CKD Flashcards

1
Q

What is CKD?

A

CKD is defined as “abnormalities of kidney structure or function present for more than 3 months with implications for health”.

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2
Q

What is the Criteria for diagnosis of CKD (either/or both of the following present for > 3 months)

A

Markers of kidney damage (one or more)

Albuminuria (AER ≥30 mg/24 hours; ACR ≥30 mg/g [≥3 mg/mmol])
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
Abnormalities detected by histology
Structural abnormalities detected by imaging
History of kidney transplantation

(ACR: Albumin to Creatinine Ratio, AER: Albumin Excretion Rate)

Decreased GFR
GFR <60 ml/min/1.73 m2 (GFR categories G3a–G5)

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3
Q

Staging of CKD

A
  1. Kidney damage with normal increased GFR > or = 90ml/min/1.73m2
  2. Kidney damage with mildly decreased GFR 60-89 ml/min/1.73m2
  3. Moderately decreased GFR 30-59 ml/min/1.73m2
  4. Severely decreased GFR 15-29 ml/min/1.73m2
  5. Kidney Failure <15 ml/min/1.73m2
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4
Q

Epidemiology of CKD

A

Prevalence of CKD Globally is 9.1 – 14%.

Nigeria (2017 GBD Report)
estimated population of CKD was 12.7 million
ranked 10th out of 195 countries,
the only African country out of 12 countries with over 10 million cases.

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5
Q

Risk Factors for CKD

A

Factors that may increase risk of chronic kidney disease include:

Diabetes mellitus
High blood pressure
cardiovascular disease
Smoking
Obesity
Race eg African, Native American or Asian-American
Family history of kidney disease
Structural abnormality of the kidneys
Advanced age

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6
Q

Aetiology of CKD: common causes

A

Hypertension (leading cause in Nigeria)
CGN (especially in a young person)
DM (the most common around the world)
Obstructive Uropathy
Cystic kidney diseases e.g ADPKD
Autoimmune diseases like SLE (causing lupus nephritis)
Infections like HIV (can cause CGN): HIV associated nephropathy (HIVAN)
Sickle cell (sickle cell nephropathy)
Chronic/acute use of of NSAIDS (analgesic nephropathy)
Amyloidosis

It’s also possible that the CKD can cause hypertension

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7
Q

Explain the Pathophysiology of CKD

A
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8
Q

What is the progression of CKD?

A

The initial injury to the kidney may result in a variety of clinical manifestations, ranging from asymptomatic hematuria to renal failure requiring dialysis.

Many individuals fully recover and subsequently suffer from little or no sequelae e.g Post-streptococcal glomerulonephritis.

In contrast, some injuries are recurring and chronic eg lupus nephritis, resulting in lasting damage.

Some in whom the initial disease is either inactive or cured may still develop progressive renal disease due to hemodynamic and other mechanisms.

The kidney is able to adapt to damage by increasing the filtration rate in the remaining normal nephrons, a process called adaptive hyperfiltration.
As a result, the patient with mild renal insufficiency often has a normal or near-normal serum creatinine concentration.

This adaptive hyperfiltration, although initially beneficial place a burden on remaining nephrons, leading to progressive glomerular sclerosis and interstitial fibrosis, suggesting that hyperfiltration may worsen renal function.

This may manifest with proteinuria and progressive renal failure.

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9
Q

What are the common clinical features of CKD? What is the hallmark of kidney damage?

A

• Symptoms develop slowly and are nonspecific

• Patients may remain asymptomatic until renal failure is far-advanced (GFR < 10-15 ml/min)

•Manifestations can include fatigue, malaise, weakness, pruritis.

GI complains of anorexia, n/v, metallic taste and hiccups are common

The hallmark of kidney damage: Protein in urine

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10
Q

Discuss Electrolyte/acid–base imbalances in CKD

A
  1. Sodium: May be normal or low
    Because of impaired excretion, sodium is retained, Water is also retained (causing dilution of sodium) leading to edema, Hypertension and congestive heart failure
  2. Potassium : Hyperkalemia
    Most serious electrolyte disorder in kidney disease
    Can lead to fatal arrhythmias (because potassium plays a role in the electrical activity of the heart, so too much can disrupts the hearts electrical activity and slow down electrical conduction making the heart beat abnormally)
  3. Calcium (hypocalcemia)
    Phosphate buildup binds calcium, reducing free calcium levels in the blood.
    • CKD reduces vitamin D activation (the kidneys activate vitamin D into calcitriol, which is needed to absorb calcium from food).
    • Low calcitriol → Less calcium absorption in the gut → Hypocalcemia.
  4. Phosphate (hyperphosphatemia) :
    Healthy kidneys remove excess phosphate from the blood.
    • In CKD (especially Stage 4-5), phosphate excretion is reduced, leading to phosphate buildup in the blood.
  5. Magnesium alterations
    Healthy kidneys remove excess magnesium from the blood.
    In CKD (especially Stage 4-5), magnesium excretion is reduced

Metabolic acidosis: Results from inability of kidneys to excrete acid load (primarily ammonia)

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11
Q

What are the effects of CKD on the Hematologic system?

A
  1. Anemia
    Due to ↓ production of erythropoietin
    From ↓ of functioning renal tubular cells
    Bleeding tendencies
  2. Defect in platelet function
  3. Infection
    Changes in leukocyte function
    Altered immune response and function
    Diminished inflammatory response
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12
Q

What are the effects of CKD on the Cardiovascular system?

A

Hypertension
Heart failure
Left ventricular hypertrophy
Peripheral edema
Arrhythmias
Uremic pericarditis

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13
Q

What are the effects of CKD on the Respiratory system?

A

Kussmaul respiration (acidotic breathing)
Dyspnea
Pulmonary edema
Uremic pleuritis
Pleural effusion
Predisposition to respiratory infections
Depressed cough reflex

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14
Q

What are the effects of CKD on the Urinary system?

A

Polyuria
Results from inability of kidneys to concentrate urine. Occurs most often at night.

Oliguria - Urine output <400-500ml per 24 hours
Occurs as CKD worsens
Anuria - Urine output <100 ml per 24 hours

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15
Q

What are the effects of CKD on the Neurologic system and what are the symptoms attributed to?

A

Expected as renal failure progresses
* Altered mental ability
* Seizures and Coma
* Peripheral neuropathy
* Restless leg syndrome (Ekbom syndrome)
* Muscle twitching
* Irritability
* Decreased ability to concentrate
* Myoclonic jerks

Neurologic symptoms are attributed to;
* Increased nitrogenous waste products (when the patient becomes uremic)
* Electrolyte imbalances
* Metabolic acidosis
* Demyelination of nerve fibers

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16
Q

What are the effects of CKD on the Reproductive system?

A

Infertility : Experienced by both sexes
Decreased libido
Low sperm counts
Sexual dysfunction

17
Q

What are the effects of CKD on the Gastrointestinal system? And what’s the main cause of them?

A

Every part of GI is affected and is due to excessive urea
Mucosal ulcerations
Stomatitis (ulceration of the mouth and lips)
Uremic fetor (urine-like odor of the breath)
GI bleeding
Anorexia
Nausea and vomiting

18
Q

What are the effects of CKD on the Musculoskeletal system?

A

CKD-MBD
Syndrome of skeletal changes
Result of alterations in calcium and phosphate metabolism
Weaken bones, increase fracture risk
Vascular calcifications

19
Q

What are the effects of CKD on the Skin?

A

Most noticeable change

Pruritus
Uremic frost (due to high levels of urea in the blood which are excreted through sweat forming white crystalline deposits on the skin, it occurs in ESRD )
Dry, pale skin
Dry, brittle hair
Thin nails
Petechiae
Ecchymoses

20
Q

What are the effects of CKD on the Physical Examination?

A

Physical Examination reveals a chronically ill-looking and pale patient.
Look for possible underlying cause (DM, lupus).
BP is commonly elevated.
Skin may be yellow, with evidence of easy bruising.
Uremic fetor (fishy breath) may be present.
Cardiopulmonary and mental status changes are frequently noted also.

21
Q

Investigations of CKD

A

May see anemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, and hyperkalemia…with both acute and chronic renal failure.

Urinalysis – proteinuria, haematuria
Abdominal USS- echogenic kidneys (kidneys that appear brighter than normal on ultrasound scan) with poor corticomedullary differentiation,other features depend on the aetiology ,e.g cystic lesions, bilaterally shrunken kidneys.
E/U/CR, Ca, PO4,
Serum protein and albumin
Renal biopsy
Fasting lipid profile
FBC
Parathyroid hormonal assay, VitD3, alkaline phosphatase
Chest X-ray-; cardiomegaly
Echocardiography- LV hypertrophy
X-ray of the hand and wrist – features suggestive of renal osteodystrophy

22
Q

Goals of management of CKD

A

Prevention of development of kidney disease / Early detection
Retardation of the progression if already established
Prevent the development of complications
Treatment of Complications
Replacement of Renal Function:
Dialysis :- Hemodialysis, Peritoneal dialysis
Renal transplantation

23
Q

How do you retard the progression in a patient with established CKD? / what are the Precipitants?

A
  • Avoid medications and agents that can lead to deterioration in kidney function i.e. NSAIDs and COX2 inhibitors, aminoglycosides (eg. Gentamicin), contrast agents, gadolinium, and herbal medications.
  • Adjust dose of drugs according to eGFR level.
  • Take enough fluid to avoid dehydration.
  • Exercise
  • Reduce proteinuria to less than 500 mg/day.
  • Diet: protein intake of 0.6 – 0.8g/kg/day
  • blood pressure lowering to less than 120mmHg systolic.
  • Blood glucose lowering to target
  • Smoking cessation
  • Bicarbonate supplementation.
24
Q

Indications for dialysis

A

Clinical:

Fluid overload
Uremic encephalopathy
Uremic pericarditis
Uremic gastritis
Restless leg syndrome

Biochemical:

SCr >600 micromol/L or daily rise > 100
Serum urea > 25mmol/L or daily rise > 10
K > 6.5mmol/L or daily rise > 1
HCO3 < 15mmol/L

25
Q

Complications of CKD

A

Anaemia
Bone Mineral Disease
Uncontrolled Hypertention
Heart Failure and Pericarditis (due to uraemia) (ask about chest pain)
Refractory Oedema
Malnutrition
Death
Uremia (ask about hematemesis, melena stool, pruitus, loss of consciousness, jerky movements, irrational talk)

26
Q

What are the Aneamia treatment options?

A

Blood transfusions
Iron therapy
Erythropoietin

27
Q

What are the treatment options for CKD-MBD (mineral bone disorder)?

A

Phosphate intake restricted to <1000 mg/day
Phosphate binders (Bind phosphate in bowel and excreted). Examples include:
- Calcium carbonate
- Sevelamer hydrochloride

Phosphate binders should be administered with each meal
Side effect: Constipation
Vitamin D supplement : Calcitriol

Serum phosphate level must be lowered before administering calcium or vitamin D

28
Q

What are the 3 common causes (at bedside) of body swelling?

A
  1. Renal disease: nephrotic syndrome, CKD
  2. Congestive heart failure
  3. Liver Cirrhosis
  4. Others; malabsorption syndrome, protein losing enteropathy
29
Q

Complications of dialysis

30
Q

Causes of acute decompensation of CKD

31
Q

Causes of polyruria

A

DM
Diabetes Insipidus
Excessive fluid intake (psychogenic polydipsia)
Diuretic use
Hypercalcemia
Hypokalemia
Early stages of CKD
Cushing syndrome
Lithium
AKI