Pyelonephritis

I. PYELONEPHRITIS
It is particular type of upper urinary tract infection (UTI) in which the renal tissue becomes inflamed due to the prolonged presence of a pathogen. The infectious microbe can be either viral or bacterial in origin, but is most commonly caused by Escherichia coli. The bacterium generally originates in the urethra, spreads to the bladder and up through the urethras, and finally impacts one or both of the kidneys.

Pathophysiology One or both kidneys may be involved. The infection extends from the ureter into the kidney, involving the renal pelvis and medullary tissue (tubule and interstitial tissue). Purulent exudate fills the kidney pelvis and calyces, and the medulla is inflamed. Abscesses and necrosis can be seen in the medulla and may extend through the cortex to the surface of the capsule. If the infection is severe, the exudate can compress the renal artery and vein and obstruct urine flow to the ureter. Bilateral obstruction is likely to result in acute renal failure. Recurrent or chronic infection can lead to fibrous scar tissue forming over a calyx, leading to loss of tubule function and hydronephrosis. If severe and bilateral, it can eventually cause chronic renal failure.

Etiology
Women are anatomically more vulnerable to infection than men because of the shortness and width of urethra, its proximity to the anus, and the frequent irritation to the tissues caused by sexual activity, bubble bath and deodorants.
Incontinence with incomplete emptying of the bladder
Retention of urine in the bladder
Obstruction to urine flow
Instruments or catheters may directly introduce into the bladder and wall, breaking the barrier to infection.
People with other renal diseases.

Signs and Symptoms
Dysuria
Flank pain
General fatigue
Fever; Chills

Diagnostic Test The tests used to diagnose pyelonephritis depend on the patient’s age, gender, and response to treatment and include the following:
Urinalysis
Urine culture
Ultrasound
Computerized tomography (CT) scan.
Voiding cystourethrogram (VCUG
Digital rectal examination (DRE).
Dimercaptosuccinic acid (DMSA) scintigraphy. DMSA scintigraphy is an imaging technique that relies on the detection of small amounts of radiation after injection of radioactive material. Because the dose of radioactive material is small, the risk of causing damage to cells is low. The procedure is performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologist. Anesthesia is not needed. Radioactive material is injected into a vein in the person’s arm and travels through the body to the kidneys. Special cameras and computers are used to create images of the radioactive material as it passes through the kidneys. The radioactive material makes the parts of the kidney that are infected or scarred stand out on the image. DMSA scintigraphy is used to show the severity of kidney infection or kidney damage, such as scarring.

Medical Management It is treated promptly with antibacterial drugs such as trimethoprim-sulfamethoxazole (Bactrim) or nitrofurantoin (Furadantin)

Nursing Intervention
1. Measure and record urine each time urination.
2. Encourage increased fluid intake.
3. Instruct to void every 2-3 hours.
4. Palpation of the bladder every 4 hours.
5. Help clients to the restroom, use bedpans / urinals.
6. Observations of changes in mental status: behavior or level of consciousness.
II. Glomerulonephritis
(Acute Poststreptococcal Glomerulonephritis)
It is a bilateral inflammation of the glomeruli that commonly follows a streptococcal infection.
There are two types of glomerulonephritis—acute and chronic. The acute form develops suddenly. You may get it after an infection in your throat or on your skin. Sometimes, you may get better on your own. Other times, your kidneys may stop working unless the right treatment is started quickly.

The early symptoms of the acute disease are: puffiness of your face in the morning blood in your urine (or brown urine) urinating less than usual.

You may be short of breath and cough because of extra fluid in your lungs. You may also have high blood pressure. If you have one or all of these symptoms, be sure to see your doctor right away.
The chronic form may develop silently (without symptoms) over several years. It often leads to complete kidney failure. Early signs and symptoms of the chronic form may include:
Blood or protein in the urine (hematuria, proteinuria)
High blood pressure
Swelling of your ankles or face (edema)
Frequent nighttime urination
Very bubbly or foamy urine

Symptoms of kidney failure include:
Lack of appetite
Nausea and vomiting
Tiredness
Difficulty sleeping
Dry and itchy skin
Nighttime muscle cramp

Glomerulonephritis may be caused by problems with the body's immune system. Often, the exact cause of glomerulonephritis is unknown.
Damage to the glomeruli causes blood and protein to be lost in the urine.

The condition may develop quickly, and kidney function is lost within weeks or months (called rapidly progressive glomerulonephritis).

A quarter of people with chronic glomerulonephritis have no history of kidney disease.
The following may increase your risk of this condition:
Blood or lymphatic system disorders
Exposure to hydrocarbon solvents
History of cancer
Infections such as strep infections, viruses, heart infections, or abscesses

Many conditions cause or increase the risk for glomerulonephritis, including:
Amyloidosis
Anti-glomerular basement membrane antibody disease
Blood vessel diseases, such as vasculitis or polyarteritis
Focal segmental glomerulosclerosis
Goodpasture syndrome
Heavy use of pain relievers, especially NSAIDs
Henoch-Schonlein purpura
IgA nephropathy
Lupus nephritis
Membranoproliferative GN

Pathophysiology
The initial reaction is usually either an upper respiratory infection or skin infection due to group A beta-hemolytic streptococcus. This leads to the formation of an antigen-antibody reaction. It is followed by the release of a membrane-like material from the organism into the body’s circulation. Antibodies produced to fight the invading organism also react against the glomerular tissue, thus forming immune complexes. The immune complexes become trapped in the glomerular loop and cause an inflammatory reaction in the affected glomeruli. Changes in the glomerular capillaries reduce the amount of the glomerular filtrate, thereby allowing passage of blood cells and protein into the infiltrate, and reducing the amount of sodium and water that is passed into the tubules for reabsorption. This affects the vascular tone and permeability of the kidney, resulting to tissue injury.

Medical Management
Because symptoms may develop slowly, the disorder may be discovered when you have an abnormal urinalysis during a routine physical or examination for another condition.

Imaging tests that may be done include:
Abdominal CT scan
Kidney ultrasound
Chest x-ray
Intravenous pyelogram (IVP)

Urinalysis and other urine tests include:
Creatinine clearance
Examination of the urine under a microscope
Urine for total protein
Uric acid in the urine
Urine concentration test
Urine creatinine
Urine protein
Urine RBC
Urine specific gravity
Urine osmolality

This disease may also cause abnormal results on the following blood tests:
Albumin
Anti-glomerular basement membrane antibody test
Anti-neutrophil cytoplasmic antibodies (ANCAs)
Anti-nuclear antibodies
BUN and creatinine

Medical Intervention
Treatment depends on the cause of the disorder, and the type and severity of symptoms. High blood pressure may be hard to control. Controlling high blood pressure is usually the most important part of treatment. Medicines that may be prescribed include:
Blood pressure medications to control high blood pressure, most commonly angiotensin-converting enzyme inhibitors and angiotensin receptor blockers
Corticosteroids
Medications that suppress the immune system
Plasmapheresis may sometimes be used for glomerulonephritis caused by immune problems. The fluid part of the blood that contains antibodies is removed and replaced with intravenous fluids or donated plasma (that does not contain antibodies). Removing antibodies may reduce inflammation in the kidney tissues.
Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts.
Sodium and fluid restriction should be advised for treatment of signs and symptoms of fluid retention (eg, edema, pulmonary edema).
Protein restriction for patients with azotemia should be advised if there is no evidence of malnutrition.

Nursing Intervention
1. Promote renal function.
Strictly measure and monitor intake and output and maintain dietary restrictions.
Encourage rest to facilitate diuresis and until renal function test levels normalize.
Administer medications as ordered and evaluate effectiveness of treatment.

2. Improve fluid balance.
Carefully monitor fluid balance and replace fluids according to patient’s fluid losses. Get daily weight.
Monitor for signs and symptoms of heart failure and hypertensive encephalopathy.
III. Urolithiasis
(Calculi/ Kidney Stones)
-small, hard deposits that form inside your kidneys
The stones are made of mineral and acid salts. Kidney stones have many causes and can affect any part of your urinary tract — from your kidneys to your bladder. Often, stones form when the urine becomes concentrated, allowing minerals to crystallize and stick together.
Kidney stones often have no definite, single cause, although several factors may increase your risk. Kidney stones form when your urine contains more crystal-forming substances — such as calcium, oxalate and uric acid — than the fluid in your urine can dilute. At the same time, your urine may lack substances that keep crystals from sticking together, creating an ideal environment for kidney stones to form.

Pathophysiology
Calculi can develop anywhere in the urinary tract. Stones may be very small or very large (.e.g. staghorn calculus, a very large stone that forms in the renal pelvis and calyces in the shape of deer’s antlers).
Calculi tend to form when there are excessive amounts of relatively insoluble salts in the filtrate, or when insufficient fluid intake creates a highly concentrated filtrate. Once any solid material or debris forms, deposits continue to build up on this nidus, or focus, and eventually form a large mass. Cell debris from infection may also form a nidus. Immobility may result in calculi in the kidney because of stasis of urine resulting in chemical changes in the urine. Increasing fluid intake can assist in removing small stones quickly from the urinary tract.
Stones usually cause manifestations only when they obstruct the flow of urine (e.g. in the ureter). Calculi may lead to infection because they cause stasis of urine in the area and also irritate the tissues. This may be an early indication of calculi formation.
When located in the kidney or ureter, calculi may cause the development of hydronephrosis, with dilation of calyces and atrophy of renal tissues related to the back pressure of urine behind the obstructing stone.
Types of kidney stones
Knowing the type of kidney stone helps determine the cause and may give clues on how to reduce your risk of getting more kidney stones. Types of kidney stones include:
Calcium stones. Most kidney stones are calcium stones, usually in the form of calcium oxalate. Oxalate is a naturally occurring substance found in food. Some fruits and vegetables, as well as nuts and chocolate, have high oxalate levels. Your liver also produces oxalate. Dietary factors, high doses of vitamin D, intestinal bypass surgery and several metabolic disorders can increase the concentration of calcium or oxalate in urine. Calcium stones may also occur in the form of calcium phosphate. Struvite stones. Struvite stones form in response to an infection, such as a urinary tract infection. These stones can grow quickly and become quite large, sometimes with few symptoms or little warning.
Uric acid stones. Uric acid stones can form in people who don't drink enough fluids or who lose too much fluid, those who eat a high-protein diet, and those who have gout. Certain genetic factors also may increase your risk of uric acid stones.
Cystine stones. These stones form in people with a hereditary disorder that causes the kidneys to excrete too much of certain amino acids (cystinuria). Other stones. Other, rarer types of kidney stones can occur.
Symptoms
A kidney stone may not cause symptoms until it moves around within your kidney or passes into your ureter — the tube connecting the kidney and bladder. At that point, these signs and symptoms may occur:
Severe pain in the side and back, below the ribs
Pain that spreads to the lower abdomen and groin
Pain that comes in waves and fluctuates in intensity
Pain on urination
Pink, red or brown urine
Cloudy or foul-smelling urine
Nausea and vomiting
Persistent urge to urinate
Urinating more often than usual
Fever and chills if an infection is present
Pain caused by a kidney stone may change — for instance, shifting to a different location or increasing in intensity — as the stone moves through your urinary tract.

Diagostic Test
If your doctor suspects you have a kidney stone, you may have diagnostic tests and procedures, such as:
Blood tests
Urinalysis
Imaging tests. Imaging tests may show kidney stones in your urinary tract. Options range from simple abdominal X-rays, which can miss small kidney stones, to high-speed computerized tomography (CT) that may reveal even tiny stones. Other imaging options include an ultrasound, a noninvasive test, and intravenous pyelography, which involves injecting dye into your arm vein and taking X-rays as the dye travels through your kidneys and bladder.
Analysis of passed stones. You may be asked to urinate through a strainer to catch stones that you pass. Lab analysis will reveal the makeup of your kidney stones. Your doctor uses this information to determine what's causing your kidney stones and to form a plan to prevent more kidney stones.

Medical Intervention
Treatment for kidney stones varies, depending on the type of stone and the cause.
Kidney stones that can't be treated with conservative measures — either because they're too large to pass on their own or because they cause bleeding, kidney damage or ongoing urinary tract infections — may require more invasive treatment. Procedures may include:
Using sound waves to break up stones. For certain kidney stones — depending on size and location — your doctor may recommend a procedure called extracorporeal shock wave lithotripsy (ESWL). ESWL uses sound waves to create strong vibrations (shock waves) that break the stones into tiny pieces that can be passed in your urine. The procedure lasts about 45 to 60 minutes and can cause moderate pain, so you may be under sedation or light anesthesia to make you comfortable. SWL can cause blood in the urine, bruising on the back or abdomen, bleeding around the kidney and other adjacent organs, and discomfort as the stone fragments pass through the urinary tract.
Surgery to remove very large stones in the kidney. A procedure called percutaneous involves surgically removing a kidney stone using small telescopes and instruments inserted through a small incision in your back. You'll receive general anesthesia during the surgery and be in the hospital for one to two days while you recover. Your doctor may recommend this surgery if SWL was unsuccessful or if your stone is very large.
Using a scope to remove stones. To remove a smaller stone in your ureter or kidney, your doctor may pass a thin lighted tube (ureteroscope) equipped with a camera through your urethra and bladder to your ureter. Once the stone is located, special tools can snare the stone or break it into pieces that will pass in your urine. Your doctor may then place a small tube (stent) in the ureter to relieve swelling and promote healing. You may need general or local anesthesia during this procedure.
Parathyroid gland surgery. Some calcium stones are caused by overactive parathyroid glands, which are located on the four corners of your thyroid gland, just below your Adam's apple. When these glands produce too much parathyroid hormone (hyperparathyroidism), your calcium levels can become too high and kidney stones may form as a result. Hyperparathyroidism sometimes occurs when a small, benign tumor forms in one of your parathyroid glands or you develop another condition that leads these glands to produce more parathyroid hormone. Removing the growth from the gland stops the formation of kidney stones. Or your doctor may recommend treatment of the condition that's causing your parathyroid gland to overproduce the hormone.

Nursing Intervention
1. Administer opioid analgesics (IV or intramuscular) with IV NSAID as prescribed.
2. Encourage and assist patient to assume a position of comfort.
3. Assist patient to ambulate to obtain some pain relief.
4. Monitor pain closely and report promptly increases in severity.
5. Encourage patient to drink enough to excrete 3,000 to 4,000 mL of urine every 24 hours.
6. If patient had surgery, instruct about the signs and symptoms of complications that need to be reported to the physician; emphasize the importance of followup to assess kidney function and to ensure the eradication or removal of all kidney stones to the patient and family.
7. If patient had ESWL, encourage patient to increase fluid intake to assist in the passage of stone fragments; inform the patient to expect hematuria and possibly a bruise on the treated side of the back; instruct patient to check his or her temperature daily and notify the physician if the temperature is greater than 38 C (about 101 F), or the pain is unrelieved by the prescribed medication.
Providing home and Follow up care after ESWL
1. Instruct patient to increase fluid intake to assist passage of stone fragments (may take 6 weeks to several months after procedure).
2. Instruct patient about signs and symptoms of complications: fever, decreasing urinary output, and pain.
3. Inform patient that hematuria is anticipated but should subside in 24 hours.
4. Give appropriate dietary instructions based on composition of stones.
5. Encourage regimen to avoid further stone formation; advise patient to adhere to prescribed diet.
6. Teach patient to take sufficient fluids in the evening to prevent urine from becoming too concentrated at night.

IV. Polycystic Kidney Disease
It is an inherited disorder in which clusters of cysts develop primarily within your kidneys. Cysts are noncancerous round sacs containing water-like fluid. The cysts vary in size and, as they accumulate more fluid, they can grow very large.
Although kidneys usually are the most severely affected organs, polycystic kidney disease can cause cysts to develop in your liver and elsewhere in your body. The disease causes a variety of serious complications.
A common complication of polycystic kidney disease is high blood pressure. Kidney failure is another common problem for people with polycystic kidney disease.
Polycystic kidney disease varies greatly in its severity, and some complications are preventable. Lifestyle changes and medical treatments may help reduce damage to your kidneys from complications, such as high blood pressure.

Pathophysiology
The main feature of ADPKD is a bilateral progressive increase in the number of cysts, which may lead to ESRD. Hepatic cysts, cerebral aneurysms, and cardiac valvular abnormalities also may occur.
Although ADPKD is a systemic disease, it shows a focal expression because less than 1% of nephrons become cystic. In ADPKD, each epithelial cell within a renal tubule harbors a germ-line mutation, yet only a tiny fraction of the tubules develop renal cysts.
It is currently held that the cells are protected by the allele inherited from the parent without ADPKD. When this allele is inactivated by a somatic event (mutation or otherwise) within a solitary renal tubule cell, the cell divides repeatedly until a cyst develops, with an aberrant growth program causing endless expansion. The severity of ADPKD is thought to be a direct consequence of the number of times and the frequency with which this cystogenic process occurs within the kidneys over the life of the patient. However this hypothesis is hard to understand in neonatal cases.
The hyperplastic cells cause an out-pocketing of the tubule wall, with the formation of a saccular cyst that fills with fluid derived from glomerular filtrate that enters from the afferent tubule segment. Progressive expansion eventually causes most of the emerging cysts to separate from the parent tubule, leaving an isolated sac that fills with fluid by transepithelial secretion. This isolated cyst expands relentlessly as a result of continued proliferation of the mural epithelium together with the transepithelial secretion of sodium chloride and water into the lumen.
The expanding fluid-filled tumor masses elicit secondary and tertiary changes within the renal interstitium evinced by thickening and lamination of the tubule basement membranes, infiltration of macrophages, and neovascularization. Fibrosis within the interstitium begins early in the course of the disease.
Cellular proliferation and fluid secretion may be accelerated by cyclic adenosine monophosphate (cAMP) and growth factors, such as epidermal growth factor (EGF). In summary, cysts function as autonomous structures and are responsible for progressive kidney enlargement in ADPKD.
A second defect, termed ADPKD type 2 (ADPKD2), is responsible for 10-15% of ADPKD cases and is found on the long arm of chromosome 4. A third genotype may exist, but no genomic locus is assigned.
PKD1 and PKD2 are expressed in most organs and tissues of the human body. The proteins that are encoded by PKD1 and PKD2, polycystin 1 and polycystin 2, seem to function together to regulate the morphologic configuration of epithelial cells. The polycystins are expressed in development as early as the blastocyst stage and are expressed in a broad array of terminally differentiated tissues. The functions of the polycystins have been scrutinized to the greatest extent in epithelial tissues of the kidneys and liver and in vascular smooth muscle
A decrease in urine-concentrating ability is an early manifestation of ADPKD. The cause is not known. Plasma vasopressin levels are increased; this increase may represent the body's attempt to compensate for the reduced concentrating capacity of the kidneys and could contribute to the development of renal cysts, hypertension, and renal insufficiency.
Bleeding
Renal cysts in ADPKD are associated with excessive angiogenesis evinced by fragile vessels stretched across their distended walls. When traumatized, these vessels may leak blood into the cyst, causing it to expand rapidly, resulting in excruciating pain. If bleeding continues, then the cyst may rupture into the collecting system, causing gross hematuria. Alternatively, the cyst may rupture into the subcapsular compartment and eventually dissect through the renal capsule to fill the retroperitoneal space.

Causes
Abnormal genes cause polycystic kidney disease, and the genetic defects mean the disease runs in families. Rarely, a genetic mutation can be the cause of polycystic kidney disease.
There are two types of polycystic kidney disease, caused by different genetic flaws:
Autosomal dominant polycystic kidney disease (ADPKD).Signs and symptoms of ADPKD often develop between the ages of 30 and 40. In the past, this type was called adult polycystic kidney disease, but children can develop the disorder.
Only one parent needs to have the disease in order for it to pass along to the children. If one parent has ADPKD, each child has a 50 percent chance of getting the disease. This form accounts for about 90 percent of cases of polycystic kidney disease.
Autosomal recessive polycystic kidney disease (ARPKD).This type is far less common than is ADPKD. The signs and symptoms often appear shortly after birth. Sometimes, symptoms don't appear until later in childhood or during adolescence.
Both parents must have abnormal genes to pass on this form of the disease. If both parents carry a gene for this disorder, each child has a 25 percent chance of getting the disease.
Researchers have identified two genes associated with ADPKD and one associated with ARPKD.
In some cases, a person with ADPKD has no known family history of the disease. However, it's possible that someone in the affected person's family actually did have the disease, but didn't show signs or symptoms before dying of other causes.
In a smaller percentage of cases where no family history is present, ADPKD results from a spontaneous gene mutation.
Polycystic kidney disease symptoms may include:
High blood pressure
Back or side pain
Headache
Increase in the size of your abdomen
Blood in your urine
Frequent urination
Kidney stones
Kidney failure
Urinary tract or kidney infections

Diagnostic Test
For polycystic kidney disease, certain tests can detect the size and number of kidney cysts you have and evaluate the amount of healthy kidney tissue, including:
Ultrasound exam.
Computerized tomography (CT) scan.
Magnetic resonance imaging (MRI) scan

Medical Management
The goal of PKD treatment is to manage symptoms. Controlling high blood pressure is the most important part of treatment. Treatment may include: pain medication blood pressure medication (angiotensin-converting enzyme (ACE) inhibitors) antibiotics (to treat UTI) a low-sodium (salt) diet diuretics (to help remove excess fluid) surgery (to drain cysts and help relieve discomfort)

With advanced PKD, dialysis and kidney transplant may be necessary. One or both of the kidneys may need to be removed.

Nursing Intervention Keeping our kidneys as healthy as possible may help prevent some of the complications of this disease. One of the most important ways we can protect our kidneys is by managing your blood pressure.
1. Monitor blood pressure and advised to take the blood pressure medications prescribed by the doctor as directed.
2. Instruct patient to eat a low-salt diet containing plenty of fruits, vegetables and whole grains.
3. Maintain a healthy weight.
4. Quit smoking.
5. Exercise regularly. Aim for at least 30 minutes of moderate physical activity most days of the week.

V. Acute Renal Failure
Acute kidney failure is the rapid loss your kidneys' ability to remove waste and help balance fluids and electrolytes in your body. In this case, rapid means less than 2 days.
-sudden decline in renal function, usually marked by increased concentrations of blood urea nitrogen (BUN; azotemia) and creatinine; oliguria (less than 500 ml of urine in 24 hours); hyperkalemia; and sodium retention.
Pathophysiology
The kidneys may fail to function for many different reasons. Either directly reduced blood flow into the kidney or inflammation and necrosis of the tubules cause obstruction and back pressure, leading to greatly reduced GFR and oliguria or anuria.
Both kidneys must be involved. The failure is usually reversible if the primary problem is treated successfully. Dialysis may be used to replace the kidney function during this period. In some cases, the kidney sustains a degree of permanent damage.
Acute kidney injury has three main causes:
A sudden, serious drop in blood flow to the kidneys. Heavy blood loss, an injury, or sepsis can reduce blood flow to the kidneys. Not enough fluid in the body also can harm the kidneys.
Damage from some medicines, poisons, or infections. Most people don't have any kidney problems from taking medicines. But people who have serious, long-term health problems are more likely than other people to have a kidney problem from medicines.

Examples of medicines that can sometimes harm the kidneys include:

Antibiotics, such as gentamicin and streptomycin.
Pain medicines, such as naproxen and ibuprofen.
Some blood pressure medicines, such as ACE inhibitors.
The dyes used in some X-ray tests.
A sudden blockage that stops urine from flowing out of the kidneys. Kidney stones, a tumor, an injury, or an enlarged prostate gland can cause a blockage.

You have a greater chance of getting acute kidney injury if:
You are an older adult.
You have a long-term health problem such as kidney or liver disease, diabetes, high blood pressure, heart failure, or obesity.
You are already very ill and are in the hospital or intensive care (ICU). Heart or belly surgery or a bone marrow transplant can make you more likely to have kidney problems.

Signs and symptoms of acute kidney failure may include:
Decreased urine output, although occasionally urine output remains normal
Fluid retention, causing swelling in your legs, ankles or feet
Drowsiness
Shortness of breath
Fatigue
Confusion
Nausea
Seizures or coma in severe cases
Chest pain or pressure

Sometimes acute kidney failure causes no signs or symptoms and is detected through lab tests done for another reason.
Diagnostic Tests
These may include:
Urine output measurements. Urinalysis.
Blood tests.
Imaging tests. Imaging tests such as ultrasound and computerized tomography (CT) may be used to help your doctor see your kidneys.
Removing a sample of kidney tissue for testing. In certain situations, your doctor may recommend a kidney biopsy to remove a small sample of kidney tissue for lab testing. To remove a sample of kidney tissue, your doctor may insert a thin needle through your skin and into your kidney.

Medical Management
Treatment for acute kidney failure typically requires a hospital stay. Most people with acute kidney failure are already hospitalized. How long you'll stay in the hospital depends on the reason for your acute kidney failure and how quickly your kidneys recover. Treating complications until your kidneys recover
Your doctor will also work to prevent complications and allow your kidneys time to heal. Treatments that help prevent complications include:
Treatments to balance the amount of fluids in your blood. If your acute kidney failure is caused by a lack of fluids in your blood, your doctor may recommend intravenous (IV) fluids. In other cases, acute kidney failure may cause you to have too much fluid, leading to swelling in your arms and legs. In these cases, your doctor may recommend medications (diuretics) to cause your body to expel extra fluids.
Medications to control blood potassium. If your kidneys aren't properly filtering potassium from your blood, your doctor may prescribe calcium, glucose or sodium polystyrene sulfonate (Kayexalate, Kionex) to prevent the accumulation of high levels of potassium in your blood. Too much potassium in the blood can cause dangerous irregular heartbeats (arrhythmias) and muscle weakness.
Medications to restore blood calcium levels. If the levels of calcium in your blood drop too low, your doctor may recommend an infusion of calcium.
Dialysis to remove toxins from your blood. If toxins build up in your blood, you may need temporary hemodialysis — often referred to simply as dialysis — to help remove toxins and excess fluids from your body while your kidneys heal. Dialysis may also help remove excess potassium from your body. During dialysis, a machine pumps blood out of your body through an artificial kidney (dialyzer) that filters out waste. The blood is then returned to your body.

Nursing Interventions:
1. Monitor 24-hour urine volume to follow clinical course of the disease.
2. Monitor BUN, creatinine, and electrolyte.
3. Monitor ABG levels as necessary to evaluate acid-base balance.
4. Weigh the patient to provide an index of fluid balance.
5. Measure blood pressure at various times during the day with patients in supine, sitting, and standing positions.
6. Adjust fluid intake to avoid volume overload and dehydration.
7. Watch for cardiac dysrhythmias and heart failure from hyperkalemia, electrolyte imbalance, or fluid overload. Have resuscitation equipment available in case of cardiac arrest.
8. Watch for urinary tract infection, and remove bladder catheter as soon as possible.
9. Employ intensive pulmonary hygiene because incidence of pulmonary edema and infection is high.
10. Provide meticulous wound care.
11. Offer high-carbohydrate feedings because carbohydrates have a greater protein-sparing power and provide additional calories.
12. Institute seizure precautions. Provide padded side rails and have airway and suction equipment at the bedside.
13. Encourage and assist the patient to turn and move because drowsiness and lethargy may reduce activity.
14. Explain that the patient may experience residual defects in kidney function for a long time after acute illness.
15. Encourage the patient to report routine urinalysis and follow-up examinations.
16. Recommend resuming activity gradually because muscle weakness will be present from excessive catabolism.

References:
Book:

Website: http://www.nursing-nurse.com/medical-and-nursing-management-of-glomerulonephritis-426/ http://www.nlm.nih.gov/medlineplus/ency/article/000484.htm http://nursingcrib.com/nursing-notes-reviewer/medical-surgical-nursing/glomerulonephritis/ http://nephrology.medicine.ufl.edu/patient-care/research/glomerulonephritis/ http://www.mayoclinic.org/diseases-conditions/polycystic-kidney-disease/basics/definition/con-20028831 http://www.healthline.com/health/polycystic-kidney-disease http://www.nlm.nih.gov/medlineplus/ency/article/000501.htm http://nursingcrib.com/nursing-notes-reviewer/acut e-renal-failure/ http://www.webmd.com/a-to-z-guides/acute-renal-failure-topic-overview http://nurseslabs.com/urolithiasis-nursing-management/ http://www.mayoclinic.org/diseases-conditions/kidney-stones/basics/definition/con-20024829