Kidney Disease, Tugas Prof Fat

8/13/2019 Kidney Disease, Tugas Prof Fat

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Diseases of the Renal

System

dr.Agustin Faizah


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An estimated 13.1% of adults ages 20 or older

(26 million adults) have physiological evidence

of chronic kidney disease (CKD) the

National Health and Nutrition Examinations

Survey between 1999 and 2004.

The medical interventions for these diseases

are among the most expensive treatments.

Introduction


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Renal

vein

Inferior

vena cava

Urinary

bladder

Urethra

Renal

artery

Kidney

Aorta

Ureter

Renal

pyramid

Renal

Cortex

Renalmedulla

Renal

Pelvis

Ureter

(b) Longitudinal section of a kidney

(a) Components of the urinary system

Anatomy

The Kidneys


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The functioning unit of the kidney is called the nephron.

Each kidney consists of approximately 1.2 million nephrons.

Each nephron is made up of a glomerulus ,which is a capillarytuft located between two arterioles (the afferent and the

efferent)

The afferent arteriole carries blood to the glomerulus and the

efferent arteriole carries blood away from it. The nephron extends through three sections of the kidney

called the cortex, outer medulla, and inner medulla .

The cortex contains the glomeruli and the proximal and distal

convoluted tubules. The medulla consists of the collecting ducts, loops of Henle,

and vasa recta.


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The primary functions of the kidney :1. Maintenance of homeostasis through control of fluid, pH, and

electrolyte balance and blood pressure.

2. Excretion of metabolic end-products and foreign substances.

3. The production of enzymes and hormones.

Urine formation is a crucial component in the maintenance ofhomeostasis.

The glomerulus the first step in urine formation occurs filters largeproteins and blood cells The ultrafiltrate , is similar in composition tothe blood.

The tubules the second phase of urine production most of its

components are reabsorbed (amino acids, glucose, selective minerals, andwater)

Vasopressin controls the final phase of urine production, as it directsconcentration of urine and assists in maintaining overall fluid balance .

Urine osmolality can vary widely from 500 mOsm to 1200 mOsm. Volumevaries as well; as little as 500 mL or as much as 12 liters of urine can be

produced to maintain normal homeostasis.

Physiological Functions


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Sodium is reabsorbed in the proximal tubule under theinfluence of aldosterone.

If serum sodium levels are elevated, sodium is

exchanged with potassium so that homeostasis isrestored.

The kidney additionally plays a significant role in bloodpressure control. Cardiac output and blood pressureare dependent on plasma volumeVasopressin,

secreted by the pituitary gland. The formation of urine also serves as the route for

excretion of waste products, including the by-productsof metabolism such as uric acid, creatinine, and urea.Other wastes excreted are drugs and environmentaltoxins.

The kidneys role in controlling both hydrogen andbicarbonate ions is a critical component of themaintenance of Ph homeostasis.


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The kidney also produces important enzymes andhormones.

Renin, is produced by the kidney and isnecessary for the initiation of the renin-angiotensin control of fluid balance.

The hormones 1,25-dihydroxycholecalciferol anderythropoietin are also synthesized by the kidney.

The active form of vitamin D is synthesized in thekidney after the inactive direct precursor 25-hydroxycholecalciferol, 25(OH)D3) is hydroxylatedin the liver.

Erythropoietin (EPO) is a glycoprotein synthesizedin the kidneys that stimulates erythropoiesis inthe bone marrow.


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Most commonly, kidney function is measured bythe glomerular filtration rate (GFR) measurethe rate at which substances are cleared from the

plasma by the glomeruli.

The normal GFR is 135200 liters per day. Of thislarge volume, 98% to 99% of filtrate is reabsorbed

with urine output, usually averaging 12 liters perday.

The GFR is used to evaluate kidney health,estimate the severity of diagnosed disease, and

monitor kidney disease progression.

Laboratory Evaluation of Kidney Function


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The two equations most frequently cited are the

Modification of Diet in Renal Disease (MDRD)

equation andthe Cockcroft-Gault equation.The Cockcroft-Gault equation:

GFR = [(140 - age) x body weight (kg) x 0.85 if female]

72 x serum creatinine (mg/dL)]

Modification of Diet in Renal Disease (MDRD) equation:

GFR = 170 x serum creatinine x age x (0.762 if female) x

(1.20 if black race) x BUN x serum albumin


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The clinical definition of CKD includes a long-term reduction in GFR, decreased creatinineclearance, and a corresponding increase inserum creatinine concentration.

Other biochemical assessments : tubularfunction tests, microscopic evaluation of theurine , radiological evaluation (intravenous

pyelogram (IVP), renal ultrasonography, renalradionuclide imaging, computing tomography,MRI, renal arteriogram), and biopsy of theorgan.

Chronic Kidney Disease


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Signs and symptoms associated withinadequate kidney function to perform thenormal homeostatic control.

Advanced impairment of kidney functionresults in edema, metabolic acidosis,

hyperkalemia, anemia, uremia, azotemia,hyperphosphatemia, oliguria, hypertension,and bone and mineral disorders.

Pathophysiology Overview


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CKD Response to Low Serum Calcium

and/or High Phosphorus


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Chronickidney disease (CKD) is a syndrome ofprogressive and irreversible loss of theexcretory, endocrine, and metabolic functions

of the kidney secondary to kidney damage.

CKD progresses slowly over time, and there

may be intervals during kidney functions

remain stable.

Chronic Kidney Disease

Definition and Medical Diagnosis


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The onset of renal failure is not usually

apparent until 50% to 70% of renal function

is lost.

The National Kidney Disease Education

Program (NKDEP) has defined CKD as

having a GFR of less than 60 mL/min/1.73

m2 for 3 months or longer and/or

albuminuria of more than 30 mg of urinaryalbumin per gram of urinary creatinine


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NKDEP describes 5 stages of CKD :

- Stage 1 : kidney damage with normal or increased

GFR . GFR 90 mL/min/1.73 m2

- Stage 2 : kidney damage with mild decrease in GFR .

GFR: 6089 mL/min/1.73 m2

- Stage 3 : a moderate decrease in GFR.

GFR: 3059 mL/min/1.73 m2

- Stage 4 : a severe decrease in GFR.

GFR: 1529 mL/min/1.73 m2.

- Stage 5 : kidney function is inadequate to sustain life

and requires initiation of renal replacement

therapy. GFR: 15mL/min/1.73 m2.


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CKD is a growing health concern.

The incidence of CKD is very high among the U.S. adultpopulation.

An estimated 11.5% of adults ages 20 or older have

evidence of CKD (The National Health and NutritionExamination Survey)

The incidence of CKD is even higher among patients withdiabetes mellitus, cardiovascular disease, andhypertension.

19902000: the number of persons with kidney failurerequiring dialysis or transplantation more than doubled

2006: > 500,000 individuals in the U S were receivingdialysis.

Epidemiology


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Diabetes, hypertension, and glomerulonephritis arethe leading causes of kidney failure.

The following additional causes and risk factors :

EthnicityAfrican-Americans 4x white Americans

Native Americans 2x white AmericansHispanic Americans 2x non-Hispanic

whites

Family history .

Hereditary factors such as polycystic kidney disease (PKD)

A direct and forceful blow to the kidneys.

Prolonged consumption of over-the-counter painkillersthat combine aspirin, acetaminophen, and other

medicines such as ibuprofen.

Etiology


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How Does Diabetes Lead to CKD?

Diabetic nephropathy is the most common cause of CKD inUS. People with either type 1 or 2 diabetes are at increased

risk. The risk is greater if blood sugars are not controlled. The earliest detectable change in the course of diabetic

nephropathy is a thickening in the glomerulus.

Increasing numbers of glomeruli are destroyed andincreasing amounts of albumin are excreted, can be

detected by a urinalysis. As the number of functioningnephrons declines, each remaining nephron must clear anincreasing solute load.

Eventually, the limit to the amount of solute that can becleared is achieved and the concentration in body fluids

increases, leading to azotemia and uremia. Because the progression is slow (microalbuminuria can

continue up to 510 years before other symptomsdevelop), the body can partially adapt to the changes.


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The goal of medical and nutritional management of kidneydisease is to treat the underlying renal pathophysiology inorder to delay the progression of the disease.

Medical and nutritional care correlates with the level ofkidney dysfunction.

Progression of the disease is highly individualized, and manypatients may remain at these initial stages for months toyears.

When CKD progresses to end-stage renal disease (ESRD orCKD stage 5) and harmful wastes build up in the blood, bloodpressure rises, and excess fl uid is retained, more extensive

treatment is needed to replace the work of the kidneys. Treatment options include hemodialysis, peritoneal dialysis,

and kidney transplantation.

Treatment


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Dialysis

Dialysis is a renal replacement procedure that removes excessiveand toxic by-products of metabolism from the blood, thus replacingthe filtering function of healthy kidneys.

It can maintain life once CKD progresses to the end stage, eventhough endocrine and metabolic functions of the kidney are nottotally replaced.

The decision to initiate dialysis depends on the severity ofsymptoms.

Symptoms considered to be definite indications for dialysis therapy

include pericarditis, uncontrollable fluid overload, pulmonary

edema, uncontrollable and repeated hyperkalemia, coma, and

lethargy. Less severe symptoms such as azotemia, nausea, and vomiting

require a subjective determination that takes into consideration thepatientsquality of life.


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Currently two major types of renal replacementtherapy are used for patients with CKD Stage 5:

hemodialysis (HD) and peritoneal dialysis (PD).The most common method is hemodialysis.

Selection the type of dialysis based on severalfactors, including underlying kidney disease and

other comorbid factors such as cardiovasculardisease, age, family support, and proximity to adialysis center.

Regardless of the modality, both methods requirea selective semipermeable membrane that allowspassage of water and small-to middle-molecularweight molecules and ions but excludes large-

molecular weight molecules such as proteins.


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The selective membrane is a man-made dialyzer sometimesreferred to as an artificial kidney.

The most common types are the hollow fiber and parallel-plate dialyzers.

Patients receiving hemodialysis first need to undergo a

procedure that allows continual access to the bloodstream. The preferred permanent access site is an arteriovenous

fistula (AVF), created surgically by fashioning in the forearmsubcutaneous joining of the radial artery and the cephalicvein

The AV fistula requires four to six weeks to become fullyfunctional. The subclavian route may be used temporarily ifHD is required before the AV fistula is ready for use.

Hemodialysis


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While blood passes through the dialyzer,dialysate simultaneously passes around the

artificial membrane.

Waste products and excess electrolytes fromthe blood to the dialysate via diffusion,

ultrafiltration, and osmosis. The filtered bloodthen returns to the patient through the venousside .

Hemodialysis treatments are typically

prescribed three times a week for an averageof 4 hours per treatment


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Although most hemodialysis treatments are doneat a dialysis center, home treatments can be an

option for some patients.

Daily home hemodialysis (DHHD) is conductedfive to seven days per week for two to three

hours at a time, and nocturnal homehemodialysis (NHHD) is performed three to sixnights per week during sleep.

The major advantage of home dialysis is the

ability to set ones own schedule; however, it isnecessary to have a trained partner and it mayalso be stressful to the patientsfamily.


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Example of a Hemodialysis System


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Access to the patientsblood supply is gained via a catheter ofsilicone rubber or polyurethane, placed surgically into theperitoneal cavity.

Dialysate is introduced into the peritoneum through theperitoneal catheter.

Solutes from the plasma circulating in the vessels and

capillaries perfusing the peritoneal wall pass across theperitoneal membrane into the dialysate, which issubsequently removed and discarded.

The dialysate for PD is available with a range of dextroseconcentrations that alter its osmolality and assist in fluidremoval.

The dwell time (i.e., how long the dialysate remains in theperitoneum) and the number of exchanges (i.e., how manybags of dialysate and the total volume of each used intwentyfour hours) also aff ect the amount of fl uid and soluteremoval.

Peritoneal Dialysis


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Peritoneal Dialysis


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Renal Transplantation

For an organ transplant to occur, theimmunological characteristics of the donatedorgan must be matched with the recipientsmedical and immunological characteristics.

The role of the major histocompatibility complex

(MHC) in determining acceptability for atransplanted organ was discussed.

MHC antigens play an important role intransplant rejection.

The immune system attacks the transplanted cellspresenting MHC antigens that are different fromthose found on the recipientstissues.


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A national databaseUnited Network for

Organ Sharingprovides the information andcoordination that allow the recipient to bematched with a potential donor.

After transplantation, patients are maintainedon a variety of immunosuppressive regimensto prevent rejection of the donated kidney.Immunosuppressive medications include

corticosteroids, cyclosporine, tacrolimus,mycophenolate mofetil, and sirolimus.


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Medical nutrition therapy (MNT) is an essential componentof medical care for early, progressive, and end-stage CKD.

Malnu trition, cardiovascular disease, bone and mineraldisorders, and anemia are the most common complications

that accompany kidney disease. Each of thesecomplications requires both medical and nutritionalintervention.

Many patients with CKD also have comorbid conditionssuch as hypertension and diabetes mellitus that also

require medical nutrition therapy. Nutrition therapy for CKD can help prevent and manage

complications as well as slow progression of the diseaseand compensate for impaired renal function and/orlimitations of treatment modalities.

Nutrition Therapy for Chronic Kidney Disease


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Nutrition Assessment

Malnutrition is very common in patients with CKD, especiallythose who are on dialysis. Evidence suggests that theprevalence of protein-energy malnutrition (PEM) ranges fromapproximately 20% to 70% among adult dialysis patients.

Signs and symptoms of malnutrition present when the GFR

declines to 30 mL/minute, and may progress to significantmalnutrition at a GFR of 10 mL/minute.

it is extremely important to evaluate the many complexfactors that contribute to poor nutritional status in patientswith CKD as part of a comprehensive nutrition assessment.

The dietary restrictions associated with CKD add to thepotential for inadequate nutrient intake. It is especiallyimportant to assess for usual dietary patterns and food intake,intolerance of specific foods, nutrient restrictions of the diet,and fear of eating wrongfoods.


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In summary, a nutrition assessment of the CKD patient should include:

Review of the medical record for comorbid conditions, drug/nutrient

interactions, or potential issues with digestion and absorption of

nutrients.

Nutrition interview for usual food/nutrient intake as well as changes in

appetite, changes in food intake with the onset/ progression of CKD, and

changes in elimination (urine output and stool).

Interview to evaluate social barriers to adequate nutritionalintake.

Physical assessment, including height, weight, frame size, subjective

global assessment and physical signs/symptoms of nutrient deficits

Review of biochemical/laboratory indices that might be affected by CKDAssessment of current food intakekcalories, protein, fat, sodium,

potassium, calcium, phosphorus, fluid, vitamins, and minerals.


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Nutrition Diagnosis

Given the complexity of nutrition implications associatedwith CKD, many nutrition diagnoses may be present.

The following is a list of possible nutrition diagnoses forpatients with CKD:

Inadequate energy intake

Inadequate oral/food beverage intake

Excessive fluid intake

Malnutrition

Excessive protein intake

Excessive mineral intake (potassium, phosphorus,sodium) Altered GI function

Altered nutrition-related laboratory values


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Food-medication interaction

Involuntary weight loss Involuntary weight gain

Food and nutrition-related knowledge deficit

Disordered eating pattern

Limited adherence to nutrition-related

recommendations

Undesirable food choices

Impaired ability to prepare foods/meals

Poor nutrition quality of life

Limited access to food


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Nutrition Intervention

CKD is not a static medical condition. Disease

progresses through a series of stages.

The nutrition goals and intervention therefore

need to be individualized based on the stages

of CKD, and overall health status of thepatient.

Nutrient recommendations frequently

provided for patients receiving renalreplacement therapies (dialysis or

transplantation).


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CKD Stages 1 and 2

Specific nutrition goals for stages 1 and 2 have notbeen identified, however nutrition therapy should

focus on the comorbid conditionsdiabetes,hypertension, and hyperlipidemiaand on slowing theprogression of potential cardiovascular disease.

Glucose control, blood pressure reduction, and lipid

management . Nutrition counseling recommendations include regular

assessment (at 13 month intervals) of the patientsnutritional status.

Interventions that maintain or improve nutritionalstatus during the progression of kidney disease areassociated with improved patient survival.


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CKD Stages 3 and 4

The KDOQIclinical practice guidelines specifically foradults with CKD who are not on dialysis (Stage 4).These guidelines outline recommended: nutritionmeasures, protein intake, energy requirements, andnutrition counseling.

Nutrition measures identified for individuals with GFR


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Recommendations for nutrition intervention for patientswith CKD (GFR


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The ability of the kidney to excrete metabolic

products of protein, regulate acid/basebalance, produce adequate amounts of

erythropoietin, activate vitamin D, and

regulate calcium, phosphorus, potassium,

sodium, and fluid excretion diminishes

modifications in calcium, phosphorus,

vitamins, minerals, and fluid are frequently

necessary.


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CKD Stage 5

The goals of nutrition therapy :

prevent malnutrition

minimize uremia and associated CKD complications(cardiovascular disease, anemia, secondaryhyperparathyroidism)

maintain blood pressure and fl uid status.

In general, the hemodialysis diet is high in protein andcontrols intake of potassium, phosphorus, fluids, and sodium.

Based on nutritional requirements, additional modifi cationsmay be needed for fat, cholesterol, and triglycerides.

Patients receiving peritoneal dialysis have a more liberalizeddiet than hemodialysis patientsthis diet is higher in protein,sodium, potassium (due to increased losses during the dialysisprocess), and fluid, but it is still limited in phosphorus.


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Nutrient Recommendations for CKD


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PROTEIN

Factors relating to higher protein requirements include:

(1) losses of approximately 10 to 12 grams free amino acids per day

and 5 to 15 grams per day of albumin

(2) altered albumin turnover

(3) metabolic acidosis, which increases amino acid degradation

(4) inflammation

(5) infection. The NKF K/DOQI guidelines on nutrition 1.2 grams of protein/kg

body weight for HD patients to ensure adequate intake of essentialamino acids.

At least 50% of the protein should be of high biological value.

The protein requirements for PD are slightly higher than for HD.During episodes of peritonitis (inflammation of the peritoneum), evenin mild cases, the dialysate protein losses increase by 50% to 100% toan average of 15 to 36 g/24 hours and have been reported to remainelevated for several weeks.


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ENERGY

Adequate energy intake is important in order to

prevent catabolism and achieve optimal nutritionalstatus. Sufficient kcal from carbohydrates and fat mayhelp to prevent muscle and visceral protein from beingutilized as energy.

The energy recommendation from the K/DOQI

Nutrition Guidelines is based on the finding that energyexpenditure is similar to or slightly higher than that ofhealthy persons .

A lower caloric requirement has been shown to beadequate for older persons who are more sedentary.Caloric requirements should be adjusted accordinglyfor those with higher activity levels, those who areunderweight and those who display catabolic stress.

There are adjusted edema-free body weight for


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There are adjusted edema free body weight for

Obese and Underweight patients to be used

when calculating protein and energy requirements

for underweight and obese patients.


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FAT

In general, patients on HD and PD are at increasedrisk for CAD (coronary artery disease) and stroke.

Hemodialysis patients typically display normallow-density lipoprotein (LDL) cholesterol, lowhigh-density lipoprotein (HDL) cholesterol, and

elevated triglyceride levels. PD patients exhibit higher total serum cholesterol

levels as well as LDL levels. Triglyceride levels areespecially increased in PD patients due to the

absorption of glucose in the dialysate. It is recommended that both PD and HD patients

adhere to the nutrient composition guidelines ofthe therapeutic lifestyle changes (TLC) diet.


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Therapeutic Lifestyle Changes for

Patients with CKD


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POTASSIUM

The potassium restriction for HD and PD patients

varies, depending on the degree of kidney function,serum potassium levels, modality, and drug therapy.

For the most part, a diet that allows 50 to 70 mmol/dayor approximately 2 to 3 g/day of potassium iscommonly prescribed in HD.

Those who are oliguric or anuric are at an increasedrisk for hyperkalemia and should have a more stringentdietary restriction.

The target range for serum potassium is 3.56.0 mEq/L. Severe hyperkalemia (serum K greater than 7.0 mEq/L)

may precipitate fatal arrhythmias.


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FLUID AND SODIUM

Fluid and sodium allowances are highly individualized andbased primarily on residual urine output and dialysis modality.

Other considerations include blood pressure control,interdialytic weight gains in HD patients, presence of edema,and congestive heart failure.

The interdialytic weight gain goal in HD patients should notexceed 5% of body weight.

Higher fluid gains can lead to sudden changes in blood volumeand hypotension during the hemodialysis treatment.

If patients become oliguric or anuric within the first 12months of hemodialysis 2 gram sodium diet with a fluidallowance of not more than 1 L (1000 mL) daily.

If urine output is greater than 1 L per day, the sodium and fluid allowance can be liberalized to approximately 2 to 4 gsodium per day and 2 L (2000 mL) of fluid per day.


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Fluid and sodium requirements for patients onPD therapy are highly individualized and

largely based on ultrafiltration.

Ultrafiltration can remove 2 to 2.5 kg of fluidper day.

Fluid and sodium restriction for the PD patientincludes a fluid allowance of 2 L per day and asodium allowance between 2 and 4 g per day.

Fluid overload

shortness of breath,hypertension, congestive heart failure, andedema.


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PHOSPHORUS

In early CKD hyperphosphatemia is preventedby an adaptive increase in renal excretion and

decreased phosphate reabsorption.

If the GFR : 20 - 30 mL/min/1.73 m2 Hyperphosphatemia.

Phosphorus restriction of 8001000 mg/day

or


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CALCIUM

Dietary calcium requirements are higher in CKD.

Low serum calcium levels often accompany CKDdue to alterations in vitamin D metabolism,decreased absorption of calcium from the gut,and elevated phosphorus levels.

Foods high in calcium are restricted, because theytend to be high in phosphorus as well.

Calcium supplements should be taken on empty

stomachbetween meals or at bedtime) . The amount of calcium from the diet plus the

amount found in supplements should not exceed2,000 mg per day.


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VITAMIN SUPPLEMENTATION

Supplementation of water-soluble vitamins due toincreased losses during dialysis,

anorexia, and poor dietary intake is typically indicatedfor HD and PD patients.

In general, the renal vitamin contains B vitamins,folic acid, and vitamin C.

Fat-soluble vitamins and minerals are not included.Preparations containing vitamin A or high doses ofvitamin C should be avoided.

Serum levels of B1 (thiamin), B2 (ribofl avin),pantothenic acid, and biotin are typically normal.

Biotin supplementation of 10 mg/day has been foundto be helpful in treating patients with peripheralneuropathy, encephalopathy, and intractable hiccups.


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Vitamin C should be limited to no more than 100mg per day.

serum vitamin A levels are elevated in HD and PDpatientssupplementation is not necessary.

Very little is known about the long-term effects ofvitamin E

Vitamin K supplementation may be needed forthose patients receiving antibiotic therapy, sincethe antibiotics may destroy the bacteria found inthe gastrointestinal tract (these bacteria are aprimary source of vitamin K).

Most HD patients receive anti-coagulationtherapy caution must be taken due to vitaminKsrole in promoting clot formation.


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MINERAL SUPPLEMENTATION

Magnesium is excreted by the kidneys.

magnesium levels are usually normal to mildly elevated indialysis patients and not generally supplemented.

Iron deficiency is common , due to the kidneys inability tomake adequate erythropoietin for production of red bloodcells

Most patients will require iron supplementation, which isindividualized depending on serum markers of ferritin, iron,total iron binding capacity, and transferrin saturation.

Some studies have indicated that impaired taste sensation,

loss of appetite, and sexual dysfunction may beameliorated with zinc supplementation.

The allowance for zinc is the same as the RDA: 15 mg perday.


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Nutritional Requirements of the Posttransplant Patient

The goal in the acute posttransplant period is :- to manage the increased metabolic demands of

transplant surgery, obesity, blood pressure, insulin

resistance, diabetes, and hyperlipidemia

- maintenance of electrolyte balance

- maximized bone health.

Nutrition therapy for kidney transplant patients

differs between the acute phase (up to 8 weeksfollowing transplant) and the chronic phase(beginning the ninth week following transplant).


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Monitoring and Evaluation


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Monitoring and Evaluation

Outcome measures for MNT in the CKD population can be

classified as clinical or patient behavioral outcomes see

table


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Definition:

ARF is a disorder characterized by abrupt cessation or reduction inGFR an accumulation of nitrogenous wastes.

Epidemiology

The prevalence of ARF is estimated at 1% for all hospitalizedpatients, 3% to 5% for general medical-surgical patients, 5% to 25%for those in intensive care units, 5% to 20% for open-heart surgery

patients, 20% to 60% for those with severe burns. Death occurs in 40% of nonsurgical patients with severe ARF, 80%

of surgical patients is associated with the degree ofhypercatabolism and infection.

Acute Renal Failure.


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Etiology

The three major types of acute renal failure are : prerenal azotemia,

intrinsic and obstructive. Prerenal azotemia :

reduce perfusion to the kidney ( ex: severe dehydration, circulatorycollapse, fluid losses from the GI tract or from extensive woundssuch as seen in burns).

Acute tubular necrosis (ATN) is the ischemia damages epithelial

cells, causing necrosis of the kidney , potentially irreversible renalfailure.

Intrinsic ARF :

refers to damage to the anatomical structure of the kidney occurafter exposure to toxins such as antibiotics, chemotherapy, orcontrast dyes used in various imaging tests, infection such asglomerulonephritis

Obstructive failure results from a blockage of the ureter or neck of thebladder could result in obstruction include kidney stones, bloodclots, or a tumor.

Pathophysiology


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Pathophysiology

In prerenal ARF the lack of blood flow to

kidneys reduction the filtrate pressure in theglomerulus uremic symptoms.

If blood flow is not restored necrosis of thecells .

Liu (2010)4 phases of ARF:1. Initiation (when GFR declines)

2. Extension (when ischemia and inflammatorydamage continue)

3. Maintenance (when GFR is at its lowest level)

4. Recovery (when epithelial cells regenerate).


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Clinical Manifestations

Normal urine output: 1 to 1.5 L per day.

GFR declines and reaches its lowest level: ARF

patients

may produce


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Decreased levels of serum potassium,magnesium, and phosphorus may also occur asa result of intracellular shifts associated withcarbohydrate delivery and anabolism.

Hypophosphatemia also occurs in the refeedingsyndrome, malnutrition, and diuretic therapy.

Serum levels of potassium, magnesium, and

phosphorus should be monitored frequentlyto assess the need for additionalsupplementation.

Nitrogen (BUN) and creatinine are elevated in ARF


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Nitrogen (BUN) and creatinine are elevated in ARF,

although the ratio of BUN to creatinine may be

normal (10:1 or higher).

Insufficient dietary kcal and protein and altered

blood levels of proteases contribute to high levels of

protein catabolism.

Dialysis may be required to remove metabolic wastesand excess water.

When recovery of renal function is expected to take

several weeks, or when wasting is severe, aggressive

dialysis is often recommended.

Medical and nutrition management typically aim to

maintain BUN in the range of 80 to 100 mg/dL.


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Treatment

Treatment options and nutrition support should bebased on ;

- the underlying cause of renal failure,

- the specific metabolic changes within each patient,

- other complications associated with the illness. Generally, continuous renal replacement therapy

(CRRT) is the mode of treatment for an individual withARF.

CRRT is the term for several different modes ofproviding dialysis over a continuous period that allowfor a significant amount of fluid (12 L/hour) to beremoved.


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Nutrition Therapy for Acute Renal Failure

It is common for the nutritional status of patients

with ARF to decline within a short period of time,owing to :nitrogen losses (up to 30 g per day), which lead to loss

of lean body mass;

toxicity-related symptoms (anorexia, nausea,vomiting, bleeding);

loss of essential and nonessential amino acids

loss of plasma proteins during intervention dialysistherapy;

metabolic disturbances (impaired glucose utilizationand protein synthesis) from uremia. Energy andprotein

malnutrition


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Energy and protein intake should meet the patients

requirementsdepends on the patients nutritional status,catabolic rate, residual GFR, and medical and/or surgicalinterventions (e.g., type of dialysis therapy).

Protein, amino acids, and energy substrates may not beutilized efficientlydifficult to maintain or improve the

nutrition status of these patients by enteral or parenteralsupport.

When feasible, patients with ARF should receive oralnutrition.

If a patient cannot eat adequately, other forms of nutrition

support should be pursued. Enteral nutrition support with standard formulations should

be considered first for patients with ARF. If necessary, specificformulas with lower electrolytes can be considered.


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General recommendations f or protein are 0.6(no dialysis) to 1.4 (dialyzed) g/kg/d.

Adequate kcal should also be provided (30 to 35kcal/kg/d).

Protein sources containing both essential andnonessential amino acids should be provided.

The patients nutrition and metabolic status andthe renal diagnosis determine the exact dose.

For patients receiving acute hemodialysis, the

recommendation is 1.2 to 1.4 g/kg of protein. For those on CRRT, protein requirements should

be estimated at 1.5 to 2.0 g/kg.

Traditional recommendations indicate that when


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Traditional recommendations indicate that whenenergy requirements cannot be measured by indirectcalorimetry, can be estimated using 25 to 35kcal/kg.

ASPEN guidelines: In all ICU patients receiving PN,mild underfeeding should be considered at leastinitially.

After energy requirements are determined, 80% of

these requirements should serve. The total fluid intake depends on the amount of

residual renal function (i.e., whether the patient isoliguric or anuric) and f uid and sodium status.

Fluid intake can be calculated by adding 500 mL (forinsensible losses) to the 24-hour urine output.

Fluid and mineral balance need to be carefullymonitored in ARF to prevent over hydration andelectrolyte disorders.


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Total fluid input is recommended to equal output from

urine and all other measured sources (e.g., nasogastricaspirate or fistula drainage) plus 400 to 500 mL per day.

If the patient is catabolic weight can be allowed to dropby 0.2 to 0.5 kg per day to avoid excessiveaccumulation of fluid.

Records of daily intake and output, weight changes,serum electrolyte levels, and blood pressure forassessment of fluid tolerance and requirements.

Supplementation of minerals, electrolytes, and traceelements monitoring serum and urine to preventexcess or deficiency states .


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Definition

NS is an abnormal condition that is marked by a deficiency ofalbumin in the blood and its excretion in the urine due to alteredpermeability of the glomerular basement membranes.

Epidemiology

About 2 : 10.000.

The prevalence is difficult to establish in adults because thecondition is usually a result of an underlying disease.

NS may occur at any age but is more prevalent in children than inadults.

In children it is most common between 1-4 y.o, males > females.

Nephrotic Syndrome


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Etiology

NS can occur with many diseases :

- Primary glomerular diseaseglomerular

dysfunction, including many conditions with avariety

of genetic and environmental causes.- Focal segmental glomerulosclerosis (FSGS)

- Diabetic nephropathy

- an infection/drug toxic to the kidneys.- autoimmune diseases (IgA nephropathy or

systemic lupus erythematosus(SLE)).


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Nephrotic syndrome is characterized by:

- proteinuria (urinary protein levels greater than

3.5 g per 1.73 m2 of body surface area per day),

- hyperlipidemia,- hypoalbuminemia


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Oliguria or acute renal failure may develop because of

hypovolemia (a decrease in the volume of the circulatingblood) and diminished renal perfusion.

Orthostatic hypotension and even shock can be seen inpediatric patients.

Protein losses in adults with NS average about 6 to 8 gramsper day.

Albumin is the principal protein lost in urine, accounting forbetween 75% and 90% of urinary protein.

In adults, serum albumin levels may be less than 2 g/dL.

Micronutrients lost in the urine include those bound toplasma proteins such as zinc, copper, vitamin D, and iron.


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Nephrotic syndrome has also been associated withincreased risk of atherosclerosis due to altered lipid

metabolism characterized : by cholesterol andtriglycerides , LDL , HDL N or

The reduction of lipoprotein lipase, an enzymeresponsible for lipoprotein metabolism, is thought to

be the reason for reduced clearance of these lipids. Atherogenic lipoprotein and fibrinogen levels due to

increased hepatic synthesiscardiovascular risk.

Hyperlipidemia alone can impair renal function .

Reducing lipid levels can slow down the progression ofrenal injury.

Treatment


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Treatment

Medical treatment of nephrotic syndrome focuses onidentifying and treating the underlying cause, reducing

high cholesterol, blood pressure, and protein in the urinediet and drugs

ACE therapy reduces proteinuria and slows down theprogression of CKD.

ACE inhibitor and angiotensin receptor blockers (ARBs)

therapy, including combination therapy reduceproteinuria in diabetic nephropathy and idiopathicnephritic syndrome.

Proteinuria may also be decreased by lowering thepatientsmean arterial pressure to levels below 92 mm Hg .

Potassium levels should be checked in those with moderateto severe renal dysfunction, because ACE inhibitors mayexacerbate hyperkalemia


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Nutrition Therapy for Nephrotic Syndrome

The goals:

- minimizing the effects of edema, proteinuria,

and hyperlipidemia

- replacing nutrients lost in the urine- reducing the risks of further renal progression

and atherosclerosis.


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Evaluate biochemical measures of renal function

(GFR, BUN, creatinine), acid-base balance, lipidprofile, fluid and electrolyte balance, proteinstatus, and vitamin/mineral status.

energy and protein needs should be calculated

using usual or ideal body weight, becauseanthropometrics will be skewed due to thepresence of edema.

Dietary assessment will focus on usual dietary

intake with a careful evaluation of protein,phosphorous, calcium, potassium, and sodiumconsumption .


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Nutrition Diagnosis

Include: increased nutrient needs, inadequate protein intake,excessive sodium intake, and food/nutrition knowledge defi cit


The nutrition therapy prescription components for NS aresummarized in Table .

Minimize edema include sodium restriction and diuretics.A

sodium restriction of 2000 mg or less per day Fluid intake is generally not restricted.

Current protein recommendations are 0.8 to 1.0 g/kg/day.Thislevel of intake is believed to decrease proteinuria without reducingserum albumin.

Several studies have suggested that soy protein or flaxseed-basedproteins may be more beneficial than high-quality proteins inreducing proteinuria, lowering lipid levels, and slowing down theprogression of renal .

There are no long-term studies to suggest the safety of low-proteindiets that provide less than 0.8 g/kg/day.

Nephrolithiasis


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Definition

Kidney stones (renal lithiasis or nephrolithiasis) form as a result ofabnormal crystallization of calcium, oxalate, struvite, cystine,hydroxyapatite, or uric acid that is unable to be excreted normally in theurine.

Epidemiology

Nephrolithiasis affects almost one million individuals in the United Stateseach year.

men > women , varies depending on ethnicity and geographic region.

Ages : 20 - 30 years.77

Risk factors for kidney stones include family history, certain medical

conditions (hypercalciuria, hyperuricosuria, hyperoxaluria); and low urinevolume.

Hypercalciuria is the cause of more than 50% of all kidney stones.

Other causes of kidney stones include gout, excess intake of vitamin D,urinary tract infections and urinary tract blockages.

Nephrolithiasis

Pathophysiology


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p y gy

Kidney stones generally consist of calcium salts,

cystine, uric acid, or struvite (a combination ofmagnesium, ammonium, and phosphate).

Generally, the development of kidney stones isnot directly related to any one cause.

Multiple factors may contribute .

Kidney stones typically do not cause anysymptoms until a stone acutely blocks urine flow.

The pain will migrate depending on the location ofthe stone.

Other symptoms : hematuria, nausea ,vomiting,pain with urination, and an urgency to urinate.

T t t


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Treatment

Depends on whether or not the patient can

pass the stone on his or her own.

Although most patients can pass the stone

with plenty of fluids and pain medication,

hospitalization may be required in some casesif the pain is severe.

If the patient cannot pass the stone, there are

several procedures available: extracorporealshockwave lithotripsy (ESWL), percutaneous

nephrolithotomy, and ureterorenoscopy.

Nutrition Therapy for Nephrolithiasis

N t iti th i t ith i i i i th f t


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Nutrition therapy can assist with minimizing the factorsthat may contribute to kidney stone formation.

A complete analysis of the stone composition is necessary

for the development of appropriate nutrition interventions.


Dietary assessment should focus on nutrient intake that

may affect the development of a specifi c stone composition.

Assessment of fluid intake is also a critical factor indevelopment of

appropriate nutrition prescriptions and interventions.

Nutrition Diagnosis

Include : excessive mineral intake, inadequate fluid intake,or food and nutrition-related knowledge deficit.



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The objectives of nutrition therapy are tominimize the supersaturation of urinarycomponents associated with the formation ofstones and to prevent stones from recurring.

The most effective preventative treatment isto increase fluid intake by 3 L per dayshould be taken in divided doses, throughout

the day and night -- > will ensure a minimumurine output of 2 L/day.


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a diet low in calcium would help prevent the

formation of calcium stones. However, it has

now been demonstrated that foods high in

calcium, including dairy products, can actually

prevent the formation of stones.

A possible explanation for this is that a

reduction in dietary calcium aids in the

intestinal absorption of oxalate, thus

increasing urinary super-saturation of calcium The goal with minimizing oxalate intake is to

decrease the bioavailability of oxalate.


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The following foods should be avoided : beets,chocolate, cola, coffee/tea, nuts/nut butters,

berries, wheat bran, spinach, and rhubarb. Avoidance of greater than 2 grams of vitamin C

should also be advised.

For stones that are composed of uric acid,avoidance of foods high in purine isrecommended.

Foods high in purine include: animal protein,

seafood, meat extracts, consomme, gravies andorgan meats.

Kidney Disease, Tugas Prof Fat

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