Chronic Kidney Disease Flashcards

1
Q

What is chronic kidney disease characterised by

A

Slow irreversible decline in renal function

Tends to be progressive and is categorised into stages according to GFR function

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2
Q

CKD staging

A

1: kidney damage but normal GFR >90
2: kidney damage mild Dec in GFR 60-89
3: moderate Dec GFR 30-59
4: severe Dec in GFR 15-29
5: kidney failure <15

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3
Q

What is the aim of treatment of chronic kidney disease

A

Previn further decline and stabilise GFR

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4
Q

Causes of CKD

A

Systemic disease such as diabetes mellitus, hypertension and immune disease
Infectious disease - HIV, TB, and hepatitis
Genetic diseases such as polycystic kidney and cystinosis
Ischaemia due to vascular disease and atherosclerosis
Obstruction due to tumours, stones and fistula

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5
Q

What results from diabetic nephropathy

A

Due to poor diabetic control and hypertension
There is thickening of the basement membrane due to increased mesangial cell expression in response to hyperglycaemia and inc TGFbeta relays therefore increased matrix production
There is also activation of the RAAS
There is glomerular sclerosis due to intraglomerular hypertension or ischaemic damage
Protein urea damages the glomerulus and increases tubular damage and fibrosis
Diabetic nephropathy there is expansion tissue in nodules lead to loss of the glomerular function it to slowly progressive changes over many years

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6
Q

What is the normal serum creatinine

A

Normal is less than 100
Continuous monitoring is 101 to 499
High is greater than 500

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7
Q

What is the negatives in measuring serum creatinine

A

See you in creatinine increases exponentially with a decrease in kidney function
It is influenced by a person‘s gender ethnicity age body mass diet exercise and pregnancy it is not a reliable way to estimate kidney function

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8
Q

What is taken into account when measuring EGFR

A

Creatinine age gender ethnicity
It is a better reflection of kidney function
It is not valid in those under 18 years of age pregnancy and AKI
It is validated in the white and Afro-Caribbean population
Is affected by extremes in weight such as in bodybuilders and in obesity

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9
Q

How is CKD classified

A

It’s classified with the GFR and albuminuria

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10
Q

What are the complications of CKD

A

To do with the kidney function
Elimination of waste can cause uraemia
Homoeostasis of water can lead to oedema
Homoeostasis of electrolytes can cause electrolyte imbalance is
Homoeostasis of acid base can cause metabolic acidosis
Homeostasis a blood pressure can cause hypertension
Control of calcium phosphate vitamin d activation and then will be reduced phosphate clearance and secondary hyperparathyroidism
In CKD patients do not convert enough vitamin di into its active form so that therefore they do not adequately secrete phosphate
Insoluble calcium phosphate forms and remove calcium from the circulation this leads to hypocalcaemia hence a secondary hyperthyroidism hope I can be there for treatment is activated vitamin d calcitriol
Also anaemia due to the lack of EPO production

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11
Q

Who requires an ultrasound scan?

Ckd

A

those that have CKD have an accelerated decline Those with visible or persistent invisible heamaturia those with symptoms of obstruction at family history of polycystic kidney disease and aged over 20 those with GFR below 30 and those who require a renal biopsy

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12
Q

When to refer people to the nephrologist

A

Those who have a GFR below 30
Or you have an ACR above 70
unless they have known diabetes and already appropriately treated
Those who have an ACR above 30 with haematuria
Those with a rare or genetic cause is known
Sustained Decrease in GFR in 12 months and 25% reduction and change in the GFR category
GFR is below 15
Poorly controlled high blood pressure requiring at least four drugs
Suspected renal artery stenosis

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13
Q

What are the risk factors for CKD progression

A
Cerebrovascular disease
Proteinuria
AKI
Poor blood pressure control
Diabetes
Smoking history
Non white ethnicity 
Chronic NSAID use
Outflow obstruction
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14
Q

How to prevent progression of CKD

A

Treat protein urea with aN ACE inhibitor or ARB
Treat hypertension according to the nice guidance
Stop smoking
Control of underlying disease through diabetes or lupus
Caution with non-steroidal anti-inflammatory use
Refer to your urology with outflow obstruction or structural abnormalities

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15
Q

If you have a diabetic nephropathy what else do you have

A

Retinopathy and neuropathy

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16
Q

Natural history of diabetic nephropathies

A

At the onset of diabetes there is increased GFR reversible Albuminurea and increasing kidney size
And between two and five years there was increase in basement membrane thickness is mesangial expansion and microalbuminuria
11 to 23 years there was onset of proteinuria and at 13-25 years there was a rise in serum creatinine and then 15-27 years it was end-stage renal failure
There is an inevitable decline in renal function over the 7 to 10 years and results on stage renal failure
With early intervention and a better glycaemic control and blood pressure control you can slow the deterioration.

17
Q

When is diabetic nephropathy diagnosed

A

When patients have had diabetes for more than 10 years
When they also have all the complications such as neuropathy and retinopathy
They have progressive increase in urine protein excretion
There was no evidence of any other cause there is no haematuria no obstruction and negative immunology and serology so there is a presumed diagnosis of diabetic nephropathies
if they don’t meet all the criteria they may need a biopsy to confirm this

18
Q

What are the functions of the kidneys

A
Elimination of waste
Homoeostasis
Blood pressure
Control of calcium and phosphate
ProDuction of red blood cells
19
Q

What is IgA nephropathy

A

It is a common glomerular disease are leads to chronic kidney disease
There is increase in mesangial cell expansion
IGA is deposited in the glomerulus

There is non-visible haematuria visible haematuria positive protein and a potential upper respiratory tract infection

20
Q

What happens in autosomal dominant polycystic kidney disease

A
Patients are screened in the early 20s
There are two main genes PKD 1 and PKD 2
There is no treatment
There is a trial of tolvaptan
The only treatment for the end-stage renal disease it causes is a transplant or dialysis
21
Q

Renal obstruction

A

Obstruction can be internal or external and
Untreated it can lead to reduced function
Intrinsic
Stones can occur in the kidney ureter or bladder
BPPH
Tumour can occur in the bladder and can obstruct the ureteric orifices
This can cause hydronephrosis
Extrinsic
Tumours of the prostate cervix or colon

22
Q

How to find the cause of CKD

A

EGFR either stable or deteriorating
Determine how reduced the EGFR is
If it’s not too reduced and stable you may not need intensive investigations

1) history and examination
Identify risk factors for CKD
Diabetes, hypertension, nephrotic medication and all the comorbidities, systemic inflam disorders, family history and urinary tract symptoms and if there is any evidence of peripheral vascular disease

2) investigations
Urine analysis to look for haematuria proteinuria if both positive this questions Glomerular disease
urinary protein loss albumin creatinines ratio, protein: creatinine ratio
Perform urine culture to exclude infection

3) immunology and serology
This is important for glomerular pathology is where there is proteinuria and he mature rear
Important history for a systemic disease
ANA antibody test for SLE
ANCA antibody test for small vessel vasculitis
Look for myeloma or MGUS looking for serum free light chains and monoclonal bands
look for HBV, HCV, HIV

4) renal imaging
Ultrasound scan look for a lower unary tract symptoms and other suspected obstruction sites
Important to biopsy if needed
Screen for polycystic kidneys
Perform a CT KUB to look for stones
Radioisotopic renogram to look for renal excretion
And MRIA to look for vessel occlusion

5) Biopsy
Look for glomerulonephritis
Maybe useful if renal function is deteriorating and no identified cause when from othert investigations
Relatively safe but not risk-free
Approximately 4% risk of bleeding
And should not be done if there is any evidence of infection or obstruction

23
Q

Failure of water and fluid homoeostasis

A

Cannot concentrate urine

Loss of diurnal rhythm of urine excretion leading to nocturia
A limited rate of water excretion
Inability to excrete water load
This leads to
Dilutional hyponatraemia
Oedema pitting and pulmonary
Hypertension
How is this treated
Diuretics-loop
Salt restriction
Fluid restriction
24
Q

Failure of electrolyte homoeostasis

A

Sodium

Loss of nephrons lead to a reduced capacity to excrete salt and water = fluid overload and hypertension