measurements, insertion of IVs, and venipuncture should NEVER be performed on the affected
extremity.
 AVGs can cause the development of distal ischemia (steal syndrome) because too much of the arterial blood is being
shunted or “stolen” from the distal extremity. Usually seen soon after surgery and may require surgical correction.
 Aneurysms can also develop at the fistula site and can rupture if left untreated.
Continuous Renal Replacement Therapy
Pros
 Acid-base status and electrolytes are adjusted slowly and continuously from a hemodynamically unstable patient.
 Causes less hypotension
 Does not require complicated equipment
 Does not require constant monitoring by a specialized HD nurse
Cons
 Risk for bleeding caused by anticoagulation used to prevent membrane clotting
Peritoneal Dialysis
Indicated for the individual who has vascular access problems or responds poorly to the hemodynamic stresses of HD
(the older pt w diabetes and CVD). Diabetic pt with ESRD does better w PD than w HD. Advantages of PD for the
diabetic pt are: better B/P control, less hemodynamic instability b/c fluid shifts are gradual, better control of BG by using
intraperitoneal insulin, and prevention of retinal hemorrhage.
Solutes and water move across the semipermeable membrane from the blood to the dialysate or from the dialysate to
the blood in accordance with concentration gradients. The principles of diffusion, osmosis, and ultrafiltration are
involved in dialysis (Fig. 47-7). Diffusion is the movement of solutes from an area of greater concentration to an area of
lesser concentration. In renal failure, urea, creatinine, uric acid, and electrolytes (potassium, phosphate) move from the
blood to the dialysate with the net effect of lowering their concentration in the blood. RBCs, WBCs, and plasma proteins
are too large to diffuse through the pores of the membrane. Bacteria and viruses that may be present in the dialysate
are too large to migrate through the pores into the blood.
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Osmosis is the movement of fluid from an area of lesser to an area of greater concentration of solutes. Glucose is added
to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood.
Ultrafiltration (water and fluid removal) results when there is an osmotic gradient or pressure gradient across the
membrane. In PD, excess fluid is removed by increasing the osmolality of the dialysate (osmotic gradient) with the
addition of glucose. In HD, the gradient is created by increasing pressure in the blood compartment (positive pressure)
or decreasing pressure in the dialysate compartment (negative pressure). Extracellular fluid moves into the dialysate
because of the pressure gradient. The excess fluid is removed by creating a pressure differential between the blood and
the dialysate solution with a combination of positive pressure in the blood compartment or negative pressure in the
dialysate compartment.
Assessment
 Daily catheter care includes application of an antiseptic solution and a clean dressing, as well as examination of the
catheter site for signs of infection.
 Assess for exit site infection – manifestations include, redness as the site, tenderness, and drainage.
 Peritonities: primary clinical manifestation is a cloudy peritoneal effluent that has a WBC count of over 100 cells. GI
symptoms may also be present including diffuse abdominal pain, diarrhea, vomiting, abdominal distention, and
hyperactive bowel sounds. Fever may or may not be present.
 Bleeding: BP and Hematocrit need to be checked if there is bloody effluent over several days.
 Pulmonary complications: assess lung sounds
Complications
 Exit site infection: generally resovles with antibiotic therapy. If not treated immediately, subcutaneous tunnel
infections usually result in abscess formation and may cause peritonitis, necessitating catheter removal.
 Peritonitis: primary clinical manifestation is a cloudy peritoneal effluent that has a WBC count of over 100 cells. GI
symptoms may also be present including diffuse abdominal pain, diarrhea, vomiting, abdominal distention, and
hyperactive bowel sounds. Fever may or may not be present. Antibiotics can be given orally, IV, or intraperitoneally.
Repeated infections may require the removal of the peritoneal catheter & termination of PD.
 Abdominal pain: may be caused by intraperitoneal irritation from low pH of the solution (which usually subsides in
1-2 wks) or peritonitis. Pain can also occur when the tip of the catheter touches the bladder, bowel, or peritoneum.
A change in position of the catheter should correct this problem. Accidental infusion of air or infusing the dialysate
too rapidly may cause referred pain in the should; if the infusion rate is decreased, the pain usually subsides.
 Outflow problems: immediately after placement – may be caused by a kink, or migration of the catheter; may
require radiologic or surgical manipulation. After catheter has settled – often the result of a full colon, bowel
evacuation frequently relieves the problem.
 Hernias: can develop because of increase abd pressure secondary to the dialysate infusion. In most situations, PD
can be resumed after hernia repair; pt must be kept supine & small dialysate volumes are used.
 Lower back problems: from increased intraabdominal pressure; orthopedic binders and a regular exercise program
for strengthening the back muscles have been beneficial for some patients.
 Bleeding: effluent drained after the first few exchanges may be pink or slightly blood tinged because of trauma from
placement. Bloody effluent over several days or the new appearance of blood in the effluent can indicate active
intraperitoneal bleeding. Check BP & Hematocrit. Blood may be present in effluent of menstruating women.
 Pulmonary complication: atelectasis, pneumonia, and bronchitis may occur from repeated upward displacement of
the diaphragm, resulting in decreased lung expansion. The longer the dwell time, the greater the likelihood of
pulmonary problems. Frequent repositioning and deep breathing exercises can help. Elevation of HOB may prevent
these problems.
 Protein loss: the peritoneal membrane is permeable to plasma proteins, amino acids, & polypeptides. Positive
nitrogen balance can be maintained with adequate protein intake.
 Carbohydrate & lipid abnormalities: continuous absorption of glucose results in increased insulin secretion &
increased plasma insulin levels. The hyperinsulinemia stimulates hepatic production of triglycerides.
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 Encapsulating sclerosing peritonitis & loss of ultrafiltration: the development of a thick fibrous membrane that
surrounds & compresses the bowel for unknown reasons. Intestinal obstruction & strangulation are common
complications. This necessitates the change to HD because of the loss of ultrafiltration.
Procedure: the three phases of the PD cycle are inflow (fill), dwell (equilibrium), and drain. The 3 phases are called an
exchange.
 The patient dialyzing at home will receive about four exchanges per day. An acutely ill hospitalized patient may
receive 12 to 24 exchanges per day. During inflow, a prescribed amount of solution, usually 2 L, is infused through an
established catheter over about 10 minutes. The flow rate may be decreased if the patient has pain. After the
solution has been infused, the inflow clamp is closed before air enters the tubing.
 The next part of the cycle is the dwell phase, or equilibration, during which diffusion and osmosis occur between the
patient's blood and the peritoneal cavity. The duration of the dwell time can last 20 to 30 minutes to 8 or more
hours, depending on the method of PD. Drain time takes 15 to 30 minutes and may be facilitated by gently
massaging the abdomen or changing position. The cycle starts again with the infusion of another 2 L of solution. For
manual PD, a period of about 30 to 50 minutes is required to complete an exchange.
Nephrectomy: surgical removal of the kidney
Procedure
 The patient should be told that there will probably be a flank incision on the affected side and that surgery will
require a hyperextended, side lying positon. This position frequently causes the patient to experience muscle aches
after surgery.
 Laparoscopic nephrectomy – can be performed in selected situations. In contrast to the open incisions of about 7
inches required in a conventional nephrectomy, a laparoscopic nephrectomy is performed using five puncture sites.
One incisions is to view the kidney and another is to dissect it. Compared to conventional, the laparoscopic approach
is less painful and requires no sutures or staples, involves a shorter hospital stay, and has a much faster recovery.
 Often requires removal of the 12th rib.
 If radical nephrectomy, steroid replacement required
Complications
 Biggest concerns are hemorrhage & adrenal insufficiency – both can cause hypotension (which is the earliest sign of
both); and both cause altered LOC.
 NEVER play contact sports again!
Nursing Priorities
 Monitor and preserve the function of the remaining kidney
- Hourly urine output X 24 hrs
- Acceptable output is 30-50 ml/hr (less than that suggests decreased renal blood flow)
- Hgb, Hct, & WBD every 6-12 hrs
- Vitals signs q4hrs
- Strict I&O
- Daily weights
- Respiratory status: adequate pain medication should be given to ensure the patient’s comfort & ability to
perform coughing & deep-breathing exercises. Frequently, incentive spirometry is used every 2 hrs when patient
is awake.
- Oral intake is restricted until bowel sounds are present; IV fluids are given until the patient can take oral fluids.
Wilm’s Tumor (nephroblastoma)
Clinical Manifestations
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 Most common – asymptomatic, mobile, palpable abdominal mass that does not cross the midline discovered by the
parent or PCP during a routine physical examination.
 While bathing or dressing child, parents notice the stomach seems swollen. Diaper no longer fits around the child’s
abdomen. Usually, the child’s activity level and appetite have not changed.
 All include microscopic or gross hematuria, hypertension, abdominal pain, fatigue, anemia, and fever.
 The lungs are the primary site for distant metastasis.
 Wilm’s tumor has been associated with other congenital abnormalities, including aniridia (absence of the irises),
hemihypertrophy, cryptorchidism, and hypospadias.
Prognosis
 Is related to stage of diease at diagnosis, histopathologic features of the tumor, and patient age.
 Categories of Wilms tumor are based on favorable and unfavorable findings; children with favorable histologic
findings (majority) have a more positive prognosis
 Survival rates for Wilms tumor are much better than for many other forms of cancer
 DO NOT PALPATE THE ABDOMEN!!
Renal Cell Carcinoma (adenocarcinoma)
Patho
 Most common type of kidney cancers occurring twice as often in men.
 Discovered between the ages of 50-70
 Cigarette smoking=most significant risk factor
 Increased incidence in 1st degree relatives
 Other risk factors=obesity, hypertension, and exposure to asbestos, cadmium, and gasoline.
 Risk is increased for those who have acquired cystic disease of the kidney associated with ESRD.
Clinical Manifestations/Diagnostic Studies
 No characteristic early symptoms; many diagnosed as incidental findings on imaging studies
 Most common presenting manifestations are hematuria, flank pain, and a palpable mass in the flank or abdomen.
Other manifestations include weight loss, fever, hypertension, anemia, and hypercalcemia.
 Most common sites of metastases include the lungs, liver, and long bones.
 Local extension into the renal vein and vena cava is common
 IVP with nephrotomography is the primary examination by which most masses are detected and evaluated.
 Angiography, percutaneous needle aspiration, CT, and MRI are also used.
 Radionuclide isotope is used to detect metastases.
Hyperparathyroidism
Manifestations
 Manifestations range from asymptomatic to overt; they include – weakness, loss of appetite, constipation, increased
need for sleep, emotional disorders, and shortened attention span.
 Major signs include – loss of calcium from bones (osteoporosis), fractures, kidney stones (nephrolithiasis).
 Neuromuscular abnormalities are characterized by muscle weakness (particularly lower extremities).
Causes
 Primary hyperparathyroidism: due to an increased secretion of PTH leading to disorders of calcium, phosphate, and
bone metabolism. The most common cause is benign tumor (adenoma) in the parathyroid gland.
 Secondary hyperparathyroidism: appears to be a compensatory response to conditions that induce or cause
hypocalcemia, the main stimulus of PTH secretion. Disease conditions associated with secondary
hyperparathyroidism include vitamin D deficiencies, malabsorption, chronic renal failure, & hyperphosphatemia.
 Tertiary hyperparathyroidism occurs when there is hyperplasia of the parathyroid gland and a loss of negative
feedback from circulating calcium levels. Thus there is secretion of PTH even with normal calcium levels. This
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condition is observed in the patient who has had a kidney transplant after a long period of dialysis treatment for a
chronic kidney disease.
Treatment
 Surgical therapy: is the most effective treatment of primary and secondary hyperparathyroidism. Surgery involves
partial or complete removal of the parathyroid glands. Autotransplantation of normal parathyroid tissue in the
forearm or near the sternocleidomastoid is usually done. This allows PTH secretion to continue with normalization
of calcium levels. If autotransplantation is not possible, or if it fails, the patient will need to take calcium
supplements for life.
 Nonsurgical therapy: This includes an annual examination with tests for serum PTH, calcium, phosphorus, and
alkaline phosphatase levels; renal function; x-rays to assess for metabolic bone loss; and measurement of urinary
calcium excretion. Continued ambulation and the avoidance of immobility are critical aspects of management.
Dietary measures also include maintenance of a high fluid intake and a moderate calcium intake.
- Drug therapy: Fosomax (inhibits osteoclastic bone resorption and rapidly normalize serum calcium levels;
estrogen or progestin therapy can reduce serum and urinary calcium levels in the postmenopausal woman and
may retard demineralization of the skeleton; phosphates (only if the pt has normal renal function for excretion);
diuretics (to increase urinary excretion of Ca+); Calcimimetic agents (Sensipar) decause PTH secretion and Ca+
blood levels, used for secondary parathyroidism in patients with chronic renal failure.
Nursing: following a parathyroidectomy
 The major postop complications are associated with hemorrhage & fluid & electrolyte disturbances. Tetany may
occur with sudden decrease in calcium levels. Mild tetany is characterized by tingling of the hands or around the
mouth, but should decrease over time.
 If tetany becomes more severe, IV calcium may be given. IV calcium should be readily available for patients following
parathyroidectomy.
 I&O monitored; Ca+, K+, phosphate, & magnesium levels assessed frequently; Chvostek’s & Trousseau’s signs;
mobility encouraged.
 If surgery is not performed – assist patient to adapt the meal plan to lifestyle, stress importance of exercise
program; keep regular appointments for test; instruct about symptoms of hypo and hypercalcemia.
Laboratory findings
 PTH, measured by radioimmunoassay, is elevated.
 Serum calcium levels usually exceed 10 mg/dl
 Serum phosphorus is usually below 3 mg/dl
 Elevations of other tests include, urine calcium, serum chloride, uric acid, creatinine, amylase (pancreatitis), and
alkaline phosphatase (bone disease).
Hypoparathyroidism
Pathophysiology
 Condition associated with inadequate circulating PTH; characterized by hypocalcemia
 The most common cause of hypoparathyroidism is iatrogenic; this may include the accidental removal of the
parathyroid glands or damage to the vascular supply of the glands during neck surgery.
 Severe hypomagnesemia also leads to a suppression of PTH secretion.
Clinical Manifestations: the clinical features are due to hypocalcemia
 Sudden decreases in calcium concentration cause tetany. This state is characterized by tingling of the lips, fingertips,
and occasionally feet and increased muscle tension leading to paresthesias and stiffness.
 Painful tonic spasms of smooth & skeletal muscles (particularly extremeties & face), dysphagia, a constricted feeling
in the throat, and laryngospasms are also present.
 Chvostek’s sign and Trousseau’s sign are usually positive.
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 Patients are usually anxious and apprehensive.
Medical/Surgical Care & Nursing
 Emergency treatment of tetany requires the administration of IV calcium
 Calcium must be infused slowly because high blood levels can cause hypotension, serious cardiac dysrhythmias, or
cardiac arrest. Thus ECG monitoring is indicated when calcium is administered. The patient who takes digoxin is
particularly vulnerable.
 IV calcium can cause venous irritation & inflammation; extravasation may cause cellulitis, necrosis, and tissue
sloughing; assess IV patency before administration
 Rebreathing may partially alleviated acute neuromuscular symptoms associated with hypocalcemia (cramps or mild
tetany).
 The patient with hypoparathyroidism needs instruction in the management of long-term drug therapy & nutrition.
Oral calcium supplements of atleast 1.5-3 g/day in divided doses are usually prescribed.
 Vitamin D is used in chronic & resistant hypocalcemia to enhance intestinal calcium absorption and bone resorption.
 A high calcium meal plan includes foods such as dark green vegetables, soybeans, and tofu.
 The patient should be told that foods containing oxalic acid (spinach, rhubarb), phytic acid (bran, whole grains), and
phosphorus reduce calcium absorption.
Parathyroidectomy
Potential Complications
 Parathyroidectomy leads to rapid reduction of calcium levels.
 The major postop complications are associated with hemorrhage and fluid & electrolyte disturbances.
 Tetany, a condition of neuromuscular hyperexcitability associated with sudden decrease in calcium levels, is another
concern.
Nursing Interventions
 IV calcium should be readily available for patients following parathyroidectomy in the event that acute tetany
occurs.
 Mobility is encouraged to promote bone calcification
 I&O are monitored to evaluate fluid status
 Calcium, potassium, phosphate, and magnesium levels are assessed frequently, as well as Chvostek’s & Trousseau’s
signs.
 If surgery is not performed, the nurse can assist the patient with hyperparathyroidism to adapt the meal plan to his
or her lifestyle.
 The nurse needs to stress the importance of an exercise program.
 Patient should be encouraged to keep regular appointments & the tests being performed should be explained.
 Instruct the patient of the symptoms of hypo & hypercalcemia.
Syndrome of Inappropriate Antidiuretic Hormone=Low & Wet
Clinical Manifestations
 Occurs more commonly in older adults. Most common cause is malignancy, especially small cell lung carcinoma
 Self limiting when caused by head trauma or drugs but is chronic in nature when associated with tumors or
metabolic diseases.
 Excess ADH increases permeability of the distal tubule and collecting duct, which leads to the reabsorption of water
into the circulation. Extracellular fluid volume expands, plasma osmolality declines, the glomerular filtration rate
increases, and sodium levels decline (dilutional hyponatremia).
 Hyponatremia causes – muscle cramps and weakness; initially thirst, dyspnea on exertion, fatigue, and dulled
sensorium may be evident.
 Low urinary output and increased body wt
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 As serum sodium falls below 120 mEq/L manifestations become more severe – vomiting, abd cramps, muscle
twitching, & seizures.
 As plasma osmolality and serum Na levels continue to decline, cerebral edema may occur, leading to lethargy,
anorexia, confusion, headache, seizures, and coma.
Diagnostic Studies
 Diagnosis made by simultaneous measurements of urine and serum osmolality
 Serum sodium <134 mEq/L, serum osmolality <280, and a urine specific gravity >1.005=dilutional hyponatremia
Treatments
 Immediate treatment goal is to restore normal fluid volume and osmolality.
 If symptoms are mild and serum sodium is greater than 125 mEq/L, the only treatment may be restriction of fluids to
800 to 1000ml per day. This should result in gradual daily reductions in weight, a progressive rise in serum sodium
concentration and osmolality, and symptomatic improvement.
 In cases of severe hyponatremia (<120), especially in the presence of neurologic symptoms such as seizures, IV
hypertonic saline may be administered. Hypertonic saline requires a very slow infusion rate.
 A diuretic such as Lasix may be used to promote dieresis, but only if the serum sodium is atleast 125 mEq/L, because
it may promote further loss of sodium.
 Water restriction of 500 ml per day is also indicated for those with severe hyponatremia.
 In chronic SIADH, water restriction of 800 to 1000ml per day is recommended. Because this may not be tolerated,
demeclocycline (Decloymycin) and lithium may be administered. They block the effects of ADH on the renal tubules,
thereby allowing a more dilute urine.
Nursing Interventions & Evaluation
 Be alert for low urinary output with a high specific gravity, a sudden weight gain without edema, or a serum sodium
decline.
 Acute onset SIADH
 Chronic SIADH
- Patient must learn to self manage treatment regimens.
- Fluids are restricted to 800-1000ml per day
- Ice chips or sugarless gum can help decrease thirst
- Patient may be treated with diuretic to remove excess fluid volume
- Diet should be supplemented with sodium and potassium, especially if diuretics are prescribed; solutions of
these electrolytes must be well diluted to prevent GI irritation or damage; they are best taken at mealtimes
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- Teach patient symptoms of fluid & electrolyte imbalances, especially those involving sodium & potassium.
Diabetes Insipidus =High & Dry
Associated with the deficiency of production or secretion of ADH or a decreased renal response to ADH. This decrease
in ADH results in fluid and electrolyte imbalances caused by increased UO and increased plasma osmolality.
TABLE 50-3 Types and Causes of Diabetes Insipidus (DI)
Medical Treatment
 Central DI: fluid and hormonal replacement.
 Acute DI: hypotonic saline or dextrose 5% in water is administered IV and titrated to replace urinary output.
 Hormone replacement is necessary because of the lack of ADH production or secretion. Desmopressin acetate
(DDAVP), is the hormone replacement of choice for central DI. It can be administered orally, IV, or as a nasal spray.
 Chlorpropamide, thought to potentiate the action of ADH & stimulate endogenous release, is considered the most
consistently effective and safest of these agents.
 Nephrogenic DI: hormone replacement & chlopropamide have little effect in the treatment of nephrogenic DI
because the kidney is unable to respond to ADH. Instead, treatment revolves around dietary measures (low sodium)
and thiazide diuretics.
- limiting sodium intake to no more than 3g per day is thought to help decrease urine output.
- thiazide diuretics (hydrochlorothiazide, Diuril) are able to slow the glomerular filtration rate, and allow the
kidney to reabsorb more water in the loop of Henle and distal tubles.
- When diet & diuretics are not effect, indomethacin (Indocin) may be prescribed; Indocin, a nonsterioidal
antiinflammatory agent, helps increase renal responsiveness to ADH
Nursing Interventions & Evaluation
 Includes early detection, maintenance of adequate hydration, and patient teaching for long-term management
 Acute central DI: administer fluids & hormone replacement; fluids are replaced orally or IV depending on patient’s
conditions and ability to drink copious amounts of fluids; keep fluids at bedside; IV glucose solutions are used,
monitor serum glucose because hyperglycemia & glucosuria can lead to osmotic diuresis which increases fluid
volume deficit.
 I&O, urine specific gravity, & daily weights are mandatory
 Administration of DDAVP
 Assess: weight gain, headache, restlessness, and signs of hyponatremia & water intoxication.
 Notify healthcare provider immediately if the individual with DI develops increased urine volume with a low specific
gravity, because this indicates need for increased dosing of DDAVP.
 Chronic DI: patient requires long-term ADH replacement and needs instruction in self-management; DDAVP can be
taken orally or intranasally. Nasal irritation may occur.
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- Headache, nausea, and other signs of hyponatremia may indicate overdosage. Failure to improve may indicate
under dosage. The patient should be instructed to report any of these symptoms
 Instruct patient to monitor daily weight
Laboratory findings
 Excretion of large quantities of urine – 5-20 L per day
 A very low specific gravity - <1.005
 Urine osmolality of <100
 Serum osmolality elevated at >295 mOsm, as a result of hypernatremia due to pure water loss from kidney
Fluid Deprivation Test
 A water deprivation test is usually done to confirm the diagnosis of central DI.
 Before a water deprivation test is done, the patient's baseline weight, pulse, urine and plasma osmolalities, urine
specific gravity, and blood pressure (BP) are obtained.
 All fluids are withheld for 8 to 16 hours. The patient may be anxious and should be reassured that the test will be
stopped if fluid volume deficit becomes severe. The patient should be observed throughout the test because of the
craving to drink.
 During the test, the patient's BP, weight, and urine osmolality are assessed hourly.
 The test continues until urine osmolalities stabilize (hourly increase less than 30 mOsm/kg [30 mmol/kg] in 3
consecutive hours) or body weight declines by 3%, or orthostatic hypotension develops.
 ADH is then given, and urine osmolality is measured 1 hour later. In central DI, the rise in urinary osmolality after
vasopressin exceeds 9%.
 Individuals with nephrogenic DI will have no response.
DRUGS
Calcium supplementation
 Intravenous:
- IV calcium gluconate or gluceptate should be readily available for patients following parathyroidectomy in the
event that acute tetany occurs.
- IV calcium chloride, calcium gluconate, or calcium gluceptate should be given slowly. Calcium must be infused
slowly because high blood levels can cause hypotension, serious cardiac dysrhythmias, or cardiac arrest. Thus
ECG monitoring is indicated when calcium is administered. The patient who takes digoxin is particularly
vulnerable. IV calcium can cause venous irritation and inflammation. Extravasation may cause cellulitis, necrosis,
and tissue sloughing. IV patency should be assessed before administration.
 Maintenance
- Oral calcium supplements of at least 1.5 to 3 g/day in divided doses are usually prescribed.
- The patient should be told that foods containing oxalic acid (e.g., spinach, rhubarb), phytic acid (e.g., bran,
whole grains), and phosphorus reduce calcium absorption.
- The patient should be instructed about the need for lifelong treatment and follow-up care including the
monitoring of calcium levels three to four times a year.
mythramycin (Mythracin): is a cytotoxic antibiotic given for chemotherapy. It inhibits bone resorption and thus lowers
the serum calcium level; used for hypercalcemia
 Given by the IV route only
 Some important side effects are: anemia, low WBC count, low platelet count, loss of appetite
calcitriol (Rocaltrol, Vitamin D): used in hypoparathyroidism to increase absorption of calcium
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 Assess: for dry mouth, metallic taste, polyuria, bone pain, muscle weakness, headache, fatigue, change in LOC,
dysrhythmias, increased respirations, anorexia, nausea, vomiting, cramps, diarrhea, constipation; may indicate
hypercalcemia
 Nutritional status, diet for sources of vit D (milk, some seafood); calcium (dairy products, dark green vegetables),
phosphates (dairy products) must be avoided
 The patient should be told that foods containing oxalic acid (e.g., spinach, rhubarb), phytic acid (e.g., bran, whole
grains), and phosphorus reduce calcium absorption. The patient should be instructed about the need for lifelong
treatment and follow-up care including the monitoring of calcium levels three to four times a year.
erythropoietin (Procrit, Epogen): used to stimulate RBC production in renal failure (anemia)
 Sufficient iron stores are needed for erythropoiesis; many patients with renal failure require oral iron supplements
 Folic acid is dialyzable, and if not adequately replaced, results in megaloblastic anemia.
 Teach: to take iron supplements, vitamin B12, folic acid as directed
vasopressin (DDAVP) the hormone replacement of choice for central DI. DDAVP can be administered orally, IV, or as a
nasal spray.
 Nursing interventions also include the administration of DDAVP. The patient should be assessed for weight gain,
headache, restlessness, and signs of hyponatremia and water intoxication. The adequacy of treatment is assessed by
monitoring fluid intake and output and by urine specific gravity. The health care provider should be notified
immediately if the individual with DI develops increased urine volume with a low specific gravity, because this
indicates need for increased dosing of DDAVP.
Lithium: used in SIADH because it blocks the effect of ADH on the renal tubules, thereby allowing a more dilute urine.
 In chronic SIADH, water restriction of 800 to 1000 ml per day is recommended. Because this degree of restriction
may not be tolerated, demeclocycline (Declomycin) and lithium may be administered.
 Lithium is one of the most common causes of nephrogenic DI
Democlocycline (Declomycin: used in SIADH because it blocks the effect of ADH on the renal tubules, thereby allowing a
more dilute urine
 In chronic SIADH, water restriction of 800 to 1000 ml per day is recommended. Because this degree of
restriction may not be tolerated, demeclocycline (Declomycin) and lithium may be administered.
Furosemide (Lasix): diuretic most commonly used as antihypertensive in CKD patients and to relieve edema in nephritic
syndrome
 Recommended as the initial therapy for non-diabetics (CKD)
Prednisone: (corticosteroid)-has been effective to varying degrees in persons with early stage nephrosis, membranous
glomerulonephritis, proliferative glomerulonephritis, and lupus nephritis.
Glucose (dextrose) and insulin: natural secretion in the body is an example of negative feedback. Increased glucose
levels in the body stimulate the secretion of insulin from the pancreas. As glucose levels decrease, the stimulus for
insulin also decreases.
 In dialysis, glucose is added to the dialysate and creates an osmotic gradient across the membrane, pulling
excess fluid from the blood.
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