Transcript Acute Renal Failure

Medical Nutrition Therapy for Renal
Disorders
.
Functions of the Kidney
 Excretory
 Acid-base balance
 Endocrine
 Fluid and electrolyte balance
.
Excretory Functions
 Removal of excess fluid and waste products
 180 L of filtrate pass through the kidneys
each day  producing 1-2 L of urine
 Wastes excreted from the body in urine
include urea (byproduct of protein
metabolism); excess vitamins and minerals;
metabolites of some drugs and poisons
.
Acid-Base Functions
 Acid-base balance is maintained through a
buffer system, which maintains blood at pH
of 7.4
 Bicarbonate carries hydrogen ions to the
kidneys where they are removed from
extracellular fluid in the tubules, returned to
the bloodstream as needed
 Phosphate buffers intracellular fluid
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney
Disease. ADA, 2004
.
Acid-Base Balance Functions
 When fluid volume is low, anti-diuretic
hormone (ADH) or vasopressin is released
from the anterior pituitary; increases
absorption of water in the collecting duct
 When extracellular volume (ECV)
decreases, the renin-angiotensin-aldosterone
system is activated  excretes less sodium
chloride
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in
Kidney Disease. ADA, 2004
.
Endocrine Functions
 1,25-dihydroxy-vitamin D3 or calcitriol is
produced in the kidney; enhances calcium
absorption
 Activation of Vitamin D and excretion of
excess phosphate maintain healthy bones
 Erythropoietin: acts on the bone marrow to
increase production of red blood cells
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in
Kidney Disease. ADA, 2004
.
The Nephron
The Most Common Kidney Diseases
 Diabetic Nephropathy damage to the nephrons in
the kidneys from unused sugar in the blood,
usually due to Diabetes.
 High Blood Pressure can damage the small blood
vessels in the kidneys. The damaged vessels
cannot filter poison from the blood as they are
supposed to.
 Polycystic Kidney Disease (PKD) is a hereditary
kidney disease in which many cysts grow in the
kidneys. These cysts may lead to kidney failure.
.
The Most Common Kidney Diseases
 Acute Renal Failure - Sudden kidney failure
caused by blood loss, drugs or poisons. If the
kidneys are not seriously damaged, acute renal
failure may be reversed.
 Chronic Renal Failure - Gradual loss of kidney
function is called Chronic Renal Failure or
Chronic Renal Disease.
 End-Stage Renal Disease - The condition of total
or nearly total and permanent kidney failure.
.
Kidney Diseases

Glomerular diseases
–
–

Tubular defects
–

Acute renal failure (ARF)
Other
–
–
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Nephrotic syndrome
Nephritic syndrome—tubular or
interstitial
End-stage renal disease (ESRD)
Kidney stones
Nephrotic Syndrome
 Alterations of the glomerular basement
membrane allows persistent loss of large
amounts of protein in the urine
 Associated with diabetes,
glomerulonephritis, amyloidosis, lupus
 High risk for cardiovascular disease
 Hypercoagulability
 Abnormal bone metabolism
.
Nephrotic Syndrome
 Albuminuria: more than 3 g/day urinary
albumin losses, with proportionally lesser
amounts for children
 Hypoalbuminemia
 Hypertension
 Hyperlipidemia
 Edema
.
Medical Mgt of Nephrotic Syndrome
 Corticosteroids
 Immunosuppressants
 ACE inhibitors/angiotensin receptor blockers
to reduce protein losses, control blood
pressure and fluid balance
 Coenzyme A reductase inhibitors to control
hyperlipidemia
.
MNT in Nephrotic Syndrome
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Protein 0.8 to 1 g/kg IBW 80% HBV
Sodium based on fluid status
Potassium and other minerals (calcium,
phosphorus) monitored and
individualized
Fluid unrestricted
Diet therapy probably not effective for
hyperlipidemia; may require medication
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
.
Nephritic syndrome
 Acute glomerulonephritis (inflammation of
the glomerulus
 Sudden onset, often after streptococcus
infections
 Symptoms include hematuria, hypertension
 Usually resolve on their own or advance to
nephrotic syndrome or ESRD
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Nephritic syndrome: Nutritional
Management
 Diet to treat underlying disease
 Restrict diet if necessary to control
symptoms
 Protein restricted in uremia
 Sodium restriction in hypertension
 Potassium restriction in hyperkalemia
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Acute Renal Failure
 Rapid, often reversible deterioration of
renal function
 GFR declines over hours to days
 Most commonly occurs during
hospitalization (5% of hospitalized pts; 30%
of ICU pts)
 Associated with major in-hospital morbidity
and mortality (7 to 80%)
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
.
Causes of Acute Renal Failure
 Pre-renal: caused by intravascular volume
depletion, decreased cardiac output
 Post-renal: benign prostatic hypertrophy,
prostate cancer, cervical cancer, colorectal
cancer, neurogenic bladder, urethral
strictures
 Intrinsic or parenchymal ARF: vascular
disease, interstitial nephritis, glomerular
disease, acute tubular necrosis
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
.
Causes of Acute Renal Failure
 Ischemic Injury (50% of all incidence) d/t loss of
blood supply to the kidneys secondary to surgical
complications, thrombosis, hypotension,
hypovolemia
 Nephrotoxic injury: medications, contrast
medium, chemotherapy, poisons (35%)
 Multiorgan system failure, particularly liver
failure
 Sepsis, especially bacterial
 Obstructive uropathy (trauma during surgery,
urolithiasis, enlarged prostate)
 Acute glomerular nephritis
.
Acute Tubular Necrosis
Most common cause of ARF
 Ischemia: due to major surgery,
hypotension, cardiogenic, septic, or
hypovolemic shock
 Nephrotoxicity: drugs, chemotherapeutic
agents, organic solvents, heavy metals,
cocaine
.
Acute Tubular Necrosis
Initiating phase
 Period between onset and established renal
failure
 Usually reversible by treating the
underlying disorder or removing offending
agent
 Time frame: hours or days
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
.
Acute Tubular Necrosis
Maintenance Phase
 Epithelial cell injury
 Urine output is at its lowest; complications
associated with uremia, fluid overload,
electrolyte imbalance (decreased sodium,
increased potassium levels)
 Time frame: 10-16 days in oliguric patients;
5-8 days in nonoliguric patients
.
Acute Tubular Necrosis
Recovery Phase
 Tubule cell regeneration and gradual return
of GFR
 BUN and creatinine return to near normal
 May be complicated by marked diuresis,
dehydration and fluid and electrolyte
imbalance (increased sodium, decreased
potassium)
 Time frame: days to months
.
Renal Replacement Therapies in ARF
 Recommended for patients with pronounced
azotemia, electrolyte imbalance, fluid
overload, severe acidosis
 Used in 85% of patients with oliguric ARF
and 30% of nonoliguric
 Purpose is to correct imbalances as well as
provide sufficient renal support to other
organs
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Renal Replacement Therapies in ARF
 Hemodialysis: standard treatment if patient
is hemodynamically stable
– However, risk of hypotension and wide swings
in body weight in unstable patients
 Continuous hemofiltration provides slow,
continuous filtration across a membrane,
driven by arterial pressure or pump
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Renal Replacement Therapies in ARF
 Continuous hemodialysis , uses an
ultrafiltrate fluid similar to plasma
– Clearance occurs through diffusion from high
concentration (blood) to low concentration
 Peritoneal dialysis: less often used in the
US; not as effective when large volume or
solute clearances needed.
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CAVH
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Chronic Kidney Disease
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Causes of Chronic Kidney Disease
Cause
Incidence (%)
Diabetes
40
Hypertension
27
Glomerulonephritis
13
Interstitial disease
4
Renal cystic disease
3
Tumors
2
Other
10
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Progression to End-Stage Renal
Disease (ESRD)
.
First
Decline in glomerular filtration rate (GFR)
Second
Adaptations in renal function, i.e.,
increase in GFR
Third
Adaptations improve renal function in short
term
Fourth
Long term loss of nephron units.
Fifth
Slow, progressive decline in renal
function
Sixth
Eventually this decline leads to renal
insufficiency, i.e., ESRD
Stages of Chronic Kidney Disease
Stage
GFR
Action
At increased risk
CKD risk
factors
Screening; CKD risk reduction
1. Kidney damage with
>90
normal or increased GFR
Tx comorbid conditions. Slow
progression. CVD risk reduction
2. Mild decrease in GFR
60-89
Estimating progression
3. Moderate decrease in
GFR
30-59
Evaluating, treating
complications
4. Severe decrease in
GFR
15-29
Prepare for kidney replacement
tx
5. Kidney failure
<15 or
dialysis
Replacement, if uremia present
National Kidney Foundation K/DOQI Clinical Practice Guidelines on CKD.
Am J Kidney Dis 2002;39(suppl 1):46.
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ESRD: Medical Management
 Dialysis
 Immunosuppressant drugs
 Kidney transplant
 Psychological support
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Uremia, a Clinical Syndrome—
Signs and Symptoms
 Malaise
 Weakness
 Nausea and vomiting
 Muscle cramps
 Itching
 Metallic taste (mouth)
 Neurologic impairment
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Stages of CKD Nutrient Recommendations
Pro Kcal
g/kg
Na+
g/day
K+
Phos
Calcium
g/day
1
.75
Based on
energy
expenditure
1-4 g to No restriction Monitor and
NAS
restrict if nec
Unless high
1.2-1.5
2
.75
Based on
energy
expenditure
1-4 g to No restriction Monitor and
NAS
restrict if nec
Unless high
1.2-1.5
3
.75
Based on
energy
expenditure
1-4 g to No restriction 800-1000
NAS
mg/day
Unless high
1.2-1.5
4
.6
30-35
kcal/kg
1-4 g to No restriction 800-1000
NAS
mg/day
Unless high
<2000
mg/day
5
0.6- 30-35
0.75 kcal/kg
1-4 g to No restriction 800-1000
NAS
mg/day
Unless high
<2000
mg/day
.
Fedje and Karalis.
Nutrition mgt in early stages of CKD. Clin Guide Nutr Care Kidney Dis, ADA, 2004
Nutrition Assessment and
Monitoring in the CKD Pt
.
Anthropometric Measurements
 % usual body weight (%UBW)
 % standard body weight (%SBW)
 Height
 Skeletal frame size
 BMI
 Skinfold thickness
 Mid-arm muscle area, circumference, or
diameter
.
Blood Urea Nitrogen (BUN)
 Measure of the nitrogenous waste products
of protein
 High BUN in CKD may reflect high protein
intake, GI bleeding or inadequate dialysis,
increased catabolism due to infection,
surgery, poor nutrition
 Decreased BUN may mean protein
anabolism, overhydration, protein loss, low
dietary protein
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease.
ADA, 2004
.
Creatinine (nl 0.5-1.4 mg/dL)
 Nitrogenous waste product of muscle metabolism
 Produced proportionate to muscle mass
 Unrelated to dietary protein intake (DPI)
 Sensitive marker of renal function: the higher the
serum creatinine, the greater the loss of renal
function; may reflect inadequate dialysis or
muscle catabolism
 A decrease in creatinine over time may reflect loss
of lean body mass
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney
Disease. ADA, 2004
.
Causes of Hyperkalemia (K+)
Goal 3.5-5.5 mEq/L
 >6 mEq/L – abnormal,
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

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
potentially dangerous
Renal failure (kidney is
primary filter)
Excessive nutritional
intake
Chronic constipation
Infection
GI bleeding
 Insulin deficiency (high BG)
.
 Metabolic acidosis
 Drug interactions
 Catabolism of
malnutrition or cell
damage caused by injury
or surgery
 Decreased urinary output
 Chewing tobacco
Causes of Hypokalemia (↓ K+)
 Vomiting, diarrhea
 Diuresis
 Potassium binder
 K+ too low in dialysate
 Urine output >1000 mL/day or serum NL,
do not need to restrict K+
.
Phosphorus (normal 3.5-5.5 mg/dL)
 As renal function decreases, phos accumulates in
the blood
  phos triggers release of PTH that releases
calcium from bone
 Phos binders prevent phosphorus from being
absorbed in the gut; form insoluble compound so
phos is excreted in stool
 ↓ phos may mean excess phos binder or poor p.o.
.
Calcium (8.4-9.5 mg/dL)
 Most abundant mineral in human body
 Nearly half of calcium is bound to albumin; if
serum calcium is low, evaluate albumin level; can
correct for low albumin
 Calcium-Phosphorus Product: multiply serum
calcium x serum phos: if >55-75, calcification can
occur
 <2000 mg/day elemental calcium from diet +
binders stage 3-4
 High ca+: calcification, nausea, vomiting, muscle
twitching may mean too much Ca+ from meds or
diet
.
Serum Sodium (nl 133-145 mEq/L)
 Not a reliable indicator of sodium intake in
CKD
 Fluid retention due to decreased urine
production can dilute an elevated level
 Serum levels must be evaluated in
conjunction with fluid status
.
Lipids
 Cardiovascular disease is the most common
cause of death in people with CKD
 Kidney disease is considered the equivalent
of a risk factor, like diabetes
 HD: often have normal LDL, TC, ↑
triglycerides, ↓ HDL
 PD: have ↑ LDL/TC + ↑ TG
 Renal Tx: ↑ LDL/TC/TG, normal HDL,
often due to medications
.
Cholesterol in CKD
 High
• High risk TC 200-300 mg/dl (non-fasting)
• LDL goal < 100 mg/dl
 Low
• <150 -180, evaluate for pro-energy malnutrition
• Increased mortality
.
Hematological Indicators
 Hemoglobin: ↓ due to lack of erythropoetin,
produced by the kidney; pts receive
synthetic EPO tx (Epogen)
 May have anemia of chronic disease
 Ferritin: may be indicator of iron overload;
↑ ferritin may mean EPO resistance
.
Glomerular Filtration Rate (GFR)
 Best index of kidney function
 Used to establish stage of CKD
 GFR is the amount of filtrate formed per minute
based on total surface area available for filtration
(number of functioning glomeruli)
 Can be determined using injected isotope (inulin)
measurement in urine
 Can be calculated from serum creatinine using
standard equations
.
.
Interdialytic Weight Gain
 Pts on dialysis gain several kg of fluid
between HD treatments
 If pts gain >5%, may reflect excessive fluid
intake, leading to hypertension, edema,
ascites, pleural effusion
 Fluid gains of <2% reflect minimal fluid
and food intake, may be losing body mass
.
Pre-ESRD (DM)
 Primary Prevention
– Glycemic control (DCCT)
• Aim for Euglycemia
• Watch for low B.S.
– B.P. control
• 130/80
• Na+ restrict
– Base on comorbidities (~2-3 g.)
– Medications may increase or decrease K+; monitor
• Wt. loss (gradual)/exercise
– Meds: ACE inhibitors and ARB’s
.
Pre-ESRD
 Secondary Prevention (overt nephropathy;
GFR ~ 25)
– Protein normalization
– 0.6 g/kg - RDA 0.8 g/kg ( minimum for DM)
– Delay need for dialysis, control uremic
symptoms, reduce acidosis
 Stage 4 CKD: monitor labs, may need to
limit K+, Phos., Ca++, Mg++
.
MNT in Patients on Hemodialysis
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Hemodialysis
 Removes concentrated molecules and
excess fluid from pts blood through
diffusion and ultrafiltration
 Three parts of the system are the dialyzer
(artificial kidney), the dialysis machine, and
the dialysate
 Requires vascular access, usually through
an AV (arteriovenous) fistula
.
AV (arteriovenous) Fistula
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ESRD: Nutritional Management
 Prevent deficiencies
 Control edema and serum electrolytes
 Prevent renal osteodystrophy
 Provide an attractive and palatable diet
.
MNT in HD: Protein
 10-12 g free amino acids lost per treatment
during dialysis
 Greater amino acid losses with glucose-free
dialysate and high flux dialyzers
 1.2 g protein/kg standard body weight
(SBW) with 50% high biological value
(meat, poultry, fish, eggs, soy, dairy)
 Most HD patients take in less than 1 g/day
NKF K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in ByhamGray, p. 45-46
.
MNT in HD: Energy
 Adults <60 years: 35 kcal/kg SBW
 Adults > 60 or obese: 30-35 kcals/kg body
weight
 Actual intakes of HD patients in studies are
lower than that (mean 23 kcals/kg in HEMO
study)
NKF K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in
Byham-Gray, p. 46
.
MNT in HD: Lipids
 HD patients at risk for lipid disorders
 Recommended fat intake<30% of calories
and saturated fat<10%; cholesterol <300
mg/day
 Optimum fiber intake 20-25 g/day
 These restrictions are difficult to achieve
along with other restrictions of HD diet
.
MNT in HD: sodium and fluid
 ≥ 1 L fluid output: 2-4 g
Na and 2 L fluid
 ≤ 1 L fluid output: 2 g Na
and 1-1.5 L fluid
 Anuria: 2 g Na and 1 L
fluid
 Restrict Na+ if ↑
interdialytic wt gain, CHF,
edema, HTN, low serum
sodium
.
MNT in HD: Potassium
 Potassium needs related to urinary output
 Most patients on HD can tolerate 2.5 g of
K+
 Stricter diet may be indicated for pts w/
insulin deficiency, metabolic acidosis,
treated with beta blockers or aldosterone
antagonists, hypercatabolic
 Individuals: 40 mg/kg edema-free IBW or
SBW
.
MNT in HD: Phosphorus
 Maintain s. phos 3.5-5.5 mg/dL
 Usually ok until GFR ↓ to 20-30 mL/min
 Dialysis removes 500-1000 mg/treatment
 Use phosphorus binders with meals: absorb
50% of dietary phosphorus
 Dietary intake: 800 to 1000 mg/day or <17
mg/kg IBW or SBW
 Identify high protein, low phos food sources
.
MNT in HD: Calcium
 High from excess Ca++ type binders,
vitamin D analogs, Ca++ fortification
 Goal 8.4-9.5 mg/dl
 Always use corrected Ca++ (adjusted
Ca++)
[ (4-alb.) x 0.8] + Ca++]
 CaXPhos product: goal <55
.
Phosphate Binders
(Taken with meals to prevent phos absorption)
Calcium acetate
PhosLo
Mg/Ca++ carbonate
MagneBind
Sevelamer hydrochloride Renagel
Aluminum carbonate
Aluminum hydrozide
Alucap, Amphogel
Calcium carbonate
TUMS, Os-Cal, calciChew, Calci-Mix
.
MNT in HD: Vitamins
 H2O soluble vitamins
 Dialyzable – take after H.D.
 B vitamins and vitamin C in renal vitamin
↑ Vit. C → ↑ oxalate → calcification of soft tissues
and stones
 Individualize need for:
– Fe++ (IV most common), Vitamin D, Ca++, Zinc.
.
MNT in HD: Vitamin D
 Vitamin D is activated in the kidney to
calcitriol, or vitamin D3
 As D3 levels fall, calcium absorption ↓ and
phos excretion ↓
 Vitamin D3 therapy helps prevent renal
bone disease but may cause hypercalcemia
 Renal pts should use calcitriol supplements
under the supervision of a physician
.
Hemodialysis
 Typical diet order
– 2000 calorie, 80 g protein, 2 g Na+, 3 g K+,
low phosphorus, 1500 cc fluid restriction
.
Skeletal Effects of Chronic
Renal Failure
 Hyperphosphatemia
 Hypocalcemia
 Hyperparathyroidism
 Low bone mass and density
 Osteitis fibrosa cystica—hyperplastic
demineralized bone
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Monitor Patient Status
1.
2.
3.
4.
5.
BP >140/90
Edema
Weight changes
Urine output
Urine analysis:
—Albumin
—Protein
.
Monitor Patient Status (cont)
6.
7.
.
Kidney function
Creatinine clearance
Glomerular filtration rate (GFR)
Blood values
BUN 10 to 20 mg/dl (<100 mg/dl)
Creatinine 0.7 to 1.5 mg/dl (10-15
mg/dl)
Potassium 3.5 to 5.5 mEq/L
Phosphorus 3.0 to 4.5 mg/dl
Albumin 3.5-5.5 g/dl
Calcium 9-11 mg/dl
Peritoneal Dialysis
.
CAPD (continuous ambulatory
peritoneal dialysis)
 Most patients do 4-5 exchanges per day
 A specific volume of dialysate (1500-3000 ml) is
infused into the peritoneal cavity via a catheter
 The dialysate dwells for 4 hours as excess fluid
and toxins diffuse through peritoneal membrane
 Dialysate and wastes are drained from the body
and the process repeated.
.
Peritoneal Dialysis (home dialysis)
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
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Blood cleansed by passive movement from
capillaries to dialysate (diffusion)
Ultra-filtration (UF): fluid removed by
osmosis due to high osmolality of dextrose in
dialysate
Better control of labs, fluid balance and B.P.
Advantages for those with heart failure, access
problems. Diet liberal, independence.
Disadvantages:, anorexia, a.a. losses in dialysate,
peritionitis→ catabolism, anorexia, long- term
wasting, high B.S., wt. gain, lack of socialization
.
MNT for PD: Energy
 Energy: 35 kcals/kg/day SBW or adjusted
body weight for pts<60 years; 30 kcals/kg
for those >60
 Calories provided in the dialysate should be
included in total intake (may absorb as
much as 1/3 of daily energy needs)
.
MNT for PD: Protein
 PD patients lose 5-15 grams of protein a
day, primarily as albumin
 Goal 1.2-1.3 g/kg SBW or ABW/day
.
MNT for PD: Sodium
 PD clears sodium very well, so sodium can
be fairly liberal
 However, high salt diets increase thirst and
may make adherence to fluid limits more
difficult
 General recommendation is 2-4 grams
sodium
.
MNT for PD
 Potassium: is easily cleared by PD; some
patients may need K+ supplementation
 Calcium: limit to 2000 mg elemental
calcium
– Generally pts get ~1500 mg from calciumbased phosphate binders
– Serum calcium should be maintained in low
normal range (8.4-9.5 mg/dl)
.
MNT for PD
 Phosphorus: limited to 800-1000 mg/day
which is difficult with high protein diet
– Use phosphate binders
 Fluid: can be adjusted by varying the
dextrose concentrations of the dialysate
– May need to be restricted if pts cannot achieve
fluid balance without frequent hypertonic
exchanges
.
PD: weight gain,
hypertriglyceridemia, hyperglycemia
 Increase exercise as allowed by MD
 Limit sodium and fluid to minimize
hypertonic exchanges
 Modify energy intake to facilitate wt loss
 Modify intake of sugars and fats, especially
saturated fats
.
PD: Protein Losses, Malnutrition
 Patient education regarding protein goals
and ways to meet them
 Suggest pt eat protein foods first and limit
fluids at mealtime
 Frequent smaller portions of protein and
easy to eat proteins such as egg white,
cottage cheese, etc
 Education on sterile technique to avoid
peritonitis
.
Kidney Transplant
1. Types: related donor or cadaver
2. Posttransplant management:
Corticosteroids
Cyclosporine
3. Diet while on high-dose steroids:
1.3 to 2 g/kg BW protein
30 to 35 kcal/kg BW energy
80 to 100 mEq Na
4. Diet after steroids:
1 g/kg BW protein
Kcal to achieve IBW
Individualize Na level
.
Well Mr. Osborne, it may not be kidney stones after all.
.
Kidney Stones
1. Particulate matter crystallizes
Ca salts (Ca oxalate or Ca phosphate)
Uric acid
Cystine
Struvite (NH4, magnesium and phosphate)
2. Ca salts in stones—Rx: high fluid; evaluate
calcium from diet; may need more!
3. Treat metabolic problem; low-oxalate diet
may be needed; acid-ash diet is sometimes
useful but not proven totally effective
.
Kidney Stones—cont’d
4. Uric acid stones
Alter pH of urine to more alkaline
Use high-alkaline-ash diet
Food list in Krause text
5. Cystine stones (rare)
6. Struvite (infection stones) antibiotics and/or
surgery
.
Acid-Ash Diet
 Increases acidity of urine (contains chloride,
phosphorus, and sulfur)
 Meats, cheese, grains emphasized
 Fruits and vegetables limited (exceptions
are corn, lentils, cranberries, plums, prunes)
.
Alkaline-Ash Diet
 Increases alkalinity of urine (contains
sodium, potassium, calcium, and
magnesium)
 Fruits and vegetables emphasized
(exceptions are corn, lentils, cranberries,
plums, prunes)
 Meats and grains limited
.
Summary
 Renal diseases—delicate balance of
nutrients
 Regular monitoring of lab values, with
altered dietary interventions accordingly
.