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Flashcards in Renal - CKD Deck (30):

What is CKD?

Reduced kidney function or kidney disease of any form that has been present for some time.
Increased prevalence - obesity and type 2 DM

Increases risk of IHD, progresses causing complications requiring renal replacement therapy, affects with drugs


Cause of death in CKD

IHD MCC of death in CKD patients on or off dialysis/ renal replacement


Changes in renal function with age

Kidney function declines with age in all people - product of age and lifestyle (obesity, type 2 DM) so many older people have low GFR but will not have specific kidney disease
- aggressive investigation of renal function in the elderly is only useful if it is outside the normal range for their age

Renal impairment (not necessarily disease) has drug consequences
- drugs normally excreted will accumulate
- NSAIDs reduce GFR in patients with already reduced renal function


Why is serum creatinine not always an accurate representation of renal function?

Creatinine does not rise above normal limits until there is a large (50%) reduction in GFR, so may not be accurate for early CKD. Is used in late CKD because GFR changes very little as creatinine rises.

GFR most commonly reported as eGFR using MDRD formula - uses "CAGE" variables:
- serum creatinine
- age
- gender
- ethnicity


Factors which affect result of eGFR

Muscle mass
Eating red meat 12 hours prior to the sample being taken

eGFR is much less accurate with relatively good renal function; interpret with caution when eGFR is predicted to be >60ml/min


CKD stages

5 stages based on eGFR
Stage 1 - greater than 90ml/min, with some sign of kidney damage on other tests
Stage 2 - 60-90ml + signs of kidney disease
Stage 3a - 45-59ml/min
Stage 3b - 30-44ml/min
Stage 4 - 15-29ml/min
Stage 5 - less than 15ml/min, established kidney failure - dialysis or kidney transplant needed


Investigating CKD

Most patients asymptomatic - usually identified on blood tests for other reasons
2 goals of assessment:
i) determine whether there is a specific cause of CKD
ii) assess severity - determines what general measures are needed (e.g. BP control)

History and examination:
- large bladder - urinary obstruction
- BP
- Urinalysis for protein and blood (low levels of proteinuria, albumin: creatinine ratio (ACR) useful, urine protein: creatinine ratio (PCR) can be used*
- USS may be useful to check anatomy and exclude obstruction

*Differs for non diabetics and diabetics - ACR of >30mg/mmol in non diabetics significant; ACR > 2.5mg/mmol in men, or >3.5mg/mmol in women is significant


End stage renal disease

Occurs when patients require renal replacement therapy with dialysis or transplantation
- number of functioning nephrons declines, surviving nephrons compensate which damages remaining nephrons and accelerates loss


What is the uraemic syndrome?

Refers to complications of chronic renal failure such as anaemia, confusion, coma, asterexis, seizures, pericardial effusions, itch and bone disease. Renal replacement therapy improves these problems, but patients with end stage renal disease have higher morbidity and mortality than rest of the population


Distinguishing between AKI and CKD

Severe acute and chronic kidney disease both raise plasma potassium, urea and creatinine and cause metabolic acidosis

Severe CKD usually evidence of chronic complications - e.g. anaemia caused by reduced EPO, bone disease (low serum Ca++, high PTH and high phosphate)

Plasma Ca++ is characteristically low in CKD unless tertiary hyperparathyroidism is present

Small kidneys on USS - key feature (atrophy and fibrosis)


Acute problems in CKD

Acute problems can occur in both acute and chronic renal failure
- emergency dialysis or haemofiltration - hyperkalaemia, severe acidosis, pulmonary oedema, and uraemic symptoms

Sudden deterioration in patients with renal impairment not on dialysis - hypertension, infection or nephrotoxic drugs (NSAIDs and ACEi cause renal deterioration by affecting renal blood flow)


Clinical features of renal bone disease

Bone pain - lower back, hips, and legs; associated with proximal myopathy and soft tissue calcification
Bone ALP usually raised


Types of renal bone disease

2 types distinguished on biopsy:
1) High bone turnover disease - excess PTH
- PTH stimulates bone resorption
- new bone has disordered collagen
- radiographs: subperiosteal resorption in phalanges, erosion of phalangeal tufts, and erosion of clavicle heads

2) Low bone turnover disease - low PTH
- low bone turnover, osteomalacia + poorly mineralised bone
- calcium intake and plasma calcium levels high enough to suppress PTH secretion below level required for normal bone turnover
- vit D levels may be low
- radiographs: multiple fractures or pseudofractures (radiolucent cortical zones perpendicular to bone surface)


Causes of high turnover renal bone disease

Main cause - renal phosphate retention and inadequate renal vitamin D production

Vit D deficiency - reduces gut calcium and phosphate absorption
- loss of 1,25 hydroxylation in CKD due to nephron loss
Kidneys retain phosphate --> net rise in phosphate and loss of calcium

Rise in phosphate further lowers calcium by causing calcium phosphate deposition in tissues
Hypocalcaemia --> PTH stimulation --> secondary hyperparathyroidism
- PTH secretion can become autonomous even when serum Ca++ returned to normal = Tertiary hyperparathyroidism

Other factors:
- high phosphate level directly stimulates PTH secretion and directly inhibits renal vit D production, normally vit D inhibits PTH (negative feedback), so deficiency causes excess PTH secretion
- acidosis stimulates bone resorption


Treating high turnover bone disease

- dialysis removes some
- low phosphate intake recommended
- phosphate binding compounds taken with food (compounds containing calcium or lanthanum or synthetic resins)

Vit D
- supplementation with calcitriol (1,25 didhydroxycholecalciferol) - inhibits PTH secretion and bone turnover; raises plasma Ca++ by increasing dietary calcium absorption
- helps bone pain and proximal myopathy

PTH levels should fall without causing low turnover bone disease. If PTH does not fall when Ca++ levels rise and vitamin D administrated, calcimimetic drugs (e.g. cinacalcet) which reduces PTH levels or surgical removal of PTH glands are required


Haematological complications of CKD

- caused by inadequate EPO production
- treated with EPO supplementation (i.v. or s.c.)
- works only if iron, vit B12 and folate levels are adequate
- antibodies can develop against administered EPO --> aplastic anaemia (rare)
- predisposes to LVH (3 x increased mortality)
- target Hb of 10-12g/dL

Bleeding time
- clotting times are normal
- platelet function is impaired --> prolonged bleeding time
- improved by dialysis, correction of anaemia and conjugated oestrogens
- synthetic vasopressin (desmopressin) increases vWF levels and transiently reduces bleeding time


eGFR that anaemia normally present in CKD

Normochromic normocytic anaemia due to lack of EPO normally occurs when eGFR is < 35ml/min (other causes of anaemia should be considered if the eGFR is >60ml/min)


Management of hypertension in CKD

Majority of patients with CKD require 2+ anti-hypertensive agents
ACEi are first line (helpful in proteinuric disease - e.g. diabetic nephropathy)
Furosemide useful when eGFR <45ml/min
- also lowers serum potassium
- high doses are usually required

Suggested target BP is 130/80mmHg for uncomplicated CKD and 125/75mmHg for CKD with proteinuria >1g/day


Why does eGFR sometimes decrease following initiation of an ACEi and what are acceptable levels of increase?

ACEi reduce filtration pressures so a rise in creatinine is expected.
NICE - decrease eGFR of up to 25% or a rise in creatinine up to 30% are acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs)

Rise greater than this could suggest renovascular disease (e.g. RAS)


Why are some patients with CKD dehydrated?

Not all patients with CKD will be oliguric. Only those patients who have CKD caused by predominantly glomerular disease will have reduced urine output. Some patients maintain some filtration, but lose tubular function, and therefore excrete very dilute urine, which can lead to dehydration.


Skin manifestations of CKD

Itch MC PC
- often occurs with secondary or tertiary hyperparathyroidism and may result from calcium phosphate deposition in tissues
- itch helped by controlling phosphate levels and creams

Uraemic frost = precipitation of urea crystals on the skin and occurs only in severe uraemia.
Skin pigmentation can occur and aneamia can cause pallor


Gastrointestinal problems associated with CKD

Gastrin levels are elevated, but peptic ulceration is no more common in patients with CKD than in the general population.

Symptoms of nausea, vomiting, anorexia, and heartburn are common
- higher incidence of oesophagitis and angiodysplasia (both of which can lead to bleeding)

Higher incidence of pancreatitis

Taste disturbance may be associated with a urine like smell to the breath


What endocrine complications can occur in CKD?

Men - loss of libido, impotence, low sperm count and motility

Women - loss of libido, reduced ovulation, infertility


Neurological and psychiatric features of CKD

- untreated end stage renal failure --> fatigue, diminished consciousness, coma, signs of neurological irritation (tremor, asterexis, agitation, meningism, increased muscle tone with myoclonus, extensor plantar responses, seizures)
- Na+/K+ ATPase activity is impaired in uraemia and PTH dependent changes in membrane calcium transport which may contribute to abnormal neurotransmission
- peripheral neuropathy; distal sensorimotor neuropathy, glove and stocking sensory loss and distal muscle weakness, usually symmetrical, isolated mononeuropathy can occur
- autonomic neuropathy
- myopathy - vit D deficiency, hypocalcaemia, hypophosphataemia, excess PTH
- sleep disturbance
- restless leg syndrome, cramps - responsive to quinine

- depression
- anxiety
- increased risk of suicide


Immunological complications of CKD

Immune function impaired - infection common
- uraemia suppresses most immune cells
- dialysis can inappropriately activate immune effectors, e.g. complement


How are lipids affected in CKD?

Hyperlipidaemia is common - esp. hypertriglyceridaemia from decreased triglyceride catabolism

Lipid levels higher in patients on peritoneal dialysis than in those on haemodialysis - loss of regulatory plasma proteins such as apoplipoprotein -A1 across peritoneal membranes.

Statins usually given to lower cholesterol


What cardiac complications can occur in CKD?

Pericarditis can occur and is more likely if urea or phosphate levels are high or there is secondary hyperparathyroidism.

Fluid overload and hypertension can cause LVH or dilated cardiomyopathy.

Large arteriovenous fistula can use up large % of cardiac output, reducing output available for the rest of the body.


What physical signs may be present on examination of a patient with CKD?

Yellow complexion
Jugular venous pressure raised in fluid overload or pericardial tamponade
Pericardial friction rub
AV fistulae for dialysis access*
Transplanted kidney with overlying scar*
Brown line pigmentation of nails
Excoriation of pruritis
Bruising easily
Peripheral neuropathy

- duel lumen central venous catheter for dialysis access*
- Tenckhoff catheter for peritoneal dialysis*


Maintenance of fluid and electrolyte balance in CKD

Patients on fluid retention should have dietary sodium intake limited to 100mmol/day, but loop diuretics may be needed to treat fluid overload.

Restrict K+ if hyperkalaemia to <70mmol/day and withdrawel of K+ sparing diuretics, ACEi and ARBs. Potassium binding resins, e.g. calcium resonium, are useful for short term only.

Correct acidosis using sodium bicarbonate supplements to keep plasma bicarb >22mmol/L may be beneficial. If the sodium load causes oedema, use calcium carbonate instead


Key aspects of management in CKD

1) Control BP - target BP <130/80 mmHg; ACEi and ARBs indicated first line (avoid duel therapy with ACEi and ARBs unless under specialist superivision)

2) Reduce proteinuria - heavy urinary protein losses are associated with an increased rate of progression in many cases of CKD; blocking RAA system slows rate

3) Dietary modification - patients with advanced CKD should maintain a normal protein and high calorie intake to avoid malnutrition in the phase leading up to RRT; protein restriction are used as conservative measure to limit uraemia in minority of patients; phosphate, Na and K restriction in CKD 4-5

4) Endocrine complications - anaemia and CKD MBD (mineral bone disease) may being in CKD 3-4, so search and treat

5) CVS prevention - statins, increased CVS mortality due to proatherogenic state and structural cardiac abnormalities

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