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Metabolic and Endocrine > Chronic Kidney Disease and Transplantation > Flashcards

Chronic Kidney Disease and Transplantation Flashcards

1
Q

what are the features nephrotic syndrome?

A
  • presence of proteinuria >3g in 24 hour
  • oedema
  • hyperlipidaemia
  • lower BP
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2
Q

what causes oedema in nephrotic syndrome?

A

due to loss of hydrostatic pressure so if the liver function is good then liver might not be as bad (albumin is a good indicator).
albumin creatinine ratio 70
protein creatinine ratio 100

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3
Q

where is the defect typically in a patient with nephrotic syndrome?

A

GBM endothelial or podocyte

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4
Q

what are the features of nephritic syndrome?

A
  • less oedema than nephrotic syndrome
  • proteinuria <3g in 24hour
  • haematuria (usually microscopic)
  • higher BP
  • low or normal albumin so fluid is intravascular so increased BP
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5
Q

why is there proteinuria but not haematuria in nephritic syndrome?

A

GBM is negatively charged so cannot allow protein through so less proteinuria but still haematuria

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6
Q

what is usually the defect in a patient with nephritic syndrome?

A

usually inflammatory condition

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7
Q

give examples of causes of nephrotic syndrome?

A
  • IgA nephropathy (can present as nephritic)
  • FSGS (focal segmental glomerular sclerosis) common in HIV patients
  • minimal change disease (most common in children)
  • membranous nephropathy (most common in adults)
  • amyloidosis
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8
Q

give examples of causes of nephritic syndrome?

A
  • good pastures
  • lupus (membranous nephropathy secondary to lupus)
  • glomerulonephritis
  • vasculitis
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9
Q

define chronic kidney disease?

A

sustained, irreversible kidney damaged (longer than 6 weeks)

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10
Q

describe how eGFR is measured?

A

NICE guidelines-blood tests taken 90 days apart
estimated GFR using creatinine
cystatin C
urea

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11
Q

describe the formula use to calculate eGFR?

A
  • MDRD (no longer used)
  • EPI (ml/min/1.73m2). need body weight and height to calculate SA, depends on factors such as gender, age, race, serum creatinine)
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12
Q

what is the role of ACE inhibitors in patients with CKD?

A

they help especially with proteinuria

they are contraindicated in pregnancy, renal artery stenosis

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13
Q

why are older people more likely to have CKD?

A

drugs
co-morbidities
ageing process
GFR-go downs per 1ml per year after 45

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14
Q

what diseases can cause CKD to go undetected?

A

amyloidosis or multiple myeloma as proteins other than albumin being produced so won’t get picked up

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15
Q

who should be referred to a renal clinic?

A

patients G3b or below

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16
Q

what are the signs and symptoms of CKD?

A
  • oedema-due to fluid overload and RAAS causing increased sodium and volume.
  • increased BP
  • metabolic acidosis
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17
Q

describe salt reabsorption in the kidney and what drugs act at each location?

A
  • 60% in PCT (carbonic anhydrase inhibitor, manntiol)
  • 30% LoH (furosemide=IV and oral, bumetanide=oral)
  • 10% DCT (thiazides, aldosterone, spironolactone, amiloride- these don’t work when GFR<45)
  • CD <1% - ADH
  • diuretic resistance-increase dose
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18
Q

what are the options for treating CKD?

A
  • conservative care

- renal replacement therapy

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19
Q

what are the methods of renal transplant therapy?

A
  • dialysis (haemodialysis, peritoneal)

- transplant (deceased either heart beating or non heart beating OR living (related, non related, altruistic)

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20
Q

define kidney failure?

A

simply a reduction in kidney function. It is identified from; a decrease in urine output, increase in serum creatinine, decrease in estimated eGFR.

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21
Q

what can kidney failure be categorised based on timescale?

A

AKI- sudden decrease in kidney function over days or weeks
CKD- persistent decline in kidney function over longer time
acute on chronic kidney failure - sudden decrease in kidney function in someone with CKD
end stage kidney disease-insufficient kidney function to maintain life without renal replacement therapy

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22
Q

what type of kidney failure is reversible and what is non reversible?

A

AKI/acute on chronic have the potential to restore kidney function
chronic /end stage -not reversible

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23
Q

what is used to determine the severity of AKI?

A

RIFLE classification

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24
Q

what is used to determine the severity of CKD?

A

GFR
Stage 1- normal GFR, applied to people with abnormality of kidney but still working normally eg autosomal dominant polycystic kidney disease or someone with diabetes and microalbuminaemia
Stage 3 is split into 2 groups important due to risk of progressive renal failure greater in patients of 3b

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25
Q

how can kidney failure be classified based on site of injury?

A

pre renal - decreased blood flow either because of fixed obstruction (renal artery stenosis) or decreased circulating volume or blood pressure
renal - injury within kidney
post renal - obstruction between pelvis and urethra, it has to affect both kidneys to cause kidney failure.

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26
Q

describe the stages in CKD severity?

A 
stage 1 - normal GFR
stage 2 - 60-89ml/min
stage 3a - 45-59ml/min
stage 3b - 30-44ml/min
stage 4 - 15-29ml/min
stage 5 - <15 ml/min or RRT
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27
Q

what are the stages in the RIFLE criteria for AKI?

A 
risk 
injury
failure
loss
end stage kidney disease
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28
Q

what are the causes of pre renal failure?

A 
True hypovolaemia (history of volume loss eg diarrhea, vomiting, burns, haemorrhag)
Relative hypovolaemia (heart failure, septic shock, hepatorenal failure)
Renovascular disease
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29
Q

what are the clues that point towards pre renal failure?

A

Clinical history and examination

  • Cause for volume depletion
  • Signs of hypovolaemia (tachycardia, hypotension esp. postural hypotension

Clues to renovascular disease

  • Atherosclerotci vascular disease
  • Hypertension
  • Vascualr bruit
  • Deteriorting renal function after ACE inhibitors or ARB
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30
Q

what medications can cause pre renal failure?

A

angiotensin 2 blockers

prostaglandin synthesis blockers

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31
Q

describe how ACE inhibition can cause volume depletion?

A

afferent arteriole pressure is generated by flow and efferent arteriole pressure is generated by resistance and usually is equal. the GFR depends on the pressure diffrence
if there is decreased flow to the afferent arteriole the pressure difference is maintained by increased resistance which is angiotensin 2 mediated vasoconstriction and GFR is maintained however if there is decreased flow to the afferent arteriole and the patient uses ACE/ARB then the pressure difference won’t be maintained and GFR will decline

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32
Q

how can NSAID use and ACE use lead to reduction in GFR?

A

pressure in afferent arteriole is maintained by pressure generated by flow which is mediated by prostaglandins causing vasodilation and pressure in efferent arteriole is generated by resistance. NSAIDs block prostaglandin synthesis and vasoconstriction results in decreased flow but the pressure is maintained by increasing resistance in efferent arteriole mediated by angiotensin 2 but with ACE/ARB the efferent arteriole cannot maintain pressure difference and subsequently there is a decreased GFR

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33
Q

what are the causes of intra-renal failure?

A

Grouped by part of nephron affected (many pathologies affect more than one area eg type 2 diabetes)

  • Glomeruli-glomerulonephritis
  • Tubules-ischaemic ATN (prolonged pre-renal/contrast nephropathy, nephrotoxic ATN (gentamycin/amphotericin/paracetamol), intratubular obstruction (crystals-urate/oxalate/aciclivar. / myoglobin, myeloma)
  • Interstitium – acute pyelonephritis / aute interstitial nephritis (drugs, infection)
  • Blood vessels – vasomotor (NSAIDs/ACE), malignant hypertension, scleroderma, vasculitis, microvascular obstruction (atheroemboli/cholesterol emboli/HUS/TTP)
34
Q

what are the clues to intra-renal failure?

A

Haematuria

  • Visible (macroscopic)- patient can see blood in urine, more commonly indicates bleeding within the urinary tract (urithelial malignancy, post streptococcal GN in children, IgA nephropathy in adults)
  • Invisible – urine dipstick positive for blood and more commonly indicates glomerular haematuria

Assess urine
Proteinuria-sign of glomerular disease
-Microalbuminuria- (albumin: creatinine ratio) – indicator of early diabetic nephropathy and capillary injry secondary to hypertension or vascular disease (urine dipstick will be negative)
-Proteinuria (measured by protein:creatinine ratio)-indicator of glomerular disease (glomerulonephritis) (positive urine dipstick

35
Q

describe post renal failure?

A

Obstruction to drainage of urine from kidney
To cause kidney failure the obstruction needs to be bilateral or to affect a single functioning kidney (eg kidney transplant)

36
Q

what are the potential sites of renal obstruction in post renal failure?

A 
Bilateral pelvicoureteric junction 
Bilateral ureteric (tumour/retroperitoneal fibrosis/bilateral stones/bilateral sloughed papilla
Bladder outflow – prostatic hypertrophy/stone/tumour/neurogenic bladder
Urethra-tumour, valves, structure, foreign body
37
Q

what clues from history would point towards post renal failure?

A

Urinary tract surgery
Pelvic malignancy/radiotherapy
Bladder symptoms
Polyuria (early obstruction)anuria (very late obstruction)

38
Q

what signs would be a clue to post renal failure?

A

Palpable bladder
Prostatic enlargement
Abnormal rectal or vaginal examination

39
Q

what would be seen on renal tract ultrasound in a patient with post renal failure?

A

Absence of hydronehrosis on ultrasound makes obstruction unlikely

40
Q

what are the key functions of the kidneys?

A 
Potassium excretion
Excretion of waste production (protein metabolism and drugs)sodium and water balance
Hormone-EPO, renin, 1, 24 dihydroxy D3
Phosphate excretion
Acid base balance
41
Q

what is uraemia?

A

a raised level in the blood of urea and other nitrogenous waste compounds that are normally eliminated by the kidneys.

42
Q

what are the signs and symptoms of uraemia?

A 
Anorexia
Change in taste
Nausea
Vomiting
Pruritis
Neuropathy
Pericarditis
Confusion
Encephalopathy
Coma
Drug accumulation leading to toxicity
43
Q

what is the treatment for severe renal failure?

A

Dialysis
Transplantation (pre-emptive, cadaveric, live donor)
Conservative care of ESRF with symptom management

44
Q

what is the consequence of sodium retention and how it can be treated?

A

Lead to peripheral or pulmonary oedema or hypertension (LVH can cause heart failure). These are treated with dietary salt restriction and loop diuretic. Hypertension managed.

45
Q

what BP medication should be used in patients with CKD?

A

Use of ACE inhibitor is more efficient than other BP medications. ACE should be used in all patients with CKD but with caution as can cause hyperkalaemia and can cause fall in GFR

46
Q

how can CKD cause anaemia, what is the treatment and what is the target Hb?

A

Hormone production-> EPO-> anaemia
Treatment-recombinant EPO by injection if symptomatic
Target HB 100-200g/l (avoid over correction as risk of CVD mortality

47
Q

how can CKD cause bone disease?

A

2 mechanism – both lead to increased PTH, secondary hyperparathyroidism leading to renal osteodystrophy and vascular calcification
-Fall in serum calcium
Due to insufficiency 1,25 dihydroxy D3, primary site of acton is on gut to allow calcium absorption
-Increase in serum phosphate
Kidney cannot excrete phosphate in most foods
High phosphate pushes calcium lower

48
Q

what is the treatment of bone disease in patients with CKD?

A 
Dietary phosphate restriction
Oral phosphate binders
Calcium based
Aluminium based
Non calcium/non aluminium
49
Q

on a basic level how do the kidneys regulate acid base balance

A

Kidney regulate acid base by excretion of hydrogen ions and generation of bicarbonate

50
Q

what happens to acid base balance as renal function worsens?

A

As renal function worsens patients tend to become acidotic, worsening renal osteodystrophy, increase protein catabolism and increase serum potasstium.

51
Q

how is the acid base inbalance in CKD patients treated?

A

Treatment with oral sodium bicarbonate-be careful with oedema and bp. Correting acidosis can delay progression of kidney failure

52
Q

what is the problem with hyperkalaemia and how can it be treated?

A

High potassium can cause arrhytmias and death
Treatment of chronic hyperkalaemai- loop diuretic, correct acidosis, consider dietary potassium restriction
Severe hyperkalaemia can cause cardiac arrest.

53
Q

what does ECG show in a patient with hyperkalaemia?

A

Tenting of T waves-first sign

Widening of QRS-indicates more severe hyperkalaemia

54
Q

what are the advantages of kidney transplant in treating CKD patients?

A

Removes burden of life long dialysis
Improves renal clearance (dialysis only provides GFR 10ml/min
Restores endocrine functions of kidney eg EPO, 1 alpha hydroxylation of vit D
Improves life expectancy

55
Q

what are the disadvantages of kidney transplant in treating CKD patients?

A

Significant perioperative mortality risk (largely cardiovascular mortality)
Lifelong burden of immunosuppression
Infection-opportunistc infection (viral, pneumocystis)
Cancer risk – non myeloma skin cancer, cervix, lymphoma
New onset post transplant diabetes in 12-20%

56
Q

what are the absolute contraindications of kidney transplantation?

A 
Active infection
Active cancer (wait 2-5 yr following cure)
Active drug misuse
Uncontrolled major psychiatric disease
Active non concordance with treatment 
Short life expectancy (<5 yrs)
57
Q

describe the basic principles of uk law surrounding kidney transplantation?

A

Organ transplantation governed by human tissue act 2004 (additional legislation in Scotland and law)
The main change to previous legislation is that facilitated live donor transplantation between unrelated people
Trafficking human tissue for transplantation is criminal offence

58
Q

what are the different sources of kidney transplant?

A

Cadaveric (deceased) donors

  • Heart beating (DBD) – brain death
  • Non heart beating (DCD)

Live donor

  • Related (Blood relationship or emotional relationship eg friend)
  • Unrelated (Paired or pooled donor – overcome blood group or HLA incompatibility)
  • Altruistic donor
59
Q

describe the role of an independent assessor in kidney transplantation?

A

For people wanting to be a live donor
Interviews donor and recipient separately and together
Ensure donors are not forced to do something against their wishes, ensure no reward, donor has capacity
Need proof of identity and proof of relationship
Criminal offense for transplant to go ahead if conditions of HTA haven’t been met

60
Q

what is the median wait time for kidney transplation?

A

2.5 years

61
Q

describe the process of kidney implantation?

A
  • Native kidneys not removed unless indicated
  • Transplant kidney in iliac fossa, extraperitoneal procedure, ureter inserted into bladder and arterial and venous blood supply come from external ilac vein and artery.
  • This is due to the blood supply of the ureter (upper 1/3rd by renal artery so when transplanting kindny can only transplant upper 1/3rd as rest will be ischaemic),
62
Q

describe the role of MHA in kidney transplantation?

A

Genes coding human leukocyte antigens
Class I antigens (HLA-A, B, Cw) expressed on nucleated cells
Class II antigens (HLA-DR, DQ, DP)-expressed on antigen presenting cels, B lymphocytes and activated T cels
Inherited-highly variable between individuals (each have 2 alleles of each gene so express 2 copies of each HLA gene)
Historically HLA types A, B and DR most important
If donor HLA type is matched to recipient HLA type then transplant survival is better
As each individual has 2 copies of each HLA type we can have a combination of 6 different HLA antigens
We express closeness of match between donor and recipient according to number of mismatches of A, B and DR.
-If HLA types are all the same = 0,0,0 mismatch
-If 1A, 1B and both DR antigen are the same then there is 1,1,0 mismatch
-If non of antigens are the same = 2,2,2, mismatch

63
Q

what would be an acceptable donor for a group O recipient?

A

no antigens expressed on red blood cells
antibodies present-anti A and B
donor =O

64
Q

what would be an acceptable donor for a group A recipient?

A

A antigens expressed on RBC
anti-B antibodies present
donor = A or O

65
Q

what would be an acceptable donor for group B recipient?

A

B antigens present on RBC
anti-A antibodies present
acceptable donor = B or O

66
Q

what would be an acceptable donor for a group AB recipient?

A

A and B antigens expressed on RBC
no antibodies present
any donor is acceptable

67
Q

what are the different kind of rejection with kidney transplant?

A

Hyperacute rejection
Acute rejection
Chronic rejection

68
Q

describe the immune response to transplanted organ?

A 
donor antigen is presented to recipient T cells by antigen presenting cells. These ay be of donor (direct) or recipient (indirect) origin. To initiate immume response, antigen must be presented with class 2 MHC molecules and co-stimulatory molecules
T cell activation, once activated the T cell will undergo IL-2 mediated clonal proliferation, produce a variety of cytokines and ell surface markers and recruit further immunoreactive cells
69
Q

describe the drugs that can be used in preventing rejection of organs?

A

Antigen presenting cell (donor or recipient) present antigen with association with MHC presented to T cell recognized by CD3 receptor (signal 1). This is associated with costimulatory molecule CD28. this activated nuclear signaling pathways including calcineurin and co stimulation and CD40, CD154 important molecular, IL2 expression and CD25 is IL2 receptor (signal 3). Cell cycle turned on leading to purine and pryidimine synthesis. And upregulates immune response
Drugs blocking calcineurin = cyclosporin, tacrolimus
mTOR blocker – sirolimus
Cell cycle disruption = azathioprine
Mycophenolic acid-interfer with purine synthesis
Leflunomide – interfers with pyridimine synthesis
Anti-CD3
Anti CD52 (alemtuzumab)
CD25-IL2 receptor antagonists)
Antibodies targeting CD40 blocking co stimulation which couldlead to graft tolerance

70
Q

give examples of immunosuppresive agents?

A 
Calcineurin inhibitors
Inhibitors of mammalian target of rapamycin (mTOR)
Antimetabolites
Monoclonal antibodies
-Anti CD3
-Anti CD52
-Anti IL2 receptor 2
Steroids
These all have side effects
71
Q

why are there so many different different drugs used to prevent rejection?

A

Act at different sites
Varying effectiveness
Different side effects
Combining lower doses of several drugs rather than large dose of one drug tends to result in lower rates of rejection with a lower incidence of side effects

72
Q

what are the potential complications from transplantation?

A

bleeding, infection, hernia, vascular thrombosis, transplant renal artery stenosis, urine leak, ureteric stenosis, new onset diabetes, electrolyte disturbance, acute calineurin inhibitor toxicity, chronic calcineurin inhibitor toxicity, glomerulonephritis, IgA nehropathy, epstein barr virus, malignancy

73
Q

describe hyperacute rejection?

A

When recipient has preformed antibodies to donor kidney (eg blood group incompatible)
Antibody binds directly to antigens on endothelium lining of capillaries of kidney
Complement activation and inflammatory cell infiltration result in endothelial damage
Platelet adhesion and vascular thrombosis lead to renal infarction

74
Q

describe acute rejection?

A

Antigen presentation leads to T cell activation
Cell mediated
Activated T cells undergo clonal proliferation
Helper T cells recruit
-Cytotoxic T cells leading to direct cellular toxicity (tubular rejection)
-B cells leading to donor specific antibody production (vascular rejection)

75
Q

what are the longterm outcomes for kidney transplantation?

A

Acute rejection can be controlled in majority of kidney transplants
Kidney transplants continue to fail over time
Major causes of late graft loss
-Chronic rejection
-Recurrent disease
-Death with functioning graft

76
Q

describe acute rejection?

A

Antibody made by b lymphocyte recognizing and binding to endotheliala and causing acute endothelial injury which can occur early
HLA incompatibility

77
Q

describe chronic rejection?

A

Largely antibody mediated

Progressive vascular damage and thickening, obliteration of lumen of blood vessels

78
Q

what is obstructive nephropathy?

A

Blockage of urinary flow which can occur at any level in urinary tract which can affect one or both kidneys depending on level of obstruction. If only one kidney is affected, urinary output may be unchanged and serum creatinine can be normal. When kidney function is affected this is called obstructive nephropathy. Hyponephrosis refers to dilation of renal pelvis and can be present with or without obstruction

79
Q

what are the causes of obstructive nephropathy?

A

urolithiasis

BPH

80
Q

what is the aim of initial treatment of obstructive nephropathy?

A

Initial treatment is directed at relieving pressure on kidneys to prevent obstructive nephropathy and irreversible renal damage. Prompt relief of obstruction usually preserves the kidneys function. This can include urethral catheter, ureteric stent or nephrostomy tube depending on level and cause of obstruction. Subsequent treatment is targeted towards underlying cause

81
Q

what are the symptoms of obstructive nephropathy?

A 
Acute urinary retention
Renal colic
Infective symptoms
Chronic urinary symptoms
Weight loss, change in bowel habits, family history, malignancy
82
Q

what investigations should be done in a patient with obstructive nephropathy?

A 
Urinary dipstick 
Renal ultrasound
Urea and creatinine
FBC
CT pyelogram
IV pyelogram
Consider
-PSA
-Tumour markers
-CT scan abdomen and pelvis
-Nuclear renography 
-Voiding cystourethrogram 
-Bladder ultrasound 
-MRI

Metabolic and Endocrine (12 decks)

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