Chronic Kidney Disease Flashcards

1
Q

what is the definition of CKD?

A

Chronic kidney disease (CKD), also known as chronic renal failure, is defined as abnormalities of kidney structure or function, present for ≥3 months, with implications for health

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2
Q

what is the epidemiology of CKD?

A

It is estimated that 9% to 13% of the adult population worldwide has CKD
The global prevalence of CKD is rising and is thought to be due to an ageing population; a higher incidence of diseases such as diabetes and hypertension, which are the most common causes in the adult population; and an increased incidence of glomerular disorders such as focal segmental glomerulosclerosis

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3
Q

what is the aetiology of CKD?

A

The most common cause in the adult population is diabetes. It is estimated that one third of patients with diabetes will develop kidney disease, as defined by albuminuria and/or a reduction in the glomerular filtration rate within 15 years after the diagnosis of diabetes.
Hypertension is the second most common cause. The interaction between hypertension and CKD is complex, with hypertension a cause and a consequence of CKD.

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4
Q

what are the risk factors for CKD?

A

Diabetes
Hypertension
>50
Childhood kidney disease

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5
Q

what is the pathophysiology of CKD?

A

In response to renal injury, there is thought to be an increase in intraglomerular pressure with glomerular hypertrophy, as the kidney attempts to adapt to nephron loss to maintain constant glomerular filtration.
An increase in glomerular permeability to macromolecules such as transforming growth factor-beta (TGF-beta), fatty acids, pro-inflammatory markers of oxidant stress, and protein may result in toxicity to the mesangial matrix, causing mesangial cell expansion, inflammation, fibrosis, and glomerular scarring.
Additionally, renal injury results in an increase in angiotensin II production, causing an upregulation of TGF-beta, contributing to collagen synthesis and renal scarring within the glomerulus.
Both the structural alterations and accompanying biochemical, cellular, and molecular changes seem to account for progressive renal scarring and loss of kidney function.
All forms of CKD are also associated with tubulo-interstitial diseases; the exact mechanism of injury is not known, but is thought to be secondary to a reduction in blood supply in addition to an infiltration of lymphocytes and inflammatory mediators that result in interstitial fibrosis and tubular atrophy.

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6
Q

what are the key presentations for CKD?

A
Risk factors
Fatigue
Oedema
Nausea
Pruritus
Restless legs
Anorexia
Infection related glomerular disease
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7
Q

what are the signs of CKD?

A

Anorexia
Infection related glomerular disease
Presence of risk factors
Enlarged prostate

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8
Q

what are the symptoms of CKD?

A
Fatigue
Oedema
Nausea
Pruritus
Restless legs
Arthralgia
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9
Q

what are the first line and gold standard investigations for CKD?

A

Renal chemistry - elevated serum creatinine; electrolyte abnormalities
Estimate GFR - <60 mL/minute/1.73 m², A GFR estimating equation using serum creatinine is recommended for initial assessment.
Serum cystatin C and cystatin C Based estimation of GFR - reduced muscle mass will lead to overestimation; increased muscle mass to underestimation of the GFR
Urinalysis - haematuria and/or proteinuria
Urinary albumin - moderately increased (AER 30-300 mg/day; ACR 30-300 mg/g)
Renal ultrasound - small kidney size; presence of obstruction/hydronephrosis; kidney stones

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10
Q

what are the differential diagnoses for CKD?

A

Diabetic kidney disease
Hypertensice nephrosclerosis
Ischemic nephropathy

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11
Q

how is CKD managed?

A

Category G1 and 2:
ACEi, dapagliflozin, statin, antihypertensive, glycaemic control, non-dihydropyridine calcium channel blockers
Category G 3 and 4:
ACEi or angiotensinII receptor agonist, dapagliflozin, statin and ezetimibe, antihypertensives, glycemic control, renal replacement therapy, non-dihydropyridine calcium channel blockers
(with anaemia): erythropoietin stimulating agent, iron, (with secondary hyperparathyroidism): dietary mods, phosphate binding drug, ergocalciferol, active vitamin D analogue, (with metabolic acidosis): oral sodium bicarb
Category G5 or with uraemia:
Dialysis, kidney transplant
(with anaemia): erythropoietin stimulating agent, iron, (with secondary hyperparathyroidism): dietary mods, phosphate binding drug, ergocalciferol, active vitamin D analogue

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12
Q

how is CKD monitored?

A

Patients with risk factors for CKD, such as diabetes, hypertension, or a family member with CKD, should be evaluated annually with serum creatinine and mathematical formulation for estimation of the glomerular filtration rate in addition to urinalysis for haematuria and/or proteinuria.
For those with established CKD, the rate of progression of CKD should be serially assessed starting in glomerular filtration rate (GFR) category G3a/G3b disease. Patients should be screened for anaemia and bone mineral disorders at least every 6 to 12 months, with a haemoglobin, calcium, phosphorus, and intact parathyroid hormone (PTH). For those in GFR category G4 disease, haemoglobin, calcium, phosphorus should be monitored every 3 to 6 months and intact PTH every 6 to 12 months. For patients in GFR category G5 CKD, anaemia should be evaluated with a monthly haemoglobin, and bone mineral disease with a calcium and phosphorus every 1 to 3 months and an intact PTH every 3 to 6 months. Lipids should be checked annually for all patients with CKD.

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13
Q

what are the complications of CKD?

A

Anaemia, renal osteodystrophy, CVD, protein malnutrition, metabolic acidosis, hyperkalaemia, pulmonary oedema

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14
Q

what is the prognosis of CKD?

A

CKD is mostly progressive and leads to end-stage renal disease (ESRD) and the need for renal replacement therapy (i.e., dialysis, transplant). Though it cannot be cured, it can be controlled and managed to a large extent. CKD is a strong cardiovascular risk factor, and the majority of patients with CKD will die prior to reaching ESRD.

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