Week 2- Renal Flashcards

(84 cards)

1
Q

Kidney physiology

A

Kidneys are retroperitoneal organs located behind abdominal peritoneum, surrounded by adipose tissue capsule and renal fascia. They are on vertebral column sides, with right kidney being lower due to liver position.

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2
Q

Anatomy of the kidneys

A

The cortex, the outermost region of the kidney, contains nephrons, glomeruli, tubules, and collecting ducts. The medulla, the inner part, consists of renal columns, pyramids, and calyces, receiving urine and connecting to the renal pelvis.

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3
Q

The Nephron

A

The nephron is a tubular structure, and each nephron contains a funnel-shaped unit called the glomerular capsule (Bowman’s capsule). The capsule has two layers - parietal and visceral. The space between the layers is referred to as the glomerular space.

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4
Q

The glomerular filtration membrane is comprised of 3 layers:

A
  • endothelium of the capillary
  • visceral layer of the glomerular capsule (contains podocytes)
  • basement membrane between the 2 layers
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5
Q

Function of the kidneys

A

The cortex, the outermost region of the kidney, contains nephrons, glomeruli, tubules, and collecting ducts. The medulla, the inner part, consists of renal columns, pyramids, and calyces, receiving urine and connecting to the renal pelvis.

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6
Q

Primary Purpose of the Kidney

A
  • Regulate body fluid volume and osmolality
  • Regulate electrolyte balance
  • Regulate acid-base balance (in conjunction with body buffer systems and respiratory system)
  • Remove metabolic wastes such as urea, creatinine, uric acid, and more
  • Regulate blood pressure
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7
Q

Maintain fluid balance
The Renin- Angiotensin- Aldosterone System

A

The kidneys maintain fluid balance by releasing renin when pressure drops, converting angiotensinogen to angiotensin I and Angiotensin II, and stimulating aldosterone release. Antidiuretic hormone (ADH) influences fluid balance by increasing water reabsorption and reducing urine output.

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8
Q

Anti-Diuretic Hormone

A
  • Also know has ‘vasopressin’
  • Secreted by posterior pituitary gland
  • Osmoreceptors (water) located in hypothalamus detecting serum osmolality levels greater than 285mOsm/kg
  • ADH released and carried to nephrons
  • Kidney distal tubules, connecting tubules and collecting ducts alter permeability to water by action of ‘aquaporins’
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9
Q

Maintain electrolyte balance- Potassium

A

Potassium is reabsorbed from the filtrate by proximal tubules and secreted back into the filtrate in the distal tubules. It’s all about the filtrate!
Factors affecting absorption and secretion of potassium:
1. Sodium deficit = potassium loss
2. Acidosis: Hydrogen into cell and potassium out to be excreted
3. Diuretics: Increased loss of potassium in the distal tubule
4. Insulin: Promotes movement if potassium into cell
5. Adrenaline: Enhances potassium resorption (this is not a typo!) from proximal tubule

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10
Q

Maintain electrolyte balance- Sodium

A

Sodium balance regulated by kidneys, adrenal glands (aldosterone secretion) and posterior pituitary gland (ADH). Most sodium reabsorption occurs in the distal tubule under the influence of aldosterone. When diuretics are administered, sodium absorption is inhibited and sodium is eliminated in the urine. This active process is regulated by site specific sodium transporters.

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11
Q

Maintain electrolyte balance- Phosphorus

A

90% of phosphorus in plasma is filtered by glomerulus and 80% is reabsorbed by the proximal tubules. This resorption is increased when phosphorus levels are low.

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12
Q

Maintain electrolyte balance- Chloride

A

is actively transported out of tubules into interstitium with sodium to help maintain the high tubular interstitial osmolality and the mechanism for concentrating the urine.

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13
Q

Maintain electrolyte balance- Bicarbonate

A

major ECF acid base buffer. Reabsorption of bicarbonate takes place primarily from the proximal tubule into peritubular capillaries. Bicarbonate is also produced in the distal tubule and reabsorbed into the blood in response to acid-base balance need.
More bicarbonate is reabsorbed when large numbers of hydrogen ions are present, and more bicarbonate is excreted when fewer hydrogen ions are present.

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14
Q

Regulation of acid-base balance

A

The kidneys, alongside the lungs, have a crucial role in maintaining the serum pH within a very narrow margin (7.35-7.45). It does this through a buffering process, altering the reabsorption and secretion of acids (H+ ions) and bases (HCO3-) when changes to pH are detected.

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15
Q

Removal of waste products

A

The kidneys play a crucial role in maintaining homeostasis by removing waste products such as urea, creatinine, uric acid, metabolic acids, bilirubin, and medications/metabolites. These waste products are influenced by the amount of protein in the diet.

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16
Q

Regulate blood pressure

A

The renin-angiotensin system regulates blood pressure and water balance. When blood volume is low, kidneys excrete renin, which stimulates the production of angiotensin I and angiotensin II. Angiotensin II increases blood pressure due to its vasoconstrictive properties. The system is influenced by blood viscosity and can be disrupted by drugs to control high blood pressure, heart failure, kidney failure, and diabetes.

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17
Q

Vitamin D activation

A

Kidneys convert Vitamin D into active form, calcitriol, which stimulates calcium absorption and resorption. Kidney failure results in lost ability to activate Vitamin D, leading to poorly absorbed calcium, bone disease, and immunological issues. PTH, secreted by parathyroid glands, overcompensates.

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18
Q

Synthesise prostaglandin

A

Kidneys produce 2 vasodilatory prostaglandins - PGE1 and PGI2.

Prostaglandins are produced in all nucleated cells.

Both vasodilators act on afferent arterioles to maintain blood flow and glomerular filtration and perfusion.

PGF2 - not produced by kidney, but acting on the kidney, contributes to vasoconstriction in times of volume depletion

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19
Q

mechanisms maintain renal blood flow and GFR:

A
  • renal autoregulation (vasoconstriction or vasodilation of renal artery)
  • tubuloglomerular feedback (afferent arteriole vasoconstriction or vasodilation based on Na+ levels)
  • sympathetic nervous system (decreased blood pressure detected by carotid sinus and baroreceptors of aortic arch leading to vasoconstriction afferent arterioles)
  • Renin-Angiotensin-Aldosterone system
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20
Q

Glomerular filtration and urine formation

A

The glomerulus filters blood to excrete waste and form urine through passive processes. The filtration membrane, lining arterioles, is fenestrated with small holes for solutes and small proteins. Filtrate, collected in Bowman’s capsule, flows through renal tubules to form urine. Reabsorption occurs passively or actively, with proximal and distal convoluted tubules and loop of Henle reabsorbing different substances.

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21
Q

Acute Kidney Injury

A

AKI is a sudden, severe impairment of renal function causing a build-up of toxins in the blood.

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22
Q

AKI are categorised as:

A
  • Pre-renal: factors external to the kidneys that reduce renal blood flow and lead to decreased glomerular perfusion and filtration. Examples of pre-renal causes of AKI include: hypovolaemia (e.g. dehydration, haemorrhage, excessive diuresis), decreased cardiac output (cardiac arrhythmias, AMI), decreased renovascular blood flow (renal thrombosis / embolus).
  • Intra-renal: conditions that result in direct damage to the renal parenchyma, causing impairment to nephron function. Examples include Acute Tubular Necrosis, renal ischaemia, nephrotoxic injury from drugs, contrast, trauma.
  • Post-renal: causes involve mechanical obstruction of urinary outflow. As the flow is obstructed, urine refluxes into the renal pelvis, impairing renal function. Examples of post-renal causes of kidney injury include: renal calculi, renal or bladder tumours, strictures of the urethra, direct trauma.
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23
Q

CKD develops as a complication of systemic diseases such as:

A
  • diabetes,
  • glomerulonephritis,
  • hypertension,
  • cardiovascular disease,
  • urinary tract obstruction/infection,
  • hereditary defects of the kidneys, or
    as a complication of renal diseases (e.g. failure to resolve AKI).
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24
Q

Stage 1 CKD

A

Kidney damage with normal or increased GFR
>90 GFR mL/min
Diagnosis and treatment
Treatment of co existing conditions
CVD risk reduction

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Stage 2 CKD
Kidney damage with mildly decreased GFR 60-89 GFR mL/min Estimation of progression
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Stage 3a CKD
Moderately decreased GFR 45-59 GFR mL/min Evaluation and treatment of complications
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Stage 3b CKD
Moderately to severe decreased GFR 30-45 GFR mL/min Frequent evaluation and aggressive treatment of complications
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Stage 4 CKD
Severely decreased GFR 15-29 GFR mL/min Preparation for renal replacement therapy
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Stage 5 CKD
Kidney failure (end stage kidney disease) <15 GFR mL/min Kidneys cannot remove metabolic waste. Renal replacement therapy required to sustain life
30
CKD pathophysiology
CKD is progressive and often goes unnoticed. In Stage 1, the patient may have polyuria (increased urine output) as the kidneys lose their ability to concentrate urine. Symptomatic changes do not usually become apparent until renal function declines to less than 25% of normal. As the disease progresses, urine output reduces to oliguria (<30mL urine / hr) and anuria <100 mL / urine / 24-hours). With a reduction in urine output, azotaemia (retention of nitrogenous waste) becomes evident, identified by increased serum urea levels, increased creatinine levels, and other more general signs and symptoms.
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Physiological effects of CKD- Creatinine
Creatinine is a by product of creatinine breakdown and is released by muscles and is exclusively excreted by the kidneys Signs of CKD: elevated levels of creatinine
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Physiological effects of CKD- Urea
Urea is the by product of protein breakdown, both dietary and metabolic. Excreted by the kidneys. Reduced kidney function causes an elevation in urea levels (uraemia)
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Physiological effects of CKD- Urea (cardiac)
Uraemic toxins causes inflammation. Which may lead to pericarditis compromising cardiac output
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Physiological effects of CKD- Urea (neurological)
Uraemic toxins produce encephalopathy. Signs and symptoms: confusion, drowsiness, impaired concentration, memory loss, impaired judgement. In end stage seizures and coma
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Physiological effects of CKD- Urea (endocrine)
Insulin resistance. The ability of the kidney to degrade insulin is reduced and insulin half life is prolonged. Signs: low BSL
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Physiological effects of CKD- Urea (Digestive)
Elevated levels of urea/ uraemic toxins are attacked by bacteria in the GIT, releasing ammonia. Signs: bad breath, nausea, vomiting, anorexia, bleeding, diarrhoea, malnutrition.
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Physiological effects of CKD- Urea (haemtological)
Uraemic toxins decrease red blood cell life span. Signs: anaemia, lethargy, dizziness, low haematocrit
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Physiological effects of CKD- Sodium and water
When GFR decreases to 25%, obligatory osmotic loss of 20-40mmol sodium per day as kidneys are unable to concentrate urine. Elevated renin stimulates secretion of aldosterone, increasing sodium reabsorption. In later CKD, kidneys are unable to regulate sodium and water balance. Both sodium and water retained
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Physiological effects of CKD- Sodium and water (cardiovascular)
increased cardiac workload due to reduced circulating volume. fluid overload Signs: Hypotension due to excess fluid loss, tachycardia. Excess sodium and water cause hypertension, cardiomyopathy due to fluid overload and anaemia
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Physiological effects of CKD- Sodium and water (respiratory)
Fluid overload, congestive heart failure. Signs dyspnoea
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Physiological effects of CKD- Sodium and water (integumentary)
Oedema
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Physiological effects of CKD- Protein
Do not pass through the fenestrations in the glomerulus. Damaged nephrons allow proteins to pass through leading to protein in the urine. Levels of serum protein reduce, with the loss of muscle mass which reduces metabolism. Signs: loss of muscle mass, muscle weakness.
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Physiological effects of CKD- Potassium
Potassium is excreted via urine and faeces is maintained until oliguria (ESKD). With oliguria, potassium levels increase to life threatening levels. Impacts cardiovascular. Signs: cardiac arrhythmias, widened QRS and peaked T waves on ECG
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Physiological effects of CKD- Bicarbonate
When GFR decreased to 20-25%, decreased bicarbonate reabsorption in tubules, a decreased hydrogen ion elimination. Metabolic acidosis. Signs: Kussmaul respirations
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Physiological effects of CKD- Calcium
When GFR decreased to 25%, calcitrol production in kidneys is impaired, and calcium absorption in the intestine is reduced. Hypocalcaemia stimulates parathyroid hormone secretion with mobilisation of calcium from bone.
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Physiological effects of CKD- Calcium (cardiovascular)
Calcium deposits reduce vascular elasticity and cause vascular calcification = vascular disease. Increased risk of heart disease, stroke and PVD
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Physiological effects of CKD- Calcium (Endocrine)
Hyperparathyriodism decreases insulin sensitivity and impairs glucose tolerance. Signs high BSLs
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Physiological effects of CKD- Calcium (metabolic bone disorder)
Increased risk of fractures
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Physiological effects of CKD- Calcium (Skin)
Calcium phosphate deposits and hyperparathyriodism associated with skin irritation inflammation, pruritus and excoriation.
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Physiological effects of CKD- Phosphate
Renal phosphate excretion decreased (hyperphosphataemia). Increased serum phosphate binds to calcium further compounding hypocalcaemia. Increased phosphate levels also increases production of parathyroid hormone. Increased production of PTH results in more calcium being released from bones into blood. This leads to weak and brittle bones
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Physiological effects of CKD- Phosphate (cardiovascular)
Can cause cardiovascular calcification, increased risk of stroke, disruption of conduction system, and cardiac arrest.
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Physiological effects of CKD- calcium (musculoskeletal)
CKD metabolic bone disorder = increased risk of fractures. Phosphate binds with calcium forming calcifications, leading to non specific symptoms such as pain and stiffness in joints.
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Physiological effects of CKD- Vitamin D
Must be activated in the kidneys before it can function to help absorb calcium and phosphate. In CKD, vitamin D in not activated, and therefore calcium and phosphate are not absorbed at usual levels. Signs: increased risk of fractures.
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Physiological effects of CKD- Red blood cells
Kidneys responsible for production of erythropoietin- as kidneys fail, erythropoietin production decreases, decreasing red blood cell production.
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Physiological effects of CKD- red blood cells (cardiovascular)
declining erythropoietin production causes anaemia, thereby increasing cardiac workload. Defective platelet aggregation increase risk of breathing. Signs: cardiomyopathy due to anaemia (and fluid overload), GI bleeding, epistaxis, cerebrovascular haemorrhage.
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Physiological effects of CKD- red blood cells (haematological)
Uraemic toxins decrease red blood cells life span. Signs: anaemia, lethargy, dizziness, low haematocrit
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Physiological effects of CKD- red blood cells (integumentary)
Anaemia causes skin pallor, and may cause bruising from increased bleeding. Signs: pale/yellowed skin, bruising
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Physiological effects of CKD- Magnesium
As the kidney is the major regulator of serum magnesium; accumulation may occur with progressive renal impairment leading to hypermagnesamia. This may cause vomiting, lethargy, muscle weakness, skin burning, hypotension and cardia arrhythmias.
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CKD - Mineral Bone Disorder
Calcium, phosphate, and vitamin D metabolism changes cause bone loss and joint destruction, contributing to CKD-MBD. Hyperparathyroidism is associated with CKD-MBD. Treatment includes limiting phosphorus intake, administering calcium supplements, and promoting vitamin D absorption.
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Bone Remodeling
Bone mass is recycled daily, with 5-7% recycled each week. Osteoblasts deposit new cells and osteoclasts re absorb them. High PTH levels increase bone turnover. Bone matrix consists of collagen, spongy bone, and compact bone, with spongy containing red bone marrow cells and osteocytes and compact containing nerve fibers and blood vessels.
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Renal Bone Disease
Renal bone disease is categorized into three major manifestations: low bone turnover due to vitamin D deficiency or parathyroid gland over-suppression, high bone turnover due to hyperparathyroidism, and mixed osteodystrophy, resulting in poorly constructed soft bone and delayed regeneration. Management involves calcium binders and phosphate binders.
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CKD MBD- signs and symptoms
* Muscle weakness and bone pain * Fractures and stiff joints * Pruritus (severe itching) * Calciphylaxis * Soft tissue calcification * Periarthritis * Skeletal deformities * Calcification of lung, skeletal muscle
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Clinical manifestations of CKD- airway and breathing
- SOB - Kussmaul respirations - Pulmonary oedema - Pleural effusion
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Clinical manifestations of CKD- circulation
- polyuria - oliguria - hypertension - cardiac arrhythmias - cardiomyopathy and heart failure - anaemia - bleeding tendencies - discolouration of skin
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Clinical manifestations of CKD- disability
- confusion/ altered state of conscious - muscle/ tissue wasting - neuromuscular twitching, cramps - weight loss - infection - increased risk of fractures
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Patient Assessment of CKD
The patient's medical history, including medications, dietary habits, and risk factors, should be assessed. They should also be evaluated for kidney disease, GFR, and risk factors for cardiovascular disease. Reduced GFR and albuminuria are independent risk factors for cardiovascular disease, which is 20 times more likely in CKD patients.
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Diagnostic Studies
Urine screening for proteinuria is crucial for kidney damage. Pathology should include serum urea, creatine, and creatinine clearance levels. GFR should be collected. Kidney ultrasound and biopsy for renal bone disease can help identify kidney size and obstructions.
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Principles of Management of CKD
* Control serum urea and creatinine * Control hyperkalaemia by restricting high-potassium foods and drugs. * Limit dietary phosphate to minimise risk of CKD-MBD. * Sodium restriction (varies from 2-4g/day) * Protein - some controversy re protein in diet. Recent evidence suggests 'avoid high protein meals, but otherwise normal protein intake' for patients who are not receiving dialysis.
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Correct / maintain fluid balance for CKD
* Patients may be dehydrated due to diuresis in early stages of CKD (inability of the kidneys to concentrate urine) or have fluid overload in later stages of CKD. * In later stages of CKD, fluid restricted to 500-600mls (insensible loss) plus an amount equivalent to previous day’s urine output. We should monitor for fluid overload, as excess fluids consumed may not be excreted. * Daily weigh will help guide fluid management
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Hypertension from CKD
Hypertension can be both a cause & consequence of CKD * Management of hypertension will: * Reduce the progression of CKD * Reduce cardiovascular risk * Target BP <130/80 * Ace inhibitor (e.g. Captopril, Ramipril) or Angiotension II receptor blocker (e.g. Irbesartan, Candesartan)
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Nutrition from CKD
* People with CKD should be encouraged to eat a balanced diet. Aim to maintain nutritional status whilst minimising the accumulation of toxic waste products. * People with GFR < 30 should have individualised diet prescribed by a dietitian. * Malnutrition may be due to anorexia, nausea, vomiting, due to CKD.
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Anaemia from CKD
Kidney failure decreases erythropoietin production, leading to anemia and decreased red blood cell life. Erythropoietin therapy can help, but is associated with cardiovascular disease risk and hypertension contraindication.
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Hyperglycaemia from CKD
* Chronic kidney disease is associated with insulin resistance, resulting in hyperglycaemia. * Hyperglycaemia can lead to increased loss of kidney function, and cardiovascular disease. * Manage hyperglycaemia – metformin should not be prescribed to patients with GFR < 30, due to possibility of fatal lactic acidosis. Other diabetic agents can be used
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Dyslipidaemia from CKD
* Dyslipidaemia is thought to be caused by a range of contributing factors in CKD, including reduced lipoprotein lipase (LPL) activity, increased concentration of apo C-III (a specific inhibitor of LPL) in plasma, secondary hyperparathyroidism, insulin resistance. * Dyslipidaemia increases the risk of cardiovascular disease. * Dyslipidaemia management – Treat with statins, e.g. atorvastatin
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Hyperkalaemia
Potassium excretion via urine and faeces is maintained until oliguria (Stage 4 and end-stage kidney disease). With oliguria, potassium levels increase to life-threatening levels, causing cardiac arrhythmias.
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Hyperkalaemia management:
* Cardiac monitor: Look for prolonged PR, wide QRS, tall peaked T waves, VT, VF * Reduce potassium in diet * Medications: Resonium, Calcium, Insulin & glucose, Sodium bicarbonate * Dialysis
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Patient Education CKD Promote self-management:
* Diet, * Medications (to take, and to avoid), * Follow-up care * Daily BP measurement * Activity intolerance due to anaemia * Energy conservation * Discuss future treatment options (dialysis, kidney transplant) * Educate patient re medication excretion, and to monitor for signs of toxicity
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Early referrals CKD
* Dietitian * Nephrologist / kidney nurse practitioner * Psychologist * Nurse Practitioners and Clinical Nurse Consultants: access, anaemia,
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Dialysis
Dialysis is an artificial process that removes waste and excess fluid from a patient's body after kidney failure, primarily for uraemia control. Urgent dialysis is necessary for complications of CKD, such as encephalopathy, neuropathies, hyperkalaemia, pericarditis, and accelerated hypertension.
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There are 3 processes involved in dialysis: diffusion, osmosis, and ultrafiltration.
1. Diffusion is the movement of solutes from an area of high concentration to an area of low solute concentration (See Figure 1). Urea, creatinine, uric acid and electrolytes move by diffusion. 2. Osmosis is the movement of fluid from an area of low concentration to an area of high concentration of solutes. Glucose is usually added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood. 3. Ultrafiltration uses the changes in pressure gradient to remove excess fluid.
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Haemodialysis
* A procedure in which blood passes by an artificial semipermeable membrane outside the body * May be intermittent dialysis or continuous renal replacement * Needs a permanent vascular access site * Requires a permanent venous access (fistula) and an external membrane * Dialysis completed via an external machine * Can be completed at home or in hospital Risks: * Shorter duration dialysis means fluids exchanged at higher speeds. Patient must be haemodynamically stable for rapid exchange.
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Peritoneal Dialysis
Key points: * Uses abdominal peritoneum as membrane * Introduce a low concentration electrolyte solution into the cavity * Blood circulates and by osmosis and diffusion toxins drawn across membrane into solution * Solution is then drained * Used more on patients with Chronic Kidney Disease Risks: * Infection at catheter site * Heat loss (if not warmed) * Raised intra-abdominal pressures * Bowel perforation * Peritonitis * Loss of amino acids
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Kidney Transplant
* The only definitive treatment for patients with End Stage Kidney Disease (ESKD) * During a transplant the donated kidney is placed inside recipient’s pelvis and attached to their blood vessels and urinary tract. Their own kidneys are usually left in place. After a successful transplant, the recipient no longer needs dialysis or special diets. * Immunosuppression required to avoid rejection, e.g. prednisolone, mycophenolate, cyclosporine
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Conservative Management
* Preserve function as long as possible * Comfort and quality of life are prioritised