w6 chronic kidney disease

Question 1

what is chronic kidney disease? (CKD)

Answer 1

progressive loss of renal function associated w/ systemic diseases such as hypertension, diabetes mellitus (most significant risk factor)
(can also be lupus, or intrinsic kidney disease etc)
-occurs when renal function declines to less than 25% of normal

Question 2

what is the intact nephron hypothesis?

Answer 2

proposes that loss of nephron mass w/ progressive kidney damage causes the surviving nephrons to sustain normal kidney function

• these nephrons are capable of a compensatory hypertrophy and expansion or hyperfunction in their rates of filtration, reabsorption and secretion and can maintain adaptive changes in solute and water regulation in the presence of overall declining GFR
• The particular location of kidney damage also can influence loss of kidney function

Question 3

what are the two factors that contribute to CKD?

Answer 3

proteinuria and angiotensin II activity

Question 4

proteinuria and CKD

Answer 4

• glomerular hyperfiltration and increased glomerular capillary permeability lead to proteinuria
• proteinuria contributes to tubulointerstital injury by accumulating in the interstitial space and activating complement proteins and other mediators and cells, such as macrophages that promote inflammation and progressive fibrosis

Question 5

angiotensin II and CKD

Answer 5

angiotensin II activity is elevated w/ progressive nephron injury

• angiotensin II promotes glomerular HTN and hyperfiltration caused by efferent arteriolar vasoconstriction and also promotes systemic HTN
• the chronically high intraglomerular pressure increases glomerular capillary permeability, contributing to proteinuria
• Angiotensin II may also promote the activity of inflammatory cells and growth factors that participate in tubulointerstitial fibrosis and scaring

Question 6

clinical manifestation of CKD- azotemia

Answer 6

is manifested by increased levels of serum urea, serum creatinine, and other nitrogenous compound r/t decreasing kidney function

Question 7

clinical manifestation of CKD- uremia

Answer 7

is a proinflammatory state with many systemic effects known as uremic syndrome and is associated with the accumulation of urea and other nitrogenous compounds and toxins

Question 8

what are symptoms of uremia?

Answer 8

Hypertension, anorexia, nausea, vomiting, diarrhea or constipation, malnutrition and weight loss, pruritus, edema, anemia, and neurologic, cardiovascular disease, and skeletal changes

Question 9

sodium and water balance

Answer 9

In chronic renal failure, sodium load delivered to nephrons exceeds normal, so excretion must increase; thus less is reabsorbed. Obligatory loss occurs, leading to sodium deficits and volume depletion. As GFR is reduced, ability to concentrate and dilute urine diminishes.

Question 10

potassium balance

Answer 10

in chronic renal failure, tubular secretion of potassium increases until oliguria develops. Use of potassium-sparing diuretics also may precipitate elevated serum potassium levels. As disease progresses, total body potassium levels can rise to life-threatening levels and dialysis is required.

Question 11

acid-base balance and metabolic acidosis

Answer 11

In early renal insufficiency, acid excretion and bicarbonate reabsorption are increased to maintain normal pH
-Metabolic acidosis begins to develop when GFR decreases to 30% to 40% of normal. When end-stage renal failure develops, the metabolic acidosis may be severe enough to require dialysis.

Question 12

calcium, phosphate, and bone

Answer 12

• bone and skeletal changes develop w/ alterations in calcium and phosphate metabolism
• these changes being when the GFR decreases to 25% of less
• hypocalcemia is accelerated by impaired renal synthesis of vitamin D3 (calcirtriol) w/ decreased intestinal absorption of calcium
• renal phosphate excretion also decrease, and the increased serum phosphate binds calcium=causing hypoclcemia
• acidosis also contributes to negative calcium balance
• the combined effect of secondary hyperparathyroidism and vitamin D deficiency can result in renal osteodystrophies and vascular calcification

Question 13

magnesium

Answer 13

Fractional excretion of magnesium increase as CKD progresses and also may contribute to cardiovascular complications

Question 14

as GFR decreases

Answer 14

serum creatinine increase (SCr)

serum creatinine as estimate of GFR limited when there is reduced muscle mass or fluid overload

Question 15

when there is a decrease in urea

Answer 15

• clearance of urea follows a pattern similar to that of creatinine, but urea is filtered as well as reabsorbed and varies with the state of hydration; it is not a good index of GFR.
• as the GFR decreases, plasma urea concentration also increases.

Question 16

Protein, carbohydrate, and fat metabolism are altered in CKD

Proteinuria and a catabolic state –>negative nitrogen balance

Answer 16

-levels of serum proteins decline including albumin, complement and transferrin and loss of muscle mass

Question 17

hyperinsulinemia and glucose intolerance-common in CKD

Answer 17

• related to insulin resistance

- hyperparathrodisim also decreases insulin sensitivity and impaired glucose tolerance

Question 18

Dyslipidemia is common CKD

Answer 18

High ratio of low-density lipoprotein (LDL) to high-density lipoprotein (HDL); high triglycerides

Question 19

Pulmonary System

Answer 19

Pulmonary edema results from fluid overload and congestive heart failure. Dyspnea is common in ESKD. Metabolic acidosis can cause Kussmaul respirations

Question 20

cardiovascular disease

Answer 20

-is a major cause of morbidity and mortality in CKD
-Declining erythropoietin production causes anemia, which reduces oxygen delivery to the myocardium
-Elevated renin level stimulates the secretion of aldosterone, increasing sodium and water reabsorption
Hypertension is the result of excess sodium and fluid volume. Dyslipidemia occurs early in CKD.
-anemia makes the heart work harder -bc it thinks it has to work faster to get oxygen in the blood

Question 21

hematologic alternations (anemia)

Answer 21

Hematologic alterations include normochromic normocytic anemia, impaired platelet function, and hypercoagulability.
- Inadequate production of erythropoietin decreases red blood cell production and is the most significant factor in contributing to anemia
Anemia contributes to decreased tissue oxygenation and to progression of kidney disease.

Question 22

hematologic alternations (part 2)

Answer 22

• Disorders of hemostasis in CKD are primarily related to defective platelet aggregation, impaired adhesion of platelets to the vascular endothelium, and alterations in coagulation factors and the fibrinolytic pathway. The consequence is either (1) an increased bleeding tendency (more common with later stages of CKD)
• or (2) excessive formation of thrombi (i.e., deep vein thrombosis, pulmonary embolism and cardiovascular events), which is more common in earlier stages of CKD.128

Question 23

treatment of anemia

Answer 23

Treatment of anemia includes erythropoiesis stimulating agents (i.e., recombinant human erythropoietin) and intravenous iron

Question 24

immune system

Answer 24

Immune system dysregulation with immune suppression, deficient response to vaccination, intestinal barrier dysfunction and dysbiosis, and increased risk for infection develop with CKD
treatment: routine dialysis

Question 25

neurologic system

Answer 25

Neurologic symptoms are common and progressive with CKD and are related to dysfunction of lower motor and sensory neurons associated with uremic toxicity, chronic hyperkalemic depolarization, and anemia. Neuromuscular irritation can cause hiccups, muscle cramps, and muscle twitching. In advanced stages of renal failure, symptoms may progress to seizures and coma
-Peripheral neuropathies also develop with impaired sensations, decreased tendon reflexes, muscle weakness, and muscle atrophy, most commonly in the lower extremities.
Treatment: Dialysis or successful kidney transplantation

Question 26

gastrointestinal system

Answer 26

Gastrointestinal complications are common in individuals with CKD. Uremic gastroenteritis can cause bleeding ulcer and significant blood loss.
Nonspecific symptoms include anorexia, nausea, vomiting, and constipation or diarrhea
Uremic fetor: Bad breath caused by the breakdown of urea by salivary enzymes
Protein-restricted diet for relief of nausea and vomiting; Na+-based alkali or alkali-inducing food

Question 27

endocrine and reproductive systems

Answer 27

Endocrine and reproductive alterations develop with progression of CKD
-Males and females have a decrease in the levels of circulating sex steroid hormones. Males often experience a reduction in testosterone levels
Oligospermia and germinal cell dysplasia can result in infertility.
Females have reduced estrogen levels, amenorrhea, and difficulty with conception and maintaining a pregnancy to term.
-decrease libido
-insulin resistance is common –> As CKD progresses, the ability of the kidney to clear adiponectin and leptin and degrade insulin is reduced, and the half-life of insulin is prolonged.
CKD also causes alterations in thyroid hormone metabolism and low thyroid hormone levels and is known as nonthyroidal illness syndrome (euthyroid sick syndrome) and increases risk for cardiovascular disease

Question 28

Integumentary System

Answer 28

Skin changes are associated with other complications that develop with CKD. Anemia can cause pallor and bleeding into the skin and results in hematomas and ecchymosis
-Retained urochromes manifest as a sallow skin color
-Hyperparathyroidism and uremic skin residues, related to calcium and phosphorus levels and alterations in opioid receptors, are associated with irritation and pruritus with scratching, excoriation, increased risk for infection, impaired sleep, and depression
Treatment: Dialysis with control of serum calcium and phosphate levels

Question 29

Evaluation

Answer 29

Early screening and evaluation: risk factors, history, presenting signs and symptoms, and diagnostic testing
Estimate GFR: Serum creatinine or cystatin C, or both
Markers of kidney damage: urine protein, particularly albumin, and examination of urine sediment

Question 30

Management

Answer 30

Management of protein intake
Supplemental Vitamin D
Maintenance of sodium and fluid
Restriction of potassium
Maintenance of adequate caloric intake
Management of dyslipidemias
Erythropoietin-stimulating agents (ESAs)
Adjuvant iron therapy

Question 31

management (2)

Answer 31

ACE inhibitors or receptor blockers: Control systemic hypertension and provide renoprotection, particularly in the presence of diabetes mellitus
Statins and fibrates are used to control hyperlipidemia
Sodium glucose cotransporter 2 (SGLT2) inhibitors

Question 32

end stage kidney disease management

Answer 32

Dialysis
Supportive therapy
Renal transplantation

Question 33

renal replacement therapy

Answer 33

Replaces the normal functions of the kidneys

Examples: Dialysis (hemo or peritoneal), hemofiltration, hemodiafiltration
Can be continuous or intermittent
Offered to patients when GFR is <15ml/min/1.73m2