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NUTRITIONAL ASPECT OF

URONEPHROLOGY SYSTEM DISEASES


Nesyana Nurmadilla
Outlines

 Basic structures and functions


 Diseases: nephron diseases, kidney failure,
end-stage renal diseases, kidney stone disease
 Epidemiology
 Etiology
 Clinical menifestation
 Medical nutrition therapy
Basic structures

Image from Williams Basic Nutrition & Therapy 2017


Functions
 Excretory and regulatory functions
 Filtration: Most particles in blood are filtered out, except
for the larger components of RBC and proteins.
 Reabsorption: As the filtrate continues through the
winding tubules, substances that the body needs are
selectively reabsorbed and returned to the blood to
maintain the electrolyte, acid-base, and fluid balances.
 Secretion: Along the tubules, additional hydrogen ions are
secreted as needed to maintain the acidbase balance.
 Excretion: Waste materials are excreted in the
concentrated urine.
Functions
 Endocrine functions
 Renin secretion: When the arteriole pressure falls, the
kidneys activate and secrete renin to reabsorb sodium and
to maintain hormonal control of the body water balance.
 Erythropoietin secretion: The kidneys are responsible
for producing 80% to 90% erythropoietin.
 Vitamin D activation: The kidneys convert inactive form
of vitamin D  active vitamin D in the proximal tubules of
the nephrons. This action is stimulated by the PTH.
General causes of kidney disease

 Infection
 Obstruction
 Damage from other diseases (hyperglycemia,
diabetes, hypertension)  damage small renal
arteries
 Toxins
 Genetic/ congenital defects

Malnutrition intensifies the rate of renal


tissue destruction and increase susceptibily of
infection
MNT in kidney diseases
During the treatment of kidney disease, MNT is based
on:
 The severity of the disease
 Length of disease
 Short term acute: Nutrition therapy is aimed at optimal nutrition
support for healing and normal growth.
 Degree of impaired kidney functions
 Progressive chronic disease: extensive MNT is required to
help maintain kidney function as long as possible. With
continuing disease, nutrient modifications are designed to
meet individual needs to address clinical symptoms.
 The presence of metabolic abnormalities
 The treatment modality (e.g., renal replacement therapy,
medications).
URONEPHRO SYSTEM DISEASES
Diseases

 Nephron diseases
 Nephritic syndrome
 Nephrotic syndrome
 Kidney failure
 Acute kidney injury
 Chronic kidney disease
 ESRD
 Dialysis, transplantation
 Kidney stone diseases
 Calcium stones, struvite stones, uric acid stones
Nephritic syndrome
• The third leading cause of stage 5 CKD
• Inflammatory process of the glomeruli
Nephritic syndrome
Clinical manifestation:
• Hematuria
• Proteinuria
• Edema
• Hypertension
• Anorexia in advanced stages  feeding problems and
malnutrition
• Oliguria or anuria (progressive)
MNT of Nephritic syndrome
• Optimal nutrition support for growth with adequate
protein.
• Diet modifications are not crucial in most patients with acute
short-term disease.
• Fluid intake is adjusted to output and insensible losses.
Nephrotic syndrome
 Also called nephrosis
 May be caused by:
 Infection
 Medications
 Neoplasms
 Preeclampsia
 Progressive glomerulonephritis
 Diabetes
 Systemic lupus erythematosus.
Disease process

Nephron tissue Filtration and


damage to the Further reabsorption
Protein pass
major filtering damage to the functions of
into the tubule
membrane of tubule the nephron
the glomerulus are disrupted
Clinical manifestation Proteinuria

 Severe edema and


ascites often mask the Hypoalbuminemia
extent of body tissue
wasting.
 Other: hyperlipidemia, Tissue protein
lipiduria, blood clotting breakdown, edema
abnormalities, and
imbalances in several
minerals (iron, copper, General
malnutrition
zinc, calcium)
MNT of Nephrotic syndrome

Directed toward:
 Controlling major symptoms
 Replacing the nutrients that are lost in the
urine
 Reducing the progression to CKD
 Decreasing the risk of atherosclerosis
MNT of Nephrotic syndrome

Protein
 Moderate (0.8 to 1.0 g/kg BW/day), with an
emphasis on protein from high biologic value sources,
including soy protein.
 Total protein intake may be modified on the basis
of BUN and GFR results (If BUN is elevated and urine
output is decreased, dietary protein may be restricted).
MNT of Nephrotic syndrome

Energy
 Total energy intake should be adequate to
support nutrition status (may be as high as 35
kcal/kg/day).
 To provide sufficient energy in kilocalories, complex
carbohydrates should be given liberally, which also
helps to combat the catabolism of tissue protein and to
prevent starvation ketosis.
MNT of Nephrotic syndrome
Fat
 Controlling the dietary intake of fat and
cholesterol may help to alleviate dyslipidemia
and the resulting risk for atherosclerosis
 Total fat intake should not exceed 30% total
kcal/day
 Cholesterol intake should not exceed 200 mg/day
 Trans fats should be limited
 Up to 10% of kilocalories should come from PUFA
MNT of Nephrotic syndrome

Sodium and potassium


 Sodium restriction of 1 to 2 g/day is advised to maintain
the sodium and fluid balance and to reduce symptoms of
edema.
 Sodium overload is difficult to treat because of the
characteristic hypoalbuminuria and hypotension;
therefore, careful monitoring is necessary.
 The renal clearance of potassium is impaired with
oliguria. Thus, potassium intake should be monitored
and adjusted in accordance with individual needs.
Acute Kidney Injury
• Healthy kidneys may suddenly shut down after
metabolic insult or traumatic injury  a life-threatening
situation.
• Occurs in as many as one in five hospitalized patients
• Significantly increases the LOS in the hospital and the
death rate.
• Risk factors for the development of in-hospital AKI
include older age, diabetes, and underlying renal
insufficiency attributable to systemic infection, organ
failure, or the use of nephrotoxic medications
• A condition in which nutrition play important supportive
roles.
MNT of AKI
• The major challenge during AKI is to improve or maintain
nutrition status while the patient is faced with marked
catabolism.
• Current standards:
• Treating the underlying cause
• Preventing further kidney damage and complications from nutrient
deficiencies
• Correcting any fluid, electrolyte, or uremic abnormalities
MNT of AKI
Protein
• Adequate protein is important for supporting kidney function
and for preserving lean tissue.
• For patients who are not receiving dialysis and who are not
experiencing catabolism, a protein intake of 0.8 to 1.2 g/kg BW
is recommended.
• For patients who are experiencing catabolism or who are on
dialysis, 1.2 to 1.5 g/kg BW of daily protein is recommended to
allow for nutrient replenishment and to account for losses.
MNT of AKI
Energy
• Energy intake in the range of 25 to 35 kcal/kg BW is suggested.
Adjusted on an individual basis (metabolic stress, nutritional
status of the patient).
• If the patient is on dialysis, energy intake from the dialysate
must be included in the total energy intake.
MNT of AKI
Sodium and potassium
• During a diuretic phase, patients may lose excessive
electrolytes.
• Losses of both sodium and potassium (2 to 3 g/day each)
should be replaced during diuretic phase. These levels are
further adjusted depending on blood pressure and the
presence of edema.
• During oliguria or anuria phases, electrolytes may need to be
restricted because of accumulation in the blood and increased
risk for hyperkalemia, a potentially fatal condition
MNT of AKI
Phosphate and calcium
• Dietary phosphorus intake is determined on the basis of body
weight, with a range of 8 to 15 mg/kg BW.
• Hyperphosphatemia during anuria phases  disturb Ca/P
equlibrium in blood  calcium resorption from bones.
• Phosphate binders taken with meals help prevent phosphate
absorption.
• Goal for calcium is to maintain serum value levels within
normal limits and to adjust dietary intake accordingly.
MNT of AKI
Vitamins and minerals
• A patient’s diet should be balanced to prevent nutrient
deficiencies by meeting the DRIs for all other vitamins and
minerals.
• If the patient is experiencing catabolism or other complications,
nutrient intakes may be modified to meet specific needs.
MNT of AKI
Fluid
• Fluid needs are highly variable with AKI.
• Treatment modality, hydration, and fluid loss should be
considered on an individual basis.
• Insensible fluid loss may increase as a result of fever, and
sensible fluid loss (e.g., urine output, vomitus, diarrhea) will
vary considerably among patients.
• A starting point recommendation is 500 mL of fluid plus
urine output daily
Chronic Kidney Disease

 A progressive breakdown of kidney tissue,


which impairs all kidney functions.
 Few functioning nephrons remain and they
gradually deteriorate.
Chronic Kidney Disease
Most commonly a result of:

Other causes: immune disease such as lupus,


obstructions such as kidney stones, chronic UTI, and
long-term use of nephrotoxic medications

Inherited diseases (polycystic kidney disease) or


congenital abnormality

Primary glomerular disease

Metabolic diseases with kidney involvement


(diabetes, hypertension, CVD, metabolic
syndrome, obesity)
Chronic Kidney Disease

Modifiable risk factors include:


 Blood pressure
 Glycemic control
 Addressing dyslipidemia
 Reducing sodium intake
 Making necessary dietary adjustments to
potassium, phosphorus, and protein intake
 Increasing physical activity
 Achieving a healthy body weight
 Quitting smoking
Clinical manifestation

 CKD changes may involve extensive scarring of


renal tissue  distorts kidney structure 
vascular damage.
 As nephrons are lost, the remaining nephrons
gradually lose their ability to sustain
metabolic balance.
 Long-term complications most commonly
include malnutrition, bone and mineral
disorders, anemia, and CVD.
Clinical manifestation

Large
amounts of
Early dilute urine Risk of
stages are produced dehydration

kidneys unable Polyuria


to reabsorb
water or to
properly
concentrate
urine
Clinical manifestation ↑ BUN,
azotemia

Oligouri,
anuria


Hyper-
activated
tension
vit D Calcium
resorption
Kidney from bone,
Edema damage abnormal
level of PTH
Proteinuri, ↑ blood
↓albumin phosphorus
in blood level

↓ produced CKD-
& survival MBD,
time of RBC osteo-
Anemia dystrophy
Clinical manifestation

associated
with ↑
loss of morbidity &
muscle and mortality
protein- visceral
energy protein
worsening wasting
malnutrition stores
Anorexia, (PEW)
and weight syndrome
nausea, and loss
vomiting
Clinical manifestation

 Progressive weakness
 Itchy skin rashes
 In advanced stages, irregular cyclic breathing
(i.e., Kussmaul’s breathing) indicates acidosis.
 Acidosis may cause mouth ulcers, a foul taste,
and bad breath in the patient.
MNT of CKD

Treatment must always be individual and adjusted


according to:
 The progression of the illness
 The type of treatment
 The patient’s response.

The nutritional status of patients with CKD should


be monitored at regular intervals to identify dietary
risk factors and to help prevent malnutrition
MNT of CKD

Protein
 The goal is to provide adequate protein to
maintain tissue integrity while avoiding excess.
 Generally limited to 0.6 to 0.8 g/kg BW/day for
individuals who are not on dialysis with a GFR of
<30 mL/min per 1.73 m2.
 Protein sources should focus on high biologic
value protein to ensure an adequate intake of
essential AA.
 Avoid high protein intakes of >1.3 g/kg BW in
adults at risk for further progression of CKD
MNT of CKD

Energy
 Carbohydrate and fat must provide sufficient
nonprotein kilocalories to supply energy and spare
protein for tissue synthesis.
 The recommended is 23 to 35 kcal/kg BW/day.
 Energy needs are less for overweight individuals with
both CKD and diabetes to allow for weight loss.
 Because cardiovascular disease is accelerated in
patients with CKD, the remaining calories should
support cardiovascular health principles (substitute to
MUFA and PUFA, reduce total cholesterol intake)
 For patients with diabetes, glycemic control is an important
part of intervention  HbA1c value of ≈7%.
MNT of CKD

Sodium and potassium


 The general recommendations for sodium (<2.4
g/day) and potassium are applicable until
complications are present.
 If hypertension and edema are present, sodium
intake is limited to 2 g/day.
 As CKD advances to stages 3 and 4, potassium is not
cleared adequately from the blood  dietary intake is
determined according to laboratory values.
 If blood levels of potassium are elevated and other
nondietary causes are eliminated, then a potassium-
restricted diet (<2.4 g/day) may be indicated.
MNT of CKD

Phosphorus and calcium


 As the kidney loses function, the activation of vitamin
D and the control of blood calcium levels are
inhibited.
 This problem is worsened by excess blood
phosphorus levels  calcium resorption from the
bone.
 Thus, moderate dietary phosphorus restriction depends
on laboratory values in the patient who is not undergoing
dialysis, and it is generally limited to 800 to 1000
mg/day when the serum phosphorus level is 4.6 mg/dL or
more or when the PTH is elevated.
MNT of CKD

Vitamins and minerals


 Recommendations are:
 To help patients meet their DRI for the B-complex
vitamins and vitamin C
 To determine the patient specific needs for vitamin D
and iron.
 Supplemental fat-soluble vitamins A and E are
not recommended, because they may accumulate to
toxic levels in patients with kidney failure.
 Excesses of vitamins D and K are contraindicated,
because the kidney cannot convert vitamin D to its active
form, and vitamin K can adversely affect clotting time.
MNT of CKD

Fluid
 Fluid intake should be sufficient to maintain
adequate urine volume in patients who are
not undergoing dialysis.
 Intake usually is balanced with output, and it
is not otherwise restricted
End-Stage Renal Disease
• Diagnosed when GFR decreases to <15 mL/min per 1.73 m2 
irreversible damage to a majority of the kidneys’ nephrons.
• At this point, the patient has two options: long-term kidney
dialysis or kidney transplant.
MNT of hemodialysis
The goal is to maintain optimal nutrition while preventing the
accumulation of excess waste products between treatments.
• Protein of 1.1 to 1.5 g/kg BW is ideal to prevent protein
malnutrition
• Energy intake are 25 to 35 kcal/kg BW/day to achieve and
maintain goal body weight.
• Sodium is limited to 2 to 3 g/day
• Potassium is restricted to 2 to 4 g/day
• Dietary intake of phosphorus is limited to 800 to 1000 mg/day
• Calcium intake should not exceed 2 g/day (include: food,
supplements, and medications)
MNT of hemodialysis
• The general recommendation for all water-soluble vitamins is
to achieve the DRI.
• Iron and vitamin D intakes are individualized per patient on the
basis of biochemical markers.
• Folate: 1 to 5 mg/day
• Vitamin E: 15 IU/day
• Zinc: 15 mg/day
• Fluid intake is limited to 1000 mL/day plus an amount equal to
urine output.
MNT of kidney transplantation
General recommendations are the same as hemodialysis except:
• Protein 0,8 to 1 g/kg BW/day
• Calcium and phosphorus are individualized based on kidney
function
• Potassium is not restricted unless there is hyperkalemia 
individualized
Kidney Stone Diseases

Table from Williams Basic Nutrition & Therapy 2017


Kidney Stone Diseases
 The most common types of kidney stones are:
calcium, struvite, and uric acid.

Image from Williams Basic Nutrition & Therapy 2017


Calcium stones
 Most common types: calcium oxalate and
calcium phosphate stones.
 The supersaturation of kidney stone
materials in the urine may result from
hypercalcemia, hypercalciuria,
hyperoxaluria, hyperuricosuria, or
hypocitraturia.
 Oxalates are derived from endogenous synthesis
and dietary sources.
Calcium stones
 A small percentage of the population are
“hyperabsorbers” of dietary oxalate and thus are
at higher risk of forming stones.
 Oxalic acid is a metabolite of ascorbic acid.
Therefore, long-term supplementation of
vitamin C in excess of the tolerable upper
intake (2000 mg/day) may pose a potential health
risk for kidney stone formation.
Calcium stones

 Adequate dietary calcium intake from all sources


is inversely associated with calcium oxalate stone
formation.
 Dietary calcium binds oxalates in the intestines,
preventing absorption and thus concentration of
oxalates in the urine.
 It was a common misunderstanding to restrict the calcium
intake of those patients who form calcium oxalate stones
Struvite stones
 Account for approximately 10% of all stones
 Composed of magnesium ammonium phosphate
and carbonate apatite.
 Often called infection stones because primarily
caused by UTI and because not associated
with any specific nutrient.
 No particular diet therapy is involved.
 Usually large “staghorn” stones that are surgically
removed.
Uric acid stones

 Approximately 9% of kidney stones


 Primary risk factors for uric acid stone
formation are:
 Overly acidic urine  diarrheal illness, type 2 diabetes,
obesity, and metabolic syndrome (acidic urine favors the
kidneys’ reuptake of uric acid whereas alkaline urine favors
the excretion of uric acid).
 Hyperuricosuria  impairment that involves the
metabolism of purine (gout, rapid tissue breakdown
during wasting disease)
 Low urine volume.
MNT of Kidney stones

Energy
 Overweight and obesity increase the risk for
kidney stone formation.
 Total energy intake should be customized to
achieve an ideal body weight.
 Diets such as the DASH diet or Mediterranean
diet are ideal.
 High-protein, low-carbohydrate diets are
specifically discouraged for individuals at risk for
stone formation
MNT of Kidney stones

Protein
 Excessive protein intake from animal sources
is a risk factor for stone formation  better
consume alkaline diet.
 Standard recommendations of 0.8 to 1.0 g/kg
BW/day.
MNT of Kidney stones

Fiber
 Should be considered in the case of calcium
stones.
 Phytate can bind calcium and thus help to
prevent the crystallization of oxalate calcium
salts.
 Phytates are found in high-fiber plant foods
such as whole wheat, bran, and soybeans.
MNT of Kidney stones

Calcium
 Low dietary calcium intake is a risk for calcium
oxalate stone formation.
 Patients should be encouraged to normalize
calcium intake to 800 mg/day for men and
1200 mg/day for women and balance intake
throughout the day.
MNT of Kidney stones

Sodium and potassium


 High sodium intake increases hypercalciuria 
increased risk of stone formation.
 All stone formers should be counseled on a low-
sodium diet (<2300 mg/day).
 Citrate and potassium are helpful in solubilizing
calcium salts and preventing calcium oxalate
stone formation.
 The diet should be rich in fruits (particularly
citrus fruits) and vegetables to provide a
potassium intake of >4.7 g/day.
MNT of Kidney stones
Oxalates
 Limiting dietary oxalates reduces urinary oxalate
excretion and the risk of calcium oxalate stone
formation.
 Intake should be <200 mg/day

Phophorus
 If a stone is made of calcium phosphate,
additional sources of phosphorus (meats,
legumes, nuts) should be controlled
MNT of Kidney stones

 All vitamin and mineral intakes should meet the


DRI.
 A large fluid intake of ≥ 2 to 3 L/day helps to
produce more dilute urine
 Exact fluid intake needs vary by patient, but
enough fluids, preferably water, should be
ingested to produce at least 2 to 2.5 L of clear
urine daily.
 For patients who consume soft drinks, reducing
softdrink intake may lower the risk of recurrent
stone formation
THANK YOU FOR YOUR
ATTENTION