Nutrition Therapy in

Diseases of Kidney
and Urinary Tract
Presented by:

Magpatoc, Jessa May C.

 Topics:
1. Review of Anatomy and Physiology of the Urinary System

2. Pathophysiology, Nutrition Therapy and Prevention of

Disorders of the Kidneys and Urinary Tract
2.1 Urinary Tract Infection
2.2 Renal Calculi
2.3 Acute and Chronic Glomerulonephritis
2.4 Nephrotic Syndrome
2.5 Acute Kidney Injury
2.6 Chronic Renal Disease
2.7 Renal Replacement Therapies: Dialysis Treatment
and Transplantation
 1. Review of Anatomy and Physiology of the Urinary System
Functions of the Urinary System
This system helps to eliminate waste products such as urea from the body, regulate electrolyte concentration, blood
pressure and pH levels. The function of the kidneys are as follows:
Filter
- Every day, the kidneys filter gallons of fluid from the bloodstream.

Waste Processing
- The kidneys then process this filtrate, allowing wastes and excess ions to leave the body in urine while returning
needed substances to the blood in just the right proportions.
Elimination
- Although the lungs and the skin also play roles in excretion, the kidneys bear the major responsibility for
eliminating nitrogenous wastes, toxins, and drugs from the body.

Regulation
- The kidneys also regulate the blood’s volume and chemical makeup so that the proper balance between water
and salts and between acids and bases is maintained.
Other Regulatory Function
- By producing the enzyme renin, they help regulate blood pressure, and their hormone erythropoietin stimulates
red blood cell production in the bone marrow.

Conversion
- Kidney cells also convert vitamin D to its active form.
 Anatomy of the Urinary System
One of the major channels for excretion
 Kidney
- a bean shaped located above the waist, each side of the spinal column.
- average weight 6 ounces, surmounted by suprarenal (adrenal) gland.
- outer layer called cortex
- middle region called medulla
- 10-15 shaped structure called pyramids
- cup-shaped tubules which drain urine called calyxes
- glistening appearance is called Fibrous capsule
- serves as cushion, called Perirenal fat capsule
- anchors the kidney, Renal fascia
- separator, Renal columns
- continuous with the ureter leaving the hilum, Renal pelvis
- arterial supply of each kidney, Renal artery
- it approaches the hilum, segmental arteries
- each segmental artery gives off several branches called interlobar arteries
- curve over the medullary pyramids, Arcuate arteries
- branch off the arcuate arteries and run outward to supply is called Cortical
radiate arteries
 Nephrons
• Nephrons. contains over a million tiny structures and they are
responsible for forming urine.
• Glomerulus. One of the main structures of a nephron, is a knot
of capillaries.
• Renal tubule. Another one of the main structures in a nephron is
the renal tubule.
• Bowman’s capsule. The closed end of the renal tubule is
enlarged and cup-shaped and completely surrounds the
glomerulus.
• Podocytes. The inner layer of the capsule is made up of highly
modified octopus-like
• Foot processes. Podocytes have long branching processes that
intertwine with one another and cling to the glomerulus.
• Collecting duct. As the tubule extends from the glomerular
capsule, it coils and twists before forming a hairpin loop and then
again becomes coiled and twisted before entering a which
receives urine from many nephrons.
• Proximal convoluted tubule. This is the part of the tubule that is near to the
glomerular capsule.
• Loop of Henle. The loop of Henle is the hairpin loop following the proximal
convoluted tubule.
• Distal convoluted tubule. After the loop of Henle, the tubule continues to coil and
twist before the collecting duct.
• Cortical nephrons. Most nephrons are located almost entirely within the cortex.
• Juxtamedullary nephrons. they are situated next to the cortex-medullary
junction, and their loops of Henle dip deep into the medulla.
• Afferent arteriole. “feeder vessel”.
• Efferent arteriole. receives blood that has passed through the glomerulus.
• Peritubular capillaries. They arise from the efferent arteriole that drains the
glomerulus.
 Ureters
- renal collects urine in its chamber and from there the urine goes down the ureter
- two slender tubes each 25 to 30 cm (10 to 12 inches) long and 6 mm (1/4 inch)
in diameter.
- runs behind the peritoneum from the renal hilum to the posterior aspect of the
bladder, which it enters at a slight angle.
 Bladder
- urine, 96 % water, is continuously produced and collected into a storage sac
- can hold half liter (2 cups) of urine at any given time
- where infections tend to persist is called Trigone
- bladder wall, Detrusor muscles,
 Urethra
- where the urine is expelled from the bladder and out of the body
- an involuntary sphincter that keeps the urethra closed when the urine is not being
passed, Internal urethral sphincter
- voluntarily controlled, External urethral sphincter
Note: Female urethra is about 3 to 4 cm (1 1/2 inches) long, and its external orifice, or
opening, lies anteriorly to the vaginal opening, while male urethra is approximately 20
cm (8 inches) long and has three named regions: the prostatic, membranous, and
spongy (penile) urethrae; it opens at the tip of the penis after traveling down its length.
 Physiology of the Urinary System

• Glomerular filtration. Water and solutes

smaller than proteins are forced through the
capillary walls and pores of the glomerular
capsule into the renal tubule.
• Tubular reabsorption. Water, glucose, amino
acids, and needed ions are transported out of
the filtrate into the tubule cells and then enter
the capillary blood.
• Tubular secretion. Hydrogen, potassium,
creatinine, and drugs are removed from the
peritubular blood and secreted by the tubule
cells into the filtrate.
 Characteristics of Urine

 Daily volume. In 24 hours, only about 1.0 to 1.8 liters of urine are produced.
 Components. Urine contains nitrogenous wastes and unneeded substances.
 Color. Freshly voided urine is generally clear and pale to deep yellow.
 Odor. When formed, urine is sterile and slightly aromatic, but if allowed to stand, it takes on an
ammonia odor caused by the action of bacteria on the urine solutes.
 pH. Urine pH is usually slightly acidic (around 6), but changes in body metabolism and certain
foods may cause it to be much more acidic or basic.
 Specific gravity. Whereas the specific gravity of pure water is 1.0, the specific gravity of urine
usually ranges from 1.001 to 1.035.
 Solutes. Solutes normally found in urine include sodium and potassium ions, urea, uric acid,
creatinine, ammonia, bicarbonate ions, and various other ions.
 Micturition

 Accumulation. Ordinarily, the bladder continues to collect urine until about 200
ml have accumulated.
 Activation. At about this point, stretching of the bladder wall activates stretch
receptors.
 Transmission. Impulses transmitted to the sacral region of the spinal cord and
then back to the bladder via the pelvic splanchnic nerves cause the bladder to go
into reflex contractions.
 Passage. As the contractions become stronger, stored urine is forced past the
internal urethral sphincter into the upper part of the urethra.
 External sphincter. Because the lower external sphincter is skeletal muscle and
voluntarily controlled, we can choose to keep it closed or it can be relaxed so
that urine is flushed from the body.
 2.1 Urinary Tract Infection
- Symptomatic bacterial infection
Bladder -- An infection in the bladder is also called cystitis or a bladder infection.
Kidneys -- An infection of one or both kidneys is called pyelonephritis or a kidney infection.
Ureters -- The tubes that take urine from each kidney to the bladder are rarely the only site of infection.
Urethra -- An infection of the tube that empties urine from the bladder to the outside is called urethritis

Risk Factors

Iatrogenic/ Behavioural Anatomic/ Genetic

Drug Physiologic

• Voiding dysfunction • Familial tendency

• Indwelling catheter • Susceptible
• Frequent or recent sexual • Vesicoureteral reflux
• Antibiotic use uroepithelial cells
intercourse • Female sex
• Spermicides • Vaginal mucus
• Pregnancy
properties
Classifications of Urinary Tract Infections:

• Uncomplicated UTI: mild UTI, without complications, occur in normal urinary tracts

• Complicated (febrile): abnormality in urinary system or individual has a health
problem that compromises host’s defenses (HIV, diabetes, kidney stones, pyelonephritis,
renal transplant)
• Recurrent UTI: three or more UTIs in 12 months or 2 or more occurrences within 6
month
-Relapse: a second UTI caused by the same pathogen within 2 weeks of first
treatment
-Reinfection: a UTI that occurs greater than 2 weeks after completing treatment for
same or a different pathogen (McCance & Huether, 2019)
Acute Cystitis
The most common site of a UTI, acute cystitis, is inflammation of the bladder. The urine is contaminated by bacteria that
make its way up to the bladder. Most commonly a UTI occurs through the reversed movement of bacteria or pathogens (most
commonly Escherichia coli) from the gut (where it usually resides) up to the urethra then to the bladder (McCance & Huether,
2019). 
Interstitial Cystitis/Painful Bladder Syndrome
creates a chronic pain related to the lower urinary tract, more specifically, the bladder. Individuals with this experience a
pain or pressure sensation symptom for greater than 6 weeks but no infection can be identified. 
Acute Pyelonephritis
Pyelonephritis is an infection of one or both upper urinary tracts. Acute pyelonephritis is usually associated with the
microorganisms E. coli, Proteus, and Pseudomonas. Urinary obstruction and reflux of urine from the bladder are the most
common risk factors, along with being a female. 
Chronic Pyelonephritis
recurrent infection of the kidney which leads to scarring. Various causes are idiopathic, chronic UTI’s, renal stones, or
recurrent episodes of acute pyelonephritis.
Risk factors for developing UTIs
Some people are at greater risk than others of developing UTIs. These include:
• women – sexually active women are vulnerable, in part because the urethra is only four centimetres long
and bacteria have only this short distance to travel from the outside to the inside of the bladder
• people with urinary catheters – such as people who are critically ill, who can’t empty their own bladder
• people with diabetes – changes to the immune system make a person with diabetes more vulnerable to
infection
• men with prostate problems – such as an enlarged prostate gland that can cause the bladder to only
partially empty
• babies – especially those born with physical problems (congenital abnormalities) of the urinary system.
Prevention of UTIs
Although not always backed up by clinical research, some women have found some suggestions useful in
reducing their risk of developing urinary tract infections, including:
• Drink plenty of water and other fluids to flush the urinary system.
• Treat vaginal infections such as thrush or trichomonas quickly.
• Avoid using spermicide-containing products, particularly with a diaphragm contraceptive device.
• Go to the toilet as soon as you feel the urge to urinate, rather than holding on.
• Wipe yourself from front to back (urethra to anus) after going to the toilet.
• Empty your bladder after sex.
• Avoid constipation.
• Cranberries (usually as cranberry juice) have been used to prevent UTIs. Cranberries contain a substance that
can prevent the E. coli bacteria from sticking to the urinary tract lining cells. However, recent research has
shown that cranberry juice does not have a significant benefit in preventing UTIs, and most people are
unable to continue drinking the juice on a long-term basis.
Glomerulonephritis
 Glomerulonephritis (GN) is inflammation of the glomeruli, which are structures in your kidneys
that are made up of tiny blood vessels. These knots of vessels help filter your blood and remove
excess fluids. If your glomeruli are damaged, your kidneys will stop working properly, and you
can go into kidney failure.

 Sometimes called nephritis, GN is a serious illness that can be life-threatening and requires
immediate treatment. GN can be both acute, or sudden, and chronic, or long-term. This condition
used to be known as Bright’s disease.
Acute Glomerulonephritis
• Acute GN can be a response to an infection such as strep throat or an abscessed tooth. It may be due to problems with

your immune system overreacting to the infection. This can go away without treatment. If it doesn’t go away, prompt

treatment is necessary to prevent long-term damage to your kidneys.

• Certain illnesses are known to trigger acute GN, including:

• strep throat

• systemic lupus erythematosus, which is also called lupus

• Goodpasture syndrome, a rare autoimmune disease in which antibodies attack your kidneys and lungs

• amyloidosis, which occurs when abnormal proteins that can cause harm build up in your organs and tissues

• granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis), a rare disease that causes

inflammation of the blood vessels

• polyarteritis nodosa, a disease in which cells attack arteries.

Chronic Glomerulonephritis
• The chronic form of GN can develop over several years with no or very few symptoms.
This can cause irreversible damage to your kidneys and ultimately lead to complete
kidney failure.
• Chronic GN doesn’t always have a clear cause. A genetic disease can sometimes cause
chronic GN. Hereditary nephritis occurs in young men with poor vision and poor
hearing. Other possible causes include:
• certain immune diseases
• a history of cancer
• exposure to some hydrocarbon solvents
 Symptoms of Glomerulonephritis
Acute GN Chronic GN
Early symptoms of acute GN include: The chronic form of GN can creep up without any

• puffiness in your face symptoms. There may be slow development of symptoms

similar to the acute form. Some symptoms include:
• urinating less often
• blood or excess protein in your urine, which may be
• blood in your urine, which turns your urine a dark
rust color microscopic and show up in urine tests

• extra fluid in your lungs, causing coughing • high blood pressure

• swelling in your ankles and face
• high blood pressure
• frequent nighttime urination
• bubbly or foamy urine, from excess protein
• abdominal pain
• frequent nosebleeds
 Pathophysiology of Acute
Glomerulonephritis
• Acute Glomerulonephritis involves both structural changes and functional changes.
• Structurally, cellular proliferation leads to an increase in the number of cells in the glomerular tuft because of
the proliferation of endothelial, mesangial, and epithelial cells.
• The proliferation may be endocapillary (i.e., within the confines of the glomerular capillary tufts) or
extracapillary (ie, in the Bowman space involving the epithelial cells).
• In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents, a
feature characteristic of certain forms of rapidly progressive GN.
• Leukocyte proliferation is indicated by the presence of neutrophils and monocytes within the glomerular
capillary lumen and often accompanies cellular proliferation.
• Glomerular basement membrane thickening appears as thickening of capillary walls on
light microscopy.
• Electron-dense deposits can be subendothelial, subepithelial, intramembranous, or
mesangial, and they correspond to an area of immune complex deposition.
• Hyalinization or sclerosis indicates irreversible injury.
• These structural changes can be focal, diffuse or segmental, or global.
• Functional changes include proteinuria, hematuria, reduction in GFR (ie, oliguria or
anuria), and active urine sediment with RBCs and RBC casts.
• The decreased GFR and avid distal nephron salt and water retention result in expansion
of intravascular volume, edema, and, frequently, systemic hypertension.
Nutrition Therapy
Treatment of acute glomerulonephritis (AGN) is mainly supportive, because there is no specific
therapy for renal disease.

• Diet. 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.

• Activity. Bed rest is recommended until signs of glomerular inflammation and circulatory
congestion subside as prolonged inactivity is of no benefit in the patient recovery process.

• Long term monitoring. Long-term studies on children with AGN have revealed few chronic
sequelae.
• Antibiotics. In streptococcal infections, early antibiotic therapy may prevent antibody response
to exoenzymes and render throat cultures negative, but may not prevent the development of
AGN.

• Loop diuretics. Loop diuretics decrease plasma volume and edema by causing diuresis. The
reductions in plasma volume and stroke volume associated with diuresis decrease cardiac
output and, consequently, blood pressure.

• Vasodilators. These agents reduce systemic vascular resistance, which, in turn, may allow
forward flow, improving cardiac output.

• Calcium channel blockers. Calcium channel blockers inhibit the movement of calcium ions
across the cell membrane, depressing both impulse formation (automaticity) and conduction
velocity.
Pathophysiology of Chronic
Glomerulonephritis
• Reduction in nephron mass from the initial injury reduces the GFR. This reduction leads to
hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of
intraglomerular hypertension. These changes occur in order to increase the GFR of the
remaining nephrons, thus minimizing the functional consequences of nephron loss. The
changes, however, are ultimately detrimental because they lead to glomerulosclerosis and
further nephron loss.
In addition to a rise in BUN and creatinine levels, the substantial reduction in the GFR
results in the following:

• Decreased production of erythropoietin, thus resulting in anemia

• Decreased production of vitamin D, resulting in hypocalcemia, secondary

hyperparathyroidism, hyperphosphatemia, and renal osteodystrophy

• Reduction in acid, potassium, salt, and water excretion, resulting in acidosis, hyperkalemia,

hypertension, and edema

• Platelet dysfunction, leading to increased bleeding tendencies

Nutrition Therapy
1. Prevent or treat uremia if products of metabolism have accumulated

2. Prevent or treat edema caused by sodium and water retention

3. Maintain nutrition, since kidney disorders are wasting diseases. The diet should be
adequate to meet the patient’s state of nutrition in terms of protein, vitamin C,
minerals, sodium, potassium and calcium should also be watched closely.

Energy. Maintenance of good nutritional statues of the patient is still the primary
consideration. Sufficient carbohydrates and fat be provided so that the energy needs of the
body can be met without the breakdown of the protein. The daily caloric needs for the
adult will usually range from 2000-3000 kcal.
Protein. A level of 40-60 g/day is recommended to reduce the amount of protein breakdown
products to be excreted. If there are signs of impending uremia, a level of 30-40 g protein or 0.5
protein/kilogram body weight may be necessary for the adult patient. The sources should give
protein of high biological value to be distributed throughout the three meals.

Sufficient levels of protein must be given as long as the kidneys can expel waste products of
protein metabolism. Protein restriction is not advisable in the case of protein malnutrition,
neoplasm, or infections. Low protein foods combined with amino acids analogs are useful in these
situations

Electrolytes and fluids. Restriction of sodium from 500-100 mg and fluids to as low as 500 ml if
there is edema or hypertension is a prophylactic measure. If electrolytes loss is excessive, these
must be replaced. Sodium restriction without edema may cause hypovolemia, reduced renal
perfusion and a drop in renal function.

A high fluid intake (about 2-3 L/day) is desirable to compensate for the kidney losses and to flush
out toxic products.

Vitamins. It is important hat the diet meets the recommended allowances for vitamins and
minerals; otherwise, supplementation will be most appropriate. Calcium and B vitamins are easily
lost in urine. Children with uremia require vitamin D3 promote growth and improve appetite.
Renal Calculi (Kidney Stone)
Renal calculi are a common cause of blood in the urine (hematuria) and pain in the
abdomen, flank, or groin. They occur in one in 11 people at some time in their lifetimes
with men affected 2 to 1 over women. Development of the stones is related to decreased
urine volume or increased excretion of stone-forming components such as calcium, oxalate,
uric acid, cystine, xanthine, and phosphate. Calculi may also be caused by low urinary
citrate levels or excessive urinary acidity.

Renal calculi present with excruciating pain and most patients present to the
emergency department in agony. A single event does not cause kidney failure but recurrent
renal calculi can damage the tubular epithelial cells, which can lead to functional loss of the
renal parenchyma.
The four major types of renal calculi include
• Calcium stones (due to hyperparathyroidism, renal calcium leak, hyperoxaluria,
hypomagnesemia and hypocitraturia)

• Uric acid stones are associated with pH less than 5, high intake of purine foods (fish, legumes,
meat), or cancer. These stones may also be associated with gout

• Struvite stones (caused by gram negative-urease positive organisms that breakdown urea into
ammonia. Common organisms include pseudomonas, proteus, and klebsiella. E coli is not
associated with struvite stones)

• Cystine stones are due to an intrinsic metabolic defect causing the failure of the renal tubules
to reabsorb cystine, lysine, ornithine, and arginine.
Pathophysiology
Most urinary stones start as Randall's plaque at the junction of the nephron's collecting tubule and the
renal pelvis in the papilla. These plaques start suburothelial and then gradually grow until they break
through into the renal pelvis. Once in continuous contact with urine, layers of calcium oxalate
typically start to form on the calcium phosphate nidus (all Randall's plaques are composed of calcium
phosphate). Calcium oxalate stones tend to form when the urinary pH is under 7.2 while calcium
phosphate will form in the more alkaline urine. Hyperparathyroidism and similar metabolic
disturbances like renal tubular acidosis typically form stones that are primarily or significantly
composed of calcium phosphate. Overly acidic urine is the primary cause of uric acid stones (not
hyperuricosuria).
The majority of renal calculi are made of calcium, followed by urare crystals. Supersaturation of the urine is
the common denominator in all cases of renal calculi. In some cases, calcium oxalate stones may deposit in
the renal papilla. Calcium phosphate stones usually precipitate in the basement membrane of the thin loop of
Henle and may erode into the interstitium. The colicky pain s usually due to the dilatation and spasm of the
ureter.
Nutrition Therapy
1. Eat plenty of cereal fiber with each meal.

2. Cut down on animal protein, particularly meat

3. Avoid refined foods, e.g., sugar and sugary foods.

4. Drink liberal amounts of fluids, 10 glasses per day at least.

Prevention
 Avoid protein intake;- usually protein is restricted to 60g/day to decrease urinary excretion of calcium and uric
acid.
 A sodium intake of 3 to 4 g/day is recommended. Table salt and high-sodium foods should be reduced,
because sodium competes with calcium for reabsorption in the kidneys.
 Low-calcium diets are not generally recommended ,except for true absorptive hypercalciuria. Evidence shows
that limiting calcium, especially in women, can lead to osteoporosis and does not prevent renal stones.
High in Urea
How to lessen oxalate in food items:
It’s possible that your chronic pain and inflammation could be caused by oxalates — chemicals found in a number of
foods, including the favorite healthy foods you eat. Most of us eat oxalates every day without a problem. When the gut
is healthy, good bacteria can metabolize oxalates and help them to be eliminated. But when oxalates encounter
damaged tissue in the body, they can bind with calcium to crystallize, resulting in serious irritation and pain.

One important tip to remember: Boil high-oxalate vegetables to naturally reduce their oxalate content.

If oxalates are destroying your health, there are three things you can do to buffer their effects on your body:
• Restore gut health. Probiotic liquids and fermented foods encourage communities of beneficial oxalate-eating
bacteria to grow.
• Address Candida overgrowth. Candida yeast can inhibit your body’s ability to break down oxalates. Fermented foods
can reduce dangerous levels of Candida in the gut.
• Consider a calcium supplement. Oxalates may bind to a citrate-based calcium supplement to improve elimination.

Drinking water can help dilute oxalate in the blood and make it easier for you to flush it out of your body, reducing
your risk of kidney stones. Drink at least 8 to 12 cups of fluid each day. Citric acid from lemons and other citrus fruits
can also help prevent the formation of calcium oxalate fluids. If you are concerned about the amount of oxalate in your
diet or are thinking of making significant dietary changes, talk to your doctor first.
List of Foods High in Uric Acid
Various factors contribute to the excessive development of uric acid in the blood. These can range from obesity to kidney problems
to diuretic or immunosuppressant use. However, various foods too can contribute to the excessive formation of uric acid in the
blood. If you suffer from gout, knowing the foods that contain high levels of purines can help you prevent a gout attack better.
• Meat - Out of all foods that are high in purines, meat is ranked the highest. Organ meats, such as liver, heart, kidney and brain,
contain the most amount of purines. If you suffer with gout, you should completely avoid the consumption of organ meats and
red meats, such as beef and pork. Bacon contains high levels of purine, and, therefore, should be strictly avoided. Poultry, such
as, chicken and turkey can be consumed only in moderation.
• Seafood - Seafood should be avoided as this too contains high purine levels. Shellfish such as crab, lobster, and shrimp, sardines,
tuna, mackerel, herring, halibut and salmon are some seafood that contains high purine levels.
• Vegetables - Although certain vegetables are high in purines, making them on the list of high uric acid foods, they are not as high
as that in organ meats and seafood. However, avoiding them or using them in moderation can be beneficial in keeping gout
attacks at bay. Some vegetables with high purines are mushrooms, black gram, beans, peas, lentils, broccoli, cauliflower, carrots,
aubergine and spinach.
• Yeast - Any food item that contains yeast should be avoided as this too contains high purine levels. Various alcoholic beverages
especially beer and breads contain excessively high amounts of purines. Gout patients should avoid these completely to prevent
attacks of gout.
• Fruits - There are also a number of fruits high in purines. These include dried fruits such as dates and figs, and fresh fruits such as
bananas, avocado, apples, kiwi fruit, gooseberry and pineapple, etc.
 How to Lower Uric Acid Levels
There are two methods that can be used to lower uric acid levels in the body, through the avoidance
of foods that contain purines and medication.

Increasing carbohydrate foods and fruits that contain high water content is beneficial in preventing
gout. Just like there are uric acid foods, there are also some foods that can help lower uric acid level, like
berry, apple, celery seed, green tea, olive oil, etc. Try to decrease your soda consumption and alcohol.
And maintain a healthy body weight to prevent an increase in uric acid levels.

While your diet can make a significant impact in maintaining proper levels of uric acid, a doctor
may also prescribe you with medications. With proper diet management and medications, you will be in
better control of your gout attacks.
References:
• Belleza, M., By, -, Belleza, M., & Marianne is a staff nurse during the day and a Nurseslabs writer at night. She is a
registered nurse since 2015 and is currently working in a regional tertiary hospital and is finishing her Master's in
Nursing this June. As an outpatient department nurse. (2021, February 11). Acute glomerulonephritis nursing CARE
planning and Management: Study guide. Retrieved April 05, 2021, from https://nurseslabs.com/acute-
glomerulonephritis/#what_is_acute_glomerulonephritis
• Belleza, M., By, -, Belleza, M., & Marianne. Urinary system anatomy and physiology: Study guide for nurses. Retrieved
March 18, 2021, from https://nurseslabs.com/urinary-system/#:~:text=Physiology%20of%20the%20Urinary%20System.
%20Every%20day%2C%20the,is%20a%20result%20of%20three%20processes%3A%20Glomerular%20filtration.
• Lees, C. (n.d.). Urinary tract infection (uti). Retrieved March 23, 2021, from http://www.pathophys.org/uti/
• Leslie, S. (2021, February 14). Renal calculi. Retrieved April 05, 2021, from
https://www.ncbi.nlm.nih.gov/books/NBK442014/
• Moro O Salifu, M. (2021, April 03). Chronic glomerulonephritis. Retrieved April 05, 2021, from
https://emedicine.medscape.com/article/239392-overview#a4
• Pathophysiology of an uti. (n.d.). Retrieved March 23, 2021, from https://u.osu.edu/utieducation/pathophysiology-of-
uti/#:~:text=Urinary%20tract%20infections%20are%20caused%20by%20bacterium%20that,way%20up%20to%20the
%20bladder%2C%20ureters%2C%20or%20kidney.