Week 8: Renal disease (2) (Pathology) Flashcards

1
Q

AKI def

A

a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.

Associated with increased mortality and morbidity

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2
Q

RF for AKI

A
  • Diabetes
  • CKD
  • IHD/CCF/CVD
  • Any major medical co-morbidity
  • Elderly >75
  • Sepsis
  • Medications – ACEi, ARBs, NSAIDs, Antibiotics
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3
Q

investigations for AKI

A
  • Urine dipstick- protein and blood
    • To look for …… perform:
      • Vasculitis: c-ANCA (PR3) and p-ANCA (MPO)
      • Lupus nephritis: anti-GBM, ANA, C3, C4
      • Myeloma: serum immunoglobulins and electrophoresis to look for myeloma
  • Daily FBC, UandEs, LFTs, bone profile, CRP, serum bicarbonate, CK
  • Urine PCR, MC+S, USS KUB
  • If suspected post-streptococcal GN- anti-streptolysin O titres
  • In case of associated thrombocytopenia consider HUS/TTP/Disseminated Intravascular Coagulopathy, request haemolysis screen - blood film, LDH, bilirubin, reticulocytes, haptoglobin, and call Renal SpR urgently.
  • Check cryoglobulins if unexplained rash, peripheral neuropathy, hypocomplementemia, known hepatitis C, history of lymphoproliferative disorder, or +ve RhF.
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4
Q

management of AKI

A
  • Discontinue nephrotoxic agents e.g. NSAID, ACEi
  • Ensure volume status and perfusion pressure
    • If dehydrated- IV fluids
    • If overloaded- diuretics
    • Aim for euvolemia
  • Be aware of third space losses
  • Urine output and daily bloods
  • Avoid hyperglycaemia
  • Treat underlying causes
  • Refer to specialist
  • Consider ICU admission
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5
Q

causes of AKI can be

A

prerenal

intrinsic

postrenal

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6
Q

prerenal causes of AKI

A
  • Hypovolemia e.g. shock
  • Decreased CO
  • Decreased effective circulating volume (CCF, liver failure)
  • Impaired autoregulation (NSAIDs, ACEi, ARB, cyclosporin)
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7
Q

intrinsic causes of AKI

A
  • Glomerular
    • Acute glomerulonephritis
    • Tubules and interstitium
      • Ischaemia
      • Sepsis/infection
      • Nephrotoxins
        • Exogenous
          • Iodinated contrast, aminoglycosides, cisplatin, amphotericin B
        • Endogenous
          • Haemolysis
          • Rhabdomyolysis
          • Myeloma
          • Intratubular crystals
    • Vascular
      • Vasculitis
      • Malignant hypertension
      • TTP-HUS
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8
Q

postrenal causes of AKI

A
  • Bladder outlet obstruction- i.e. stones, stenosis, tumour
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9
Q

staging of AKI

A
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10
Q

Renal replacement therapy for AKI indication

A
  • Hyperkalaemia refractory to medical therapy
  • Metabolic acidosis refractory to med therapy
  • Resistant fluid overload
  • Uraemic pericarditis
  • Uraemic encephalopathy- vomiting, confusion, drowsiness, reduced consciousness
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11
Q

glomerulonephritis

A

nephrotic/ nephriitc syndorme

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12
Q

nephrotic syndrome presentation

A
  • Oedema
  • Albumin <30
  • Urine PCR >350 (more than 3.5 grams of protein in 24 hours)
    • Hypercholesteraemia
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13
Q

Complications of Nephrotic syndrome include

A
  • Higher risk of Infection
  • Venous thromboembolism - DVT
  • Progression of CKD
  • Hypertension
  • Hyperlipidaemia
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14
Q

causes of nephotic syndrome

A
  • Minimal Change Disease – most common form of GN in children
  • Focal Segmental Glomerulosclerosis – Idiopathic or secondary to infection, malignancy, drugs etc.
  • Membranous Nephropathy – Idiopathic or secondary to infection, malignancy, drugs etc.
  • Membranoproliferative Glomerulonephritis (more commonly presents as nephritic syndrome)
  • Amyloidosis/Myeloma/Diabetes may have nephrotic range proteinuria but not necessarily other nephrotic features
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15
Q

nephritic syndrome presentation

A

Presentation can vary in a combination of some or many of the following:

  • AKI (sometimes GFR can drop drastically)
  • On urine dipstick: blood +/- and/or protein+/- Mild to moderate oedema
  • Proteinuria <3.5g/24 hours
  • Hypertension
  • Sometimes visible haematuria
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16
Q

causes of nephritic syndrome

A
  • Post streptococcal GN (post-infective)
    • Weeks after group A B-haemolytic streptococci infection
    • Children aged 3-12
  • IgA nephropathy
  • Vasculitis (ANCA associated vasculitis)
  • Anti-GBM disease (Goodpasture syndrome)
    • 2 peaks
    • Antibodies against type IV collagen
    • Associated issues with pulmonary basement membrane
  • Alport syndrome
    • X-lined
    • Related to collagen (type V)
    • Associated hearing loss and eye abnormalities
    • ESRF
  • Lupus nephritis
    • Complication fo SLE
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17
Q

management of glomerulonephritis

A
  • Supportive
    • Control BP: ACEi/ARB for proteinuria
    • Salt and water restriction if overloaded
    • Diuretics
    • If hypalbuminaemia <20g/dl then higher risk for VTE- consider LMWH
    • Statins for hypercholesterolaemia
  • Immunosuppressive therapy
    • oral corticosteroids
    • methylprednisolone
    • cyclophosphamide
    • tacrolimus
    • ciclosporin
    • rituximab
    • MMF
    • Azathioprine
  • Invasive therapy
    • Renal replacement therapy
    • Plasma exchange
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18
Q

define chronic kidney disease

A

CKD is defined as the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months.

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19
Q

classification of CKD

A

KDIGO looks at

  • eGFR
  • albumin/creatinine ratio
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20
Q

causes of CKD

A
  • Diabetes
  • Hypertension
  • Glomerulonephritis
  • Renovascular Disease
  • Polycystic Kidney disease
  • Obstructive nephropathy – urological problems
  • Chronic/recurrent Pyelonephritis
  • Others
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21
Q

complications of CKD

A
  • Anaemia of Chronic Kidney Disease
  • Chronic Kidney Disease – Mineral & Bone Disease
  • Secondary & Tertiary hyperparathyroidism
  • Hypertension
  • Cardiovascular Disease – No 1 cause of Mortality
  • Malnutrition/sarcopenia
  • Dyslipidaemia
  • As CKD progresses
    • Electrolyte disturbances
    • Fluid overload
    • Metabolic acidosis
    • Uraemic pericarditis
    • Uraemic encephalopathy (indication for replacement therapy)
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22
Q

MDT management in CKD

A
  • Renal physicians
  • General practitioners
  • Renal specialist nurses/ home care team
  • Dieticians
  • Pharmacists
  • Vascular/transplant surgeons
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23
Q

management for CKD is based around

A
  • treating underlying disease
  • reduce CCD risk
  • reduce progression
  • prevent complications
  • plan for the future
24
Q

CKD- treat underlying disease

A
  • Treat and monitor diabetic control
  • Treat hypertension
  • Treat infections promptly
  • Tolvaptan if meets criteria for ADPKD
  • Immunosuppression for GN if appropriate
25
Q

CKD- reducing cvd risk

A
  • Start on statin
  • Control BP
  • Improve control of diabetes
  • Advise weight loss
  • Advise exercise
  • STOP SMOKING
26
Q

how to reduce progression of CKD

A
  • Reduce proteinuria – ACEi/ARB
  • Monitor blood tests
  • Control BP
27
Q

preventing complications of CKD

A
  • Dietary advice regarding low phosphate/low potassium diet
  • Phosphate binders
  • IV Iron/Folate/Vit B12 replacement
  • EPO (Erythropoesis stimulating agent)
  • Replace Vitamin D deficiency
  • Consider Calcimimetics for tertiary hyperparathyroidism
  • Dietician input
28
Q

planning for the future in CKD

A
  • Start discussions of what options they have if they reach ESRF
  • Home care team input
  • Discuss disadvantages & advantages of types of RRT
    • Home therapies – APD, CAPD, Home HD
    • Unit-based therapies – Nocturnal HD, conventional HD
    • Active conservative management
    • Transplant
  • Refer for fistula
    • Venous mapping
  • Refer for PD tube insertion
  • Work-up for transplant
    • Further tests
    • Refer to Transplant work-up clinic
29
Q

renal replacmeent therapies

A
  • Haemodialysis
  • Peritoneal dialysis
  • Renal transplant.
30
Q

how does haemodialysis work

A

The dialysis machine pumps blood from the patient, through disposable tubing, through a dialyser, or artificial kidney, and back into the patient. Waste solute, salt and excess fluid is removed from the blood as it passes through the dialyser.

31
Q

Getting blood out of a patient for dialysis

A

venous fistula

central venous line

32
Q

creating a venous fistula for haemodialysis

A
  • Take radial artery and join it up with cephalic vein and overtime the cephalic vein becomes arterialised
  • This can them be used to cannulate x3 times per week
  • Will be able to feel a thrill and hear a bruit

If fistulas fail or in a rush….. move onto a venous line

33
Q

warning signs of venous fistula

A
  • shiny
  • thin looking
    *
34
Q

advanatges of PD

A
  • Quality of life
  • It is often an excellent first choice for patients starting dialysis, particularly when they still have some residual native renal function
  • PD regimes are designed on a much more individualised basis than patients on HD.
35
Q

types of HD

A

Home HD – offer training at home for more frequent HD

  • *Nocturnal HD** – Overnight slow, long HD
  • *CRRT –** continuous renal replacement therapy mainly used in acute setting (ITU/HDU)
36
Q

active conservative management of ESRF

A

Decision made after discussion with patient and family members – often after multiple clinic visits and after patient is fully informed of risks & benefits of each mode of therapy

Evidence suggests that if

  1. Age >80 OR
  2. WHO performance score of 3 or more
    …then RRT offers no survival benefit
  3. Often these patients may be unsuitable for or choose to not have invasive therapy such as PD/HD/Transplantation
37
Q

advatantages of dialysis

A
  • Efficient form of dialysis
  • Unit-based – plenty of support from staff
38
Q

disadvantages of dialysis

A
  • Dialysis access needs to be secured
  • Infection/Bacteraemia
  • Haemodynamic instability
  • Reactions to dialysers
  • Haematomas/risk of bleeding
  • Muscle cramps
  • Anaemia due to clotted lines/Haemolysis
  • AVF steal syndrome
  • SVCO from central lines
39
Q

types of PD

A

Automated PD

  • Carried out with an automated cycler machine performed at night.
  • 10-12L usually exchanged, over 8-10 hours.
  • Lifestyle advantages – Leaves the daytime free

Continuous Ambulatory PD

  • Usually consisting of 4-5 dialysis exchanges per day (usually 2 litres each)
  • Exchanges are performed at regular intervals throughout the day, with a long overnight dwell.

Assisted Automated PD

Trained healthcare assistants visit the patient’s home to help with setting up APD.

40
Q

how does peritoneal dialysis work

A
  • Home based therapy
  • Reliant on the patients’ own peritoneal membrane acting as the dialysis membrane.
  • Solutes (electrolytes, urea, creatinine) move from the patient’s blood, across the peritoneal membrane, down the concentration gradient into the dialysate fluid.
  • Osmotic gradient is created by high concentration of glucose (occasionally amino acid or glucose polymer solutions are used) in the dialysate fluid, which removes water from the patient.
41
Q

Contraindications for kidney transplantation

A
  • Active infection or malignancy
  • Severe heart disease not suitable for correction
  • Severe lung disease
  • Reversible renal disease
  • Uncontrolled substance abuse, psychiatric illness
  • On-going treatment non-adherence
  • Short life expectancy
42
Q

advantages of renal transplant

A
  • Near normal lifestyle
  • Better mortality/morbidity
43
Q

transplantation

A

Treatment of choice for most patients with ESRF

44
Q

central venous line and haemodialysis

A

Blood can be taken a t a flow rate of 200ml/minute from the superior vena cava.

  • High risk of infection from skinendocarditis
45
Q

disadvantages of PD

A
  • Patients need to be able to manage technical aspects of dialysis
  • Unsuitable in patients with stoma/previous surgery
  • Risk of infection (PD peritonitis)
  • Complications – drainage problems, malposition, leaks, herniae, hydrothorax, long term use associated with encapsulating peritoneal sclerosis
46
Q

living unrelated donor

A
  • 4 forms:
    • a)live-donor paired exchange,
    • b) live- donor/deceased-donor exchange,
    • c)live-donor chain,
    • d)altruistic donation
    • Usually have comparable outcomes to live-related donors
    • Time to transplantation can happen in months
47
Q

disadvantages of renal transplant

A
  • Criteria to meet suitability to safely undergo operation
  • Compliance with medication lifelong
  • Risk of rejection
  • Risk of malignancies over time
  • Risk of infection (on immunosuppression)
    • CMV, hepatitis B, herpes, varicella zoster, EBV, aspergillus, pneumocystis jiroverccii, listeria, MTB
  • Long waiting times for cadaveric organ
  • New onset diaebetes
48
Q

types of renal transplant

A
  • living related donor
  • living related
  • deceased donor
49
Q

living related donor

A
  • Best
  • Good compatibility
  • Time to transplantation can happen in months
50
Q

deceased donor

A
  • Approximately 60% of the transplants in the UK fall into this category
  • Patients receive a kidney (or two from the same donor) with little time for preparation, so transplant protocols are important to keep updated regularly
  • Time to transplantation happen in years
  • Survival of kidney allograft and patients are significantly low compared to live donor transplantation.
51
Q

Simultaneous kidney transplantation

A
  • Liver-kidney: patients with liver failure or cirrhosis and ESRF can be candidates for simultaneous transplant
  • Pancreas-kidney: selected patients with Type 1 diabetes mellitus. Can be done simultaneous or sequential
  • Patients with kidney transplant who progress into ESRF can be re-transplanted
52
Q

induction treatment in transplantation

A

Immunosuppressive drugs to create tolerance of the graft

  • Methylprednisolone with any of the following:
    • Basiliximab
    • Thymoglobulin
53
Q

maintenance treatment in transplantation

A

Prevent acute rejection

  • Steroids: prednisolone
  • Calcineurin inhibitors (CNI): tacrolimus, cyclosporine, voclosporin
  • Antimetabolite medications: mycophenolate, azathioprine
  • T cell regulation: belatacept and belimumab
54
Q

long term care in renal transplantation

A
  • Regular follow ups
    • GFR
      CNI levels
    • Proteinuria
    • Calcium, phosphate and PTH
    • Lipids
    • Glucose
  • Screen for infections
  • Vaccination (except live or live attenuated)
  • Monitor and control CVD
  • Screen for malignancies
  • Contraception obligatory in first yes and counsel about pregnancy one year after
55
Q

mortality after transplant-ion related to

A
  • Cardiovascular disease
  • Infections
  • Malignancy