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Medicine year 4 CDM > Block 4: glomerulonephritis and RRT > Flashcards

Block 4: glomerulonephritis and RRT Flashcards

1
Q

Anti-GBM autoantibodies= cause of nephritic syndrome

A
  • An immune-mediated pathology involving antibodies directed against glomerular basement membrane antigens (anti-GBM antibodies)
  • Investigations: Immunohistochemistry (IgG deposits along the basement membrane of the glomerulus), Antibodies (anti-GBM antibodies)
  • Management: high dose immunosuppression (IV prednisolone, cyclophosphamide and plasmapheris)
  • The antigens are located in the glomeruli and in the alveoli of the lungs causing nephritic syndrome and alveolar haemorrhage presenting as haemoptysis. If both lungs and kidneys are involved its Goodpastures
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2
Q

Nephrotic syndrome

A

Triad of:

  • Heavy proteinuria >3.5g/day
  • Hypoalbuminaemia (<35 g/L)
  • Peripheral oedema
  • May be accompanied by Hyperlipidaemia and thrombotic disease
  • Can develop AKI but less common then in nephritic
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3
Q

Non-proliferative (structural) nephrotic syndrome

A

Glomerular damage characterised by structural changes and often sclerosis (scarring of the glomeruli). May show diffuse scarring or only subtle changes under electron microscope. Typically associated with excess protein loss and nephrotic syndrome.

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4
Q

Causes of nephrotic syndrome

A
  • Primary: due to renal glomeruli injury. Minimal change disease, Focal segmental glomerulosclerosis, Membranous nephropathy
  • Secondary: Glomeruli injury due to wider systemic injury. For example diabetes mellitus, Amyloidosis, HIV
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5
Q

Nephrotic syndrome: investigations

A
  • Gold standard: renal biopsy
  • Urine: dipstick (detects albumin), Urine protein:creatinine ratio (normal is <30mg/mmol), 24 hour urinary collection (urine is collected over 24 hours to determine the protein content. Normal is <0.2g)
  • Blood tests: FBC, U&E’s, bone profile, HbA1c, blood gas, lipid profile (hyperlipidaemia in nephrotic syndrome)
  • Imaging: renal ultrasound or CT KUB
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6
Q

Symptoms of nephrotic syndrome

A
  • Fatigue
  • Poor appetite
  • Peripheral oedema, Periorbital oedema: less protein so loss of oncotic pressure and increased movement of fluid into the interstitial space
  • Shortness of breath: typically from pleural effusions and/or
    pulmonary oedema
  • Foamy urine: due to excess protein loss
  • Signs: ascites, effusion (dull percussion note and reduced air entry)
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7
Q

Complications of nephrotic syndrome

A
  • Thrombotic: both arterial and venous, causes DVT and PE
  • Hyperlipidaemia: fall in oncotic pressure increases lipoprotein synthesis causing higher levels of cholesterol. Reduced triglyceride metabolism due to reduced activity of lipoprotein lipase
  • Recurrent infections: due to loss of immunoglobulins through glomeruli
  • AKI
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8
Q

Minimal change disease

A
  • Cause of nephrotic syndrome- majority of cases in young children
  • Mostly idiopathic but can be due to Drugs (NSAID’s), malignancy (lymphoproliferative disorders), infections (syphilis).
  • Due to fusion of podocyte processes causing immune dysfunction and disruption of the filtration barrier
  • In children assume minimal change and start treatment, in adults need renal biopsy
  • Management: systemic glucocorticoids (prednisolone). Second line is further courses of prednisolone or more intensive immunosuppresants
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9
Q

Glomerulonephritis cause: Focal segmental glomerulosclerosis

A
  • Causes of nephrotic syndrome- common cause in adults
  • Refers to sclerosis in parts of at least one glomerulus
  • Primary FSGS: due to a circulating factor that damages podocytes causing them to spread out, reducing the effectiveness of the filtration barrier
  • Secondary FSGS: an adaptive response to renal injury, causes less proteinuria and renal impairment. Causes glomerular hypertrophy and hyperfiltration. Causes: severe obesity, reflux nephropathy and reduction in kidney mass
  • Diagnosis: renal biopsy
  • Management: primary FSGS is treated with immunosuppressive medication and steroids. Secondary FSGS is about treating the underlying cause i.e. weight loss in obesity
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10
Q

Membranous nephropathy

A
  • Most common cause of nephrotic syndrome in adults
  • Glomerular basement membrane thickening without significant cellular proliferation
  • Primary MN: an autoimmune reaction against antigens in the filtration barrier. Development of autoantibodies, formation of immune deposits and thickening of glomerular basement membrane. Primarily antibodies against phospholipase A2 receptor (PLA2R)
  • Secondary: due to underlying infection, drug use or systemic disorder i.e. SLE, viral hepatitis, prostate cancer, NSAID’s
  • Management: some have spontaneous remission. If high risk but no irreversible damage then use immunosuppressive agents in primary. In secondary target underlying cause
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11
Q

Renal amyloidosis

A
  • Cause of nephrotic syndrome- extracellular deposition of fibrils that contain proteins
  • There are two systemic forms: AL amyloidosis (excess light chains due to
    plasma cell disorders) and AA amyloidosis (excess precursor protein due to chronic inflammation).
  • Amyoid fibrils contain insoluble proteins that form beta pleated sheets that are resistant to degradation and deposit in organs- some are genetic
  • Diagnosis: renal biopsy with identification of amyloid fibrils using Congo red staining, can sample tissue from another site as its systemic
  • Management: depends on cause i.e. AA amyloidosis, hereditary amyloidosis. In renal involvement supportive management is needed. In end stage dialysis may be used
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12
Q

Renal screen nephrotic syndrome

A
  • Complement: typically low in vasculitis
  • Anti-nuclear antibody (ANA)
  • Anti-neutrophil cytoplasmic antibody (ANCA)
  • Anti-glomerular basement membrane antibody (GBM)
  • Anti-dsDNA: raised in systemic lupus erythematosus
  • Myeloma screen: serum free lights chains, protein electrophoresis
  • Anti-PLA2R autoantibody: raised in membranous nephropathy
  • Virology: Hepatitis B, Hepatitis C and Human immunodeficiency virus
  • Cryoglobulins: immunoglobulins that precipitate at low temperatures
  • Creatine kinase: may be raised in rhabdomyolysis
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13
Q

Management in glomerular disease

A
  • Regular monitoring
  • Treat underlying causes: corticosteroids in minimal change disease and immunosuppressors in ANCA associated vasculitis
  • Treat complications: i.e. nephrotic syndrome causes hyperlipidaemia and nephritic syndrome has extra-renal manifestations i.e. pulmonary haemorrhage
  • Consider renal replacement therapy
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14
Q

Renal replacement therapy definition

A

Term used to encompass life supporting treatment for renal failure. Includes all types of dialysis and kidney transplantation

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15
Q

Dialysis techniques

A
  • Continuous hemofiltration
  • Continuous haemodialysis
  • Peritoneal dialysis
  • Intermittent haemodialysis
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16
Q

Dialysis time scale

A

Can be intermittent or continuous. Continuous therapy is used in an AKI when it has benefits over intermittent therapy due to improved tolerability due to slower removal of solute and water

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17
Q

Haemodialysis

A
  • Blood comes into contact with a semi-permeable membrane (in the dialyser) which contains dialysate on the other side, substances diffuse across
  • Works as an artifical kidney
  • The solutes are removed with the dialysate
  • Can be performed in hospital or at home. In hospital its 4 hours 3 times a week
  • Require either an arteriovenous fistula (takes around 6-8 weeks to become usable after formation) or a tunnelled central venous catheter
  • Arteriovenous fistula: Preferred dur to more complications with lines (particularly infection)
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18
Q

AV fistula

A

Small surgery allows blood to be diverted from an artery to a vein, high pressure arteriole blood causes the vein to enlarge and thicken. So, two large bore needles can be inserted regularly. Provides better quality dialysis

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19
Q

Complications of Haemodialysis

A
  • Access-related: infection (including bacteraemia leading to endocarditis, discitis), venous stenosis, access failure
  • Haemodynamic instability
  • Nausea and vomiting
  • headache
  • cramps, particularly leg cramps
  • Reactions to dialysis membranes
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20
Q

Peritoneal dialysis

A
  • The vascularised peritoneum acts as the dialysis membrane
  • Dialysis fluid in the peritoneal cavity creates osmotic gradients causing water removal (ultrafiltration), convection and diffusion of solutes across the membrane
  • After several hours the used fluid is drained out and fresh fluid is installed
  • Just as effective as haemodialysis and is performed for 8-12 hours a day, usually overnight and in their own home
  • The dilatate contains varying amounts of glucose which creates a high osmotic pressure helping to draw out extra fluid from the body that the patient doesn’t require
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21
Q

Peritoneal dialysis: process

A
  • A catheter (e.g. Tenckhoff catheter) is inserted into the abdominal cavity, which allows the infusion of the dialysate.
  • The dialysate then dwells within the abdomen using the peritoneum as a semi-permeable membrane for the transfer of
    waste products.
  • The dialysate is then removed
  • Requires a functional peritoneal membrane so may not be suitable if previous intra-abdominal pathology (previous peritonitis, surgery, adhesions)
22
Q

Types of peritoneal dialysis

A
  • Continuous ambulatory peritoneal dialysis (CAPD): manual dialysate exchanges are typically performed four times per day. Takes about 20-40 minutes each time.
  • Automated dialysis (APD): a machine performs exchanges overnight. Often fluid is left in the peritoneal cavity in the day to increase effectiveness of dialysis. Requires a small machines
  • Done at home
23
Q

Complications of peritoneal dialysis include

A
  • Bacterial or fungal peritonitis (usually detected by cloudy PD fluid or effluent)
  • Catheter problems: infection, blockage, kinking, leaks, displacement (more likely if a patient becomes constipated)
  • Weight gain
  • Worsening glycaemic control in patients with diabetes
  • Failure of peritoneal membrane requiring a switch to haemodialysis
  • Encapsulating peritoneal sclerosis
24
Q

Peritoneal dialysis peritonitis

A
  • Bacterial peritonitis is the most serious complication
  • Presents as abdominal pain of varying severity: can cause guarding
  • Cloudy effluent from the cavity
  • If severe can cause vomiting, nausea and paralytic ileus (sometimes bowel perforation)
  • Treat with intra-peritoneal antibiotics
25
Q

Kidney transplant

A
  • the gold standard for RRT. Treatment of choice for anyone with ESRD who is fit enough.
  • Need induction and maintenance immunosuppression to prevent graft rejection
  • Old kidney left in situ, new one is placed in either the right or left iliac fossa
  • Transplantation has best outcomes, removes need for dialysis, normalises anaemia and renal bone disease and improves QoL and long term survival
26
Q

Types of kidneys transplant

A
  • May be from living or non-living donors as long as there is MHC compatibility
  • Non living: Donors after cardiac death (DCD), Donors after brain death (DBD)
27
Q

Contraindications to kidney transplant

A
  • Active or recent malignancy
  • Active infection
  • Significant co-morbidity
28
Q

Complications of renal transplantation 1

A
  • Operative complications: infection, bleeding, arterial or venous thrombosis, problems with ureteric anastomosis
  • Stenosis of graft artery or ureter
  • Side effects from immunosuppressive therapy: nephrotoxicity and hypertension secondary to tacrolimus or ciclosporin
  • Opportunistic infections particularly Cytomegalovirus (CMV)
  • Malignancy: Epstein Barr virus-driven non-Hodgkin B cell lymphomas, and non-melanoma skin cancers (squamous cell and basal cell carcinomas)
29
Q

Complications of renal transplantation 2

A
  • Recurrence of original renal disease in the transplant
  • Hyperacute graft rejection: untreatable and should not occur if appropriate cross-matching has been performed
  • Acute graft rejection: presents with creatinine rise, diagnosed by graft biopsy, initial treatment normally with intravenous steroids
  • Chronic allograft nephropathy: can occur for multiple reasons, does not usually respond to increased immunosuppression
30
Q

The three types of tissue rejection

A
  • Hyperacute rejection occurs a few minutes after the transplant when the antigens are completely unmatched. The tissue must be removed right away so the recipient does not die. For example, giving the wrong blood
  • Acute rejection may occur any time from the first week after the transplant to 3 months afterward. All recipients have some amount
    of acute rejection.
  • Chronic rejection can take place over many years. The body’s constant immune response against the new organ slowly damages the transplanted tissues or organ.
31
Q

How oral absorption may be reduced in renal impairment

A
  • Gut oedema: may have to give IV furosemide
  • Uraemia symptoms: nausea and vomiting
  • Reduced gut motility
  • Increased gut pH
  • Concurrent medication: phosphate binders- allows phosphate to be removed in the GI tract and not renally, reduced gut absorption in some diabetic meds
32
Q

How drug distribution can be affected in renal impairement

A
  • Oedema: Large volume of distribution into the water soluble compartment
  • Changes in hydration station
  • Long term malnutrition and muscle mass: reduced protein and tissue binding
33
Q

How metabolism and excretion is affected in renal impairment

A

Metabolism: overall drug metabolism is slowed down in CKD, specific drugs i.e. vitamin D and insulin.

Excretion: any drug predominantly excreted by the kidneys will accumulate in renal impairment. Causing increased therapeutic effects, side effects and toxic effects

34
Q

What makes a drug nephrotoxic

A
  • Direct- inflammation and damage to the structure within the kidney: i.e. Aminoglycosides (tubular cell toxicity), Trimethoprim/ Penicillin/ Vancomycin/ NSAID’s (acute interstitial nephritis). Immune modulators (nephropathies, tubular damage, acute interstitial nephritis)
  • Indirect- altered haemodynamics compromising perfusion of kidneys i.e. ACEi/ARB, diuretics, vasodilators
35
Q

Ideal drugs for the renally impaired

A
  • Not metabolised or excreted by the kidneys
  • Wide therapeutic index or can monitor levels
  • Few side effects
  • Does not interact with other drugs
  • Not affected by hydration status
  • low protein binding, low sodium content, low infusion volume
36
Q

CKD supportive medicines

A
  • Renal Anaemia; IV iron, EPO
  • Bone chemistry: Alfacalcidol (vitamin D), phosphate binders, cinacalcet (treats tertiary hyperparathyroidism), etelcalcitide
  • Acid/base balance: Sodium bicarbonate
  • Analgesia: Simple analgesia, suitable opiates
  • Antidepressants
  • Extra vitamins: Renavit for intermittent haemodialysis patients
  • Laxatives: Particularly important for peritoneal dialysis patients
37
Q

Drug dosing in renal impairement

A
  • Calculate CrCl
  • Look up in the renal drug handbook
  • If drug is renally excreted give smaller doses and/or less often
  • Reduce Statin dose
  • ACEi can increase Potassium so important to monitor
  • Oxycodone is a renal friendly opiate but should be given on half dose in dialysis
  • If drug is renally excreted give in smaller doses and less often
38
Q

Continuous veno-venous haemofiltration (CVVH)

A

Done in ICU, continuous dialysis which works by convection. The eGFR changes drastically between the different types of dialysis. For example, in haemodialysis it rises rapidly but because the rest of time its zero you assume its always less than 10.

39
Q

Drug dosing in RRT

A
  • Drug factors: molecular weight (if too large to fit through membrane pores wont be removed), protein binding (if high wont be removed), water solubility (if high will be removed), adsorption of drug molecule onto dialysis membrane- will be removed
  • Dialysis factors: duration of dialysis (if long more is removed), flow rate of blood and dialysate (more drug removal), type of membrane used (permeability)
  • Dont calculate CrCl for patients on dialysis- not accurate assume <10ml/min
40
Q

Diabetic kidney disease (DKD) definition and symptoms

A

Diabetic kidney disease (DKD) normally occurs in patients with long-standing diabetes (>10 years) with albuminuria and/or reduced estimated glomerular filtration rate (eGFR) in the absence of signs or symptoms of other primary causes of kidney damage.

Symptoms: may not be present till disease is advances include fatigue, anorexia and swelling of extremities

41
Q

DKD investigations

A
  • Reduced eGFR without albuminuria is becoming more common
  • Characteristically have proteinuria and later deterioration in renal function
  • A nephrotic syndrome
  • Progression of DKD may occur even in well controlled diabetes
  • Kidney biopsy- mesangial expansion and nodular glomerulosclerosis. Kidney biopsy rarely needed
  • Can diagnose clinically with albuminuria (>3.4 mg/mmol [30 mg/g]) and progressive reduction in eGFR with long duration of diabetes (>10 years in type 1, may be present on diagnosis in type 2). Typically associated with retinopathy
42
Q

DKD treatment

A
  • Intensive control of hyperglycaemia and hypertension with ACEi, ARB’s and other antihypertensives
  • Lipid reduction and smoking cessation
  • SGLT 2 inhibitors are effective at glycaemic control and slow progression of DKD
  • GLP-1 mimetics are highly effective
43
Q

DKD risk factors

A

Poor control of blood glucose, uncontrolled high blood pressure, Type 1 diabetes with onset before 20, past or current smoking, family history of diabetic nephropathy, Afro-caribbean.

44
Q

What investigations would be helpful in a patient with suspected pulmonary renal syndrome

A

CXR, urine microscopy, pulmonary function tests, immunology and antibodies

45
Q

Good pastures diagnosis

A

Confirmed by detecting anti-GBM antibodies in the blood or deposited in the kidney

Renal biopsy: RBC in the urine caused by ruptured glomerular capillaries and abnormal crescent shaped accumulation of cells in the urine surrounding the glomerulus (crescent)

46
Q

What fluids are advised in AKI

A

Fluid resuscitation with 0.9% sodium chloride at a rate of 10-15ml/kg/hr to achieve high urinary flow rates (>100ml/hr), with the cautious addition of sodium bicarbonate 1.4% to maintain urinary pH> 6.51 (monitor fluid status and take care not to precipitate pulmonary oedema)

47
Q

How is hypocalcaemia caused by CKD

A

Kidneys fail= unable to activate Vit D= functional Vit D deficiency= unable to absorb Ca from the gut= decreased Ca (then goes on to cause secondary hyperparathyroidism to draw Ca out of the bone so Ca may be normal)

48
Q

What causes Hyperphosphatemia in CKD

A

Kidney failure= inability to activate Vit D= unable to absorb Ca from the gut= low Ca= PTH release= draws Ca and phosphate out of the bone, phosphate cannot be excreted due to renal impairment= high serum phosphate

49
Q

At what eGFR is anaemia likely to be an issue in CKD and treatment

A

<30 (<45 in diabetics)

Treatment: EPO treatment after normalisation of haematinics (particularly iron stores- iron metabolism is impaired in CKD so IV iron is often used)

Target iron: 10.5-12.5

50
Q

Medication to help treat CKD

A

Reduce proteinuria: ACEi and ARB
Reduces progression: SGLT2- only use if diabetic

50
Q

What might be seen on renal biopsy in CKD

A

Renal fibrosis (accumulation of myofibroblasts in the interstitium= laying down fibrotic tissue in the kidney= increased matrix deposition, separation of tubules and loss of peritubular capillaries= tubular atrophy and loss of function, and glomerulosclerosis)

Medicine year 4 CDM (44 decks)

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