RENAL MEDICINE Flashcards
1
Q
What blood tests may you order to investigate a patient’s renal function? (For each you can think of, state what you might be looking for. )
A
FBC - signs of anaemia, infection
Haematinics - iron, folate, b12 deficiency
U&E - Potassium, urea, creatine, bicarbonate
Bone profile - Calcium, phosphate, PTH, Alkaline Phosphatase, Albumin
CRP - Infection, Inflammation
HbA1c - diabetic control
2
Q
What urinary tests may you order to investigate a patient’s renal function? (For each you can think of, state what you might be looking for. )
A
Urine dipstick - infection (leukocytes, nitrites), any pathology of glomerulus (blood, protein)
Urine protein:creatinine ratio - quantifies amount of protein in urine
Urine albumin:creatinine ratio - quantifies amount of albumin
Urine microscopy, culture and sensitivity (MC&S)
3
Q
What imaging may you order to investigate a patient’s renal function?
A
US KUB - good for peri-nephric (i.e. around the kidney) collections, size of the kidneys, corticomedullary differentiation, hydronephrosis
4
Q
What would VBG show for metabolic acidosis?
A
pH would be low
Bicarb would be low
pCO2 would be normal (maybe low if compensation)
5
Q
What would VBG show for metabolic alkalosis?
A
pH would be high
Bicarb would be high
pCO2 would be normal
6
Q
What causes metabolic alkalosis?
A
GI losses - vomiting.
Renal losses - primary hyperaldosteronism, tubular transporter defects, diuretics
Intracellular shifts - Hypokalaemia
7
Q
What is a normal anion gap range?
A
8-12
8
Q
What are specific causes of metabolic acidosis? (Split into causes of lactic acidosis, ketoacidosis, GI losses, renal losses and toxins)
A
Lactic acidosis - due to sepsis, anaerobic exercise, organ ischaemia
Ketoacidosis - diabetic, starvation, alcohol abuse
GI losses of bicarb - diarrhoea
Renal losses of bicarb - renal tubular acidosis, Addison’s
Toxins - Aspirin, Isoniazid (used in TB), see others on pg5 of booklet
9
Q
Why may a patient have a metabolic acidosis? (HINT: 2 main overarching reasons)
A
Due to having increased acid OR acidosis due to reduced alkali
10
Q
What are RF for AKI?
A
DM
CKD
IHD, CCF (congestive heart/cardiac failure),CVD
Liver disease
Elderly 75+ (Z2F says 65+)
Sepsis
Cognitive impairment
Nephrotoxic Meds - ACEi, ARBs, NSAIDs, Abx
Use of contrast medium e.g. during CT scans
11
Q
How many stages of AKI are there?
A
3
12
Q
How can causes of AKI be grouped?
A
Pre renal
Intrinsic
Postrenal
13
Q
Name pre renal causes of AKI
A
Z2F: Dehydration, Hypotension(shock), HF
Renal Booklet: Hypovolameia
Decreased cardiac output
Decreased effective circulating volume - in CCF, Liver failure
Impaired renal autoregulation - due to NSAIDs, ACEi, ARBs, Cyclosporine
14
Q
Name intrinsic/renal causes of AKI
A
Z2F: Glomerulonephritis, Interstitial nephritis, Acute Tubular necrosis
Renal booklet: Acute glomerulonephritis
Ischamia
Sepsis / infection
Vasculitis
Malignant HTN
Nephrotoxins - e.g contrast, haemolysis, cisplatin, aminoglycosides e.g. gentamicin
15
Q
Name post renal causes of AKI
A
Z2F: kidney stones, masses, ureter or urethral strictures, BPH, prostate cancer
Renal booklet: Bladder outlet obstruction e.g. renal calculi, BPH
Pelvoureteral obstruction
16
Q
What is the most important investigation in suspected AKI?
A
URINE DIP - look for abnormal proteins and blood
(This is according to renal booklet)
Z2F: Urinalysis - protein and blood (for acute nephritis), leucocytes and nitrites (for infection), glucose (for diabetes)
17
Q
What investigations would you want to do in patient with suspected AKI?
A
Urine dip
FBC, U&E, LFTs, bone profile, CRP
Urine PCR, Urine MC&S,
USS KUB - look for obstruction
18
Q
Potential presenting complaint in AKI
A
Symptoms: Nausea, vomiting, diarrhoea, tiredness/fatigue, changes to urine colour
19
Q
How is AKI managed?
A
Treat underlying cause (prerenal, itrinsic, post renal). Send off investigations
Stop any nephrotoxic agents
Dehydrated? IV fluids
Overloaded? Diuretics
Monitor urine output (catheterise if needed) and daily bloods
Avoid hyperglycaemia
20
Q
What are indications for renal replacement therapy?
A
Hyperkalaemia even after medical therapy
Metabolic acidosis even after medical therapy
Fluid overload which is not helped by diuretics
Uraemic pericarditis
Uraemic encephalopathy
Intoxications
21
Q
What is uraemia?
A
High urea.
Waste products that should be removed via urination accumulate in the blood. This is due to reduced kidney function
22
Q
What are signs of uraemic encephalopathy?
A
Vomiting, confusion, drowsiness, reduced consciousness
23
Q
What triad of signs are characteristic of nephrotic syndrome?
A
Oedema
Albumin <30
Unine PCR (protien:creatinine ratio) >350 aka more than 3.5g/24hrs
24
Q
What are the complications of nephrotic syndrome?
A
Higher risk of infection
VTE
Progression to CKD
Hypertension
Hyperlipidaemia
25
What can cause nephrotic syndrome?
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis
Amyloidosis, Myeloma, DM
26
Who does minimal change disease affect?
Children under 6yrs.
27
Describe the pathophysiology of membranous glomerulonephritis
(AR of Urinary module)
Subepithelial deposition of immune complexes - i.e. these deposit between the basement membrane and podocytes.
This causes thickening of the BM
28
What conditions can predispose to secondary focal segmental glomerulosclerosis?
Sickle cell disease
HIV
Heroin abuse
Kidney hyper perfusion
29
Define AKI
An acute drop in kidney function
30
How is AKI diagnosed?
By measuring the serum creatinine
31
What are NICE criteria for AKI?
Rise in creatinine of 25< micromol/L in 48hrs
Rise in creatinine of 50%< in 7 days
Urine output of <0.5ml/kg/hr for more than 6 hours
32
What are complications of AKI?
Hyperkalaemia
Fluid overload, HF, pulm oedema
Metabolic acidosis
Ureaemia
33
What are features of nephritic syndrome?
Haematuria
Oliguria
Proteinuria <3.5g/24hr
Fluid retention
Its may also have hypertension
34
What is the most common cause of primary glomerulonephritis?
IgA nephropathy aka Berger's disease
35
What is the most common cause of nephrotic syndrome in:
a) children?
b) adults?
a) Minimal change disease
b) Focal segmental glomerulosclerosis or in older people = diabetes
36
A patient with post-streptococcal glomerulonephritis may have ____what?____ in their recent PMH?
Hint: there are 2.
1-2 weeks after tonsillitis/pharyngitis
3-4 weeks after impetigo/cellulitis
37
What are main treatments for most types of glomerulonephritis?
Immunosupression using steroids
Blood pressure control - ACEi/ARBs
38
A patient has IgA nephropathy. What may be present in their PMH?
URTI: 1-2 days ago
GI infection
Strenuous exercise
Associated with: alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura
39
In what age groups do Goodpastures syndrome incidence peak?
30s - usually male
60+ - usually female
40
What is the pathophyisology of Goodpastures Syndrome?
Antibodies against type 4 collagen (in glomerular basement membrane) develop .
41
What are complications of Goodpastures?
Pulmonary haemorrhage
Rapidly progressive glomerulonephritis
42
Define CKD
Chronic kidney damage which is permanent and progressive.
Have:
- abnormal albumin excretion / decreased kidney function
- present for more than 3 months
43
What can cause CKD?
DM, HTN, age (decline as age +), glomerulonephritis, polycystic kidney disease, medications - NSAIDs, PPIs, lithium. Obstructive nephropathy. Recurrent pyelonephritis
44
What are RF for CKD?
Older age, HTN, DM, smoking, medications which affect kidney
45
How does CKD present?
Asymptomatic
Pruritis (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN
46
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
47
A patient has haematuria. What are your differentials?
Bladder cancer, prostate cancer, CKD, kidney stones, UTI, pylenonephritis, period, acute protastitis, BPH, trauma (depends on context of hx)
48
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
49
In CKD, what is the A score based on?
The ALBUMIN: creatinine ratio
50
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
51
What eGFR is needed for a diagnosis of CKD?
less than 60
OR proteinuria has to be present
52
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
53
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
54
What are main aims of management in CKD?
Slow progression of disease
Reduce CVD risk
Reduce risk of complications
Treat complications
55
What can be implemented to slow down progression of CKD?
Optimising diabetic control
Optimising HTN control
Treat infections promptly
Immunosuppression for GN
56
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
57
What dose of atorvastatin is offered for primary prevention of CVD?
20mg
58
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
59
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
60
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
61
What features may be present in CKD MBD (mineral bone disease)?
Osteomalacia
Osteoporosis
Osteosclerosis `
62
CKD MBD is a complication of CKD. How would you manage this?
Vit D
63
ESRD is a complication of CKD. How would you manage this?
Dialysis
Renal transplant
64
What is the most important antigen to match in renal transplant?
HLA-DR
65
How does Anti-glomerular basement membrane disease (Goodpastures) present?
Typically with haemoptysis + AKI/proteinuria/haematuria
66
How does an acute graft rejection present?
Presents like infection: fever, rigors Usually picked up by rising creatinine, pyuria and proteinuria
67
What part of the kidney does Nephrotic syndrome affect?
Glomerulus or Bowman's capsule
68
What does proteinuria and/or haematuria indicate?
Damage to the glomerulus
69
A patient is losing > to 3g in 24hrs of protein in their urine. what conditions could it be?
Diseases that cause Nephrotic syndrome:
Diabetes
Minimal changes disease
Membranous
Focal segmental glomerular sclerosis
Amyloid
70
What is nephrotic syndrome symptoms?
Oedema- often periorbital swelling
Proteinaemia (> 3g in 24hrs)
Hypoalbuminaemia
Hyperlipidaemia
Hypercoagulable state
71
What is nephrotic syndrome proteinuria range?
>3g in 24hrs
72
What are nephritic syndrome symptoms?
Haematuria
Proteinuria (less than 3g over 24hrs)
Hypertension
73
What diseases present with nephritic syndrome?
IgA nephropathy
Lupus
Mesangial proliferative glomerulonephritis
Vasculitis
74
What is the difference between nephrotic and nephritic syndrome?
Both manifestations of glomerulonephritis, different diseases present as either one but they are both due to damage to the glomerulus/bowmans capsule
75
How is kidney function affected by glomerulonephritis?
V often kidney function is not affected, the damage is to the glomerulus
76
What investigations would you do for a patient with suspected glomerulonephritis?
Urine dip- protein:creatinine, 24 hr- nephrotic syndrome: diagnostic criteria is 300. If less than this may be nephritic syndrome
Bloods- U&Es, FBC,Bone, serum glucose
Imaging
77
What is the pathophysiology of minimal change syndrome?
Podocytes become flattened- lose ability to control amount of protein that goes into the urine
78
After diabetes and hypertension, what is the most common glomerulonephritis?
IgA nephropathy
79
What type of kidney injury can vasculitis cause?
Acute
80
How may vasculitis present?
Non-blanching rash
Knee/ankle pain
Inflammation of blood vessels in ENT
Neuro conditions
Pt with vague symptoms, haematuria and presence of ANCA
81
What type of kidney injury does glomerulonephritis cause?
Mostly chronic, however some may cause acute e.g. vasculitis
82
How is vasculitis treated?
Plasma exchange- take blood from pt and pass through filter which removes the antibodies driving the condition
Cyclosporin
Tacrolimus
Mycophenate motefil
Cylcophosphamide
83
What antibody is implicated in vasculitis?
p-ANCA- anti-neurophil anti-cytoplasmic antibodies, they target neutrophil nucleus
c-ANCA- attaches to cytoplasm of nucleus
84
Name three investigations you would do for suspected glomerulonephritis
Urine dip - protein creatinine ratio
Bloods - U&Es, FBC, Bone, Serum glucose
Imaging - USS of renal system
85
What is common clinical presentation of minimal change disease in children/young adults?
Swelling - facial - peri-orbital swelling
86
What are ddx for swelling/odema in pt with pmh of proteinuria and angina?
Nephrotic syndrome, HF, Liver disease
87
What do patients with nephrotic syndrome need to help find cause?
Renal biopsy
88
A lady attends a&e with DVT and oedema. What renal condition must you rule out?
Nephrotic syndrome - dvt can be first sign; pts with nephrotic syndrome are at risk of dvt and stroke
89
How can you check pt with MCD is responding to steroids given?
Look at serum albumin - should be increasing if steroids are working.
90
What are risks of steriods?
Risk of osteoporosis
Risk of DM
Weight gain
Skin thinning
Risk of infection
91
What risk is associated to kidney biopsy?
Heamatoma - biopsy can damage kidney and pt presents with heamaturia
92
What antibodies can cause vasculitis?
P-ANCA
C-ANCA
93
What extra renal complications are related to AKPD?
Liver cysts
Berry aneurysms - check FHx of sudden death
94
What are complications of AKPD?
Renal failure
Hypertension
Infection
Pain
95
Why isn't it useful doing genetic testing for AKPD?
High number of mutations - i.e. can not just test for ne mutation, have to test for 100s.
96
What is inheritance pattern of AKPD?
Autosomal dominant
97
Where is the mutation in Adult Polycystic Disease?
Polycystine gene, on chromosome 16 and chromosome 4
98
How is Adult polycystic disease inherited?
Autosomal dominant
99
How do you diagnose adult polycystic ovary syndrome?
Family history
Ultrasound- done over the age of 16 as cysts too small to be seen before then
100
What are the features of adult polycystic kidney disease?
Bilateral cysts on the kidneys
HTN
Risk of berry aneurysms
101
What are the complications of adult polycystic kidney disease?
Pain
Discomfort
Haematuria
Kidney failure
102
What are the extra renal involvements of adult polycystic kidney disease?
Liver- doesn't affect function too much, but pts may feel bloated and uncomfortable
Berry aneurysms
103
What major complications result in patients needing dialysis?
Hyperkalaemia- give calcium gluconate and dextrose
Pulmonary oedema
104
What are the aims of renal replacement therapy?
Remove toxic metabolites
Normalise electrolyte disturbances
Correct volume deficit
105
What is Renal Replacement Therapy?
Dialysis- Peritoneal or Haemodialysis
Renal transplant
106
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
107
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
108
What are the types of AvF
Radial artery joined to cephalic vein
Brachial artery joined to cephalic vein
109
How do you know if the AvF is working?
You can feel a thrill or hear a bruit
110
When do you use a central line in dialysis?
When you can't get a AvF
111
Where does the end of the central line sit?
Superior vena cava
112
What is the risks with central line for dialysis?
Endocarditis
SVC obstruction
113
How often do you need to do PD?
peritoneal dialysis
4 x a day, every day, as less efficient
114
What is the biggest complication of PD
Peritonitis due to infection
115
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
116
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
117
How do you try to avoid hyperparathryoidism?
vit D
Or parathyroidectomy--> give calcium in the long time
118
What is renal anaemia?
Reduction in EPO
Normocytic anaemia
119
How do you treat renal anaemia?
Oral iron tablets, if that doesn’t work give
Give EPO injection
IV Iron
120
What is the complication to giving EPO?
May increase BP
Too much Hb can lead to viscous blood leading to hypercoaguable state
121
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
122
What do you need to suppress during transplantation?
CD4 + T helper cell--> can't produce NKC or B cells
123
What are the complications of immunosuppression for kidney transplant?
Opportunistic infection e.g. miliary TB
Cancer: melanoma, lymphoma
Karposi sarcoma
124
What drugs do you give to immunosuppress a patient prior to transplant?
Mycophenolate
Azathioprine
Calcineurin inhibitors- tacrolimus and cyclosporin
Steroids
125
What are some long term side effects of ciclosporin?
Nephrotoxicity- tubular atrophy and fibrosis
Gum hypertrophy
Hypertension
Atherosclerosis
126
What is the rule of thirds in membranous glomerulonephritis?
1/3 get better
1/3 have a relaxing and remitting condition
1/3 progress to ESRD
127
What metabolic abnormality does alcohol poisoning cause?
Raised anion gap metabolic acidosis
128
What metabolic abnormality Renal tubular acidosis cause?
Normal anion gap metabolic acidosis
129
What metabolic abnormality does renal failure cause?
Raised anion gap metabolic acidosis
130
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.
131
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).
132
Important differentials of CKD?
Diabetic kidney disease
Glomerulonephritis
Obstructive uropathy
133
Indication for dialysis in CKD patient?
CKD stage 5 - end stage renal disease
134
Which protein is lost in nephrotic syndrome?
Antithrombin III
135
Features of osteomalacia?
bone pain, proximal myopathy, and waddling gait
136
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
137
First line management of CKD induced osteomalacia?
Limit dietary phosphate
138
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.
139
Why would a patient with Nephrotic syndrome develop a DVT /PE ?
Nephrotic syndrome is associated with a hypercoagulable state due to loss of antithrombin III and plasminogen via the kidneys
Antithrombin III inhibits coagulation by inhibiting the action of thrombin while plasminogen is involved in fibrinolysis.
140
Which is higher in nephrotic syndrome LDL or HDL?
LDL
141
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
142
Who is at risk of diabetic nephropathy?
T1 DM or long duration of T2 DM patients
143
A patient has diabetic nephropathy. What 2 additional microvascular complications may be present?
Retinopathy
Peripheral neuropathy
144
What is glomerulosclerosis?
In Diabetic nephropathy - chronic high levels of glucose pass through glomerulus and cause scarring = glomerulosclerosis
145
What is key feature of diabetic nephropathy?
Proteinuria
146
Why do we get proteinuria in diabetic nephropathy?
Glomerulus is damaged - so allows protein to be filtered from the blood into the urine.
147
What is involved in screening for diabetic nephropathy ?
Urine Albumin:creatinine ratio
U&Es
148
What does albumin:creatinine ration show for patient with diabetic nephropathy?
Raised urine albumin:creatinine ratio
149
How is diabetic nephropathy managed?
Key: want to optimise blood sugar levels and blood pressure.
ACEi/ARB - reduces proteinuria and controls blood pressure
CVS risk modification (may involve lifestyle changes)
Continue screening for microvascular complication of diabetes e.g. retinal screening, foot checks.
150
What should always be started in patients with diabetic nephropathy, regardless of their BP reading?
ACEi (even if BP is normal)
151
Signs present in patient with diabetic nephropathy?
Presence of RF: Hyperglycaemia, HTN, FHx of DM, obesity, smoker
Retinopathy, odema, foot ulcers.
152
Drugs that cause acute interstitial nephritis?
Penicillin
Rifampicin
NSAIDS
Allopurinol
furosemide
153
Most common complication of haemo-dialysis?
Diaslysis induced hypotension
154
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
155
What is alport syndrome?
X-linked (usually affects males) Mutation in gene coding for Type V collagen
Associated with hearing loss and abnormalities of the eyes
Often leads to ESRF
156
Presentation of alport syndrome?
Persistent microscopic haematuria with intermittent visible haematura Sensorineural hearing loss Biopsy: splitting of GBM and alternating thickening & thinning of GBM
Genetic studies – family history
157
Clinical features of pyelonephritis?
Fever, rigors
Loin pain
Vomiting
White cell casts in urine
158
Hb target for CKD patients being treated for anaemia?
Hb 100-120
159
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
160
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
161
A pt with CKD has a low bone turnover. What could this mean they have?
Adynamic bone disease
Osteomalacia
162
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
163
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
164
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
165
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
166
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
1. Fibroblast growth factor-23 = Increased
2. ALP = Increased
3. Phosphate = Increased
4. PTH = Increased
5. Serum calcium = Decreased
6. Vit D = Decreased
167
Define tertiary hyperparathyroidism
Occurs when PTH release continues despite raised serum Calcium levels
168
What is Secondary hyperparathyroidism?
* elevation of parathyroid hormone (PTH) secondary to hypocalcaemia.
169
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.
170
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
171
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.
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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.
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