chapter 22 nutrition and renal diseases

Nutrition and Renal Diseases

2222

Copyright © 2017 Cengage Learning. All Rights Reserved.

© Cengage Learning 2017

Introduction

• Kidneys– Filter the blood and remove excess fluid and

wastes for elimination in urine– Nephron: functional unit of the kidney

• Glomerulus: filters water and solutes from the blood

• Bowman’s capsule: surrounds the glomerulus; collects the filtrate that is passed to the tubules



Introduction (cont’d.)

• Kidneys– Regulate the extracellular fluid volume

• Control osmolarity, electrolyte concentrations, and acid-base balance

– Excrete metabolic waste products• Urea and creatinine; various drugs and toxins

– Secrete renin, produce erythropoietin, and convert vitamin D to active form


© Cengage Learning 2017Copyright © 2017 Cengage Learning. All Rights Reserved.

The Kidneys and Nephron Function


Nephrotic Syndrome

• Syndrome caused by significant proteinuria (>3-3.5 g/day)– Damage to glomeruli increases their

permeability to plasma proteins• Causes

– Glomerular disorders, diabetic nephropathy, immunological and hereditary diseases, infections (kidney or other), etc.



Nephrotic Syndrome (cont’d.)

• Consequences of nephrotic syndrome– Attempting to compensate, liver increases

synthesis of various plasma proteins • Some or the proteins produced in excess

– Edema• Hypoalbuminemia: contributes to a fluid shift from

blood plasma to the interstitial spaces • Impaired sodium excretion: sodium and water

retention




• Consequences of nephrotic syndrome– Blood lipid and blood clotting abnormalities

• Elevated levels of LDL, VLDL, and lipoprotein(a)• Increased risk of deep vein thrombosis

– Other effects of nephrotic syndrome• Susceptibility to infection• Increased risk of rickets (children)• PEM and muscle wasting



Effects of Urinary Protein Losses in Nephrotic Syndrome




• Treatment of nephrotic syndrome– Requires diagnosis and management of the

underlying disorder– Medications for complications

• Diuretics, ACE inhibitors or angiotensin receptor blockers, lipid-lowering drugs, anti-inflammatory drugs, and immunosuppressants

– Nutrition therapy• Helps to prevent PEM, correct lipid abnormalities,

and alleviate edema



Nephrotic Syndrome: Treatment (cont’d.)

• Protein and energy– Adequate to meet needs: helps minimize

muscle tissue losses– Why are high-protein diets not advised?

• Lipids– Dietary measures usually inadequate for

controlling blood lipids– Lipid-lowering medications may be prescribed



Nephrotic Syndrome: Treatment (cont’d.)

• Sodium and potassium– Sodium restriction (1-2 g/day) helps control

edema (Table 22-1)– Foods rich in potassium encouraged

• Vitamins and minerals: supplementation– Iron and vitamin D– Calcium (1000-1500 mg/day) may be advised



Acute Kidney Injury

• Kidney function deteriorates rapidly, over hours or days– Reduced urine output and build-up of

nitrogenous wastes in blood• Causes of acute kidney injury

– Often a consequence of critical illness, sepsis, major surgery



Acute Kidney Injury:Causes of Acute Kidney Injury (cont’d.)

• Prerenal factors: cause a severe reduction in blood flow to the kidneys– Often involve a severe stressor such as heart

failure, shock, or blood loss• Intrarenal causes: factors that damage

kidney tissue– Infections, toxicants, drugs, or direct trauma



Acute Kidney Injury:Causes of Acute Kidney Injury (cont’d.)

• Postrenal factors: prevent excretion of urine due to urinary tract obstructions



Acute Kidney Injury (cont’d.)

• Consequences of acute kidney injury– Altered composition of blood and urine

• Kidneys unable to regulate levels of electrolytes, acid, and nitrogenous wastes in the blood

• Oliguria or anuria– Fluid and electrolyte imbalances

• Sodium retention and edema• Hyperkalemia: alters heart rhythm; heart failure• Hyperphosphatemia: leads to bone calcium losses




• Consequences of acute kidney injury– Uremia

• Nitrogen-containing compounds and various other waste products may accumulate in the blood

• Uremic syndrome: cluster of disorders caused by impairments in multiple body systems




• Treatment of acute kidney injury– Combination of drug therapy, dialysis, and

nutrition therapy • Restores fluid and electrolyte balances• Minimizes blood concentrations of toxic waste

products– Highly individualized– Oliguric patients may experience diuresis

during recovery



Acute Kidney Injury: Treatment of Acute Kidney Injury (cont’d.)

• Drug treatment for acute kidney injury– Why may it be necessary to lower doses of

some usual medications, while others may need to be increased?

– Nephrotoxic drugs must be avoided until kidney function improves




• Drug treatment for acute kidney injury– Drugs prescribed depend on cause of illness

and complications• Immunosuppressants: inflammatory conditions• Diuretics: edema• Potassium-exchange resins and possibly insulin:

hyperkalemia• Phosphate binders: high serum phosphorus• Bicarbonate: acidosis




• Energy and protein– Sufficient energy and protein to preserve

muscle mass, but avoid overfeeding– Protein recommendations influenced by

kidney function, degree of catabolism, and use of dialysis

– 20-35 kcal/kg/day with monitoring– 0.8-1.0 g protein/kg/day (noncatabolic)– 1.0-1.7 g/kg/day for catabolism, dialysis




• Fluids– Estimate needs: measure urine output and

add 400-500 mL for water lost from skin, lungs, and perspiration

• Electrolytes– Serum electrolyte levels monitored closely– Potassium, phosphorus, sodium restrictions

may be needed




• Enteral and parenteral nutrition– In cases requiring additional nutritional

support, why is enteral support preferred over parenteral nutrition?

• Box 22-3 presents an example case



Chronic Kidney Disease

• Gradual, irreversible deterioration• Kidneys have a large functional reserve

– Chronic disease typically progresses over many years without causing symptoms

• Most common causes– Diabetes mellitus and hypertension– What are other causes of chronic kidney

disease?



Chronic Kidney Disease (cont’d.)

• Consequences of chronic kidney disease– Early stages

• Nephrons compensate by enlarging to handle the extra workload

– End-stage renal disease• Advanced stage in which dialysis or a kidney

transplant is needed to sustain life– Many symptoms are nonspecific

• Delays diagnosis of the condition



Chronic Kidney Disease: Consequences (cont’d.)

• Assessing kidney function– Glomerular filtration rate (GFR)

• Rate at which the kidneys form filtrate• Estimated using predictive equations based on

serum creatinine levels, age, gender, ethnicity, and body size

• Categorized into stages (Table 22-4)– What other tests can assess kidney function?




• Altered electrolytes and hormones– As GFR falls, remaining nephrons increase

activity to maintain electrolyte excretion• Electrolyte disturbances may not develop until third

or fourth stage of chronic kidney disease– Hormonal adaptations to regulate electrolyte

levels create new complications• Increased aldosterone ► hypertension• Parathyroid hormone ► renal osteodystrophy




• Uremic syndrome– Hormonal imbalances

• Lead to anemia (erythropoietin), bone disease (active vitamin D), other problems

– Altered heart function/increased heart disease risk

– Neuromuscular disturbances• Malaise, irritability, sensory deficits, seizures, etc.




• Uremic syndrome– Other effects

• Defects in platelet function and clotting factors• Increased skin pigmentation and severe pruritus• Suppressed immune responses




• Protein-energy malnutrition– Anorexia: contributes to the poor food intake

• Due to hormonal disturbances, restrictive diets, uremia, depression, other illnesses

– Nutrient losses• Dialysis, blood draws, GI bleeding

– Negative nitrogen balance due to low-grade inflammation




• Treatment of chronic kidney disease– Treatment goals

• Slow disease progression• Prevent or alleviate complications

– Drug treatment for chronic kidney disease• Antihypertensive drugs• Erythropoietin (epoetin) for anemia• Others: phosphate binders, sodium bicarbonate,

and cholesterol-lowering drugs



Chronic Kidney Disease: Treatment (cont’d.)

• Dialysis: removes excess fluid and wastes from the blood– Hemodialysis: blood is circulated through a

dialyzer– Peritoneal dialysis: dialysate infused into the

peritoneal cavity, then drained• Nutrition therapy for chronic kidney

disease (Table 22-5)




• Energy– High-energy density foods if at risk for PEM– Peritoneal dialysis dialysate provides kcal

• Protein: enough to meet needs and prevent wasting– Between 0.6 and 0.75 g/kg/day in later stages– At least 50% from high-quality sources




• Lipids: restrict intakes of saturated fat, trans fat, refined sugars, and alcohol– Why are persons with chronic kidney disease

often encouraged to consume high-fat foods?• Sodium and fluids

– Mild sodium restriction may be beneficial– Fluids: not restricted until urine output

decreases– What water intake restrictions apply during

dialysis?Copyright © 2017 Cengage Learning. All Rights Reserved.



• Potassium– Stages 1-4: normal potassium intake levels– Restrictions with hyperkalemia, diabetic

nephropathy, stage 5– Potassium supplementation with potassium-

wasting diuretics– Dialysis patients must control potassium

intakes (see Table 22-6 for a guide)




• Phosphorus, calcium, and vitamin D– Serum phosphorus and calcium levels

monitored to minimize bone disease risk– Elevated phosphorus levels

• Dietary restriction, sometimes phosphate binders– What accounts for the risk of hypercalcemia?– Vitamin D supplements




• Vitamins and minerals– Multivitamin/mineral supplements typically

recommended– Limit supplemental vitamin C to 70 mg/day– Vitamin A supplements not recommended– Hemodialysis patients: intravenous iron along

with erythropoietin therapy




• Enteral and parenteral nutrition– Formulas: more kcalorically dense, lower

protein and electrolyte concentrations than standard formulas

– What is intradialytic parenteral nutrition?• Used mainly in patients with PEM who have not

responded well to oral supplements– Dietary compliance: probably the most

challenging aspect of treatment for patients




• Kidney transplants– Benefits

• Restores kidney function, allows a more liberal diet, and frees the patient from routine dialysis

– What are barriers to kidney transplants?– Immunosuppressive drug therapy

• Prevents tissue rejection following transplant surgery

• Be aware of diet-drug interactions (Box 22-8)



Chronic Kidney Disease:Kidney Transplants (cont’d.)

• Nutrition therapy after kidney transplant– Most nutrients can be consumed at levels

recommended for the general population– Primary reason for dietary adjustments: side

effects of drugs• Serum electrolyte levels monitored• Calcium supplementation recommended with

corticosteroids



Kidney Stones

• Kidney stone: crystalline mass that forms within the urinary tract

• Formation of kidney stones– Stone constituents become concentrated in

urine• Allowing crystals to form and grow

– Most common constituent: calcium oxalate• Less common: calcium phosphate, uric acid,

cystine, magnesium ammonium phosphate



Kidney Stones:Formation of Kidney Stones (cont’d.)

• Factors predisposing an individual to stone formation:– Dehydration or low urine volume– Changes in urine acidity– Metabolic abnormalities– Obstruction




• Calcium oxalate stones– Hypercalciuria is most common abnormality– Hyperoxaluria also promotes formation

• Uric acid stones– Urine is abnormally acidic, contains excessive

uric acid, or both– Frequently associated with gout – Diet rich in purines raises uric acid levels




• Cystine and struvite stones– Cystine stones form in people with inherited

disorder cystinuria– Struvite stones

• Composed primarily of magnesium ammonium phosphate

• Form in alkaline urine



Kidney Stones (cont’d.)

• Consequences of kidney stones– Renal colic

• Severe, stabbing pain when stone passes through the ureter

• Hematuria: blood in urine– Urinary tract complications

• Urination urgency, frequent urination, or inability to urinate

• Urinary tract obstruction, infection, acute kidney injury



Kidney Stones (cont’d.)

• Prevention and treatment of kidney stones– Drink 12 to 16 cups of fluids daily

• Maintain urine volumes of at least 2-2½ L per day– Calcium oxalate stones

• Reduce urinary calcium and oxalate levels• Adjust calcium, oxalate, protein, and sodium

intakes• Medications: diuretics; drugs to inhibit crystal

formation; and drugs to reduce uric acid production



Kidney Stones: Prevention and Treatment of Kidney Stones (cont’d.)

• Uric acid stones– Diets restricted in purines may help to control

urinary uric acid levels– Drug treatments: allopurinol to reduce uric

acid levels and potassium citrate to reduce urine acidity




• Cystine and struvite stones– Cystine stones:

• High fluid intakes• Medications may be needed

– Penicillamine, tiopronin; potassium citrate

– What is a central strategy in preventing struvite stones?




• Medical treatment for kidney stones– Medications

• Relax ureter• Increase urine flow

– Extracorporeal shock wave lithotripsy• High-amplitude sound waves degrade the stone

– Surgical methods• Higher success rate• More invasive



Nutrition in Practice: Dialysis

• Overview of how dialysis works• Separation of solutes from blood• Removal of fluid from blood• Frequency and duration of treatments• Monitoring efficacy of dialysis• Hemodialysis complications• Overview of how peritoneal dialysis works



Nutrition in Practice: Dialysis

• Advantages and disadvantages of peritoneal dialysis

• Features of continuous renal replacement therapy


chapter 22 nutrition and renal diseases

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