Chapter 70: Care Of Patients With Renal Disorders Flashcards
Etiology and risk of PKD
Those with the recessive form usually die in early childhood. 5 to 10% show no family history.
There is no way to prevent it, early detection can help slow the progression. Genetic counseling is needed.
More common in white people.
Pathophysiology of polycystic kidney disease
Fluid filled cysts develop in the nephrons.
In the inherited dominant form only a few nephrons have cysts until the person reaches the 30s. In the recessive form nearly 100% of nephrons have cysts from birth. The cysts become larger and more widely distributed. They damage the glomerular and tubular membranes. They are filled with fluid and enlarge and the kidney function deteriorates. The kidneys become very large, 2 to 3 times the normal size. The abdominal organs are displaced the patient has pain. The cysts are at risk for infection, rupture, and bleeding. Most patients have high blood pressure. The Renin/angiotensin system leads to hypertension also. Cysts can also occur in the liver and reduce liver function. Cerebral aneurysms are higher in these patients. Heart valve problems, left ventricular hypertrophy, colonic diverticula are common.
Manifestations of PKD
Abdominal or flank pain. Hypertension. Nocturia. Increased abdominal girth. Constipation. Bloody or cloudy urine. Kidney stones
Gently palpate the kidneys which are usually easily felt. Dull aching pain is caused by increased kidney size with distention or by infection within the cyst. Sharp intermittent pain occurs when cyst ruptures or a stone is present. When a cyst ruptures, the patient may have bright red or cola colored urine. If it is cloudy or foul-smelling infection is suspected. Nocturia is an early manifestation because of decreased concentrating ability.
As renal function further declines the patient has increasing hypertension, edema, anorexia, nausea and vomiting, pruritus, and fatigue. Berry aneurysms can occur and may cause a severe headache with or without neurologic or vision changes.
Diagnostic tests for PKD
Urinalysis shows the protein urea, hematuria, possibly bacteria.
Creatinine and BUN rises.
Creatinine clearances decrease.
Sodium up or down
Renal sonography, CT, MRI.
Treatment of polycystic kidney disease
Pain management however NSAID’s are used cautiously. Aspirin is avoided to avoid bleeding.
Antibiotics such as Cipro or Bactrim. Monitor creatinine levels because of nephrotoxicity. Dry heat promote comfort. Needle aspiration and drainage of a cyst.
Constipation: increase fluids, increase fiber, exercise. Use the stool softeners and a careful use of a laxative.
Control blood pressure. Drink at least 2 L to prevent dehydration. Restrict sodium. Antihypertensive agents and diuretics may be used.
.
Patient teaching for PKD
Teach patient to measure blood pressure, monitor weight daily, self administer medications. Protein intake may be limited
Take your temperature. Limit intake of salt. Notify your doctor if your urine is foul-smelling or if there is blood. Notify if you have a headache that does not go away or if you have visual disturbances. Monitor bowel movements to prevent constipation
Hydronephrosis
The kidney enlarges as urine collects in the pelvis and kidney tissue. The capacity is normally only 5 to 8 mL. Obstruction in the pelvis or at the point where the ureter joins the renal pelvis quickly distends. In only a matter of hours the blood vessels in renal tubule can be damaged
Hydroureter
Enlargement of the ureter with an obstruction lower in the urinary tract. This usually obstructed where the iliac vessels cross or where the ureter enters the bladder. Ureter dilation occurs and enlarges as urine collects.
Urethral stricture
The obstruction is very low in the urinary tract, causing bladder distention before hydroureter and hydronephrosis. It still needs prompt treatment.
Urinary obstruction
Pressure builds on the kidney and can cause failure. Nitrogen waste products such as urea, creatinine, and uric acid as well as electrolytes such as sodium, potassium, chloride, and phosphorus are retained. Acid-base is impaired. Causes can be tumors, stones, trauma, structural defects, and fibrosis, radiation, surgical treatment.
Creatinine and BUN increase with reduced GFR.
CT, IV urography, or sonography.
Treatment for urinary obstruction
Remove the stone. Cystoscope or retrograde urogram. Nephrostomy can be performed. A nephrostomy diverts urine externally to prevent kidney damage
Nephrostomy
NPO, clotting studies, and moderate sedation. Patient is placed prone, kidney located under ultrasound or fluoroscope, local anesthesia. A needle is placed into the kidney. A catheter is inserted into the renal pelvis and the external is connected to a drainage bag. It remains in place until the obstruction is resolved.
Post op monitor I and O. Some urine will still drain through a Foley catheter. Assess amount hourly for the first 24 hours. If the drainage decreases and the patient has back pain, the tube maybe clogged. Notify the doctor immediately. Monitor for leaking urine or blood and notify Dr. A red tinge in the urine may last for 12 to 24 hours.w
Pathophysiology of Pyelonephritis
Bacterial infection of the kidney and the renal pelvis/the upper urinary tract. Acute pyelonephritis is the active bacterial infection. Chronic pyelonephritis results from repeated or continued upper UTIs. Chronic is usually from a tract defect, obstruction, or most commonly when you’re in refluxes from the bladder into the ureters.
Reflux occurs at the vesicoureteral junctions where the ureter joins the bladder.
Abscesses may occur anywhere in the kidney. Inflammation and fibrosis lead to deformity of the renal pelvis and calyces. Repeated infection create scar tissue changing blood vessel. Glomerular, and tubular structure. Filtration, reabsorption, and secretion are impaired and renal function is reduced
Etiology and risk of pyelonephritis
Reflex as a child can cause scarring which then leads to chronic pyelonephritis. If they do not have reflux as a child it usually comes from a spinal cord injury, bladder tumor, prostate enlargement, or stones. At risk if you have had manipulation of the urinary tract, diabetes mellitus, chronic renal stones, overuse of analgesics. NSAIDS can lead to reflux
E. coli is the most common. If it is blood-borne which is rare the most common is Staphylococcus arias and Candida and salmonella
More common in women Until the age of 65 and then it is more common in men because of prostatitis
Manifestations of acute pyelonephritis
Fever, chills, tachycardia, tachypnea, flank back or groin pain, tender costal vertebral angle, abdominal discomfort, nausea and vomiting, general malaise or fatigue, burning urgency or frequency of urination, nocturia
Manifestations of chronic pyelonephritis
Hypertension, inability to conserve sodium, decreased urine concentrating ability/nocturia, tendency to develop hyperkalemia and acidosis. It is less dramatic. Ask about vague symptoms and history.
Diagnostic tests for pyelonephritis
Urinalysis shows positive leukocyte esterase and nitrate. Presence of white blood cells and bacteria. Culture and sensitivity is needed. Blood cultures may be obtained along with C reactive protein and ESR. X-rays of the KUB and IV urography can diagnose stones or obstructions. Cystourethrogram maybe indicated. Examining the urine for antibody coated bacteria may help.
assessment gallium scan to identify active pyelonephritis or abscesses, or tests to examine anti-body coated bacteria in urine, to identify patients who may need long term antibiotic therapy.
Treatment for pyelonephritis
Acute pain is treated with antibiotics and antiseptic drugs. Increase fluids 2 to 3 L per day and ensure adequate calories from all food groups. Surgical interventions to correct the problem. Conserve kidney function as long as possible. Teach to adhere to drug therapy. Control blood pressure. Possible protein restriction. Balance rest and activity
- Pyelolithotomy (stone removal from kidney)
- Nephrectomy (removal of the kidney) last resort
- Ureteroplasty ureteral diversion, or reimplantation of ureter to restore proper bladder drainage.
Hypertension and renal failure
ØBlood pressure is necessary to reduce cardiovascular complications and slow progression of kidney dysfunction. Educate to promote self management and understanding
ØUrge patient to drink 2 L of fluid per day to prevent dehydration, and decrease urine concentration with nocturia.
ØRestricting sodium intake to control blood pressure. Antihypertensives and diuretics, ACE inhibitors, calcium channel blockers, beta blockers, and vasodilators. ACE inhibitors may help control growth aspects of PKD
Immunologic renal disorders/ glomerular nephritis
Glomerulonephritis (GN) is the third leading cause of end-stage kidney disease (ESKD).
Whether the disease starts in the kidney or occurs as the result of other health problems, the glomeruli are usually injured.
For disease that starts in the kidney, a genetic basis and immune problem are common. In addition, systemic diseases and infections can have kidney effects and cause glomerular injury. Conditions that lead to glomerular disease include systemic lupus erythematosus and diabetic nephropathy.
Each type of disease or syndrome has a specific pathophysiology and clinical manifestations. Their glomerular effects are caused by injury to the glomeruli and result in proteinuria, hematuria, decreased glomerular filtration rate (GFR) edema, and hypertension.
Pathophysiology of acute glomerular nephritis
An infection (group A beta-hemolytic Streptococcus, staphylococcal or gram-negative bacteremia or sepsis, pneumococcal, syphilis, hepatatis B, measles, mumps, refer to table 70-3), often occurs before the kidney manifestations of acute glomerulonephritis (GN). The onset of symptoms is about 10 days from the time of infection. Usually, patients recover quickly and completely from acute GN. The incidence of acute GN is unknown, and GN after a systemic streptococcal infection is more common in men.
Manifestations of acute Glomerulonephritis
Patient assessment
ØConnection with sore throat? Skin or upper respiratory tract, recent travel or other exposures to viruses, bacteria, fungi, or parasite, recent illness or surgery, or systemic diseases. Recent incisions body piercing
Physical assessment/clinical manifestations: look for edema in face eyelids, hands, and othr area, assess for fluid overload and circulatory congestion (which may accompany the sodium and fluid retention), difficulty breathing or shortness of breath, assess for crackles in the lung, an S3 gallop rhythm and neck vein distention.
Changes in urination pattern and urine color smoky, reddish brown, rusty, or cola colored, dysuria, oliguria. Weigh to assess for fluid retention.
Baseline blood pressure. They usually have mild to moderate hypertension because of sodium and fluid retention. Fatigue, lack of energy, anorexia, nausea and vomiting if urea from kidney failure is present.
Test for acute glomerulonephritis
Laboratory assessment
ØUrinalysis shows RBCs (hematuria) and protein (proteinuria). Early morning specimen of urine is preferred for urinalysis because urine is most acidic and formed elements are more intact at that time.
ØSerum and urine creatinine measured by 24-hour urine test for creatinine clearance, BUN
ØSpecimens from the blood, skin, or throat are obtained for culture.
Other diagnostic tests
ØKidney biopsy
Treatment of acute glomerular nephritis
Interventions focus on managing infection, preventing complications, and providing appropriate patient education.
Management of infection begins with appropriate antibiotic therapy such as PCN, erythromycin, or azitromycin. To prevent spread of infection, antibiotics for people in immediate close contact with the patient also may be prescribed. Stress personal hygiene and basic IC principles such as handwashing, and complete entire course of antibiotics.
Prevention of complications
ØFluid overload, hypertension, and edema, diuretics and a sodium and water restriction are prescribed. Antihypertensive drugs to control hypertension. Fluid allowance is equal to the 24-hour urine output plus 500-600 mL.
ØOliguria may have increased serum levels of potassium and blood urea nitrogen (BUN). Potassium and protein intake may be restricted to prevent hyperkalemia and uremia as a result of the elevated BUN.
Dialysis is necessary if if uremic symptoms or fluid volume excess cannot be controlled.
Plasmapheresis is the removal and filtering of the plasma to eliminate antibodies.
Patient education for acute glomerulonephritis
Patient education includes teaching about the purpose of prescribed drugs, the dosage and schedule, and potential adverse side effects. Understand dietary or fluid restrictions and how to recognize fluid overload. Weight and daily blood pressure, peritoneal or vascular access care and dialysis schedules.
Pathophysiology of rapidly progressive glomerulonephritis
A type of acute glomerulonephritis. There are crescent shaped cells in the Bowmans capsule. Developed over several weeks or months and causes loss of kidney function. Patient become quite ill and quickly have manifestations of renal failure such as fluid volue excess, hypertension, Oliguria, electrolyte imbalances, uremic symptoms. May have lupus and it usually progresses to end-stage kidney disease.
Manifestations of Chronic Glomerulonephritis
AKA chronic nephrotic syndrome
Develops over period of 20 to 30 years or longer. Exact cause unknown and kidneys are atrophied.
Assessment
Mild protein urea, hematuria, hypertension, fatigue, occasional edema
Assess for circulatory overload, auscultate lung fields for crackles, rate, depth of respirations, BP, and weight. Auscultate heart for rate, rhythm, and presence of S3 heart sound. Neck for engorgement, edema in lower extremities. Uremic symptoms of slurred speech, ataxia, tremors, yellowish skin, bruises, rashes, itching.
Tests for chronic glomerulonephritis
Urine output is decreased but appears normal. Protein appears. Specific gravity is fixed at a constant level about 1.01 red blood cells and casts maybe seen. Creatinine clearance is low. Serum creatinine is high >6 up to 30 BUN > 100-200 Na retention usually Hyperkalemia Hyperphosphatemia Acidosis h ion retention and bicarbonate loss X-ray small kidneys Renal biopsy
Treatment of Chronic Glomerulonephritis
Interventions:
ØSlowing progression, preventing complications
ØDiet changes
ØFluid intake sufficient to prevent reduced blood flow volume to kidneys
ØDrug therapy to control the problems from uremia
ØDialysis, transplantation to prevent death from uremia.
Manifestations of nephrotic syndrome
Massive protein urea, hypoalbuminemia, edema, lipiduria, hyperlipidemia, increased coagulation, renal insufficiency
Nephrotic syndrome
Condition of increased glomerular permeability; allows larger molecules to pass through the membrane into urine and be excreted
Severe loss of protein into urine, edema formation, and decreased plasma albumin levels
The most common cause of glomerular membrane changes is an immune or inflammatory process.
Treatment of nephrotic syndrome
ØImmunosuppressive agents steroids and cytotoxic agents
ØACE inhibitors can decrease protein loss in the urine, and cholesterol-lowering drugs can improve blood lipid levels.
ØHeparin may reduce urine protein loss and improve kidney function.
ØDiet changes are often prescribed. (Protein)
ØMild diuretics and sodium restriction may be needed to control edema and hypertension.
Nephrosclerosis
Thickening in nephron blood vessels; results in narrowing of vessel lumen. This decreases renal bloodflow and the tissue is hypoxic.
Occurs with all types of hypertension, atherosclerosis, diabetes mellitus
Rarely seen if blood pressure is below 160/110
Collaborative management—control high blood pressure, preserve kidney function
It is the cause of end stage kidney disease and kidney failure in about 30% of patients requiring renal replacement therapy
Renovascular disease
Processes affecting renal arteries; may severely narrow lumen, greatly reduce blood flow to kidneys
Assessment
They often have a sudden onset of hypertension particularly if older than 50.
Significant, difficult to control high blood pressure
Poorly controlled diabetes or sustained hyperglycemia
Elevated serum creatinine
Decreased creatinine clearance
Treatment renovascular disease
Interventions
Drugs to control high blood pressure and by procedures to restore blood supply to the kidney.
Balloon angioplasty with or without stent placement to open renal vessels is less risky.
Renal artery bypass is a major procedure and requires 2 or more months to recover.
Renal angioplasty
Synthetic blood vessel graft.
Stages of progression of type one diabetic renal disease
Stage one, at the time diabetes is diagnosed. Kidney size and GFR are increased. Blood sugar control can reverse the changes
Stage two, 2 to 3 years after diagnosis. Glomerular and tubular capillary basement membrane changes result in microscopic changes with loss of filtration surface area and scar formation. Glomerular changes are referred to as glomerulosclerosis
Stage three, 7-15 years after diagnosis. Microalbuminuria is present. GFR is normal or increased
Stage four. Albuminuria is detectable by dipstick. GFR is decreased. Blood-pressure is increased, and retinopathy is present
Stage five. GFR decreases at an average rate of 10 mL per minute per year
Pathophysiology of diabetic nephropathy
Diabetes mellitus is the leading cause of end-stage kidney disease (ESKD) among white people in North America. About 36% of patients requiring dialysis or kidney transplantation have diabetes mellitus
Diabetic neuropathy (microvascular changes) occurs in either type 1 or type 2 diabetes mellitus, and the severity of diabetic kidney disease is related to the degree of hyperglycemia the patient experiences.
With poor control of hyperglycemia, the complicating problems of atherosclerosis, hypertension, and neuropathy(which promotes loss of bladder tone, urinary stasis, and UTI) are more severe and more likely to cause kidney damage.
Manifestations of diabetic nephropathy
First manifestation: persistent albuminuria as shown by dipstick or a urinary albumin excretion rate above 0.3 g/dL, without evidence of other kidney disease. Diabetic kidney disease is progressive. Refer to Table 70-4 The Stages of Progression of Type 1 Diabetic Kidney Disease
If possible, nephrotoxic agents (e.g., radiopaque contrast media or aminoglycosides) and dehydration are avoided.
Patients with worsening kidney function may have frequent hypoglycemic episodes and a reduced need for insulin or antidiabetic medication.
When kidney function is reduced, the insulin is available for a longer time and therefor less is needed. Many patients believe this means their diabetes is improving. The result is a more rapid progression of ESKD.
Real cell carcinoma
Adenocarcinoma of kidney is the most common type of kidney cancer.
Systemic effects occurring with the cancer type are called paraneoplastic syndromes and include:
ØAnemia
ØErythrocytosis
Related to large amounts of EPO
ØHypercalcemia
PTH production causes it
ØLiver dysfunction
ØIncreased sedimentation rate
ØHypertensionNephrectomy
Blood loss is a major concern and artery supplying the kidney may be embolized by radiation prior.
Place patient side with kidney to be removed uppermost. Removal of the 11th or 12th. Maybe needed. Sometimes the lymph nodes are removed.
Monitor for hemorrhage and adrenal insufficiency. Inspect abdomen for distention. Symptoms include hypotension, decreased urine output, and altered level of consciousness.
Adrenal insufficiency has a large urine output followed by hypotension and over urea. IV replacement of fluids and possibly red blood cells. Second kidney usually provides adequate function within a couple weeks.
Signs of pneumonia include fever, chills, thick sputum, or decreased breath sounds. Pain management usually requires opioid analgesics given parenterally.
Steroid replacements may be needed for insufficient glucocorticoids.
Assessment of renal cell carcinoma
Patient history
ØAge, known risk factors (e.g., smoking or chemical exposures), weight loss, changes in urine color, abdominal or flank discomfort, and fever, and family history of kidney, bladder, ureter, prostate gland, uterus or ovary.
Physical assessment/clinical manifestations
Ø5% to 10% of patients with renal cell cancer have flank pain, obvious blood in urine, and a kidney mass that can be palpated.
ØBloody urine is a late common sign.
ØSkin for pallor, darkening of the nipples, breast enlargement (gynecomastia) caused by changing hormone levels, muscle wasting, weakness, poor nutritional status, and weight loss.
Tests for renal cell carcinoma
Diagnostic assessment
ØUrinalysis with RBCs, CBC decreased hgb/hct, hypercalcemia, ESR, increased levels of adrenocorticotropic hormone, HCG, cortisol, renin, parathyroid hormone
ØIV urogram, surgical exploration, nephrograms, sonography, CT, MRI
Treatment renal cell carcinoma
Nonsurgical management
ØRadiofrequency ablation guided with MRI
ØChemotherapy limited use
BRMs and IL interleukin and interferon, TNF
Surgical management
Usually treated with a nephrectomy (removal of kidney)
Kidney trauma
Minor injuries—contusions, small lacerations
Major injuries—lacerations to cortex, medulla, or branches of renal artery
Collaborative management
Nonsurgical management—drug therapy is used for bleeding prevention or control. The need for clotting factors such as vitamin K and platelets is assessed, and given as needed.
Fluid therapy is given to restore circulating blood volume and ensure adequate blood flow to the kidneys. Crystalloid solutions replace water and some electrolytes. When bleeding is extensive, whole blood or PRBCs to restore hgb amd promotes oxygenation. Plasma volume expanders, such as dextran or albumin, help restore plasma oncotic pressure and reduce fluid shift to the interstitial fluid space.
Note: If the urethral opening is bleeding, consult with the physician before attempting urinary catheterization
Surgical management—nephrectomy or partial nephrectomy
