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MEDICINE - Renal > AKI, CKD & GN > Flashcards

AKI, CKD & GN Flashcards

1
Q

What are the different KDIGO classifications of an AKI?

A

Stage 1:

Serum Creatinine 1.5-1.9x baseline,

Urine output <0.5ml/kg/hr for 6-12 hours

Stage 2:

Serum Creatinine 2.0-2.9x baseline,

Urine output <0.5ml/kg/hr for >12 hours

Stage 3:

Serum Creatinine 3x baseline,

Urine Output <0.3ml/kg/hr for >24 hours OR

Anuria for >12 hours

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2
Q

What are some modifiable and non-modifiable risk factors for AKI?

A

Modifiable

  • Dehydration
  • Sepsis
  • Diabetes
  • Nephrotoxic drugs
  • Drugs eg. ACEi, ARBs, NSAIDs, Antibiotics

Non-Modifiable

  • >75 years old
  • CKD
  • HF
    Peripheral vascular disease
  • Chronic Liver Disease
  • LUTS Hx
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3
Q

How would AKI present?

A
  • symptoms of uraemia eg. anorexia, nausea, pruritis, vomiting. Then drowsiness, fits, coma, confusion
  • GI bleeds, epistaxis
  • Hyperkalaemia (particularly in sepsis or muscle trauma)
  • Metabolic acidosis
  • Pulmonary Oedema
  • Hyponatraemia
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4
Q

What is acute tubular necrosis?

A

sustained underperfusion and reduced renal blood flow of renal tubules, resulting in tubular death

OR

nephrotoxins causing direct injury/cell death in renal tubules

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5
Q

What are some pre-renal causes of AKI?

A

RENAL HYPOPERFUSION

  • Hypovolaemia (bleeding, dehydration, etc)
  • Decreased effective circulating vol (congestive heart failure, liver failure)
  • Decreased cardiac output
  • decreased intake/ dehydration
  • Hepatorenal syndrome (portal HTN results in splanchnic vasodilation which triggers RAAS and causes renal vasoconstriction)
  • Systemic vasodilation/ Shock eg. anaphylactic, cardiogenic, hypovolaemic, mechanical
  • Renal artery stenosis
  • Impaired renal autoregulation eg. NSAIDs (afferent vasoconstriction), ACEI/ARBs (efferent vasodilation), Cyclosporin
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6
Q

What are some Intrinsic Renal causes of AKI?

Split into those affecting Glomerular, Tubules, Vascular

A

Glomerular - Acute glomerulonephritis

  • Membranous (adults)
  • Minimal change (children)
  • IgA Nephropathy (children)
  • Focal segmental Glomerulosclerosis

Tubules/Interstitium - Acute Tubular Necrosis​ caused by

  • Exogenous Nephrotoxins (iodinated contrast, aminoglycosides, cisplatin, amphotericin B, gentamicin)
  • Endogenous Nephrotoxins (Haemolysis, Rhabdomyolysis, Myeloma, Intratubular crystals)
  • Sepsis/Infection/Ischaemia

Vascular

  • Vasculitides eg. Wegeners, Goodpastures, SLE, HSP, Vasculitis
  • Malignant Hypertension
  • TTP, HUS
  • pre-eclampsia
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7
Q

Describe how rhabdomyolysis happens?

A

This is “crush syndrome”

skeletal muscle injury causes the release of intracellular myoglobin, which is a direct tubular toxin leading to ATN

Causes eg. trauma, compartment syndrome, excessive exertion (eg. marathon runners), status epilepticus, muscle toxins (eg. antimalarials, snake venom)

Results in a really high CK.

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8
Q

What are some post-renal causes of AKI?

Split into External, Lumen and Wall obstructions.

A

External causes of obstruction

  • Retroperitoneal fibrosis, aneurysms, tumours, diverticulosis, BPH, blocked catheter

Causes of obstruction in the wall

  • Ureteric strictures, BPH

Causes of obstruction in the lumen of ureters/kidneys/bladder

  • Clots, calculi, papillary necrosis, tumours
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9
Q

What investigations would you do in a suspected AKI?

A
  • Urine dipstick and MC&S
    • PRE = normal
    • RENAL = protein/blood on dipstick and RBC casts on microscopy is GN
      • If protein/blood +ve, do c-ANCA and p-ANCA for vasculitis, anti-GBM, ANA, C3 and C4 for lupus nephritis, serum immunoglobulins and electrophoresis for myeloma
    • ATN = muddy brown granular casts
    • POST = sometimes blood on dipstick
  • Assess volume status = pulse, bp, cap refill, JVP
  • FBC, U&Es, LFTs, Bone profile, CRP, (CK if rhabdo suspected)
  • Post-Strep GN (Anti-Streptolysin O Titres)
  • USS KUB to rule out obstruction
  • US of kidneys to differentiate between CKD and AKI
  • In case of thrombocytopaenia consider HUS/TTP/DIC. Request haemolysis screen.
  • Abdo exam can feel palpable bladder = outflow obstruction
  • Neutrophil Gelatinase associated Lipocalin rises hours after AKI. (Better than Creatine which rises 48-72 hours after and by then it might be irreversible)
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10
Q

How would you manage an AKI?

A
  • discontinue nephrotoxic agents
  • if dehdyrated = fluids
  • if overloaded = diuretics
  • Monitor urine output/daily bloods (catheterise if necessary)
  • Treat underlying cause
  • Refer to specialist for consideration of renal replacement therapy
  • Monitor creatinine
  • Consider ICU admission
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11
Q

When would you consider renal replacement therapy for an AKI?

A
  • Unresponsive Hyperkalaemia
  • Unresponsive Metabolic Acidosis
  • Fluid overload unresponsive to diuretics
  • Uraemic pericarditis
  • Uraemic encephalopathy (vomiting, confusion, drowsiness, reduced consciousness)
  • Removal of drugs causing AKI (ethylene glycol, methanol, gentamicin, lithium, severe aspirin overdose)
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12
Q

How would you classify CKD?

A

Stage 1 = eGFR>90 = normal

Stage 2 = eGFR 60-89 = mild

Stage 3 = eGFR 30-59 = moderate

Stage 4 = eGFR 15-29 = severe

Stage 5 = eGFR <15 = kidney failure

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13
Q

What are some early symptoms of CKD? (urea <40mmol/L)

A

early on it is mostly asymptomatic but some experience:

  • Malaise
  • loss of appetite
  • Itching (high urea)
  • Nocturia/Polyuria (inability to concentrate urine)
  • Nausea, Vomiting, Diarrhoea
  • Paraesthesia and tetany due to hypocalcaemia
  • Restless Leg Syndrome
  • Peripheral/Pulmonary oedema (salt and water retention)
  • anaemia
  • erectile dysfunction in men, amenorrhoea in women
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14
Q

How would CKD present in more advanced uraemia? (50-60mmol/L)

A

CNS symptoms like Mental slowing, clouding of consciousness, seizures

Myoclonic twitching (myoclonus)

uraemic pericarditis (saddle ST elevation)

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15
Q

What signs on examination are there of CKD?

A
  • short stature in children
  • pallor due to anaemia
  • increased photosensitive pigmentation
  • brown colouration of nails
  • pericardial friction rub
  • flow murmurs (mitral regurg due to mitral annular calcification, aortic/pulmonary regurg due to vol overload)
  • glove and stocking peripheral sensory loss
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16
Q

What are some of the risk factors for CKD?

A
  • CVS disease
  • Diabetes
  • Smoking
  • HTN
  • AKI
  • Chronic NSAID use
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17
Q

What are some common causes of CKD?

A
  • Diabetes (most common in UK) = 20-40%
  • HTN = 5-25%
  • Glomerulonephritis = 10-20%
  • Renovascular disease (Renal artery stenosis) = 5%
  • Polycystic Kidney Disease or other congenital = 5%
  • Obstructive nephropathy or urological problems
  • Chronic/Recurrent pyelonephritis
  • Systemic inflammatory disease eg. SLE/Vasculitis = 5%
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18
Q

How would you differentiate between AKI and CKD?

A
  • CKD kidneys would be small and scarred with the presence of cysts. AKI has normal sized kidneys
  • CKD presents with anaemia (normochromic normocytic)
  • AKI has a low BP, CKD has a high BP
  • CKD has CNS symptoms later
  • CKD presents with oligouria very late. Early on it is polyuria and nocturia.
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19
Q

What are the main complications of CKD?

A
  • Anaemia of chronic disease
  • Mineral and bone disease
    • results in bone pain and fractures
  • Secondary/Tertiary Hyperparathyroidism
    • bone pain and fractures
  • Hypertension
    • can result in HF, CVS disease
  • CVS Disease !!!!!!
  • Malnutrition/Sarcopenia
  • Dyslipidaemia
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20
Q

What are some later complications of CKD?

A

Electrolyte disturbances

Fluid overload

Metabolic acidosis

Uraemic pericarditis

Uraemic encephalopathy

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21
Q

How would you manage the Hypertension?

A

ACEI (check K first via U&Es. Not if K+>5)

For dialysis patients, do low salt diet and ultrafiltration

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22
Q

How would you manage the Mineral & Bone disease?

A

Give Bisphosphonates and Vitamin D

This is diagnosed if there are:

  • abnormalities in calcium/phosphate/alkaline phosphatase/PTH or Vit D metabolism.
  • Vascular/soft tissue calcification
  • Abnormalities in bone turnover/metabolism/volume/linear growth/strength
    • Low turnover states = adynamic bone disease, Osteomalacia
    • High turnover states = Osteitis Fibrosa (Increased bone remodelling but new bone is nonlamellar or non nutrient supplied and weak)
23
Q

How would you manage the Anaemia of Chronic Disease?

A

presents as lethargy, intolerance to cold, decreased stamina.

Measure Vit B12, ferritin, iron, folate, transferrin saturation, CHr regularly.

Replace them if deficient! (IV iron tolerated better than PO sometimes)

Aim for Hb 100-120

Treat with erythropoietin stimulating agents (contraindicated in HTN though as SE is increased BP)

24
Q

How would you manage the secondary/Tertiary Hyperparathyroidism?

A

Measure calcium, phosphate, PTH 3 monthly.

Control of phosphate:

  • dietary restrictions of phosphate
  • take phosphate binders with meals eg. calcium carbonate/acetate
  • Nicotinamide (alternative to phosphate binders), blocks intestinal sodium/phosphate co-transporter

Control of PTH:

  • Treat with Vitamin D (Cholecalciferol or ergocalcierol)
  • If Vit D has been replaced but bone problems persist, offer calcitriol or vitamin D analogue (alfacalcidol)
  • calcimimetics
25
Q

Describe the PTH, phosphate and Calcium levels in Primary, Secondary and Tertiary Hyperparathyroidism

Primary = adenoma

Secondary = parathyroid hyperplasia in CKD

Tertiary = continued hyperplasia but fixed CKD

A
26
Q

How would you manage the electrolyte imbalances and chronic acidosis?

A

Hyperkalaemia = calcium gluconate for the heart, then glucose + insulin, reduce fruit/chocolate/coffee, dialysis if >7

Acidosis = NaHCO3 tablets

Na+ = Loop diuretics, avoid binge drinking, replace fluid losses eg. from sweating, dietary Na+ and K+ restriction sometimes

27
Q

When would you refer the CKD to a specialist?

A
  • eGFR<30
  • Albumin Creatinine Ratio >70 unless being treated or due to DM
  • ACR>30 + haematuria
  • Accelerated progression of disease
    • decrease of eGFR by 25% or more + change in category of disease within <12 months
  • HTN poorly controlled despite atleast 4 anti-HTN meds
  • suspected renal artery stenosis
  • suspected rare/genetic CKD causes
  • CKD + renal outflow obstruction (refer to urology)
28
Q

How would you reduce the CVS risk in CKD?

A
  • smoking cessation, exercise, weightloss
  • Start on statins
    • start on atorvastatin 20mg
  • B12 and folate supplementation
    • Check folate and b12 in stage 5/6 patients ever 6 months
    • Check every 3 months in dialysis patients
  • Aspirin sometimes
  • Oral anticoagulants if indicated eg. non-valvular AF
    • rivaroxaban preferred to warfarin
29
Q

How would you plan ahead for CKD treament?

A
  • stop nephrotoxic drugs!!!
    • Tetracyclines, gentamicin (excreted by kidneys), NSAIDs, K+ sparing eg. amiloride/spironolactone
  • Provide influenza and pneumococcas vaccinations
  • Assess urine ACR, U&Es annually
  • start discussing options for if they reach end stage renal failure
  • home care team input
  • discuss disadvantages/advantages of different renal replacement therapies
    • home = APD, CAPD, Home HD
    • unit = Nocturnal HD, conventional HD
    • Active conservative management
    • transplant
  • Refer for fistula = venous mapping
  • Refer for PD tube insertion
  • Refer to transplant work-up clinic
30
Q

How would you manage diabetic nephropathy?

A
  • ACE I/ARB to reduce proteinuria
  • Anti-hypertensives for BP control
  • deal with CVS risk factors
  • continue Eye checks and foot checks
31
Q

Chronically raised BP can cause nephrosclerosis.

However, by the time you’re at advanced renal disease it’s hard to decide whether the HTN caused the renal disease or if the renal disease caused secondary HTN.

How would you investigate this?

(Hint investigate the causes of HTN)

A
  • 24 hour urinary metanephrines (phaeochromocytoma)
    Aldosterone:Renin ratio (primary aldosteronism)
  • Cortisol & Dexmethasone suppression test (Cushings)
  • TSH (Hyperthyroidism)
  • MRA (Renal Artery Stenosis)
32
Q

Polycistic Kidney Disease.

How does it present?

Why is it a big deal? Ie Risks.

How would you treat it?

A

Presentation:

  • family history!!!!!
  • Usually diagnosed on US
  • Asymptomatic sometimes
  • Or if there is infection of cysts = flank pain, haematuria, fever

Significant as it increases the risk of intracranial aneurysms and heart valve abnormalities!

Treatment:

  • Control BP = ACE I or ARBs
  • Manage as you would CKD
  • Tolvaptan (vasopressin receptor 2 antagonist)
  • Genetic counselling and testing
  • Fluids, reduced salt, no excessive protein
33
Q

Explain to me how anaemia of chronic disease happens in CKD?

A
  • decreased erythropoietin production in kidneys
  • iron deficiency due to poor absorption and malnutrition
  • blood loss due to occult gi bleeding, platelet dysfunction, etc
  • shortened RBC lifespan in uraemia, haemodialysis also results in some haemolysis
  • bone marrow suppression from uraemia
  • medication induced sometimes eg. ACE I
  • haematinic deficiency = vit b12 and folate deficiency
34
Q

What are the 4 main signs of nephrotic syndrome?

A

Oedema

Hypoalbuminaemia (alb<30)

Hypercholesteraemia

Urine PCR >350 (heavy proteinuria >3.5g of protein in 24 hours)

35
Q

How would a nephrotic syndrome patient physically?

A

New onset oedema = periorbital, then peripheral, genitals, ascites, pleural effusions

Low albumin = fatigue, leuchonychia

Breathless = pleural effusions, acute renal failure

Dysipidaemia = erruptive xanthomata, xanthelasma

Frothy proteinuria

36
Q

What are the 5 main causes of nephrotic syndrome?

A
  • Minimal Change Disease
  • Focal Segmental Glomerulosclerosis
  • Membranous Nephropathy
  • Membranoproliferative Glomerulonephritis (presents as nephritic syndrome)
  • Amyloidosis/Myeloma/Diabetes can have the proteinuria but not necessarily the other nephrotic features
37
Q

What are some drugs and diseases that cause secondary nephrotic syndrome?

A

Drugs

  • NSAIDs, lithium, antimicrobials, pencilamine, tamoxifen, catopril

Diseases

  • DM, SLE, amyloidosis, myeloma and lymphoma, Congenital (alports, piersons, etc), Infections (HIV, Hep B/C, malaria, schistosomiasis)
38
Q

What are some complications of Nephrotic syndrome?

A
  • Venous thromboembolism
    • hypoalbuminaemia results in loss of anticoagulation factors in urine. Liver overcompensates to replace albumin, ends up making more clotting factors too.
  • Higher infection risk
    • due to loss of immunoglobulins
  • Progression to CKD
  • Hypertension
  • Hyperlipidaemia
    • elevated lipoproteins to compensate for loss of album = increased cholesterol and triglycerides = lipiduria (fatty casts)
39
Q

How would you vaguely differentiate between the 5 main causes of nephrotic syndrome?

A

Minimal Change Disease

  • most common in children
  • associated with tumours eg. Hodgkin Lympnoma
  • Electron Microscopy = effacement of foot processes

Focal Segmental Glomerulosclerosis

  • Most common in black populations
  • Associated with heroin abuse, HIV, obesity, sickle cell
  • Light Microscopy = segmental sclerosis
  • Immunoflorescent Microscopy = IgM and C3
  • EM = effacement of foot processes
  • presents similarly to MN but will almost always have a lowered eGFR

Membranous Nephropathy

  • Most common cause in white populations
  • Primary = anti-phospholipase A2 receptor antibodies
  • Secondary = associated with infections (Hep B/C), SLE, tumours, drugs
  • LM = Basement membrane thickened
  • IM/EM = subepithelial deposits in “spike and dome” appearance

Membranoproliferative Glomerulonephritis

  • Immune mediated proliferation of the mesangium
  • EM = basement membrane thickening, GBM splitting = “Train Track appearance”
  • IM = IgG deposits on BM

Diabetes

  • LM = Kimmelstiel-Wilson Nodules

Amyloidosis

  • associated with multiple myeloma or chronic inflammatoyr disease eg. RA
  • LM = Congo red stain shows apple green birefringence under polarised light
40
Q

Describe why there is such massive proteinuria in nephrotic syndrome

A

Structural damage of glomerular filtration barrier, so there is a massive loss of protein through the kidneys.

There is a loss of negative charge of the GBM so the selective permeability is lost.

Podocyte damage and fusion results in non-selective proteinuria. (Except in minimal change, which presents with selective glomerular proteinuria)

41
Q

How would you investigate a nephrotic syndrome?

A
  • Urinalysis
    • Dipstick for protein
    • Lipiduria, fatty casts appear as “maltese cross” sign under polarised light
    • Renal tubular epithelial casts
  • 24 hour urine collection shows heavy proteinuria (>3.5g/24hours)
  • Bloods
    • decreased serum protein/albumin/AT3/Immunoglobulins
    • Increased choelsterol/triglycerides
42
Q

How would a Nephritic Syndome present?

A
  • AKI
  • Dipstick = blood/protein/mild to moderate oedema
  • Proteinuria <3.5/24 hours (frothy urine)
  • Hypertension
  • Sometimes visible haematuria
43
Q

Describe how Post-Strep GN presents, how you would investigate it and treat it

A
  • occurs weeks after GroupA/B Haemolytic Strep infections
    • 1-2 weeks post tonsillitis/pharyngitis
    • 3-4 weeks post impetigo/cellulitis
  • Usually affects kids 3-12 years old

Investigate:

  • Positive anti-streptococcal antibodies (ASO titre)
  • Low serum C3
  • Biopsy = immune complex IgG, IgM, C3 deposits

Treat:

  • HTN/Proteinuria = ACEI/ARB
  • Low sodium diet
  • Renal Replacement Therapy if it progresses to ESRF
44
Q

Describe when you would suspect IgA Nephroapthy, how you would investigate it, and how you would treat it

A
  • Episodic Gross Haematuria during or right after URTI or GI infection or Strenous Exercise
  • Male>Female
  • typically 20-40 years old

Investigate:

  • Microhaematuria with intermittent visible haematuria
  • Increase in serum IgA
  • Normal C3 and C4
  • Biopsy = mesangial immune complex deposits in glomeruli

Treat:

ACEI/ARB for proteinuria/HTN

45
Q

GN with an URTI with coca cola urine!!! What do you suspect?

A

Coca-Cola Urine is haematuria.

I would suspect IgA and Post-Strep GN.

I would differentiate between them, as IgA would happen during/right after the infection, while Post-Strep GN would happen weeks after.

46
Q

What are the three types of small vessel ANCA vasculitis and how would you differentiate them?

A

Granulomatosis with Polyangiitis (wegeners)

  • Pulmonary + Nasopharyngeal involvement (haemoptysis and nasal ulcers/polyps)
  • Investigate = cANCA (PR3)

Microscopic Polyangiitis

  • Mild resp symptoms
  • Investigate = pANCA (MPO)

Eosinophilic Granulomatosis with Polyangiitis

  • patients have asthma/ allergic rhinitis/ purpura/ peripheral neuropathy
  • Investigate = pANCA, Bloods show eosinophilia, Biopsy shows focal segmental necrotising GN
47
Q

How would you treat vasculitis?

A

Steroids eg. prednisolone + immunosuppression eg. Cyclophosphamide

(mycophenolate mofetil, rituximab, methotrexate sometimes used instead)

48
Q

How does Goodpastures Syndrome present, how would you investigate it and how would you treat it?

A
  • peaks in 30s (mainly male) and >60s (mainly female)
  • Antibodies against type 4 collagen react with the pulmonary basement membrane causing haemoptysis
  • Can lead to Rapidly Progressing Glomerulonephritis

Investigate:

  • Anti-GBM antibodies
  • CXR shows pulmonary infiltrates
  • Biopsy = linear deposits of igG along basement membrane

Treat:

  • plasma exchange
  • immunosuppression (prednisolone + cyclophosphamide)
49
Q

You get a patient presenting with haemoptysis and renal symptoms. (pulmonary-renal)

What do you suspect and how do you investigate it?

A

I suspect ANCA vasculitis and Goodpastures!

Microscopy shows a crescent GN, indicating Rapid Progressive Glomerulonephritis.

I would do immunostaining:

  • Goodpastures = linear igG deposits
  • Vasculitis = Pauci-immune GN, you would get pANCA and cANCA
50
Q

What is Thin Basement Membrane Disease, how does it present and how would you treat it?

A

It is a hereditary abnormality of Type 4 collagen.

Investigate:

  • persistent microscopic haematuria
  • possibly intermittent visbile haematuria
  • Biopsy = diffuse thinning of GBM

Treat:

  • monitor renal function
  • supportive treatment
51
Q

What is Alports syndrome, how does it present, how would you investigate it and how would you treat it?

A

It is an X linked (usually affects males) mutation in Type 5 collagen.

Associated with hearing loss and eye abnormalities.

Often leads to ESRF.

Investigate:

  • persistent microscopic haematuria with intermittent visible haematuria
  • Sensorineural hearing loss
  • Biopsy = abnormally split and laminated GBM

Treat:

  • Renal Replacement Therapy
  • Renal Translplant (sometimes leads to Goodpastures)
52
Q

How would you investigate a lupus nephritis and how would you treat it?

A
  • ANA and anti-dsDNA positive
  • Treat with high dose corticosteroids + immunosuppression
    • eg. prednisolone + Mycophenolate Mofetil

(fewer SE than cyclphosphamide. Can use in younger people as it does not cause infertility)

53
Q

How would you treat glomerulonephritis?

A
  • Treat Oedema
    • limit dietary Na+, Loop diuretics eg. furosemide (can add thiazide or K+ sparing)
  • Treat Proteinuria/HTN
    • ACEI, ARB, single/bilateral nephrectomy or renal embolisaiton if uncontrolled
  • Treat Dislipidaemia
    • reducing proteinuria should help
    • statins for hypercholesterolaemia
  • High risk for VTE if hypoalbuminaemic <20g/dl
    • Therapeutic LMWH
  • Immunosuppressive therapy if needed
  • Invasive therapy eg. renal replacement therapy/haemodialysis if ESRF or severe AKI
  • Plasma exchange for Goodpastures and ANCA
    *

MEDICINE - Renal (3 decks)

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