Ppt highlighted about the Nutritional Management of Kidney disorders.

1. Physiology And Functions Of
Kidney

2. The Structure Of The Mammalian Kidney
• The kidneys are a pair of bean-shaped organs found in the lower back
region behind the intestines. They are 7-10cm long and are the major
excretory and osmoregulatory organs. Along with the ureter, bladder and
urethra, they make up the urinary system. It is in this system that urine is
produced and excreted by the body via urination (micturition).
• The renal artery brings blood with waste products to the kidney to be
cleansed. After the blood is cleansed, it returns to the heart via the renal
vein. Wastes flow through the ureter as urine to the bladder to be stored.
When the bladder is full, stretch receptors in its wall trigger a response, the
muscles in the wall contract and the sphincter muscles relax, allowing the
urine to be excreted through the urethra. The kidneys are enclosed with a
protective fibrous capsule that shows distinct regions

3. Diagram of kidney

4. The Internal Structure Of The Kidney
• Cortex: The outer region. It has a more uneven texture than the
medulla. The Renal capsule, proximal convoluted tubule and distal
convoluted tubule of the nephron are located here.
• Medulla: The inner region, consisting of zones known as pyramids
which surrounds the pelvis. The Loop of Henle and collecting ducts of
the nephron are located here.
• Pelvis: The central cavity. Urine formed after blood is cleansed is
deposited here. This cavity is continuous with the ureter so the urine
goes directly to the bladder

5. The structure of Nephron

6. The nephron is the functional unit found within the kidneys.
Each kidney is made up of millions of microscopic nephrons,
each with a rich blood supply. To fully understand the function
of the kidney, the function of the nephron must be studied and
understood since it is the structure that carries out excretion
and osmoregulation.
Each nephron has the following structures:
• Bowman’s capsule (renal capsule)
• Proximal convoluted tubule
• Distal convoluted tubule
• Collecting duct

7. Structure Of Bowman’s Capsule

8. Bowman’s Capsule
• Glomerulus: A mass of capillaries enclosed by the Bowman’s capsule.
• Afferent arteriole: A branch of the renal artery that supplies the
glomerulus with blood.
• Efferent arteriole: Takes blood away from the glomerulus.
• Malpighian body: The structure consisting of the Bowman’s capsule
and the glomerulus.

9. • There is a hydrostatic pressure in the glomerulus due to the strong
contraction of the left ventricle of the heart and the fact that the
diameter of the afferent arteriole is larger than that of the efferent
arteriole. The difference in diameters between the two vessels raise the
hydrostatic blood pressure. This causes blood to filter into the
Bowman’s capsule under pressure in a process called ultrafiltration. As
a result, only molecules with RMM less than 68,000 can enter the
capsule (water, glucose, amino acids, hormones, salt, urea), while the
larger molecules like plasma proteins and blood cells remain in the
blood and exit the Malpighian body via the efferent arteriole. The
blood must pass several filtrating barriers before it can enter the
capsule.

10. The Proximal Convoluted Tubule
• This is the longest part of the nephron and is located in the cortex of
the kidney. It is surrounded by many capillaries that are very close to
the walls. Approximately 80% of the glomerular filtrate is reabsorbed
here via selective reabsorption. Cubical epithelial cells line the tubule
walls and have many microvilli on their free surfaces which increase
the surface area of the wall exposed to the filtrate.
Fact: The total surface area of the Human proximal tubule cells is 50m2.

11. The Loop Of Henle
• This hairpin-bend structure has a descending limb and an ascending
limb and is found in the medulla of the kidney. The descending limb
has thin walls permeable to water and penetrates deep into the medulla
but the ascending limb has thicker, relatively impermeable walls that
returns to the cortex. Surrounding the loop is a network of capillaries,
one part of which has the same hairpin structure and is called the vasa
recta.

12. • Need to know : The loop of Henle works by making the concentration
of the interstitial tissues of the medulla hypertonic (greater solute
concentration) to the filtrate by actively transporting chloride ions out
of the filtrate into the surroundings. Sodium ions passively follow. This
occurs in the thick part of the ascending limb. The deeper part of the
medulla near the pelvis is the most concentrated and therefore has the
lowest water potential

13. Distal Convoluted Tubule
• The cells of the wall of the distal convoluted tubule are similar to
those of the proximal convoluted tubule, having numerous microvilli
and mitochondria and carries out active transport. However, this
tubule reabsorbs varying quantities of inorganic ions in accordance
with the body's needs. It can also secrete substances into the filtrate to
maintain a particular condition (example: control of pH). The walls of
the distal convoluted tubule are permeable to water only if the ADH
(anti-diuretic hormone), otherwise, it is impermeable to water. If it is
permeable, water exits the filtrate and enters the bloodstream and an
isotonic filtrate enters the ducts. If it is not permeable, a hypotonic
filtrate enters the collecting ducts.

14. The Collecting Duct
• The distal convoluted tubule ends in the collecting duct. (Several
nephrons can share one collecting duct.) Final modifications are made
to the filtrate which is then emptied into the pelvis of the kidney as
urine. Like the walls of the distal convoluted tubule, the walls of the
collecting ducts are only permeable to water if ADH is present,
otherwise, it is impermeable to water.

15. Functions of the kidney
Overview Of Kidney Functions
• Excretion of wastes and other foreign substances.
• Regulation of blood ionic composition
• Regulation of blood pH
• Production of hormones and biosynthesis of vitamin D
• Regulation of blood pressure
• Regulation of blood volume
• Maintenance of blood osmolarity
• Regulation of blood glucose level

16. 1. Excretion Of Wastes And Other Foreign Substances
By forming urine, the kidneys help excrete wastes- substances that have no
useful function in the body.
Some wastes excreted in urine result from metabolic reactions in the body.
These include:
Bilirubin from the catabolism of haemoglobin.
 Ammonia and urea from deamination of amino acids.
Creatinine from the breakdown of creatinine phosphate in muscle fibres.
 Uric acid from the catabolism of nucleic acids.
Other wastes include foreign substances from the diet, such as drugs and
environmental toxins.

17. 2. Regulation Of Blood Ionic Composition And PH
• The kidney can correct any imbalances by:
• Removing excess acid (hydrogen ion) or bases (bicarbonate) in the urine and
• Restoring the bicarbonate concentration in the blood to normal.
• The kidney cells produce a constant amount of hydrogen ion and bicarbonate
because of their own cellular metabolism (production of carbon dioxide).
Whether the kidney removes hydrogen ions or bicarbonate ions in the urine depends
upon the amount of bicarbonate filtered in the glomerulus from the blood relative to
the amount of hydrogen ions secreted by the kidney cells. If the amount of filtered
bicarbonate is greater than the amount of secreted hydrogen ions, then bicarbonate
will be lost in the urine. Likewise, If the amount of secreted hydrogen ion is greater
than the amount of filtered bicarbonate, then hydrogen ions will be lost in the urine
(i.e. acidic urine).

18. 3. Production Of Hormones
The human kidney secretes two hormones:
1. Erythropoietin (EPO)
2. Calcitriol (1,25[OH]2 Vitamin D3
Erythropoietin a Glycoprotein it acts on the bone marrow to increase the
production of red blood cells. Stimuli such as bleeding or moving to high
altitudes (where oxygen is scarcer) trigger the release of EPO. People with
failing kidneys; dialysis. Without a source of EPO, these patients suffer from
anaemia.

19. Calcitriol: Calcitriol is 1,25[OH]2cholecalciferol, Vitamin D3, the active form of
vitamin D. It is derived from
• Calciferol ( cholecalciferol, vitamin D3) which is synthesized in skin exposed to the
ultraviolet rays of the sun
• Precursors (cholecalciferol, vitamin D3 and ergocalciferol, vitamin D2 ) ingested in
the diet, Which are biologically inert
Calciferol in the blood is converted into the active vitamin in two steps: calciferol is
converted in the liver into 25[OH] vitamin D3 this is carried to the kidneys where it
is converted into calcitriol. This final step is promoted by the parathyroid hormone
(PTH) Calcitriol acts on: * The cells of the intestine to promote the absorption of
calcium and phosphate from food
* Bone to mobilize calcium from the bone to the blood

21. 4. Regulation Of Blood Pressure And Blood Volume
RENIN : One of the functions of the kidney is to monitor blood pressure and take
corrective action if it should drop. The kidney does this by secreting the proteolytic
enzyme renin. Renin acts on angiotensinogen, a plasma peptide, splitting off a
fragment containing 10 amino acids called angiotensin I. Angiotensin I is cleaved by
a peptidase secreted by blood vessels called angiotensin converting enzyme (ACE)
— producing angiotensin II, which contains 8 amino acids. Angiotensin II
 Constricts the walls of arterioles closing down capillary beds
 Stimulates the proximal tubules in the kidney to reabsorb sodium ions
 Stimulates the adrenal cortex to release aldosterone. Aldosterone causes the
kidneys to reclaim still more sodium and water.
Increases the strength of the heartbeat
Stimulates the pituitary to release the vasopressin . All of these actions lead to an
increase in blood pressure and blood volume

23. 5. Maintenance Of Blood Osmolarity
By separately regulating loss of water and loss of solutes in the urine,
the kidneys maintain a relatively constant blood osmolarity close to 300
milliosmoles per litre.
6. Regulation Of Blood Glucose Level
Like the liver, the kidneys can use the amino acid glutamine in
gluconeogenesis, the synthesis of new glucose molecules. They can
then release glucose into the blood to help maintain a normal blood
glucose level.

24. Acute Kidney Injury/Acute Renal Failure

25. ACUTE KIDNEY INJURY (ACUTE RENAL FAILURE)
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. These causes
are generally classified into three categories:
(1) Inadequate renal perfusion (prerenal)
(2) diseases within the renal parenchyma (intrinsic)
(3) Urinary tract obstruction (postrenal)

26. • Acute renal failure (ARF) is a rapid loss of renal function due to damage to the
kidneys, resulting in retention of nitrogenous (urea and creatinine) and non-
nitrogenous waste products that are normally excreted by the kidney.
• Depending on the severity and duration of the renal dysfunction, this
accumulation is accompanied by metabolic disturbances, such as metabolic
acidosis (acidification of the blood) and hyper-kalaemia (elevated potassium
levels), changes in body fluid balance, and effects on many other organ
systems. It can be characterized by oliguria or anuria (decrease or cessation of
urine production), although non-oliguric ARF may occur.
• It is a serious disease and treated as a medical emergency
• Acute renal failure, in fact is a sudden loss of the ability of the kidneys to
excrete waste, concentrate urine and conserve electrolytes. It is a serious
condition characterized by a sudden shutdown of kidney function as mentioned
above due to decreased renal flow, acute glomerular or a tubular damage. It
results in a decline in glomerular filtration rate (GFR), usually associated with
azotemia (accumulation of nitrogenous waste products in the blood) and a fall
in urine output

27. Classifications of AKI
RIFLE Classification
Stage Creatinine Urine output
Risk renal failure Cr. x 1.5 normal or
UO < 0.5ml / kg /
hour for 6 hours
Injury to kidney Cr. x 2 normal or
UO < 0.5ml / kg /
hour for 12 hours
Failure of kidney fxn Cr. x 3 normal or Anuric for 12 hours
Loss kidney fxn Need renal replacement therapy x 4 weeks
End stage renal
disease
Need renal replacement therapy for > 13 weeks

28. Stage Creatinine criteria Urine output criteria
1
Cr. x 1.5 - 2 baseline or
↑Cr.≥150-200%
or <0.5 mL/kg/h for > 6 hours
2
Cr. x 2 -3 from baseline or ↑Cr.
≥200-300%
or <0.5 mL/kg/h for >12 hours
3
Cr. x 3 baseline OR ↑ Cr.
≥300%
Cr. ≥ 354 µmol/l (≥4mg/dl)
↑ ≥44µmol/l(≥5mg/dl) OR
need RRT
or
UO <0.3 mL/kg/h for 24hours OR
anuria for 12 h OR
need for RRT
AKIN Classification(Acute Kidney Injury Network)

29. KDIGO Classification(Kidney Disease Improving Global Outcome)
Stage Serum creatinine Urine output
1
1.5 to 1.9 times multiplied by
baseline
OR
↑ ≥26 µmol/L in 48hrs
<0.5ml/Kg/h for 6-12
hours
2
2 to 2.9 times multiplied by
baseline
<0.5 ml/Kg/h for ≥12
hours
3
3 times multiplied by baseline
OR
↑ ≥354 µmol/L
OR
Initiation of renal replacement
therapy
OR, in patients <18 yrs, ↓in eGFR
to <35 ml/min per 1.73m2
<0.3 ml/Kg/h for ≥24
hours
OR
Anuria for ≥12 hours

30. Etiology
• Several conditions can lead to ARE These include:
Prerenal AKI
• Prerenal AKI results from decreased blood supply to the kidney. here the kidney is structurally and functionally normal. Just
because it does not get enough blood supply it cannot throw out all the nitrogenous waste products resulting in, rise in BUN and
creatinine ( azotemia).
• Decreased blood supply to the kidney can from, Circulatory shock, large blood loss and reduced renal blood flow as in traumatic
injury, shock, severe burns, surgery, septicemia, dehydration followed by vomiting and loose motions and also fluid loss.
• If decreased blood flow to the kidney persist for a long period, it can lead to the ischemic injury to the tubules of the kidney, a
condition called as ischemic acute tubular necrosis.
Renal (intrinsic) AKI
• Structural injury in the kidney is the hallmark of intrinsic AKI. Structural components of the kidney include: vessels, glomeruli,
tubules and interstitium. Involvement of any component will lead to intrinsic AKI.
• Vascular injuries like vasculitis, thrombotic micro angiopathy, atheroembolic renal disease. Glomerular injuries like,
glomerulonephritis. And also tubular injuries like, ischemic acute tubular necrosis.
Post renal AKI
• Mechanical obstruction of the urinary system, including the renal pelvis, ureters, bladder or urethra results in obstructive
uropathy or post renal AKI.
Causes of obstruction include, stone disease, stricture, intraluminal, extraluminal or intramural tumors
• Mismatched blood transfusions
• Nephrotoxins like carbon tetrachloride, certain poisonous mushrooms,
• Infections, snake bite, bee stings etc.
• Immunological reactions to drugs like certain antibiotics.

31. Clinical and Metabolic Manifestations
The onset of ARF is sudden, with the course of the disorder having two phases, namely:
a) oliguria or initial acute phase
b) diuretic phase.
• The latter indicates restoration of renal function, although it may still remain poor for several days.
• The major clinical features of ARF are oliguria or anuria (urine output 20-200 ml), due to drastic reduction of GFR
to 1-2% of normal. Along with this, haematuria and proteinuria are usually present.
• There is an elevation of serum urea nitrogen and creatinine due to reduced GFR and tissue protein breakdown.
• Uremia may develop along with associated symptoms like disorientation, lethargy, nausea, vomiting and anorexia.
Blood pressure elevation, increased levels of potassium, phosphate and sulphate occurs with lowered levels of
sodium and bicarbonate.
• Water balance is a crucial factor and unless controlled, the condition can prove fatal mostly due to potassium
intoxication or excess fluid retention leading to cardiac failure.
• Return to renal function is characterized by an increase in urine output or diuresis. When diuresis is established, the
urine volume gradually increases to between 3 to 5 litres/day and the excretion of sodium, potassium, urea and
other solutes also increase. The blood urea falls to normal in 7 to 10 days, indicating that glomerular filtration has
effectively improved.
• Although the excretory function of kidney is restored, the recovery of regulatory function of the tubules is slower.
• The internal environment of the patient is still at risk because of excessive losses of water, sodium, potassium,
bicarbonate and magnesium. In majority of patients, the kidneys will recover with little or no residual damage if the
patient can survive the oliguric phase. However, in a few cases, residual damage of tubular function may sometimes
be detected even long after the blood urea has returned to normal levels.

32. Dietary Management In ARF
The common nutritional problems include:
(1) Poor appetite
(2) Inability to take food or fluids orally due to intubation
(3) Hyper-catabolism (increased metabolism) due to underlying illnesses such as infection,
postoperative healing.
Principles of diet therapy in AKI: low protein, low sodium, low potassium and fluid restricted
diet ( High protein for dialysis)
Goals of dietary treatment AKI
• Preventing further damage to the kidney
• Re-establishment of fluid electrolyte balance
• Maintenance of acceptable levels of blood urea and creatinine while supporting tissue healing
and making up catabolic losses
• Preventing infection
With conservative medical and diet treatment, recovery may occur within a few days or weeks.
However, if oliguria continues with a rise in nitrogenous wastes and potassium, aggressive
therapy including hemodialysis may be required with nutritional support. Thus dietary
management is a challenge and plays an important role. Oral feeding is best, but if nutritional
support is needed, caution is necessary to avoid fluid overload and uremia.

33. The Dietary Guidelines for Acute Renal Failure
• Calories: In most adults, energy requirement amounts to 30-40 Kcal/kg body weight with
up-to 40-45 Kcal /kg for hyper-catabolic cases. The major source of energy is carbohydrates
followed by fat. An intake of 100-200 g or more of sugar /glucose per 24 hours is
administered when the oral intake is poor because of vomiting and diarrhoea. Children need
enough calories to support growth. In some cases enteral or parental non-protein
concentrated calories sources may have to be provided because of fluid restriction.
• Protein: This needs restriction and intake is dependent on GFR and extent of hyper
catabolism. Initially the intake may range from 0.5 to 0.6g/kg IBW, subsequently, increased
to 0.8-1.2 g/kg IBW/day. Therefore, depending on the degree of protein catabolism 0.5-
lg/kg/day of protein may be given. With improvement, at least 60- 70% of good quality
proteins are recommended to reduce unnecessary nitrogen load. In case total parenteral
nutrition (TPN) is required, a balanced amino acid solution containing both essential and
nonessential amino acids should be administered. In addition to essential amino acids,
arginine, histidine, serine, taurine and tyrosine may be recommended.
Foods included: On dialysis- high quality protein, such as meat, fish and eggs are
recommended
Foods avoid: dals, beans, low quality proteins

34. Sodium: During the oliguric phase, sodium may need to be restricted to 500-
1000 mg (20-40 mEq) daily. It can be liberalized with onset of diuresis.
How to monitor sodium intakes
• Always read food labels. Sodium content is always listed.
• Pay close attention to serving sizes.
• Use fresh, rather than packaged meats.
• Choose fresh fruits and vegetables or no-salt-added canned and frozen produce.
• Avoid processed foods.
• Compare brands and use items that are lowest in sodium.
• Use spices that do not list “salt” in their title (choose garlic powder instead of
garlic salt.)
• Cook at home and do NOT add salt.
• Avoid table salt

35. Sodium content of some foods

36. Potassium: Since, hyperkalaemia is a life-threatening complication of acute renal failure, it needs to
be treated urgently. Potassium intake is restricted to 1000-2000 mg (25 to 50 mEq) and should be monitored
strictly and regularly. As the renal function improves, the intake may be increased.
How can patients monitor their potassium intake?
When the kidneys no longer regulate potassium, a patient must monitor the amount of potassium that enters
the body.
•Talk with a renal dietitian about creating an eating plan.
•Limit foods that are high in potassium.
•Limit milk and dairy products to 8 oz per day.
•Avoid salt substitutes & seasonings with potassium.
•Read labels on packaged foods & avoid potassium chloride.
•Pay close attention to serving size.

38. • Fluid: Intake is based on fluid balance but is usually restricted to a basic allowance of
500 ml/day for an average adult with addition made for losses via other routes
(500ml+losses through urine).
• The fluid allowance is usually regulated in accordance with urinary output and any
additional losses from vomiting or diarrhea.
• Strict monitoring of fluid balance is important, the patient's weight and blood sodium
levels are good indicators of fluid balance, and the amount of fluid required. If fluid
intake is not adequate for excretion of metabolic wastes, dialysis is usually
recommended.

39. Chronic kidney Disease
• Chronic renal failure is a slow progressive loss of renal function over a period of
months or years and defined as an abnormally low glomerular filtration rate, which is
usually determined indirectly by the creatinine level in blood serum.
• CRF, therefore, is a condition that arises due to advanced and progressive damage of
kidneys with impairment of renal function.
• Few functional nephrons remain and CRF results in what is usually termed uremia.
Uremia, is a toxic condition resulting from renal failure, when kidney function is
compromised and urea, a waste product normally excreted in the urine, is retained in
the blood. Unlike acute renal failure, with its sudden reversible failure of kidney
function, chronic renal failure is a gradual and progressive loss of the ability of the
kidneys to excrete wastes, concentrate urine, and conserve electrolytes.
• CRF can range from mild dysfunction to severe kidney failure. CRF that leads to
severe illness and requires some form of renal replacement therapy (such as dialysis) is
called end-stage renal disease (ESRD)
• The National Kidney Foundation (NKF) divides CKD into five stages related to the
estimated GFR (eGFR) the rate at which the kidneys are filtering wastes (mentioned in
Table ). Stages 1 and 2 are early stages with markers such as proteinuria, hematuria, or
anatomic issues. Stages 3 and 4 are considered advanced stages. Stage 5 results in
death unless dialysis or transplantation is initiated.

40. Stage GFR (mL/min/1.73 m2) Description Action plan*
1 ≥ 90 Kidney damage with
normal or increased GFR
Treat primary and
comorbid conditions
Slow CKD progression,
CVD risk reduction
2 60-89
Kidney damage with mild
reduction of GFR
Estimate rate of
progression of CKD
3 30-59
Moderate reduction of
GFR
Evaluate and treat
complications
4 15-29 Severe reduction of GFR
Prepare for kidney
replacement therapy
5 < 15 (or dialysis) Kidney failure
Kidney replacement
therapy
Table 1: NKF classification of the stages of chronic kidney disease (CKD).
NKF: The National Kidney Foundation; GFR: Glomerular Filtration Rate (millilitres per minute per
1.73-meter square of body surface area);
CVD: Cardiovascular Disease. *The actions that are listed in the more severe stages of CKD also
include actions from less severe stages.

41. Causes
Diseases and conditions that cause chronic
kidney disease include:
• Type 1 or type 2 diabetes
• High blood pressure
• Glomerulonephritis: an inflammation of the
kidney's filtering units (glomeruli)
• Interstitial nephritis: an inflammation of the
kidney's tubules and surrounding structures
• Polycystic kidney disease or other inherited
kidney diseases
• Prolonged obstruction of the urinary tract,
from conditions such as enlarged prostate,
kidney stones and some cancers
• Vesicoureteral reflux: a condition that
causes urine to back up into your kidneys
• Recurrent kidney infection, also called
pyelonephritis
Risk factors
Factors that can increase your risk of
chronic kidney disease include:
• Diabetes
• High blood pressure
• Heart (cardiovascular) disease
• Smoking
• Obesity
• Being Black, Native American or
Asian American
• Family history of kidney disease
• Abnormal kidney structure
• Older age
• Frequent use of medications that can
damage the kidneys

42. Complications
Potential complications include:
• Malnutrition
• Fluid retention, which could lead to swelling in your arms and legs, high blood pressure, or fluid in
your lungs (pulmonary edema)
• A sudden rise in potassium levels in your blood (hyperkalemia), which could impair your heart's
function and can be life-threatening
• Anemia
• Heart disease
• Weak bones and an increased risk of bone fractures
• Decreased sex drive, erectile dysfunction or reduced fertility
• Damage to your central nervous system, which can cause difficulty concentrating, personality
changes or seizures
• Decreased immune response, which makes you more vulnerable to infection
• Pericarditis, an inflammation of the saclike membrane that envelops your heart (pericardium)
• Pregnancy complications that carry risks for the mother and the developing fetus
• Irreversible damage to your kidneys (end-stage kidney disease), eventually requiring either dialysis
or a kidney transplant for survival

43. Clinical and Metabolic Manifestations
• Progressive loss of nephrons with a decreased renal blood flow and glomerular filtration results in a
marked impairment of not only excretory but also metabolic and endocrine functions of the kidney. It
leads to decreased ability of the kidneys to maintain body water balance, concentrate solutes in body fluid
(osmolality) and electrolyte and acid- base balance, Other clinical manifestations that develop may relate
to almost every system of the body due to an overall pervasive metabolic derangement of the body.
• Increased solute load of metabolic wastes results in osmotic diuresis initially, due to an impaired ability of
the kidney to concentrate urine. This leads to loss of sodium and potassium. However, with continued
renal damage and reduced GFR, sodium, potassium and nitrogenous wastes tend to be retained in the
body. This contributes to oedema, hypertension, hyperkalemia and azotemia, respectively, Azotemia is the
buildup of nitrogen waste products in the blood.
• Retention of phosphate, sulphate and organic acids causes metabolic acidosis due to loss of bicarbonate.
• Impaired calcium and phosphorus balance due to decreased vitamin D 3 and consequent secondary
hyperparathyroidism leads to renal osteodystrophy or renal bone disease, with bone and joint pains.
Calcification of soft tissues is another complication that can develop.
• Other clinical features include anaemia due to impaired RBC synthesis. Hypertension arises due to
stimulation of the renin angiotensin system by the reduced renal blood flow, resulting in vasoconstriction.
The resultant cardiovascular damage worsens renal function.
• Other related symptoms are shortness of breath and fatigue. Azotemia and other metabolic changes cause
anorexia, weight loss, gastrointestinal irritability, nausea, vomiting and diarrhoea.
• Subcutaneous nasal or GI bleeding can occur due to increased capillary fragility. Mouth ulceration, taste
changes, neurological symptoms, increased susceptibility to infection due to malnutrition also commonly
observed

44. Medical Management : Dialysis
Haemodialysis
• HD requires permanent access to the bloodstream
through a fistula created by surgery to connect an artery
and a vein . If the patient’s blood vessels are fragile, an
artificial vessel called a graft may be implanted
surgically. Large needles are inserted into the fistula or
graft before each dialysis and removed when dialysis is
complete.
• Temporary access through subclavian catheters is
common until the patient’s permanent access can be
created or can mature; however, problems with
infection make these catheters undesirable
• The HD fluid and electrolyte content is similar to that
of normal plasma. Waste products and electrolytes
move by diffusion, ultrafiltration, and osmosis from the
blood into the dialysate and are removed. Filtered blood
is then returned to the body.
• Outpatient HD usually requires treatment of 3 to 5
hours three times per week in a dialysis unit
Peritoneal dialysis
• PD makes use of the body’s own semipermeable
membrane, the peritoneum. A catheter is implanted
surgically through the abdomen and into the
peritoneal cavity.
• Dialysate containing a high-dextrose concentration is
instilled into the peritoneum, where diffusion carries
waste products from the blood through the peritoneal
membrane and into the dialysate; water moves by
osmosis. This fluid then is withdrawn and discarded,
and new solution is added multiple times each day.
Several types of PD exist.
• In CAPD, the dialysate is left in the peritoneum and
exchanged manually, by gravity. Exchanges of
dialysis fluid are done four to five times daily,
making it a 24-hour treatment. In APD, patient
treatments are done at night by a machine that
mechanically performs the exchanges. During the day
these patients sometimes keep a single dialysate
exchange in the peritoneal cavity for extended
periods (called a long dwell), perhaps the entire day.
Several combinations of CAPD and APD are possible
and are referred to here as PD

46. Dietary Management
• The primary objectives of MNT are to manage the symptoms associated with the syndrome (edema,
hypoalbuminemia, and hyperlipidemia), decrease the risk of progression to renal failure, decrease inflammation,
and maintain nutritional stores. Patients are treated primarily with statins to correct hyperlipidemia, low-sodium
diets, and diuretics. Patients with an established severe protein deficiency who continue to lose protein may
require an extended time of carefully supervised nutritional care. The diet should attempt to provide sufficient
protein and energy to maintain a positive nitrogen balance and to support tissue synthesis while not overtaxing
the kidneys. In most cases, sufficient intake from carbohydrate and fats is needed to spare protein for anabolism.
• Feeding is a challenge in CRF as anorexia and taste changes reduce food intake. The main focus of dietary
management is on protein, sodium, potassium, phosphate, water and adequate non-protein calories. Individual
modifications are required based on clinical profile, treatment and response of the patient. Keeping in mind the
general objectives of diet treatment in renal disease, the following modifications are required.
• Energy : About 2000-2500 Kcal/day are recommended or 30-40 Kcal/day for adults and about 100-150
Kcal/kg/day for children. If the calorie intake is inadequate, endogenous protein catabolism and gluconeogenesis
occur to supply energy and further aggravate uremia. Therefore, 300-400 g of carbohydrates are recommended
• Protein: Protein needs to be restricted. However, enough has to be provided to minimize tissue catabolism.
About 0.5 g/kg/day is recommended but has to be regulated depending on declining renal function. A protein
intake of 35-40 g (day (60-70% of high biological value protein) with liberal calorie intake can maintain the
nitrogen equilibrium for long periods while reducing azotemia. If BUN rises, the protein intake may need to be
restricted to 20 g/day. High biological value proteins from milk and eggs are recommended to provide all the
essential amino acids. To reduce the nitrogen load, in advanced cases, mixture of essential amino acids or
nitrogen free precursors of the essential amino acids like a keto or a hydroxy analogs may be recommended. The
potential benefits of protein restriction include: Decreases glomerular hyperfiltration, which may slow
progression of glomerulosclerosis. Protein restricted diets are phosphorus restricted, which delays onset of renal
secondary hyperparathyroidism and may slow progression of glomerulosclerosis, Reduces proteinuria in
glomerulopathies. Reduce net acid load. May reduce serum lipids. Improves the symptoms of uremia

47. • Sodium: Sodium intake will vary between 500 mg to 2.0 g/day. Weight loss and
decreasing urine volume usually indicate a need for additional sodium, whereas
if hypertension and oedema are present, the sodium intake needs to be restricted.
• Potassium: The failing kidney cannot excrete potassium adequately and
therefore intake is kept at about 1500 mg/day (35 to 40 mEq /day). The
potassium intake has to be adjusted to maintain normal levels in blood. In severe
vomiting and diarrhoea, significant losses of potassium can occur and in these
conditions, careful potassium supplementation may be needed.
• Calcium and phosphorus: To maintain calcium and phosphorus balance and
prevent or delay renal bone diseases, calcium supplements (1-2 g/day) are
recommended and phosphate is restricted to 800-1200 mg/day. Phosphate
binding agents may be used if required to reduce absorption. Calcium carbonate
supplements can help buffer metabolic acidosis, if present. It is important to
remember not to start calcium supplements, unless phosphate is restricted, to
avoid soft tissue calcification.
• Vitamin: Multivitamin supplements are recommended for a diet with < 40 g/ day
of protein. Supplements of vitamin D3 may be recommended, based on need.
• Fluid: Intake is dependent on urine output and water balance. Fluid intake should
be adequate to stimulate urine output for excretion of wastes but should avoid
excess fluid retention at the same time.

48. Nutritional Management of CKD on Dialysis
Hemodialysis : Low K, low PO4, low Na, moderate protein, fluid restriction
Peritoneal dialysis : High K, low PO4, low Na, high protein, moderate fluid restriction
Once dialysis is started, the diet in ESRD or CKD can be liberalized, taking care that accumulation of
metabolic wastes and water is prevented between treatments and biochemical balance is maintained. The
objectives of diet management thus are to maintain balance of protein, energy, fluid and electrolytes,
calcium and phosphorus, while making up losses of water-soluble nutrients lost in the dialysate. The
dietary guidelines include:
• Energy: Up to 35-40 Kcal/kg/day for adults and 100 Kcal or more kg/day for children is recommended
to meet the body needs and minimize tissue protein breakdown. Fats and carbohydrates are the main
energy sources used. Some restriction of total and saturated fats may be needed, as dialysis patients are
prone to cardiovascular disease.
• Protein: The requirement is increased due to losses in the dialysate. In haemodialysis, 1.2g/kg/day is
required in PD 1.5-2.0g/day . At least 70% of the protein given should be of high biological value from
eggs, fish, chicken and milk, though milk may need to be limited being a rich source of potassium. This
protein intake helps to maintain positive nitrogen balance, replace losses and prevent undue
accumulation of nitrogen wastes, between treatments. Amino acid replacement may also be required in
case of large losses.
• Sodium: A daily intake of 1500 to 2000 mg may be permitted to control fluid retention and
hypertension in HD and 1.5-4 g/day in PD . This restriction helps to prevent pulmonary oedema or
congestive heart failure because of fluid overload. Regular assessment of the kidneys ability to handle

49. • Potassium: A daily intake of 2-3 g /day is prescribed to prevent hyperkalcmia in
HD and 3-4 g/day in PD. Potassium accumulations easily cause cardiac
arrhythmias or cardiac arrest.
• Phosphorus: This may need some restriction.0.8 -1.2g/day or <17mg/kg IBW
• Vitamins and Minerals: A daily supplement of water-soluble vitamins and
minerals are usually given, as these are lost in the dialysate. Fat-soluble
vitamins may be retained. Thus, their supplements are avoided except vitamin
D. Supplements of minerals like calcium, iron and zinc are recommended.
• Fluid: Usually 400-500 ml (basal losses) plus the urine output is recommended
in HD and minimum of 1000ml plus losses from urine in PD . The fluid intake
must take into account all sources of fluid input and output to maintain balance.
Mild fluid retention between treatments usually occurs. Patient counseling and
support is an important part of dietary management to help renal patients
understand their dietary modifications, the foods permitted and those to be
avoided. Counseling about the ways to increase the palatability of the restricted
diets can encourage the patient to increase their dietary intake.

50. Kidney Transplantation
Kidney transplantation, is a procedure that surgically places a healthy kidney
from a donor into the recipient's body. This new kidney does the work of the failed
kidneys.
Donated kidneys may come preferably from blood relatives, after tissue and blood
matching.
Success of kidney transplant has improved with the use of immunosuppressive
drugs and steroids to prevent organ rejection and infection.
Post transplant nutritional support is required for this major surgical procedure.
Optimal energy and protein intake are important for recovery, Initially, while on
medication, some restriction of sodium, simple sugars, total fat, cholesterol and
saturated fat may be required. This is because of the side effects of
immunosuppressant and steroids.
With recovery and reduction or withdrawal of medication, the diet can be
normalized.

51. The nutritional care of the adult patient who has received a transplanted kidney is based
mainly on the metabolic effects of the required immunosuppressive therapy.
 Medications typically used for the long term include azathioprine (Imuran),
corticosteroids (e.g., prednisone), calcineurin inhibitors ,cyclosporine A, Sandimmune,
tacrolimus , everolimus (Zortress), mycophenolate mofetil and mycophenolic acid.
 Corticosteroids are associated with accelerated protein catabolism, hyperlipidemia,
sodium retention, weight gain, hyperglycemia, osteoporosis, and electrolyte
disturbances.
Calcineurin inhibitors are associated with hyper-kalemia, hypertension, hyperglycemia,
and hyper-lipidemia.
The doses of these medications used after transplantation are decreased over time until a
“maintenance level” is reached.
During the first 6 weeks after surgery, a high-protein diet is often recommended (1.2 to
1.5 g/kg ideal body weight [IBW]) with an energy intake of 30 to 35 kcal/kg IBW, to
prevent negative nitrogen balance.
 A moderate sodium restriction of 2 to 3 g/day during this period minimizes fluid
retention and helps to control blood pressure.
After recovery, protein intake should be decreased to 1 g/kg IBW, with calorie intake
providing sufficient energy to maintain or achieve an appropriate weight for height.
A balanced low-fat diet aids in lowering cardiac complications, whereas sodium intakes
are individualized based on fluid retention and blood pressure.

52. Hyper-kalemia warrants a temporary dietary potassium restriction.
After transplantation, many patients exhibit hypophosphatemia and mild
hypercalcemia caused by bone resorption; this is associated with persistent
hyperparathyroidism and the effects of steroids on calcium, phosphorus,
and vitamin D metabolism.
The diet should contain adequate amounts of calcium and phosphorus
(1200 mg of each daily) and cholecalciferol (vitamin D3, 2000 IU daily).
Supplemental phosphorus also may be necessary to correct
hypophosphatemia
Hydration must also be monitored closely after transplantation. Because
most kidney recipients required a fluid restriction while on dialysis, they
must be reminded of the importance of maintaining fluid intake after
transplant. Typically, patients are encouraged to drink 2 L/day, but their
overall needs depend on their urine output.

53. The majority of transplant recipients have elevated serum triglycerides or
cholesterol for a variety of reasons. Intervention consists of medications,
calorie restriction for those who are overweight, cholesterol intake limited
to less than 200 mg/day, and limited total fat
In patients with glucose intolerance, limiting carbohydrates and a regular
exercise regimen are appropriate.
Tissue weight gain with resultant obesity is common after transplantation.
 Medication side effects, fewer dietary restrictions, and the lack of physical
exercise can contribute to post-transplant weight gain.
Because of immunosuppression, care must be taken with food safety
similar to other significantly at risk groups. Handwashing, food temperature
monitoring, and avoidance of uncooked foods remain appropriate infection
control behaviors

54. Kidney Stones (Nephrolithiasis)
Nephrolithiasis, the presence of kidney stones, is a significant health problem.
• The prevalence of kidney stones from the National Health and Nutrition
Examination Survey (NHANES) 2007 to 2010 data is 8.8% (Scales et al, 2012).
• 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.
• Thought to be a predominantly male disease, its prevalence is fast increasing in
women (7.1%) and in men at 10.6%, changing the male/female ratio. Kidney
stones affect people of all ethnic groups.

55. 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.

56. • 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

57. Types of stones
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
Cystine Stones. Cystine stones represent 1% to 2% of urinary calculi and are caused by
homozygous cystinuria
• 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 cystine 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

58. 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 results in overproduction of oxalate and a urinary oxalate
concentration three to eight times normal.
• 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

59. 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 undissociated uric acid,
which occurs at urinary pH less than 5.5.
• Inflammatory bowel disease results in chronically acidic urine, usually from
dehydration. GI bicarbonate loss from diarrhoea 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.

60. 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
• Struvite stones are mostly due to urinary tract infection (UTI)
Clinical Symptoms :
• The kidney stones may not produce symptoms until they begin to move
down the ureter, causing pain.
• The pain is usually severe and often starts in the flank region, then moves
down to the groin.
• The patient experiences blood in the urine, severe pain, weakness and in
some cases fever. Laboratory examination and chemical analysis can help
determine location, size and main constituent of stones to determine the
treatment.

61. Dietary Management
• The goal of treatment of renal calculi is to relieve symptoms and prevent
further complications.
• Treatment, therefore, varies depending on the type of stone and the extent
of symptoms or complications.
• Kidney stones usually pass on their own. In acute stage with stones less
than 5 mm in diameter, it may pass in the urine by drinking large quantities
of fluid especially water and needs no specific treatment. Stones more than
7 mm in diameter may require surgical treatment or lithotripsy by which
large stones are broken down and excreted in the urine.
• Although, role of diet in the formation of urinary stones is not well
established, it is advisable to have liberal fluid intake, a balanced diet and
restrict foods based on the main constituent of the stones.

62. Different stones and their corresponding diet restriction
Main constituent Diet restrictions Urine pH
Calcium stones
- Phosphate
- Oxalate
Struvite stones
Calcium – 400-600mg
Phosphorous -1000-1200mg
Low phosphorous diet
Acid
Acid
Uric acid stones Low purine diet Alkaline
Cystine stones Low methionine diet Alkaline

63. Recommendations for Diet and 24-Hour Urine Monitoring in Kidney Stone
Disease
Diet Component
Protein
Calcium
Oxalate
Intake Recommendation
Normal intake: avoid excess
Normal intake:1000 mg if age
<50 years; 1200 mg if age >50
years Divide intake between
three or more eating sessions.
Choose from dairy or non
dairy sources
Avoid moderate- to high-
oxalate foods if urinary
oxalate is high
24-Hour Urine
Monitor urinary urea
Calcium <150 mg/L (<3.75
mmol/L)
Oxalate <20 mg/L (<220
µmol/L)

64. Fluid
Purines
Vitamin C
Vitamin D
Vitamin B6
Sodium
2.5 L or more; assess type of
fluids consumed; provide
guidelines
Avoid excessive protein
intake; avoid specific high-
purine foods
Avoid supplementation
Meet DRI for vitamin D
intake
Use supplements to reach
DRI
40 mg or more per day
reduces risk. No
recommendation made
<100 mmol/day
Volume > 2 L/day
Uric acid <2 mmol/L (<336
mg/L)
Monitor urinary oxalate
Serum 25(OH)D3 in
acceptable range
Monitor urinary sodium

65. Dietary Sources of Various Constituents of the Renal Stones
Dietary sources of potassium, sodium, calcium, oxalate and uric acid are given in this section. We
begin our study with the dietary sources of potassium.
A. Directions / Methods for leaching Potassium
Method I — Wash, peel and cut vegetables into small pieces. Soak in warm water for 2-3 hours.
Discard water. Add large volume of fresh water and cook the vegetables. Discard water.
Method II — Peel vegetables and cut into small pieces. Bring to boil in a large quantity of water.
Discard excess water and cook in a large volume of fresh water. Discard excess water.
B. Sources of Sodium
Food items with a high sodium content (these food items should be avoided):
• Salt
• Baking powder /Bicarbonate of soda
• Canned, preserved and processed food items as processed cheese, sauce, margarine, etc.
• Bacon, ham and sausages
• Meat and yeast extracts like marmite
• Salted chips, nuts, popcorn and biscuits
• Commercial salad dressings and sauces Soup cubes
• Malted beverages like Boost, Bournvita and Proteinex.
• Flavour enhancers such as Monosodium glutamate (MSG)

66. C. Sources of Calcium, Oxalate and Uric Acid
Calcium: Beans, cauliflower, egg yolk, figs, milk and milk products like
cheese, , curds, molasses and potatoes.
Oxalate: cashew nuts, chickoo, chocolate, cocoa, custard apple,
groundnuts, spinach, strawberries, tomatoes and tea.
Uric Acid: Fish herring, fish roe, salmon, sardines, kidney, liver, meat, red
meat ,meat extracts and soups, and sweet bread.