chapter 021

Williams' Basic Nutrition & Diet Therapy

Chapter 21Kidney Disease

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14th Edition

Lesson 21.1: Kidney Anatomy, Physiology, and Disease

Kidney disease interferes with the normal capacity of nephrons to filter waste products of metabolism.

Short-term kidney disease requires basic nutrition support for healing rather than dietary restriction.

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Introduction (p. 425)

100,000 Americans diagnosed with end-stage renal disease each year

84,000 die per year Reduced kidney function often undiagnosed Requires extensive medical nutrition therapy Dialysis extends lives but carries high costs

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Basic Structure and Function of the Kidneys (p. 425)

Kidneys filter about 1.2 L of fluid per minute Structures

Nephron• Glomurulus: cluster of capillaries filters the blood• Tubules: carries filtered fluid to kidney medulla

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Basic Structure and Function of the Kidneys (cont’d) (p. 427)

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Tubules (p. 426)

Proximal tubule: reabsorbs needed nutrients and returns them to blood

Loop of Henle: exchanges sodium, chloride, water Distal tubule: secretes hydrogen ions as needed Collecting tubule: produces concentrated urine

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Function (p. 427)

Excretory and regulatory functions Filtration: removes most particles from blood

except proteins and RBCs Reabsorption: substances body needs are

reabsorbed and returned to blood Secretion: additional hydrogen ions secreted as

needed to maintain acid-base balance Excretion: waste materials excreted in

concentrated urine

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Endocrine Functions (p. 428)

Renin secretion: maintains hormonal control of body water balance

Erythropoietin secretion: stimulate RBC production within bone marrow

Vitamin D activation: converts inactive form to final active vitamin D

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Disease Process and Dietary Considerations (p. 428)

General causes of kidney disease Infection and obstruction: bladder infections,

kidney stones Damage from other diseases: diabetes mellitus,

hypertension Toxins: environmental agents, animal venom,

certain plants, heavy metals, drugs Genetic or congenital defects: cystic diseases,

congenital abnormalities

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General Causes of Kidney Disease (p. 428)

Risk factors Diabetes, hypertension, CVD Older than 60, smoke, obese Family history of kidney disease

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Case Study

Mrs. Hendricks is a 65-year-old female who has poor glycemic control with her Type 2 diabetes of 32 years, hypertension, and smokes 1 pack of cigarettes per day.  Her most recent glomerular filtration rate is 22 mL/min.

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Case Study (cont’d)

What are Mrs. Hendrick’s risk factors for chronic kidney disease (CKD)?

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Case Study (cont’d)

What clinical assessment parameters would be useful to find out from Mrs. Hendricks?

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Medical Nutrition Therapy in Kidney Disease (p. 429)

Based on the nature of the disease process and individual responses Length of disease: acute or chronic

• Long term: more specific nutrient modifications Degree of impaired renal function

• Extensive: extensive nutrition therapy required Individual clinical symptoms

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Nephron Diseases (p. 429)

Acute glomerulonephritis or nephritic syndrome Disease process: affects glomeruli Clinical symptoms: hematuria, proteinuria,

possible edema, mild hypertension Medical nutrition therapy: diet modifications

usually not crucial

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Nephrotic Syndrome (Nephrosis) (p. 430)

Disease process: nephron tissue damage allows protein to pass into tubule

Clinical symptoms: hypoalbuminemia, edema, ascites, distended abdomen, reduced plasma protein level

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Nephrotic Syndrome (Nephrosis) (cont’d) (p. 430)

Medical nutrition therapy: Protein: moderate Energy: adequate to support nutrition status Sodium, potassium: restricted and monitored Calcium, phosphorus: 1 to 1.5 g/day calcium,

maximum 12 mg/day phosphorus Fluid: restricted according to output and losses

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Lesson 21.2: Treatment of Kidney Disease

The progressive degeneration of chronic kidney disease requires dialysis treatment and nutrient modification according to individual disease status.

Current therapy for kidney stones depends more on basic nutrition and health support for medical treatment than on major food and nutrient restrictions.

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Kidney Failure (p. 431)

Acute kidney injury Disease process

• Prerenal: inadequate blood flow to kidneys and subsequent reduced GFR

• Intrinsic: damage to a part of the kidney• Postrenal obstruction: obstruction of urine flow

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Acute Kidney Injury (p. 431)

Clinical symptoms: RIFLE classification system assesses severity of: Risk Injury Failure Loss End-stage kidney disease

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Acute Kidney Injury (cont’d)(p. 431)

Medical nutrition therapy Basic objective: improve or maintain nutrition

status Principle: prevent protein catabolism, electrolyte

and hydration disturbance, acidosis, uremic toxicity

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Chronic Kidney Disease (CKD) (p. 432)

Disease process: Progressive breakdown of kidney tissue Most often results from

• Primary glomerular disease• Metabolic diseases with kidney involvement• Inherited diseases• Other causes: immune diseases, obstruction, infection,

hypertension

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Clinical Symptoms (p. 433)

Water balance: large amounts of dilute urine Electrolyte balance: metabolic acidosis Nitrogen retention Anemia Hypertension Azotemia

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General Signs and Symptoms(p. 433)

Progressive weakness Shortness of breath General lethargy Fatigue Possible thirst, anorexia, weight loss, diarrhea,

vomiting

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Medical Nutrition Therapy(p. 433)

Basic objectives: monitor at regular intervals Principles

Protein: generally limited to .0 to 0.8 g/kg body weight Energy: 35 kcal/day for those under 60 with GFR less than

25 ml/min Sodium/potassium: may be restricted Phosphorus/calcium: phosphorus may be restricted, calcium

1.0 to 1.5 g/day Vitamins/minerals: help patients meet needs for B-complex

vitamins and vitamin C Fluid: intake balanced with output

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Case Study (cont’d)

Mrs. Hendricks is in what stage of chronic kidney disease?

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Case Study (cont’d)

Outline appropriate medical nutrition therapy plan of care for Mrs. Hendricks.

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End-Stage Renal Disease(p. 434)

Disease process Patient, family, physician face life-support

decisions Irreversible damage to majority of nephrons Options are long-term dialysis for kidney

transplant

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Hemodialysis (p. 434)

Artificial kidney machine removes toxins and restores metabolites and nutrients

Three to six treatments per week Medical nutrition therapy

Protein: major concern of patients on dialysis Energy: 35 kcal/day for patients <60 years Sodium/potassium: may be restricted Phosphorus/calcium: monitored and limited Vitamins/minerals: achieve the DRI

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Peritoneal Dialysis (p. 437)

About 6% of patients Exchange of fluids occurs within the body,

allows mobility Medical nutrition therapy

Protein: increased slightly Energy: maintain lean body weight Sodium/potassium: intake slightly more liberal Phosphorus/calcium, vitamins/minerals: same as

for hemodialysis

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Peritoneal Dialysis (cont’d)(p. 437)

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Transplantation (p. 438)

Improves quality of life and survival More cost effective than maintenance dialysis Waiting lists can be long Donor matches difficult to find

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Transplantation (cont’d) (p. 439)

Transplantation Complications: bone disorders, malnutrition,

anemia, hormonal and blood pressure imbalances, depression, reduced quality of life

Nutrition support: enteral or parenteral feedings customized to dialysis

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Transplantation (cont’d) (p. 439)

Osteodystrophy Bone disease and disorders common with CKD Decreased activation of vitamin D has cascade

effect Neuropathy

Central and peripheral disturbances common at initiation of dialysis

Patients should be periodically assessed

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Kidney Stone Disease (p. 442)

Basic cause is unknown Factors relating to urine or urinary tract

environment contribute to formation Present in 5% of U.S. women and 12% of

U.S. men Major stones are formed from one of three

substances: Calcium Struvite Uric acid

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Calcium Stones (p. 442)

Most common type: 80% of cases High levels of urinary oxalate Long-term megadosing of vitamin C Dietary calcium intake inversely related to stones

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Struvite Stones (p. 442)

10% of all stones Caused primarily by urinary tract infection No diet therapy Usually surgically removed

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Uric Acid Stones (p. 443)

Caused by impairment of purine metabolism with some diseases

Account for 9% of stones Other stones

Due to inherited disorders or complications of medications

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Clinical Symptoms and Medical Nutrition Therapy (p. 443)

Clinical symptoms Severe pain Urinary symptoms Weakness, fever

Medical nutrition therapy Protein: no more than DRI Calcium: normal calcium intake Sodium: no more than 2300 to 3450 mg/day Oxalates: avoid Vitamins/minerals: limit to DRI Fluid: high intake

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Objectives Specific to Type of Stone (p. 444)

Calcium stones: reduce dietary intake of stone constituents, consider fiber intake

Uric acid stones: raise urinary pH, maintain healthy weight, limit animal protein

Cystine stones: reduce intake of cystine and dilute urine

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