KINNAIRD COLLEGE FOR WOMEN UNIVERSITY,

LAHORE

FINAL PROJECT

SUBMITTED BY: Ayesha Masood

Hafiza Momina Irfan
Hira Asad
Laiba Akhtar
Liza Kamran
SUBMITTED TO: Miss Nida Tasneem Khan
COURSE TITLE: Human Physiology
SECTION: A
SEMESTER: 4
SESSION: 2019-23
MAJOR: Food Science & Human Nutrition
DATE OF SUBMISSION: 21st May, 2021

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 KIDNEY DISORDERS

Contents
KIDNEY DISEASES .................................................................................................................................. 3
RENAL DISEASES .................................................................................................................................... 4
Nephrolithiasis (Kidney stones) ............................................................................................................. 4
ACUTE RENAL FAILURE..................................................................................................................... 11
DISEASES OF TUBULES AND INTERSTITIUM............................................................................... 13
Chronic Interstitial Nephritis .............................................................................................................. 13
Fanconi’s Syndrome ............................................................................................................................. 14
Renal Tubular Acidosis ........................................................................................................................ 15
Pyelonephritis ........................................................................................................................................ 16
GLOMERULAR DISEASE ..................................................................................................................... 18
CHRONIC KIDNEY DISEASE (CKD) .................................................................................................. 21
END STAGE RENAL DISEASE (ESRD) .............................................................................................. 26
LIFESTYLE MANAGEMENT FOR THE PREVENTION AND TREATMENT OF KIDNEY
DISORDERS ............................................................................................................................................. 30
REFERENCES .......................................................................................................................................... 37

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 KIDNEY DISEASES
The kidneys are amazing organs that play a major role in keeping our body clean and healthy by
flushing out unwanted wastes and toxic materials. Though their
primary function is to remove toxins from the body, it is not
their only function. The kidneys also play a crucial role in
regulating blood pressure, the volume of fluid and electrolytes
in the body. Although most of us are born with two kidneys,
just one suffices to effectively carry out all important tasks.

In recent years, there has been a disturbing increase in the

number of patients suffering from diabetes and hypertension
that has led to a noticeable increase in the number of patients
suffering from chronic kidney disease. This calls for better
awareness and understanding of kidney diseases, their
prevention and early treatment.

You have two kidneys, each about the size of your fist. They are near the middle of your back,
just below the rib cage. Inside each kidney there are about a million tiny structures called
nephrons. They filter your blood. They remove wastes and extra water, which become urine. The
urine flows through tubes called ureters. It goes to your bladder, which stores the urine until you
go to the bathroom.

Kidney disease is a term used to include any abnormality of the kidneys. Many diseases can
affect the kidneys, and can be described as acute (rapid in onset) or chronic (longer term) kidney
disease.

Most kidney diseases attack the nephrons. This damage may leave kidneys unable to remove
wastes. Causes can include genetic problems, injuries, or medicines. You have a higher risk of
kidney disease if you have diabetes, high blood pressure, or a close family member with kidney
disease. Chronic kidney disease damages the nephrons slowly over several years. Other kidney
problems include

 Cancer

 Cysts

 Stones

 Infections

Your doctor can do blood and urine tests to check if you have kidney disease. If your
kidneys fail, you will need dialysis or a kidney transplant.

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 RENAL DISEASES
The manifestations of renal disease are significant. They can be ordered by degree of severity:
(1) kidney stones, (2) acute kidney injury (AKI), (3) chronic kidney disease (CKD), and (4) end-
stage renal disease (ESRD).

Nephrolithiasis (Kidney stones)

Kidney stones (renal lithiasis or nephrolithiasis)
form as a result of abnormal crystallization of
calcium, oxalate, struvite, cystine,
hydroxyapatite, or uric acid that is not excreted
normally in the urine. It is characterized by frequent
occurrences during the fourth and fifth decades of
life and a high recurrence rate. The risk doubles in
those with a family history of kidney stones; stone
formers often have first-degree relatives with kidney
stones. Increased frequency of obesity, diabetes, and
metabolic syndrome have resulted in increasing rates of nephrolithiasis.

Risk factors associated with kidney stones

Risk factors for kidney stones include family history; previous stone formation; certain medical
conditions, such as hypercalciuria, hyperuricosuria, and hyperoxaluria; low urine volume; and
malabsorption. Hypercalciuria, the cause of more than 50% of all kidney stones, is defined as
urinary calcium excretion greater than 300 mg per 24 hours in men or 250 mg per 24 hours in
women. Other causes of kidney stones include gout, excess intake of vitamin D, urinary tract
infections, and urinary tract blockages. The most significant risk factor for development of
kidney stones is low urine output.

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Pathophysiology
Kidney stone formation is a complex process that consists of saturation; supersaturation;
nucleation; crystal growth or aggregation; crystal retention; and stone formation in the presence
of promoters, inhibitors, and complexors in urine.

Calcium stones are the most common: 60% of stones are calcium
oxalate, 10% calcium oxalate and calcium phosphate, and 10%
calcium phosphate. Other stones are 5% to 10% uric acid, 5% to
10% struvite, and 1% cystine.

Obese stone formers excrete increased amounts of sodium, calcium,

uric acid, and citrate, and have lower urine pH. Obesity is the
strongest predictor of stone recurrence in first-time stone formers. As
body weight increases, the excretion of calcium, oxalate, and uric
acid also increases. Patients with a higher body mass index (BMI)
have a decrease in ammonia excretion and impaired hydrogen ion
buffering. With increasing BMI, uric acid stones become more
dominant than calcium oxalate stones, especially in men. Based on
urinary supersaturation index and urinary risk factors total body fat
and truncal fat mass are associated more strongly with uric acid
stones than total body weight and lean body mass.

Uric acid stones are common in the presence of type 2 diabetes. Hyperinsulinemia also may
contribute to the development of calcium stones by increasing urinary calcium excretion.

In postmenopausal women as the amount not the intensity of physical activity increases, the risk
of incident stones declines.

Weight control may be considered one of the preventive modalities and in stone formers, a BMI
of 18 to 25 kg/m2 is recommended.

With malabsorptive bariatric procedures such as Roux-en-Y gastric bypass (RYGB), urolithiasis
is higher than in obese controls, probably because of the increased prevalence of hyperoxaluria
and hypocitraturia in RYGB patients. However, restrictive gastric surgery (i.e., gastric banding
or sleeve gastrectomy) is not associated with increased risk of kidney stones.

Agents added intentionally or unintentionally to food or drug products have led to the appearance
of new types of stones containing melamine and indinavir.

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  Calcium stones
One third to one half of patients with calcium stones are hypercalciuric. Hypercalciuria
describes a value of calcium in excess of 300 mg (7.5 mmol) per day in men, 250 mg (6.25
mmol) per day in women, or 4 mg (0.1 mmol)/kg/day for either in random urine collections of
outpatients on unrestricted diets. The classic definition of hypercalciuria of upper normal limit of
200 mg per day is based on a constant diet restricted in calcium, sodium, and animal protein.

Idiopathic hypercalciuria (IH) is a familial disorder characterized by abnormal serum calcium

in the absence of known causes of hypercalciuria, such as primary hyperparathyroidism,
sarcoidosis, excess vitamin D intake, hyperthyroidism, glucocorticoid use, or renal tubular
acidosis (RTA). Ninety percent of patients with IH never
form a kidney stone. However, they are more sensitive to
forming stones, as relatively small increases in urine
calcium increase calcium oxalate supersaturation.

Formation of a stone in a person with IH can be triggered

by an excessive dietary calcium intake, increased intestinal
absorption of calcium that may or may not be vitamin D–
mediated, decreased renal tubular reabsorption of calcium,
or prolonged bed rest. Increased gut absorption of calcium
even when on a restricted calcium, sodium and animal
protein diet is noted particularly in patients with absorptive hypercalciuria. Urinary calcium
levels higher than normal at any level of net calcium absorption suggests that some of the urine
calcium is derived from the bone. Negative calcium balance appears to be greater in stone
formers than in non–stone formers.

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When challenged with a very-low-calcium diet, the loss of more calcium in the urine than is in
the diet indicates a net loss of total body calcium. The source of this additional calcium is the
skeleton. Patients with IH tend toward negative phosphorus balance even on normal intakes. The
defective phosphate metabolism may lead to increased 1, 25 (OH)2 D3 levels, and increased
intestinal calcium absorption.

Bone loss can be high in patients with IH in whom low calcium intake exaggerates bone loss
from increased net acid excretion (NAE). For decades low-calcium diets were recommended to
reduce the hypercalciuria in these stone formers. However, chronic prolonged calcium
restriction, deficient calcium intake, and increased losses from hypercalciuria decrease bone
mineral density. The decreased BMD also correlates with an increase in markers of bone
turnover as well as increased fractures. Vertebral fracture risk increases fourfold among
urolithiasis patients in comparison with the general population.

Undesirable bone resorption may be enhanced by a high protein intake of nondairy origin. An
inadequate calcium intake along with high protein intake induces metabolic acidosis, increases
calcium excretion, and lowers urinary pH. This acid load inhibits the renal reabsorption of
calcium. A reduction in nondairy animal protein may be recommended.

Calcium supplements do not have the same protective effect against stone formation as dietary
calcium. Widespread use of calcium supplements to prevent osteoporosis corresponds to an
increase in kidney stones in women. A trial of combined calcium–vitamin D supplementation to
prevent bone loss and fractures led to a 17% increase in new stone formation in women who
increased their calcium intake to 2000 mg a day by adding a 1000 mg calcium supplement to
their baseline diet.

If calcium is taken as a supplement, timing is important. Calcium supplements taken with meals
increase urinary calcium and citrate, but decrease urinary oxalate; thus the increase in citrate and
decrease in oxalate counterbalance the effects of elevated urinary calcium. Therefore, if used by
patients who cannot tolerate dairy products because of lactose intolerance, allergies, or
preference, calcium supplements should be taken with meals. Urine calcium should be measured
before starting the supplement and afterward to see the effect; if urine calcium increases, patients
should increase fluid intake to dilute the urine concentration of calcium.

Higher dietary calcium from either nondairy or dairy foods is independently associated with a
lower kidney stone risk. Therefore, based on DRI recommendations for age, patients may select
calcium from dairy or nondairy choices. Given recent concerns for increased risk for
cardiovascular disease and kidney stones with increased use of calcium supplements, women
should aim to meet DRI recommendations from a calcium-rich diet, taking calcium supplements
only if needed to reach DRI goals. Calcium should be taken in divided doses, choosing a source
with each meal to maximize oxalate binding. Low-fat dairy choices are good options for their
lower saturated fat content.

 Oxalate stones
Hyperoxaluria (more than 40 mg of oxalate in urine per day) plays an important role in calcium
stone formation and is observed in 10% to 50% of recurrent stone formers. Primary
hyperoxaluria is a feature of an autosomal recessive genetic defect of a hepatic enzyme that

7
results in overproduction of oxalate and a urinary oxalate concentration three to eight times
normal. Multiple stones occur in these children, causing
renal failure and early death.

Patients with inflammatory bowel diseases or gastric

bypass often develop hyperoxaluria related to fat
malabsorption. The bile acids produced during the
digestive process normally are reabsorbed in the
proximal gastrointestinal (GI) tract, but when this fails to
occur, bile salts and fatty acids increase colonic
permeability to oxalate. The unabsorbed fatty acids also
bind calcium to form soaps, decreasing availability of
calcium in a soluble form. With less calcium available to bind oxalate in the gut and prevent its
absorption, serum oxalate and thus urinary oxalate levels increase.

Urinary oxalate also comes from endogenous synthesis, proportional to lean body mass.
Ascorbic acid accounts for 35% to 55%, and glyoxylic acid accounts for 50% to 70% of urinary
oxalate. In patients with CKD, excessive vitamin C intake may lead to stone formation. Oxalate
synthesis is not increased with a high protein diet. Because pyridoxine acts as a cofactor in the
conversion of glyoxylate to glycine, its deficiency could increase endogenous oxalate
production. The bioavailability of food oxalate and urine oxalate are affected by salt forms of
oxalate, food processing and cooking methods, meal composition, and the presence of
Oxalobacter formigenes (OF) in the GI tract. Stone-forming patients who lack this bacteria have
significantly higher urinary oxalate excretion and stone episodes compared with patients
colonized with the bacteria. There is a 70% risk reduction in calcium-oxalate stone formers when
there is OF colonization of their stool.

Administration of O. formigenes as enteric-coated capsules significantly reduces urine oxalate in

patients with primary hyperoxaluria. Dietary advice for reducing urinary oxalate should include
use of this probiotic and reduction of dietary oxalate, if needed, and simultaneous consumption
of calcium rich food or supplement to reduce oxalate absorption.

 Uric acid stones

Uric acid is an end product of purine metabolism from food, de novo synthesis, and tissue
catabolism. Approximately half of the purine
load is from endogenous sources and is
constant. Exogenous dietary sources provide
the other half, accounting for the variation in
urinary uric acid. The solubility of uric acid
depends on urine volume, the amount
excreted, and urine pH. Uric acid stones form
when urine is supersaturated with un-
dissociated uric acid, which occurs at urinary
pH less than 5.5.

The most important feature in uric acid stone

formers is low urine pH resulting from increased NAE and impaired buffering caused by reduced

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urinary ammonium excretion. The former can be a result of low intake of alkali-producing foods
or increased consumption of acid-producing foods.

Inflammatory bowel disease results in chronically acidic urine, usually from dehydration. GI
bicarbonate loss from diarrhea may predispose these patients to uric acid stones. Uric acid stones
also are associated with lymphoproliferative and myeloproliferative disorders, with increased
cellular breakdown that releases purines and thus increases uric acid load. Diabetes, obesity, and
hypertension appear to be associated with nephrolithiasis; diabetes is a common factor in uric
acid stone development. Besides diabetes management for patients with uric acid lithiasis and
hyperuricosuric calcium oxalate stones, dietary purines also should be restricted.

Meat, fish, and poultry are rich in purines and acid ash and thus should be used in moderation to
meet DRI for protein. Purines and metabolism of sulfur-rich amino acids, cysteine and
methionine, in animal protein confer an acid load to the kidney, thus lowering urine pH. PRAL
value is assigned to groups of foods in terms of their positive or negative effect on acidic load.
Foods specifically high in purines should be avoided, including organ meats, anchovies, herrings,
sardines, meat-based broth, and gravy (see Box 39-3). Dietary noncompliance or persistence of
hyperuricosuria warrants use of medication such as allopurinol. Uric acid stones are the only
stones amenable to dissolution therapy by urine alkalinization to a pH of 6 to 6.5. Potassium
citrate has been used as the therapy of choice. Sodium bicarbonate increases urinary
monosodium urate and calcium and should not be used as a supplement.

 Cysteine stones
Cystine stones represent 1% to 2% of urinary calculi and are caused by homozygous cystinuria.
Whereas normal individuals daily excrete 20 mg or less of cystine in their
urine, stone-forming cystinuric patients excrete more than 250 mg/day.
Cystine solubility increases when urine pH exceeds 7; therefore an alkaline
urine pH must be maintained 24 hours per day, even while the patient sleeps.
This is achieved almost always with the use of medication. Fluid intake of
more than 4 L daily is recommended to prevent cysteine crystallization.
Lower sodium intake may be useful in reducing cystine in the urine.
Restriction of animal protein is associated with lower intake of cystine and
methionine, a precursor of cystine. Ingestion of vegetables and fruit high in citrate and malate,
such as melons, limes, oranges and fresh tomato juice, may help alkalinize the urine.

 Melamine and Indinavir stones

Kidney stones, ARF, and death have been reported in young children who received melamine-
contaminated infant formula. Melamine is an organic base synthesized from urea. When added to
liquid milk or milk powder, it deceptively increases the protein content. Melamine precipitates in
the distal renal tubules, forming crystals and sandlike stones. Hydration and urine alkalinization
help with stone passage.

The treatment of human immunodeficiency virus infection with protease inhibitors has led to the
appearance of another previously unknown urinary calculus: indinavir. Hypocitraturia is

9
universal in all patients with indinavir
stones as well as decreased solubility in a
low urine volume with a low pH. These
stones are soft, gelatinous, and radiolucent
and are not amenable to basket removal or
ureteroscopy. Intravenous (IV) hydration
and temporary cessation of indinavir
should be the first choice of treatment.

 Struvite stones
Struvite stones are composed of magnesium ammonium phosphate and carbonate apatite. They
are also known as triple-phosphate or infection stones. Unlike most urinary stones, they occur
more commonly in women than in men, at a ratio of 2:1. They form
only in the presence of bacteria such as Pseudomonas, Klebsiella,
Proteus mirabilis, and Urealyticum, which carry urease, a urea-splitting
enzyme. Urea breakdown results in ammonia and carbon dioxide (CO2)
production, thus raising urine pH and the level of carbonate. Struvite
stones grow rapidly to large staghorn calculi in the renal pelvic area.
The mainstay of treatment is extracorporeal shockwave lithotripsy
(ECSWL) with adjunctive culture-specific antimicrobial therapy that
uses urease inhibitors. The goal is to eliminate or prevent urinary tract infections by regularly
screening and monitoring urine cultures. Because of their infectious origin, diet has no definitive
role except avoidance of urine alkalinization.

Treatment of kidney stones

Uric acid stones are the only type amenable to dissolution therapy, or dissolving of the stone by
alkalinization of the urine. This is done with consumption of a more vegetarian diet, lower in
purines, or use of medication. Shockwave lithotripsy and endourologic techniques almost have
replaced the open surgical procedures of stone removal of 20 years ago. Struvite stones also are
treated with adjunctive culture-specific antimicrobial therapy that uses urease inhibitors.
Management strategies are now aimed at kidney stone prevention.

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 ACUTE RENAL FAILURE
Acute kidney failure occurs when your kidneys suddenly become unable to filter waste products
from your blood. When your kidneys lose their filtering ability, dangerous levels of wastes may
accumulate, and your blood's chemical makeup may get out of balance.

Acute kidney failure also called acute renal failure or acute kidney injury, develops rapidly,
usually in less than a few days. Acute kidney failure is most common in people who are already
hospitalized, particularly in critically ill people who need intensive care.

Pathophysiology
Acute kidney injury (AKI), formerly acute renal failure (ARF), is characterized by a sudden
reduction in glomerular filtration rate (GFR), the amount of filtrate per unit in the nephrons, and
altered ability of the kidney to excrete the daily production of metabolic waste. AKI can occur in
association with oliguria (decreased output of urine) or normal urine flow, but it typically occurs
in previously healthy kidneys. Duration varies from a
few days to several weeks. The causes of AKI are
numerous and can occur simultaneously. The causes are
generally classified into three categories:

1. Inadequate renal perfusion (prerenal),

2. Diseases within the renal parenchyma (intrinsic),
and
3. Urinary tract obstruction (post renal).
A new form of classification to help clinicians assess the
severity and progression of acute kidney injury, using the
acronym RIFLE (Risk, Injury, Failure, Loss and ESRD),
indicates the likelihood of a patient recovering or progressing to chronic renal failure. This, in
turn, helps dietitians knows whether to increase protein intake goals or be more moderate to
preserve kidney function.

Symptoms

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
 Shortness of breath
 Fatigue
 Confusion
 Nausea
 Weakness

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  Irregular heartbeat
 Chest pain or pressure
 Seizures or coma in severe cases
Diagnosis

If your signs and symptoms suggest that you have acute kidney failure, your doctor may
recommend certain tests and procedures to verify your diagnosis. These may include:

 Urine output measurements.

Measuring how much you urinate in 24 hours may help your doctor determine the cause
of your kidney failure.
 Urine tests.
Analyzing a sample of your urine (urinalysis) may reveal abnormalities that suggest
kidney failure.
 Blood tests.
A sample of your blood may reveal rapidly rising levels of urea and creatinine. two
substances used to measure kidney function.
 Imaging tests.
Imaging tests such as ultrasound and computerized tomography may be used to help your
doctor see your kidneys.
 Removing a sample of kidney tissue for testing.
In some situations, your doctor may recommend a kidney biopsy to remove a small
sample of kidney tissue for lab testing. Your doctor inserts a needle through your skin
and into your kidney to remove the sample.
Treatment
Treatment for acute kidney failure involves identifying the illness or injury that originally
damaged your kidneys. Your treatment options depend on what's causing your kidney failure.

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

In case of excessive water: diuretics
In case of lack of water: intravenous fluids
 Medications to control blood potassium, calcium, glucose or sodium polystyrene
sulfonate
 Medications to restore blood calcium levels
Infusion of calcium
 Dialysis to remove toxins from your blood.

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 DISEASES OF TUBULES AND INTERSTITIUM
Chronic Interstitial Nephritis
Interstitial nephritis, also known as tubule-interstitial nephritis, is inflammation of the area of the
kidney known as the renal inter-stitium, which consists of a collection of cells, extracellular
matrix, and fluid surrounding the renal tubules.

Chronic interstitial nephritis is a nonspecific diagnosis of a pattern of kidney injury, which may
occur due to any of many conditions that initially cause an acute interstitial nephritis. The
diagnosis is made when specific underlying causes cannot be identified.

Symptoms

Blood in the urine.

 Fever.
 Increased or decreased urine output.
 Mental status changes (drowsiness, confusion, coma)
 Nausea, vomiting.
 Rash.
 Swelling of any area of body.
 Weight gain (from retaining fluid)
Diagnosis

If your doctor suspects your kidneys aren’t functioning properly, they’ll take a detailed medical
history. They’ll ask you about your family’s history of medical problems. They’ll also ask you:

Make certain to tell your doctor about all drug use, including OTC pain relievers and dietary
supplements. These drugs can have significant impact on the kidneys.

Your doctor will also listen to your heart and lungs. Fluid in your lungs is a common sign
of kidney failure. It can be detected by changes in breath sounds. High blood pressure is also a
potential sign of kidney problems, as well as weight changes.

Following tests are used to identify the problems or functioning of kidneys

 Blood tests ( CBC, BUN, BC, BG )

 Urinalysis
 Biopsy
 Abdominal ultrasound
Treatment

Treatment consists of addressing the cause, such as by removing an offending drug. There is no
clear evidence that corticosteroids help. Nutrition therapy consists of adequate fluid intake,
which can require several liters of extra fluid.

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 Fanconi’s Syndrome
Fanconi syndrome is a rare disorder of kidney tubule function that results in excess amounts of
glucose, bicarbonate, phosphates (phosphorus salts), uric acid, potassium, and certain amino
acids being excreted in the urine.

Symptoms
Symptoms of inherited FS can be seen as early as infancy. They include:

 excessive thirst
 excessive urination
 vomiting
 failure to thrive
 slow growth
 frailty
 rickets
 low muscle tone
 corneal abnormalities
 kidney disease
Symptoms of acquired FS include:

 bone disease
 muscle weakness
 low blood phosphate concentration (hypophosphatemia)
 low blood potassium levels (hypokalemia)
 excess amino acids in urine (hyperaminoaciduria)
Diagnosis
Infants and children with inherited FS

Usually the symptoms of FS appear early on in infancy and childhood. Parents may notice
excessive thirst or slower than normal growth. Children may have rickets or kidney problems.

Your child’s doctor will order blood and urine tests to check for abnormalities, such as high
levels of glucose, phosphates, or amino acids, and to rule out other possibilities. They may also
check for cystinosis by looking at the child’s cornea with a slit lamp examination. This is
because cystinosis affects the eyes.

Acquired FS

Your doctor will ask for your or your child’s medical history, including any drugs you or your
child is taking, other diseases present, or occupational exposures. They’ll also order blood and
urine tests.

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In acquired FS, you may not notice the symptoms right away. Bones and kidneys may be
damaged by the time a diagnosis is made.

Acquired FS can affect people at any age.

Treatment
 Drinking sodium bicarbonate
 Fanconi syndrome cannot be cured, but it can be controlled with proper treatment.
Effective treatment can keep the damage to bones and kidney tissue from getting worse
and in some cases correct it. The high acid level of the blood (acidosis) may be
neutralized by drinking sodium bicarbonate. People with low potassium levels in the
blood may need to take potassium supplements by mouth.
 Bone disease requires treatment with phosphates and vitamin D supplements given by
mouth.
 Kidney transplantation may be lifesaving if a child with the disorder develops kidney
failure, but if cystinosis is the underlying disease, progressive damage may continue in
other organs and eventually result in death.

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the
body due to a failure of the kidneys to appropriately acidify the urine.

Symptoms
Many people have no symptoms. Most others develop symptoms only after the disorder has been
present for a long time. Which symptoms eventually develop depend on the type of renal tubular
acidosis.

 Types 1 and 2
When potassium levels in the blood are low, as occurs in types 1 and 2, neurologic problems
may develop, including muscle weakness, diminished reflexes, and even paralysis. In type 1,
kidney stones may develop, causing damage to kidney cells and, in some cases, chronic kidney
disease. In type 2 and sometimes in type 1, bone pain and osteomalacia may occur in adults and
rickets may occur in children.

 Type 4
In type 4, potassium levels typically increase, although it is uncommon for the level to rise high
enough to cause symptoms. If the level becomes too high, irregular heartbeats and muscle
paralysis may develop.

Diagnosis

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Followings are the tests to diagnose RTA

 Blood tests
 Urine tests
A doctor considers the diagnosis of type 1 or type 2 renal tubular acidosis when a person has
certain characteristic symptoms (such as muscle weakness and diminished reflexes) and when
tests reveal high levels of acid and low levels of bicarbonate and potassium in the blood.

Type 4 renal tubular acidosis is usually suspected when high potassium levels accompany high
acid levels and low bicarbonate levels in the blood. Tests on urine samples and other tests help to
determine the type of renal tubular acidosis.

Treatment

 Drinking sodium bicarbonate daily

Treatment depends on the type.

Types 1 and 2 are treated by drinking a solution of sodium bicarbonate (baking soda) every day
to neutralize the acid that is produced from food. This treatment relieves the symptoms and
prevents kidney failure and bone disease or keeps these problems from becoming worse. Other
specially prepared solutions are available, and potassium supplements may also be required.

In type 4, the acidosis is so mild that bicarbonate may not be needed. High potassium levels in
the blood can usually be kept in check by restricting potassium intake, avoiding dehydration,
using diuretics that increase potassium loss, and substituting different drugs or adjusting drug
dosages.

Pyelonephritis
Pyelonephritis is inflammation of the kidney, typically due to a bacterial infection.

Acute pyelonephritis is a sudden and severe kidney infection. It causes the kidneys to swell and
may permanently damage them. Pyelonephritis can be life-threatening.

When repeated or persistent attacks occur, the condition is called chronic pyelonephritis. The
chronic form is rare, but it happens more often in children or people with urinary obstructions.

Symptoms
Symptoms usually appear within two days of infection. Common symptoms include:

 a fever greater than 102°F (38.9°C)

 pain in the abdomen, back, side, or groin

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  painful or burning urination
 cloudy urine
 pus or blood in the urine
 urgent or frequent urination
 fishy-smelling urine
Other symptoms can include:

 shaking or chills
 nausea
 vomiting
 general aching or ill feeling
 fatigue
 moist skin
 mental confusion
Symptoms may be different in children and older adults than they are in other people. For
example, mental confusion is common in older adults and is often their only symptom.

People with chronic pyelonephritis may experience only mild symptoms or may even lack
noticeable symptoms altogether.

Diagnosis
Following test are done for the diagnosis of pyelonephritis

 Urine test
 Imaging test
 Radioactive imaging
Treatment
 Antibiotics
- Levofloxacin
- Ciprofloxacin
- Co-trimoxazole
- Ampicillin
 Hospital admission
 Surgery
Recurrent kidney infections may result from an underlying medical problem. In those cases,
surgery may be required to remove any obstructions or to correct any structural problems in the
kidneys. Surgery may also be necessary to drain an abscess that doesn’t respond to antibiotics.

In cases of severe infection, a nephrectomy may be necessary. In this procedure, a surgeon

removes part of the kidney.

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 GLOMERULAR DISEASE
Nephritic Syndrome
Nephritic syndrome is an inflammatory process that is defined as the presence of one or more of
the following

 Hematauria (leakage of RBCs, which stick together and form red blood cell cast in the
renal tubules) with acanthocytes
 RBCs casts in urine
 Proteinuria ( leakage of proteins)
 Hypertension
 Mild to moderate edema (swelling from
injury or inflammation)
 Sterile pyuria
 Oliguria (inflammatory infiltrates reduce
fluid movement across the membrane)
 Azotemia (inflammation prevents
sufficient filtering and excretion of urea)
Symptoms

 Blood in the urine (urine appears dark, tea-colored, or cloudy)

 Decreased urine output (little or no urine may be produced)
 Swelling of the face, eye socket, legs, arms, hands, feet, abdomen, or other areas.
 High blood pressure.
Diagnosis
 Urinalysis
- Hematuria
- Acanthocytes
- Red blood cells cast
- Sterile puyria with WBC cast
- Mild to moderate proteinuria
 Blood tests
- Increased creatinine with decreased GFR (glomerular filtrate rate)
- Azotemia with increased blood urea nitrogen
- Complement ANA, ANCA, anti GBM antibodies
Treatment
Supportive therapy

 Low sodium diet

 Water restriction
Medical therapy

18
  In case of proteinuria and hypertension
Angiotensin-converting enzyme inhibitor or angiotensin receptor blocker
 Severe hypertension or edema
Diuretics
 RPGN from anti GBM antibodies
Plasmapheresis
 Sometimes immunosuppressive therapy is indicated ( e.g. in lupus nephritis)
 Severe renal insufficiency or kidney failure
Renal replacement therapy e.g. hemodylisis, possibly transplantation
 Membrano-proliferative glomerulonephritis (type 1 and type 2 MPGN)
RAAS inhibitors are often added to treatment
Prednisone alone or combination with other immunosuppressant ( cyclosporine)

Nephrotic Syndrome
Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your
urine. It is characterized by massive proteinuria (> 3.5g/ 24 hours), hypoalbuminemia and
edema.

Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your
kidneys that filter waste and excess water from your blood. The condition causes swelling,
particularly in your feet and ankles, and increases the risk of other health problems

Symptoms
Signs and symptoms of nephrotic syndrome include:

 Severe swelling (edema), particularly around your eyes and in your ankles and feet
 Foamy urine, a result of excess protein in your urine
 Weight gain due to fluid retention
 Fatigue
 Loss of appetite
Diagnosis
Tests and procedures used to diagnose nephrotic syndrome include:

 Urine tests. A urinalysis can reveal abnormalities in your urine, such as large amounts of
protein. You might be asked to collect urine samples over 24 hours.
 Blood tests. A blood test can show low levels of the protein albumin and often decreased
levels of blood protein overall. Loss of albumin is often associated with an increase in
blood cholesterol and blood triglycerides. The creatinine and urea nitrogen levels in your
blood also might be measured to assess your overall kidney function.

19
  Kidney biopsy. Your doctor might recommend removing a small sample of kidney tissue
for testing. During a kidney biopsy, a needle is inserted through your skin and into your
kidney. Kidney tissue is collected and sent to a lab for testing.
Treatment
Treatment for nephrotic syndrome involves treating any medical condition that might be causing
your nephrotic syndrome

 Diuretics
 Anticoagulants
Heparin, warfarin, dabigatran, apixaban and rivaroxaban
 Immune system-suppressing medications.
Rituximab (Rituxan), cyclosporine and cyclophosphamide.
 Blood pressure medications
Enalapril, captopril, benazepril
 Cholesterol reducing medication.

20
 CHRONIC KIDNEY DISEASE (CKD)
“Chronic kidney disease (CKD) is a syndrome of progressive and irreversible loss of the
excretory, endocrine, and metabolic functions of the kidney secondary to kidney damage”.

The National Kidney Disease Education Program (NKDEP) has defined CKD as having a GFR
of less than 60mL min1 .73m 2// for 3 months or longer and/or albuminuria of more than 30 mg
of urinary albumin per gram of urinary creatinine. CKD progresses slowly over time, and there
may be intervals during which kidney functions remain stable.

Prevalence:

 The prevalence of CKD is now estimated at approximately 10% of adults in the United
States, or greater than 20 million Americans.
 This estimated prevalence of CKD shows that 1 in 3 people with diabetes and 1 in 5
people with hypertension have CKD.
Diagnosis:

Kidney function is assessed based on the glomerular filtration rate, which is reflected in
clearance tests that measure the rate at which substances are cleared from the plasma by the
glomeruli. The onset of renal failure is not usually apparent until 50%–70% of renal function is
lost.

Many states now urge clinical laboratories reporting serum creatinine also to report the patient’s
eGFR. Patients with a low calculated eGFR do not necessarily have CKD. They must have
several blood samples drawn 3 months apart that are consistently low (showing eGFR of less
than 60). This testing alerts primary care physicians to monitor for possible presence of kidney
disease. Further research using eGFR cystatin C followed by eGFR pairing cystatin C and
creatinine is now recognized as the most precise measure

Stages of CKD:

 Stage 1 and 2
They are defined as kidney damage with normal or increased GFR and kidney damage with mild
decrease in GFR, respectively.

 Stage 3
It is defined as a moderate decrease in GFR with a specific range of 30 59mL min1 .73m 22/ /.

 Stage 4
It is defined as a severe decrease in GFR with a specific range of 15 29mL min1 .73m 22/ /.

 Stage 5

21
Stage 5 of CKD is defined as kidney function that is inadequate to sustain life, results in uremia,
and requires initiation of renal replacement therapy (RRT). Stage 5 results in death unless
dialysis or transplantation is initiated.

Pathophysiology
It is thought that, in response to a decreasing GFR, the kidney undergoes a series of adaptations
to prevent decline. Although in the short term this leads to improvement in filtration rate, in the
long term it leads to an accelerated loss of nephrons and progressive renal insufficiency. The
nature of these adaptations involves a change in the hemodynamic characteristics of the
remaining glomeruli, specifically leading to increased glomerular pressure. Factors that increase
glomerular pressure tend to accelerate this process, whereas factors that decrease glomerular
pressure tend to alleviate it.

Causes (The Etiology):

Diabetes is the leading risk factor for CKD followed by hypertension and glomerulonephritis. In
addition, the following are potential causes of and risk factors for CKD:

 Ethnicity; African Americans are nearly four times as likely to develop kidney failure
as white Americans; Native Americans are nearly two times as likely, and Hispanic
Americans have nearly twice the risk of non-Hispanic whites.
 Family history; CKD runs in families, so one’s risk is greater if a family member has
kidney failure.
 Hereditary factors such as polycystic kidney disease (PKD)
 A direct and forceful blow to the kidneys
 Prolonged consumption of over-the-counter painkillers that combine aspirin,
acetaminophen, and other medicines such as ibuprofen.

Treatment

22
 1. Dialysis
Dialysis is a renal replacement procedure that removes excessive and toxic by-products of
metabolism from the blood, thus replacing the filtering function of healthy kidneys. It can
maintain life once CKD progresses to the end stage, even though endocrine and metabolic
functions of the kidney are not totally replaced. The decision to initiate dialysis depends on the
severity of symptoms

Symptoms of indications for dialysis therapy:

 Pericarditis
 Uncontrollable fluid overload
 Pulmonary edema
 Uncontrollable and repeated hyperkalemia
 Coma
 Lethargy
 Less severe symptoms such as azotemia, nausea, and vomiting require a subjective
determination that takes into consideration the patient’s quality of life.
Currently two major types of renal replacement therapy are used for patients with CKD stage 5:
hemodialysis (HD) and peritoneal dialysis (PD). The most common method is hemodialysis.

Hemodialysis
For Dialysis to be done a
permanent access site called an
arteriovenous fistula (AVF),
created surgically by fashioning in
the forearm a subcutaneous
joining of the radial artery and the
cephalic vein or a tunneled
catheter. If the patient’s veins are
not adequate for this procedure,
an arteriovenous graft (AVG) can
be created with a catheter. Blood
travels through a needle placed into the arterial side of the graft. The needle is attached to tubing
that leads to the hollow fibers of the dialyzer. While blood passes through the dialyzer, dialysate
simultaneously passes around the artificial membrane. Because the electrolyte content of the
dialysate is similar to that of normal plasma, this results in the removal of waste products and
excess electrolytes from the blood to the dialysate via diffusion, ultrafiltration, and osmosis. The
filtered blood then returns to the patient through the venous side.

How often should it be done?

 Hemodialysis treatments are typically prescribed three times a week for an average of 4
hours per treatment.

23
  Although most hemodialysis treatments are done at a dialysis center, home treatments are
an option for some patients. Daily home hemodialysis is conducted 5–7 days per week
for 2–3 hours at a time, and nocturnal home hemodialysis is performed three to six nights
per week during sleep.
Advantage of this type of Dialysis:

The major advantage of home dialysis is the ability to set one’s own schedule; however, it is
necessary to have a trained partner and it may also be stressful to the patient’s family.

Peritoneal Dialysis:
In peritoneal dialysis, access to the patient’s
blood supply is gained via a catheter of silicone
rubber or polyurethane, placed surgically into the
peritoneal cavity. In this procedure, dialysate is
introduced into the peritoneum through the
peritoneal catheter. Solutes from the plasma
circulating in the vessels and capillaries
perfusing the peritoneal wall pass across the
peritoneal membrane into the dialysate, which is
subsequently removed and discarded. The
dialysate for PD is available with a range of
dextrose concentrations that alter its osmolality
and assist in fluid removal. In addition, the dwell
time (i.e., how long the dialysate remains in the peritoneum) and the number of exchanges (i.e.,
how many bags of dialysate and the total volume of each used in 24 hours) also affect the
amount of fluid and solute removal.

Types:

There are two main types of PD:

 Continuous Ambulatory Peritoneal Dialysis (CAPD)

CAPD requires no machine. The usual dwell time is 4–6 hours, followed by the draining of used
dialysate and its replacement with fresh solution, requiring an additional 30–40 minute. Most
patients change the dialysate solution at least four times a day and sleep with the solution in their
abdomens at night.

 Continuous Cycling Peritoneal Dialysis (CCPD)

CCPD does require a machine called a cycler to fill and empty the abdomen three to five times
during the night. One exchange is then done during the day with a dwell time that lasts the entire
day. An additional exchange can be added in the afternoon for some patients.

2. Renal Transplantation
The final treatment for Stage 5 patients is Renal Transplantation. In order for an organ transplant
to occur, the immunological characteristics of the donated organ must be matched with the

24
recipient’s medical and immunological characteristics. The antigens for Major
Histocompatibility Complex (MHC) (often referred to as human leukocyte antigens [HLAs])
provide the basis for the MHC haplotype (a combination of closely linked genes on a
chromosome inherited as a unit from one parent). MHC antigens play an important role in
transplant rejection, since the presence of a MHC antigen on the transplanted organ or tissue that
is different from the MHC antigens on the recipient’s tissues signals the presence of the
transplanted tissue and initiates an immune response. The immune system attacks the
transplanted cells presenting MHC antigens that are different from those found on the recipient’s
tissues. After transplantation, patients are maintained on a variety of immunosuppressive
regimens to prevent rejection of the donated kidney. Immunosuppressive medications include
corticosteroids, cyclosporine, tacrolimus, mycophenolate mofetil, and sirolimus.

25
 END STAGE RENAL DISEASE (ESRD)
It reflects the kidney’s inability to excrete waste products, maintain fluid and electrolyte balance,
and produce certain hormones. As renal failure slowly progresses, the level of circulating waste
products eventually leads to symptoms of uremia. Uremia is a clinical syndrome of malaise,
weakness, nausea and vomiting, muscle cramps, itching, metallic taste in the mouth, and
neurologic impairment that is brought about by an unacceptable level of nitrogenous wastes in
the body.

Pathophysiology
ESRD can result from a wide variety of different kidney diseases. Currently 90% of patients
reaching ESRD have chronic (1) diabetes mellitus, (2) hypertension, or (3) glomerulonephritis.
The manifestations are somewhat nonspecific and vary by patient. No reliable laboratory
parameter corresponds directly with the beginning of symptoms. However, as a rule of thumb,
BUN of more than 100 mg/dl and creatinine of 10 to 12 mg/dl are usually close to this threshold.

Medical Treatment
Once the patient progresses from stage 4 to stage 5 CKD, options for treatment for ESRD
include dialysis, transplantation, or medical management progressing to death. Patients do best if
they have some control and choice over their options.

Treatment
1. Dialysis
Dialysis is a renal replacement procedure that removes excessive and toxic by-products of
metabolism from the blood, thus replacing the filtering function of healthy kidneys. It can
maintain life once CKD progresses to the end stage, even though endocrine and metabolic
functions of the kidney are not totally replaced. The decision to initiate dialysis depends on the
severity of symptoms

Symptoms of indications for dialysis therapy:

 Pericarditis
 Uncontrollable fluid overload
 Pulmonary edema
 Uncontrollable and repeated hyperkalemia
 Coma
 Lethargy
 Less severe symptoms such as azotemia, nausea, and vomiting require a subjective
determination that takes into consideration the patient’s quality of life.
Currently two major types of renal replacement therapy are used for patients with CKD stage 5:
hemodialysis (HD) and peritoneal dialysis (PD). The most common method is hemodialysis.

26
 Hemodialysis
For Dialysis to be done a permanent access site called an
arteriovenous fistula (AVF), created surgically by
fashioning in the forearm a subcutaneous joining of the
radial artery and the cephalic vein or a tunneled catheter.
If the patient’s veins are not adequate for this procedure,
an arteriovenous graft (AVG) can be created with a
catheter. Blood travels through a needle placed into the
arterial side of the graft. The needle is attached to tubing
that leads to the hollow fibers of the dialyzer. While
blood passes through the dialyzer, dialysate
simultaneously passes around the artificial membrane.
Because the electrolyte content of the dialysate is similar
to that of normal plasma, this results in the removal of
waste products and excess electrolytes from the blood to
the dialysate via diffusion, ultrafiltration, and osmosis. The filtered blood then returns to the
patient through the venous side.

 Hemodialysis treatments are typically prescribed three times a week for an average of 4
hours per treatment.
 Although most hemodialysis treatments are done at a dialysis center, home treatments are
an option for some patients. Daily home hemodialysis is conducted 5–7 days per week
for 2–3 hours at a time, and nocturnal home hemodialysis is performed three to six nights
per week during sleep.
Advantage:

The major advantage of home dialysis is the ability to set one’s own schedule; however, it is
necessary to have a trained partner and it may also be stressful to the patient’s family.

Peritoneal Dialysis:
In peritoneal dialysis, access to the patient’s blood supply is gained via a catheter of silicone
rubber or polyurethane, placed surgically into the peritoneal cavity. In this procedure, dialysate is
introduced into the peritoneum through the peritoneal catheter. Solutes from the plasma
circulating in the vessels and capillaries perfusing the peritoneal wall pass across the peritoneal
membrane into the dialysate, which is subsequently removed and discarded. The dialysate for PD
is available with a range of dextrose concentrations that alter its osmolality and assist in fluid
removal. In addition, the dwell time (i.e., how long the dialysate remains in the peritoneum) and
the number of exchanges (i.e., how many bags of dialysate and the total volume of each used in
24 hours) also affect the amount of fluid and solute removal.

Types:

27
There are two main types of PD:

 Continuous Ambulatory Peritoneal Dialysis

(CAPD)
CAPD requires no machine. The usual dwell time is 4–6
hours, followed by the draining of used dialysate and its
replacement with fresh solution, requiring an additional
30–40 minutes. Most patients change the dialysate
solution at least four times a day and sleep with the
solution in their abdomens at night.

 Continuous Cycling Peritoneal Dialysis

(CCPD)
CCPD does require a machine called a cycler to fill and
empty the abdomen three to five times during the night. One exchange is then done during the
day with a dwell time that lasts the entire day. An additional exchange can be added in the
afternoon for some patients.

 End-Stage Renal Disease in Patients with Diabetes

Because renal failure is a complication of diabetes, approximately 40% to 50% of all new
patients starting dialysis have diabetes. The need to control blood sugar in these patients requires
specialized diet therapy. The diet for diabetes management can be modified for the patient on
dialysis. In addition, the diabetic patient on dialysis often has other complications such as
retinopathy, neuropathy, gastroparesis, and amputation, all of which can place this patient at high
nutritional risk. Increased osmolality caused by high serum levels of glucose may cause water
and potassium to be pulled out of cells, with resultant hyperkalemia. Interpretation of commonly
used laboratory values will change when a diabetic patient develops renal failure. Hemoglobin
A1C (Hgb A1C) measures the glycosylation of hemoglobin. The shortened half-life of red blood
cells from uremia and the losses in the dialysis process cause Hgb A1C values to appear lower
than they really are.

 Chronic Kidney Disease and End-Stage Renal Disease in Children

Although CKD may occur in children at any age, from the newborn infant to the adolescent, it is
a relatively uncommon diagnosis. Causal factors in children include congenital defects, anatomic
defects (urologic malformations or dysplastic kidneys), inherited disease (autosomal-recessive
polycystic kidney disease), metabolic disorders that eventually result in renal failure (cystinosis
or methylmalonic aciduria), or acquired conditions or illnesses (untreated kidney infections,
physical trauma to kidneys, exposure to nephrotoxic chemicals or medications, hemolytic anemia
resulting from E. coli 0157 ingestion, or glomerular nephritis). As with all children, the major
concern is to promote normal growth and development. Without aggressive monitoring and
encouragement, the child with renal failure rarely meets his or her nutritional requirements. If the
renal disease is present from birth, nutrition support needs to begin immediately to avoid losing

28
the growth potential of the first few months of life. Growth in children with CKD usually is
delayed. Although no specific therapy ensures normal growth, factors capable of responding to
therapy include metabolic acidosis, electrolyte depletion, osteodystrophy, chronic infection, and
protein-calorie malnutrition. Energy and protein needs for children with chronic renal disease are
at least equivalent to the DRIs for normal children of the same height and age. If nutrition status
is poor, energy needs may be even higher to promote weight gain and linear growth. Feeding by
tube is required in the presence of poor intake, particularly in the critical growth period of the
first 2 years of life. Gastrostomy tubes almost always are placed in these children to enhance
nutritional intake and facilitate growth. PN rarely is initiated unless the GI tract is nonfunctional.

Control of calcium and phosphorus balance is especially important for maintaining good growth.
The goal is to restrict phosphorus intake while promoting calcium absorption with the aid of
1,25-(OH)2D3. This helps prevent renal osteodystrophy, which can cause severe growth
retardation. Use of calcium carbonate formulations to supplement the dietary intake enhances
calcium intake while binding excess phosphorus. Persistent metabolic acidosis is often associated
with growth failure in infancy. In chronic acidosis the titration of acid by the bone causes
calcium loss and contributes to bone demineralization. Bicarbonate may be added to the infant
formula to counteract this effect. Restriction of protein in pediatric diets is controversial. The so-
called “protective” effect on kidney function must be weighed against the clearly negative effect
of possible protein malnutrition on growth. The recommended dietary allowance for protein for
age is usually the minimum amount given.

Each child’s diet must be must according to his/her own preferences, family eating patterns, and
biochemical needs. This is often not an easy task. In addition, care must be taken not to place too
much emphasis on the diet to avoid food becoming a manipulative tool and an attention-getting
device. Special encouragement, creativity, and attention are required to help the child with CKD
consume the necessary energy. When possible, PD is given intermittently during the day and
continuously at night because it allows liberalization of the diet. The child is more likely to meet
nutritional requirements with fewer dietary restrictions and therefore experience better growth.
Other treatments that help renal disease in children include the use of rHuEPO and recombinant
deoxyribonucleic acid– produced human growth hormone. EPO usually is started when the
child’s serum hemoglobin falls below 10 g/dl, with a goal of maintaining hemoglobin between
11 and 12 g/dl. Correction of anemia with the use of rHuEPO may increase appetite, intake, and
feeling of well-being, but it has not been found to affect growth, even with seemingly adequate
nutrition support.

29
 LIFESTYLE MANAGEMENT FOR THE PREVENTION AND
TREATMENT OF KIDNEY DISORDERS
Lifestyle management is a key for a healthy, wealthy and
a happy life. In today’s life where everyone is busy in the
race of earning wealth, do not realize that health is their
actual wealth.

Adaptation of unhealthy lifestyle has elevated the

prevalence of disease dramatically. Lifestyle
diseases share risk factors similar to prolonged exposure
to three modifiable lifestyle behaviors that are
smoking/alcohol/drug abuse, unhealthy diet, and physical
inactivity this result in the development of
chronic diseases, specifically heart disease, stroke, diabetes, obesity, hypertension and eventually
Kidney diseases.

Fortunately, the risk of these diseases can be reduced without drugs or expensive medical facilities.
However, preventing these diseases will require changes in behaviors related to smoking, physical
activity, and diet; investments in education, food policies, and urban physical infrastructure are
needed to support and encourage these changes.

Prevention is always better than cure, adapting healthy lifestyle can not only prevent diseases but
also help in the treatment and reduction of risk and severity of diseases.

How kidney disease impact your life?

Healthy kidneys are important to our overall health, as they act as body cleanser, removing wastes
and toxins from the blood. If kidney stop working and disease gets worse, wastes can build to high
levels in the blood and make the person feel sick. One may develop complications like high blood
pressure, anemia, weak bones, poor nutritional health and nerve damage. Also, kidney disease
increases risk of heart and blood vessel disease. Psychosocial factors including depression, anxiety
and lower social support are common in patients with chronic kidney disease (CKD).

Risk Factors

Anyone can get kidney disease, but the following risk factors make it more likely to happen to
certain people.

 Approximately 1 of 3 adults with diabetes and 1 of 5 adults with high blood pressure may
have CKD.

 In addition to diabetes and high blood pressure, other problems that put you at greater
chance of kidney disease include: heart disease, obesity (being overweight), and a family
history of CKD. Kidney infections and a physical injury can also cause kidney disease.

30
How to know your risk?

As kidney diseases do not show early symptoms, get yourself tested if you have any risk factors
or you observe any changes in your regular health.

Screening

 Urine test
 Blood test
 Lipid levels
 Hemoglobin
 Blood markers for bone and mineral health

Lifestyle Management
Kidney disease can often be prevented or if one already have kidney disease, he can take steps to
keep kidney damage from getting worse. Even small changes can make a big difference. Lifestyle
changes include:

 Controlling Diabetes
 Monitoring Blood pressure
 Healthy eating
 Being active
 Limiting alcohol and tobacco
 Working with your doctor

1. Controlling Diabetes:
High blood glucose levels make kidney diseases worse.
Diabetes can harm the kidneys by causing damage blood
vessels inside kidneys. The filtering units of the kidney are
filled with tiny blood vessels. Over time, high sugar levels
in the blood can cause these vessels to become narrow and
clogged.

 Monitor blood sugar levels by regular testing.

 Dietary changes.
 Medicines can be prescribed by doctors to help keep blood glucose in a safe range.

2. Controlling Blood Pressure

The nephrons in the kidneys are supplied with a dense network of blood vessels, and high volumes
of blood flow through them. Over time, uncontrolled high blood pressure can cause arteries around
the kidneys to narrow, weaken or harden. These damaged arteries are not able to deliver enough

31
blood to the kidney tissue hindering the organs’ ability to remove waste and excess fluid from the
body. Excess fluid can, in turn, raise blood pressure even more

 Monitor blood pressure regularly

 Improve diet, eat more vegetables and fruit, reduce sodium and potassium in diet while
increasing water intake.
 Medications as prescribed by doctor
 Regular exercise
 Reduce stress by adapting healthy lifestyle, yoga, meditation and adapting habits like
reading or planting etc.
 Diuretics are key to BP control

3. Healthy eating
What you eat and drink affects your health. A kidney-friendly diet is a way of eating that helps
protect your kidneys from further damage. Tis include limiting some foods and fluids so other
fluids and minerals like electrolytes do not build up in the body. At the same time, making sure to
get the right balance of protein, calories, vitamins, and minerals.

32
 Reduce Sodium
This mineral is found naturally in many foods. It’s most common in table salt.

Sodium affects blood pressure. It also helps to maintain the water balance in your body. Healthy
kidneys keep sodium levels in check. But in CKD, extra sodium and fluids build up in your body.
This can cause a number of problems, like swollen ankles, high blood pressure, shortness of breath,
and fluid buildup around your heart and lungs. One must aim for less than 2 grams of sodium in
daily diet.

Simple steps to cut the sodium in diet:

 Avoid table salt and high-sodium seasonings (soy sauce, sea salt,
garlic salt, etc.).
 Cook at home - most fast foods are high in sodium.
 Try new spices and herbs in place of salt.
 Stay away from packaged foods, if possible. They tend to be high
in sodium.
 Read the labels when shopping, and choose low-sodium foods.
 Rinse canned foods (veggies, beans, meats, and fish) with water
before serving.

 Limit Phosphorus and Calcium

These minerals are necessary for healthy and strong bones. Healthy kidneys remove the excessive
phosphorus. However damaged kidneys are unable to excrete excessive phosphorus which result
in too high levels of phosphorus, adding risk for heart and renal disease. Moreover, calcium levels
begin to drop. To make up for it, body pulls it from bones. This can make them weak and easier to
break.

The person suffering from late-stage CKD, doctor may advise to get no more than 1,000 milligrams
(mg) of phosphorus mineral each day. This can be achieved by:

 Choosing foods with low levels of phosphorous (look for “PHOS” on the label)
 Eating more fresh fruits and vegetables
 Choosing corn and rice cereals
 Cutting back on meat, poultry, and fish
 Limiting dairy foods
Foods that are high in calcium also tend to be high in phosphorus. The doctor might suggest to cut
back on calcium-rich foods. Dairy foods that are lower in phosphorus include:

 Brie or Swiss cheese

 Regular or low-fat cream cheese or sour cream
 Sherbet

33
 Reduce Your Potassium Intake
Potassium helps nerves and muscles work properly. CKD limits filtration of out extra potassium.
Excessive potassium in blood can lead to serious heart problems.

Potassium is found in a lot of fruits and vegetables. These foods can affect potassium levels in the
blood. However one must consult the doctor or a dietitian before limiting these foods, they may
recommend low-potassium foods

 Eat The Right Amount And The Right Types Of Protein

People who have been diagnosed with chronic kidney
disease and are not receiving dialysis treatment may be
advised to eat less protein. When the kidneys aren’t
functioning properly, they may not be able to filter
protein, causing an unhealthy buildup in the urine called
proteinuria.
 Eat small portions of protein foods.

 Protein is found in foods from plants and animals.

Most people eat both types of protein. Talk to dietitian
about how to choose the right combination of protein
foods for you.

34
 Eat Less And Correct Fat (choose unsaturated over saturated fat)
 Choose lean meats, like chicken, turkey or fish. Remove the skin and trim the fat off
meats before cooking.
 Bake, grill or broil instead of frying.
 Shop for fat-free or low-fat dairy products, salad dressing and mayonnaise
 Try olive or canola oil instead of vegetable oil
 Choose egg whites or egg substitute instead of whole eggs

 DASH Diet
DASH stands for Dietary Approaches to Stop Hypertension. It’s a
diet rich in fruits, vegetables,

low-fat dairy products, whole grains, fish, poultry, beans, seeds,

and nuts. It’s low in sodium, sugars and sweets, fats, and red
meats. One must consult a doctor before making these changes.

 Drink Enough Water.

Drinking enough eater prevent kidney diseases as water helps
the kidneys remove wastes from your blood in the form of urine. Water also helps keep your
blood vessels open so that blood can travel freely to your kidneys, and deliver essential
nutrients to them. Dehydration reduces blood flow to your kidneys, which can damage them.

4. Limiting alcohol and tobacco

Drinking alcohol in large amounts can make your blood pressure go
up, which can lead to kidney disease. By drinking less, you can help
keep your blood pressure under control. Here are healthy guidelines:

 For men, no more than two drinks per day

 For women, no more than one drink per day
Do not smoke or use tobacco. Using tobacco (smoking or chewing) can make high blood
pressure and kidney problems worse. It also causes many other serious health problems such as
cancer, heart disease and stroke. If you use tobacco, quitting can help lower your chance of
getting kidney disease or help prevent your kidney disease from getting worse.

5. Being Active
Being active can help you stay healthy and:

 Lose weight
 Keep a healthy blood sugar level
 Improve your heart and lung health
 Lower your blood pressure
 Lower your total cholesterol level and increase your HDL
(“good” cholesterol) level
Set a goal to be active for at least 30 minutes, 5 days a week.

35
6. Use Less Painkillers And Avoid Excessive Medication
Avoid taking large amounts of painkillers, especially drugs containing a combination of caffeine,
acetaminophen and aspirin. Combination agents such as these have been associated with an
increased risk of kidney disease. Drugs containing acetaminophen alone can also be dangerous to
the kidneys, although these are less harmful. All of these drugs can damage the inner parts of the
kidneys, a condition known as interstitial nephritis. It has been observed that eight to ten tablets
or capsules of acetaminophen alone can damage the kidneys over a five-year period.

Conclusion
Small lifestyle changes can make a big difference in helping to prevent kidney disease. Many of
the same changes that help control diabetes and high blood pressure can also help prevent kidney
disease or keep it from quickly getting worse.

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 REFERENCES

https://www.healthline.com/health/kidney-health/how-to-prevent-kidney-failure#what-it-is
https://www.cdc.gov/kidneydisease/prevention-risk.html
https://www.cdc.gov/kidneydisease/pdf/CKD_TakeCare.pdf
https://www.winchesterhospital.org/health-library/article?id=103158
https://www.kidney.org/news/newsroom/newsreleases/0314
Kidney Disease Introduction | Kidney Structure and Kidney Function (kidneyeducation.com)
Kidney Diseases | Renal Disease | MedlinePlus
Introduction - ScotPHO

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