RENAL: CKD Flashcards
What are indications for renal replacement therapy?
Hyperkalaemia even after medical therapy
Metabolic acidosis even after medical therapy
Fluid overload which is not helped by diuretics
Uraemic pericarditis
Uraemic encephalopathy
Intoxications
What is uraemia?
High urea.
Waste products that should be removed via urination accumulate in the blood. This is due to reduced kidney function
What are symptoms of uraemic encephalopathy?
- Vomiting,
- confusion,
- drowsiness,
- reduced consciousness
Define CKD
Chronic kidney damage which is permanent and progressive.
Have:
- abnormal albumin excretion / decreased kidney function
- present for more than 3 months
What can cause CKD?
- DM,
- HTN,
- age (decline as age +),
- glomerulonephritis,
- polycystic kidney disease,
- medications - NSAIDs, PPIs, lithium.
- Obstructive nephropathy.
- Recurrent pyelonephritis
What are RF for CKD?
- Older age,
- HTN,
- DM,
- smoking,
- medications which affect kidney
How does CKD present?
Asymptomatic
Pruritis (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN
What investigations would you do for suspected CKD?
1) U&Es - to check eGFR. Need to be 2 tests 3 months apart to confirm ddx of CKD
2) Urinanalysis - urine albumin:creatinine ratio. >3mg/mmol is significant
3) Urine dipstick - haematuria
4) Renal USS
Write out/speak aloud stages of CKD (the G score):
G1 = eGFR ?
G2 = eGFR ?
G3a = eGFR ?
G3b = eGFR ?
G4 = eGFR ?
G5 = eGFR ?
G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15
In CKD, what is the A score based on?
The ALBUMIN: creatinine ratio
What are the stages involved in the A score in proteinuria?
A1 = ?
A2 = ?
A3 = ?
A1 = <3mg/mmol so normal to mildly increased
A2 = 3-30mg/mmol so moderately increased
A3 = 30+ mg/mmol so severely increased
What eGFR is needed for a diagnosis of CKD?
less than 60
OR proteinuria has to be present
What are complications of CKD?
Anaemia of chronic disease
Renal bone disease
CVD = number 1 cause of mortality!!!
Hyperparathyroidism (secondary or tertiary)
HTN
Malnutrition
Dialysis related problems
Who is needed in MDT meeting to manage patients with CKD?
Renal physicians
GPs
Renal specialist nurses/home care teams
Dieticians
Pharmacists
Vascular/Transplant surgeons
What are main aims of management in CKD?
Slow progression of disease
Reduce CVD risk
Reduce risk of complications
Treat complications
What can be implemented to slow down progression of CKD?
Optimising diabetic control
Optimising HTN control
Treat infections promptly
Immunosuppression for GN
How to reduce the risks of CKD complications?
Main complication is CVD, so advice on this is appropriate:
- Exercise, weight loss/maintain healthy weight,
- Stop smoking
- control BP - so dietary advice regarding sodium and water intake (+potassium and phosphate)
-Advise on starting statin
What dose of atorvastatin is offered for primary prevention of CVD?
20mg
Why do potassium levels need to be monitored in patient with CKD?
CKD can cause hyperkalaemia
ACEi used to treat HTN in CKD also cause hyperkalaemia
Describe how CKD causes anaemia
(the main reasoning taught in Urinary module)
Kidney cells produce erythropoietin (EPO)
EPO is a hormone that stimulates production of RBC
In CKD, kidney cells are damaged = can not produce as much EPO = can not produce as many RBC = anaemia
How can anaemia in CKD be managed?
Measure haematincis - Vit B12, folate, ferritin, iron, transferrin saturation, reticulocyte Hb. If deficient in any of these, replace these first.
- Note: IV iron may be better tolerated than PO
If this does not treat anaemia, discuss with renal team to offer EPO stimulating agents - e.g. exogenous EPO
Aim for Hb of 100-120
What features may be present in CKD MBD (mineral bone disease)?
Osteomalacia
Osteoporosis
Osteosclerosis `
CKD MBD is a complication of CKD. How would you manage this?
Vit D
ESRD is a complication of CKD. How would you manage this?
Dialysis
Renal transplant
What is the most important antigen to match in renal transplant?
HLA-DR
How does an acute graft rejection present?
Presents like infection: fever, rigors Usually picked up by rising creatinine, pyuria and proteinuria
What major complications result in patients needing dialysis?
Hyperkalaemia- give calcium gluconate and dextrose
Pulmonary oedema
What are the aims of renal replacement therapy?
Remove toxic metabolites
Normalise electrolyte disturbances
Correct volume deficit
What is Renal Replacement Therapy?
Dialysis- Peritoneal or Haemodialysis
Renal transplant
How does haemodialysis work?
Movement of solute across semi-permeable membrane- molecules that shouldn’t be there ie. ‘dirty’ molecules move across into water, thus cleaning blood Driven by osmotic pressure
3x weekly 4 hr treatment
Why do you need a AvF in haemodialysis?
To get blood out of the patient, most veins will collapse so need to arterialise the vein
What are the types of AvF
Radial artery joined to cephalic vein
Brachial artery joined to cephalic vein
How do you know if the AvF is working?
You can feel a thrill or hear a bruit
When do you use a central line in dialysis?
When you can’t get a AvF
Where does the end of the central line sit?
Superior vena cava
What is the risks with central line for dialysis?
Endocarditis
SVC obstruction
How often do you need to do PD?
peritoneal dialysis
4 x a day, every day, as less efficient
What is the biggest complication of PD
Peritonitis due to infection
What is encapsulating sclerosing peritonitis?
In PD- Peritoneal membrane becomes thickened due to constant exposure due to sugar water, becomes a fibrosis capsule so bowel cannot move- sx of small bowel obstruction
What is renal bone disease?
Renal failure- cannot hydroxylate Vit d–> means they cannot reabsorb calcium from gut–> serum calcium falls–> parathyroid hormone activated–>uses osteoclastic activity to increase serum calcium
Parathyroid goes out of control–> tertiary hyperparathryoidism–>Parathyroid increases calcium even when it doesn’t need to–> hypercalcaemia
How do you try to avoid hyperparathryoidism?
vit D
Or parathyroidectomy–> give calcium in the long time
What is renal anaemia?
Reduction in EPO
Normocytic anaemia
How do you treat renal anaemia?
Oral iron tablets, if that doesn’t work give
Give EPO injection
IV Iron
What is the complication to giving EPO?
May increase BP
Too much Hb can lead to viscous blood leading to hypercoaguable state
Why are pts on dialysis at risk of not surviving transplantation?
Due to cardio complications- pts likely to have diabetes or HTN which leads to increase CVS risk
What do you need to suppress during transplantation?
CD4 + T helper cell–> can’t produce NKC or B cells
What are the complications of immunosuppression for kidney transplant?
Opportunistic infection e.g. miliary TB
Cancer: melanoma, lymphoma
Karposi sarcoma
What drugs do you give to immunosuppress a patient prior to transplant?
Mycophenolate
Azathioprine
Calcineurin inhibitors- tacrolimus and cyclosporin
Steroids
What are some long term side effects of ciclosporin?
Nephrotoxicity- tubular atrophy and fibrosis
Gum hypertrophy
Hypertension
Atherosclerosis
Important differentials of CKD?
Diabetic kidney disease
Glomerulonephritis
Obstructive uropathy
Indication for dialysis in CKD patient?
CKD stage 5 - end stage renal disease
Features of osteomalacia?
bone pain, proximal myopathy, and waddling gait
Link between CKD and osteomalacia?
phosphate is renally excreted, if there is impaired renal function - phosphate will build up, ‘dragging’ the calcium out of the bones resulting in osteomalacia
First line management of CKD induced osteomalacia?
Limit dietary phosphate
Aside from diet, how else can you manage CKD induced osteomalacia?
phosphate binder e.g Sevelamer- non-calcium-based phosphate binder, it binds to dietary phosphate and prevents its absorption.
What is Dialysis disequilibrium syndrome?
Rare
Usually caused by cerebral oedema- treat by reducing ICP
Neurological symptoms due to rapid removal of urea
Headache, nausea, vomiting, disturbed consciousness, convulsions, coma
Most common complication of haemo-dialysis?
Diaslysis induced hypotension
Hb target for CKD patients being treated for anaemia?
Hb 100-120
What factors contribute to anaemia in CKD?
Decreased production of EPO from kidney
Absolute iron deficiency - poor absorption/malnutrition
Functional iron deficiency - inflammation/infection
Blood loss
Shortened RBC survival
Bone marrow suppression from uraemia
Medication induced anaemia
Deficiency of B12 or folate
What needs to be present for CKD-MBD to be diagnosed in a pt with CKD?
Evidence of one or more of:
- Abnormal metabolism of vitamin D or levels of PTH, calcium, phosphate, alkaline phosphatase
- Vascular and/or soft tissue calcification
- Abnormal bone turnover, metabolism, volume, linear growth or strength
A pt with CKD has a low bone turnover. What could this mean they have?
Adynamic bone disease
Osteomalacia
What is Osteitis Fibrosa?
1. give the features
2. Give symptoms
Features:
* loss of bone mass
* weakening of bones and calcified structures - this is replaced with fibrous tissue (peritrabecular fibrosis)
* formation of small cyst-like brown tumours
Symptoms:
* Bone pain
* tenderness
* fractures
* skeletal deformities
A patient has CKD which has progressed. Describe the levels of the following as either increased or decreased:
1. Fibroblast growth factor-23
2. ALP
3. Phosphate
4. PTH
5. Serum calcium
6. Vit D
- Fibroblast growth factor-23 = Increased
- ALP = Increased
- Phosphate = Increased
- PTH = Increased
- Serum calcium = Decreased
- Vit D = Decreased
Define tertiary hyperparathyroidism
Occurs when PTH release continues despite raised serum Calcium levels
How is CKD-MBD managed?
Reduce the severity/occurrence of renal bone disease
Reduce CVS morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload.
AIM: control serum phosphate, calcium and vit D levels.
* Dietary phosphate reduction
* Phosphate binder
* Vit D supplemenation (if low) / vit D analaogue
* Ca - treat if hypo/hyper (can be either) either by supplementing or binder
* Persistently elevated PTH - parathyroidectomy or calcimimetic therapy is indicated.
When do you use Ramipril in kidney disease?
In patients with proteinuria, an ACE inhibitor such as ramipril is used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol.
They are also used regardless of a patient’s blood pressure if the ACR is > 70 mg/mmol.
What causes Osteotits fibrosa cystica?
Cause: Unchecked hyperparathyroidism
* overproduction of PTH
* PTH causes Ca release from bones - blood - reabsorption of calcium in kidney
* this results in hypercalcaemia
What conditions might lead a pt to develop hyperparathyroidism and therefore develop a complication such as Osteitis fibrosa cystica ?
- Parathyroid adenoma (majority)
- Genetics -( i.e. familiar hyperarathyroidsim, MEN type 1)
- Parathyroid carcinoma
- Renal - End stage renal disease
Why does End stage renal disease lead to hyperparathyroidism?
- In ESRD the kidneys fail to produce calcitriol (a form of vitamin D)
- Vit D facilitates the absorption of calcium into bones.
- When calcitriol levels decrease, parathyroid hormone levels increase
- This causes calcium to be removed from the bones and released into the blood
What is Secondary hyperparathyroidism?
- elevation of parathyroid hormone (PTH) secondary to hypocalcaemia.
What causes secondary hyperparathyroidism ?
- Any disorder that results in hypocalcaemia will elevate parathyroid hormone.
- CKD - MOST COMMON
- malabsorption syndromes
- chronic inadequate sunlight exposure, acting via alterations in vitamin D, phosphorus, and calcium.
Secondary hyperparathyroidism (SHPT) is a complication of CKD. This is important in the pathogenesis of CKD-mineral bone disorder (MBD).
Define CKD-MBD
- a systemic disorder of mineral and bone metabolism due to CKD.
This is due to either one or a combination of the following:
* abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism
* abnormalities in bone turnover, mineralisation, volume, linear growth, or strength
* vascular or other soft tissue calcification
Potential clinical findings in pt with AKI?
Signs: Reduced urine output (oliguria), dehydrated (NO moist mucous membranes, reduced skin turgor, sunken eyes). Confusion, drowsiness,
Who: over 65, RF present (see BS on this), Hx off AKI.
Differentials of AKI?
CKD (i.e. a progression of CKD staging/acute on chronic kidney disease)
BMJ also states 1) increased muscle mass which shows elevated Cr. 2) Drug side effect leading to elevated creatinine (trimethoprim).
What are principals of management in AKI?
Find and treat causes (e.g. sepsis, drugs, obstruction):
Bloods/Blood Cultures, urine dip, bladder scan, ultrasound renal tract, ECG
Stop renotoxic drugs
Give IV fluid
Treat complications
Consider dialysis if indicated
How to test for proteinuria. What values are significant?
1) Albumin: creatine ratio
2) >3mg/mol = proteinuria
3-30mg/mol moderately increases
>30mg/mol severely increased
When to refer to a nephrologist for a pt with Proteinuria?
- a urinary albumin:creatinine ratio of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
- a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
- consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease
Management of proteinuria?
- ACEi > 30mg/mol if they have HTN, >70mg/mol regardless of BP
- consider SGLT
