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Medicine (Year 5) > Renal (Other conditions) > Flashcards

Renal (Other conditions) Flashcards

1
Q

Renal artery stenosis (RAS)

A

describes the narrowing of the renal arteries and is most commonly due to atherosclerosis, followed by fibromuscular dysplasia (FMD). RAS generally presents with accelerated or difficult-to-control hypertension.

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2
Q

Pathogenesis of hypertension in RAS

A

Narrowing of the renal artery lumen can lead to decreased perfusion to the kidneys. This leads to the activation of the renin-angiotensin-aldosterone system (RAAS) which leads to the secretion of renin. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II acts on the adrenal glands leading to aldosterone secretion, which leads to sodium and water retention and increased blood pressure.

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3
Q

Renal artery stenosis in <30

A

fibromuscular dysplasia

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4
Q

Renal artery stenosis in >55

A

suggests RAS due to atherosclerosis

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5
Q

presentation of RAS

A

many asymptomatic or only have hypertension

  • Severe, accelerating, and/or difficult-to-control hypertension
  • Biochemical and/or clinical evidence of renal dysfunction when starting ACE inhibitors or angiotensin II receptor blockers (ARBs) – they reduce renal perfusion even more
  • Sudden or unexplained recurrent acute heart failure in a hypertensive patient (‘flash’ pulmonary oedema)
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6
Q

investigations for RAS

A

UEs
- urea and creatinine may be deranged
- potassium may be low or low-normal due to RAAS activation

Aldosterone:renin ration
- >20 (renin>aldosterone) -> rules out primary hyperaldosteronism

CT angiography or MR angiography
- first line if FMD suspected
- may show string of beads appeaance

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7
Q

management of RAS

A

Management involves optimising cardiovascular risks (e.g. smoking cessation, control of blood pressure, lipids and blood glucose etc.), avoiding ACE inhibitors or ARBs, and avoiding other nephrotoxic medications. Other management steps include:

  • Atherosclerotic RAS: angioplasty with stenting, particularly in flash pulmonary oedema. It may be considered in refractory or severe hypertension
  • FMD: percutaneous transluminal angioplasty with balloon dilatation with or without stenting
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8
Q

complications of RAS

A
  • Chronic kidney disease
  • Acute kidney injury – e.g. if rapidly worsening or another cause of renal dysfunction is present
  • End-organ damage due to hypertension
  • Flash pulmonary oedema
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9
Q

Acute interstitial nephritis (AIN)

A

describes inflammation of the kidney interstitium usually triggered by a hypersensitivity reaction to drugs.

It classically presents with a triad of

  • rash
  • fever
  • eosinophilia
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10
Q

common drugs which can cause acute intestitial nephritis

A
  • Nearly all penicillins and cephalosporins
  • NSAIDs
  • Rifampicin
  • Proton pump inhibitors
  • Allopurinol
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11
Q

non-drug causes of AIN

A
  • Infections (e.g. HIV and Epstein-Barr virus (EBV))
  • Systemic autoimmune diseases (e.g. systemic lupus erythematosus (SLE) and Sjögren’s syndrome)
  • Idiopathic
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12
Q

presentation of AIN

A

Patients classically have a reduction in kidney function without oliguria within days of starting a causative drug. Other features include:

The classic triad of AIN – rarely appears as all three (<10% of cases):

  • Rash
  • Fever
  • Eosinophilia
  • Elevated serum immunoglobulin E (IgE)
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13
Q

acute interstitial nephritis vs acute tubular necrosis

A

Acute tubular necrosis (ATN)
* Eosinophilia, rash, and elevated IgE make ATN less likely
* Urinalysis may show muddy brown casts in ATN

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14
Q

investigations of AIN

A

UEs
- urea and creatinine are elevated

Urinalysis
- may show sterile pyuuria - white cells with negative bac culture
- mild- mod proteinuria

Full blood count
- eosinophilia

Trail of discontinuing suspected causative medication
- AKI resolves

Kidney biopy- only test for definitive diagnosis
- only if AKI does not improve when medication stopped or if treatment involving immunosuppessants e.g. steroids is being considered

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15
Q

management of AIN

A
  • Withdrawal of the offending drug
  • Supportive care (e.g. correcting derangements in U&Es and fluid balance)
  • Corticosteroids may be considered in some cases
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16
Q

complication of AIN

A

CKD

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17
Q

Acute tubular necrosis (ATN)

A

is the most common cause of acute kidney injury (AKI). It describes the death of tubular epithelial cells in the kidney and occurs due to ischaemia or nephrotoxic drugs. The presence of ‘muddy brown casts’ is pathognomonic for ATN.

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18
Q

causes of acute tubular necrosis

A
  • Any scenario causing hypoperfusion, such as haemorrhage, sepsis, or excessive fluid loss – can lead to ischaemia
  • Exposure to nephrotoxic agents such as NSAIDs, ACE inhibitors, aminoglycosides (e.g. gentamicin), radiocontrast media, and ethylene glycol
  • Rhabdomyolysis – the release of myoglobin can lead to ATN
  • Causes of increased uric acid (e.g. gout or tumour lysis syndrome)
  • Causes of increased light chain proteins (e.g. multiple myeloma)
19
Q

presentations of acute tubular necrosis

A

Patients may not have any symptoms except for an AKI on blood tests.

  • Oliguria and/or anuria may be present
  • ATN responds poorly to fluids
20
Q

investigations for ATN

A

Urea and electrolytes (U&Es):
* Urea and creatinine may be elevated
* Hyperkalaemia may be present

Urea:creatinine ratio – calculated by dividing urea by creatinine, ensuring units are the same:
* A ratio of <40:1 suggests a renal cause

Urinary sodium:
* Elevated – tubular dysfunction leads to increased sodium excretion

Urinalysis:
* Shows muddy brown casts

21
Q

management of ATN

A

Management is supportive (correcting electrolyte and acid-base abnormalities, and maintaining volume status)

22
Q

rhabdomyolysis

A

Rhabdomyolysis describes any disease process that leads to skeletal muscle damage and breakdown, leading to the release of intracellular components such as potassium ions, myoglobin, and creatine kinase (CK).

Release of these components into the bloodstream can lead to electrolyte disturbances, acute kidney injury (AKI), metabolic acidosis, and disseminated intravascular coagulation (DIC).

Myoglobin is directly nephrotoxic to the kidneys and can precipitate within them, leading to AKI.

23
Q

causes of rhabdomyloysis

A

Any condition that can cause damage to muscle tissue can cause rhabdomyolysis:

  • Any overexertion of muscle
  • Trauma and compartment syndrome
  • Epilepsy, particularly status epilepticus
  • Burns
  • Chronic alcohol excess
  • Drugs, such as statins (especially if co-prescribed with macrolides)
  • Myositis
  • Collapses and falls, particularly in the elderly and those who have had a long lie
24
Q

presentation of rhabdomyolysis

A
  • ‘Tea-coloured’, dark urine – due to myoglobinuria
  • Myalgia and muscle weakness
  • Fever, malaise, nausea, and vomiting

Features of complications:
* DIC – shock, easy bruising, and bleeding
* Hyperkalaemia – arrhythmia and palpitations
* Hypocalcaemia (myoglobin binds to calcium) – arrhythmia and tetany

25
Q

investigations for rhabdomyolysis

A

Urine dipstick:
* May be positive for blood

Urine microscopy:
* Generally negative for red blood cells

Urea and electrolytes (U&Es):
* Increased potassium – due to release from skeletal muscle tissue
* Hypocalcaemia – due to myoglobin binding to calcium
* Disproportionately elevated creatinine – suggesting intrinsic renal damage

Serum or urinary myoglobin levels:
- Increased

Serum creatine kinase (CK) – the most specific test to diagnose rhabdomyolysis:
* Must be increased to >5 times normal or >1,000 IU/L

26
Q

management of rhabdomyolysis

A
  • 1st-line: fluid rehydration – dilutes nephrotoxins and reduces myoglobin-induced renal damage
  • Treat hyperkalaemia
  • Urinary alkalinisation is sometimes considered
  • Renal replacement therapy may be necessary
27
Q

Fanconi syndrome

A

Fanconi’s syndrome (FS) describes dysfunction of resorption in the proximal renal tubules of the kidney. It leads to the urinary loss of substances that would normally be reabsorbed, including glucose, amino acids, phosphate, and bicarbonate.

It is associated with type 2 renal tubular acidosis, which describes the failure of bicarbonate reabsorption in the proximal renal tubules.

28
Q

causes of fanconi syndrome

A

Inherited causes include:

  • Idiopathic
  • Cystinosis – most common in children
  • Wilson’s disease

Acquired causes include:

  • Sjögren’s syndrome
  • Rejected renal transplants
  • Multiple myeloma
  • Intrinsic kidney diseases (e.g. acute tubular necrosis and interstitial nephritis)
  • Hyperparathyroidism
  • Some drugs (e.g. aminoglycoside antibiotics)
  • Some toxins (e.g. glue sniffing and heavy metals)
29
Q

presentation of fanconis syndrome

A

Patients may present with:

  • Polyuria
  • Polydipsia
  • Dehydration
  • Rickets/osteomalacia – due to excess urinary calcium loss secondary to impaired urine acidification. Calcium tends to deposit at higher pHs
  • Failure to thrive
30
Q

management of fanconis syndrome

A

Management involves treating the underlying cause and replacing the substances lost in the urine.

31
Q

polycystic kidney disease

A

Polycystic kidney disease (PKD) is an inherited disorder in which the renal tubules form cysts and become non-functional, which fill with fluid and exert pressure on adjacent normal tubules, damaging them.

Cysts may also form in other areas, including the** liver, pancreas, and spleen.**

32
Q

types of Polycystic kidney disease

A

1) Autosomal dominant polycystic kidney disease (ADPKD) – subdivided into:

  • PKD1 – around 85% of cases with an abnormality on chromosome 16
  • Encodes for polycystin-1, symptoms are generally more severe
  • PKD2 – around 15% of cases with an abnormality on chromosome 4
  • Encodes for polycystin-2, symptoms are generally less severe
  • PKD3 – no gene locus has been identified yet

2) Autosomal recessive polycystic kidney disease (ARPKD)

33
Q

polycystic kidney disease epidemiology

A
  • ADPKD tends to present between the ages of 30-60 years
  • ARPKD tends to present from birth and may be prenatally diagnosed
  • ARPKD is much less common than ADPKD
  • ARPKD has a prevalence of around 10 per 100,000 births
  • PDK makes up for ~10% of people on dialysis
  • Prevalence in Europe is around 4 per 10,000
34
Q

how to ADPKD and ARPKD present differently

A

autosomal recessive is more serious with cysts starting to form in infancy or perinatally

autosomal dominant may only become apparent due to refractory hypertension

35
Q

ADPK presentation

A
  • Haematuria
  • Polyuria
  • Loin pain – due to renal cysts or extra-renal cysts (e.g. hepatic cysts and enlargement)
  • Bilateral kidney enlargement – may be noticed on an abdominal examination
  • Hypertension
  • Recurrent urinary tract infections (UTIs)
  • Renal stones

Features of extra-renal manifestations:

  • Hepatomegaly due to liver cysts – most common
  • Pancreatitis due to pancreatic cysts
  • Intracranial berry aneurysms – affects up to 16% of people and may lead to a subarachnoid haemorrhage if they rupture
  • Mitral valve prolapse
  • Aortic root dilatation
36
Q

presentatio of ARPKD

A

The presentation of ARPKD varies significantly:

Perinatal features:

  • Abdominal distention due to renal enlargement
  • Oligohydramnios and pulmonary hypoplasia
  • Potter’s facies (flattened nose, micrognathia, low-set ears) – due to oligohydramnios

Neonatal features – at birth:

  • Palpable kidneys
  • Mild liver disease

Features in infancy and childhood:

  • Palpable kidneys
  • Hepatomegaly – may progress to portal hypertension and varices, hypersplenism, and hepatosplenomegaly

Marked liver disease

37
Q

investigations for polycystic kidney disease

A

Screening: if relatives with ADPKD

Others

Full blood count (FBC):

  • May show elevated haemoglobin as polycystic kidneys can produce excess erythropoietin

Urea and electrolytes (U&Es) and estimated glomerular filtration rate (eGFR):

  • Creatinine and eGFR may be normal in early stages

**Renal ultrasound scan **– the test of choice. ADPKD is diagnosed if there is a positive family history and:

  • ≥2 unilateral or bilateral renal cysts at <30 years
  • ≥2 cysts in each kidney at 30-59 years
  • ≥4 cysts in each kidney at >60 years
  • If no family history, then >10 cysts must be present in each kidney

MRI/CT:

  • May be considered if a renal ultrasound is equivocal
  • May also be considered to identify intracranial berry aneurysms

Genetic testing:

  • Not routinely performed
38
Q

management of polycystic kidney disease

A
  • Blood pressure control
  • Management of complications such as UTIs, renal stones, and loin pain
  • Renal replacement therapy may be necessary if end-stage renal disease (ESRD) develops
  • Tolvaptan (a vasopressin V2 receptor antagonist) may be considered if:
  • Patients have chronic kidney disease stage 2 or 3 at the start of treatment
  • There is evidence of rapidly progressive disease
39
Q

complications of polycystic kidney disease

A
  • chronic kidney disease
  • hepatic cysts
  • cardiovascular disease secodnary to hypertension
  • Berry aneurysms
  • Pregnancy complications such as pre-eclampsia
40
Q

Alport’s syndrome (AS)

A

is a genetic disorder that is mostly inherited in an x-linked dominant pattern, however, may also be inherited in an autosomal recessive fashion. It is caused by an inherited defect in type IV collagen, which is found in the ears, eyes, and kidneys. It can lead to chronic kidney disease (CKD).

41
Q

alport syndrome presentation

A
  • Microscopic haematuria
  • Proteinuria
  • Bilateral sensorineural deafness
  • Lenticonus – bulging of the lens capsule
42
Q

investigations for alport syndrome

A

Urinalysis and microscopy:

  • Microscopic/macroscopic haematuria is the earliest and commonest sign of AS
  • Proteinuria worsens with age
  • May show red blood cells and red cell casts

Renal biopsy:

  • Light microscopy: mesangial cell proliferation and capillary wall thickening
  • Electron microscopy: glomerular basement membrane lamina densa splitting and lamellation

Audiometry:

  • Sensorineural hearing loss

Molecular genetic testing:

  • Identifies mutations
43
Q

management of alport syndrome

A

There is no definitive treatment for AS. Management involves:

  • ACE inhibitors – reduce proteinuria and renal disease progression
  • Management of CKD
44
Q

alport syndrome complications

A
  • Nephritic syndrome
  • Nephrotic syndrome
  • End-stage renal disease (ESRD): at around 15-40 years

Medicine (Year 5) (34 decks)

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