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Year 2 - Renal > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Myeloma - signs and symptoms (including classical presentation)

A

Classical presentation - back pain and renal failure

Signs

  • Anaemia
  • Hypercalcaemia
  • Renal failure
  • Amyloidosis
  • Recurrent renal infections

Symptoms

  • Bone pain
  • Fatigue
  • Weight loss
  • Weakness
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2
Q

CKD - symptoms

A

Uraemia

  • nausea and vomiting
  • anorexia and weight loss
  • fatigue
  • itch
  • altered taste
  • restless legs and muscle twitching
  • difficulty concentrating and confusion

Anaemia

  • fatigue
  • muscle weakness

Pain

  • bony
  • neuropathic
  • ischaemic
  • visceral
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3
Q

Minimal Change Nephropathy is the most common cause of nephrotic syndrome in children/adults

What is the target in minimal change? What are the investigations and treatment?

Does this condition cause progressive renal failure?

A

Minimal Change Nephropathy is the most common cause of nephrotic syndrome in children

The podocyte is the target of an unknown antigen and antibody

Investigations - light microscopy and immunofluorescence of renal biopsy will appear normal, but electromicroscopy will show foot process fusion of podocytes

Treatment - 94% have complete remission with oral steroids. Second-line is cyclophosphamide

No, this condition does NOT cause progressive renal failure

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4
Q

Renal Artery Stenosis - diagnosis and treatment

A

Diagnosis

  • Clinical history - e.g. patient will be a little older and likely have signs of general atherosclerosis
  • Imaging
    • Renal USS
    • CT/MR/Conventional angiography

Treatment

  • Pharmacological - Statins, antiplatelets, ACE inhibitors
  • Surgical intervention - angioplasty +/- stenting
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5
Q

What are some of the life-threatening complications of an AKI?

A

Hyperkalaemia

Fluid overload (resulting in pulmonary oedema)

Severe acidosis (pH <7.15)

Uraemic pericardial effusion

Severe uraemia (Ur >40)

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6
Q

If dysmorphic red cells were noted on urinoscopy, where would the bleeding likely be coming from?

A

Bleeding likely coming from the kidneys themselves - dysmorphic appearance is due to the red cells being squeezed through the tubules at the glomerulus

If the blood cells were normal, the bleeding would be likely from a structure further down the renal system e.g. the bladder

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7
Q

GN treatment - what are some of the non-immunosuppressive options?

A

Anti-hypertensives (target of <130/80, or <120/75 if proteinuria)

ACE inhibitors/ARBs to reduce both BP and proteinuria

Diuretics if the patient is fluid overloaded

Statins if the patient has hypercholesterolaemia

Anticoagulants/Aspirin/Antiplatelets?

Some evidence for Omega 3 fatty acids and fish oil

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8
Q

What % of patients with lupus will have associated renal dysfunction, and what is the most commonly seen sign?

A

Up to 50% of patients with SLE will present with renal involvement, and up to 60% will develop it over the course of their condition

Most frequently observed abnormality is proteinuria

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9
Q

What type of vasculitides to nephrologists typically deal with?

A

small-vessel e.g. MPA/GPA/eGPA

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10
Q

What gene and on what chromosome is involved in ARPKD?

What is the classical presentation?

A

PKDH1 on chromosome 6

Classic presentation is young children and a constant association with hepatic lesions.

Kidneys are always palpable

Again, hypertension is common

Patients also experience recurrent UTIs

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11
Q

What are the two types of reabsorption that can occur?

A

Transcellular

Paracellular, using the tight junctions

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12
Q

How is Pre-Renal AKI treated?

A

1) Assess hydration of patient

  • Clinical observations (BP, HR and urinary output)
  • JVP, cap refill time, oedema
  • Pulmonary oedema

2) Fluid challenge for hypovolaemia

  • Crystalloid (0.9% NaCl) or Colloid (Gelofusin)
    • NB - do not use 5% dextrose
  • Give a fluid bolus, then reassess and continue as necessary
  • Seek help if over 1,000 mls given and no improvement
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13
Q

When leaving the proximal tubule, what is the osmolarity of the tubular fluid?

A

300 mosmol/l

The tubular fluid is iso-osmotic with the surrounding interstitial fluid

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14
Q

Give some examples of substances that are a) reabsorbed and b) secreted in the proximal tubule

A

Reabsorbed in the PT

  • sugars
  • amino acids
  • phosphate
  • sulphate
  • lactate

Secreted in the PT

  • H+
  • Hippurates
  • Neurotransmitters
  • Bile pigments
  • Uric acid
  • Drugs e.g. atropine, morphine, penicillin etc.
  • Toxins
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15
Q

Where is aldosterone secreted from?

When is it secreted?

What effect does it have?

A

Secreted from the adrenal cortex

Secreted in response to rising K+ or falling Na+ in the blood, or in response to activation of the renin-angiotensin-aldosterone system

Stimulates Na+ reabsorption (= increased blood volume and pressure) and K+ secretion

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16
Q

Diabetic nephropathy - diagnosis (also, what is the earliest clinical sign?)

A

Long history of diabetes (this is not an acute condition!)

Presence of albuminuria/proteinuria (NB - earliest sign is microalbuminuria)

Presence of other diabetic complications e.g. retinopathy, ulcers etc.

Renal impairment (late finding, not a good sign)

NB - need to regularly screen diabetic patients for microalbuminuria and closely monitor renal function

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17
Q

CKD - signs

A

Anaemia -> pallor

Weight loss

Advanced uraemia

  • jaundice
  • twitching
  • encephalopathy
    • confusion
    • flapping tremor
  • pericardial rub/haemorrhagic pericardial effusion
  • Kussmaul breathing (due to metabolic acidosis)
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18
Q

How is glomerulonephritis classified histologically?

A

Proliferative or non-proliferative (usually referring to the presence or absence of proliferation of mesangial cells)

Focal/Diffuse - are more or less than 50% of the glomeruli affected?

Global/Segmental - is all or part of the glomerulus affected?

Crescentic - presence of a crescent shape of endothelial cells around the glomerulus e.g. RPGN in vasculitis

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19
Q

What confounding factors are taken into account when calculating the estimated GFR (eGFR)?

A

Sex

Age

Ethnicity

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20
Q

What are the three categories of renal tubular dysfunction? Give an example of each

A

Pre-renal (reduced renal perfusion) - blood loss/hypovolaemia

Renal (intrinsic kidney tissue damage) - glomerulonephritis or nephrotoxins

Post-renal (ureteric/urethral obstruction) - stones or malignancy

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21
Q

What is the most common form of glomerulonephritis globally?

How might it present?

What other condition is it associated with?

A

IgA nephropathy is the most common GN in the world

May have asymptomatic microhaematuria, with or without proteinuria

This may become macroscopic haematuria, especially if the patient has recently suffered from a resp/GI infection (due to excess IgA being deposited in the kidney)

IgA nephropathy is associated with Henoch-Schonlein Purpura (HSP)

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22
Q

What substances do the kidneys (usually) reabsorb?

A
  • fluid (99%)
  • salt (99%)
  • glucose (100%)
  • amino acids (100%)
  • urea (50%)
  • creatinine (0%)
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23
Q

When determining urine protein, what is the gold standard test?

What tends to be done instead? Why?

What are the cutoffs for grading proteinuria based on this other test?

A

24 hour urine collection is the gold standard (normally <150mg/24 hours)

Instead, urine protein/creatinine ratio tends to be used (50mg/mmol, ~0.5g/24 hours). This is because it can be done on the spot and is easier on patients, however it only gives an indication and so is not the gold standard

Asymptomatic/low grade proteinuria - urine protein/creatinine ratio of <1 g/day

Heavy proteinuria - urine protein/creatinine ratio of 1-3 g/day

Nephrotic range - urine protein/creatinine ratio of > 3g/day

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24
Q

Clinical scenario - 24 year old man incidentally found to have ++ blood and + protein on dip, BP 148/92

Protein quantified at 0.7g/day, creatinine 72

What glomerular cells are likely to be affected?

A

Mesangial cells - slow, gradual process and red cells are present

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25
Q

What condition is associated with glomerular crescents on biopsy?

Is this a treatable cause of acute renal failure?

Name some of the conditions that this form of GN is associated with

A

Rapidly Progressive Glomerulonephritis (RPGN)

This is treatable

Associated with both ANCA-positive and ANCA-negative conditions

ANCA-positive

  • Systemic vasculitis
  • GPA
  • MPA

ANCA-negative

  • Goodpasture’s disease
  • HSP
  • SLE
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26
Q

What are some of the consequences of CKD-MBD?

A

Secondary/tertiary hyperparathyroidism

Vascular calcification

Bone pain

Fractures

CV events

Reduced QoL

High morbidity and mortality

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27
Q

What hormones are involved in the regulation of ion and water balance? What does each do?

A

ADH

  • increases water reabsorption (and therefore decreases urine output)

Aldosterone

  • increases Na+ reabsorption (Na+ rises)
  • increases H+ and K+ secretion (H+ and K+ lowers)

Atrial Natriuretic Hormone

  • decreases Na+ reabsorption (effectively has the opposite effect to aldosterone on sodium)

Parathyroid hormone

  • increases Ca2+ reabsorption
  • decreases PO43- reabsorption
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28
Q

How might hyperkalaemia present on an ECG?

A

With tall, peaked T waves

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29
Q

Renal artery stenosis - aetiology

A

Tends to appear in older patients (>50yrs)

M > F

Same risk factors as for generalised atherosclerosis

Very common, prevalence of 4-20% on autopsy

Usually unilateral, and rarely only renal - usually there’ll be other appearances of atherosclerosis elsewhere in the body

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30
Q

What are the survival %s of dialysis like in patients with diabetes?

A

Not good.

5 year survival T1DM - 24%

5 year survival T2DM - 20%

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31
Q

What amount of glucose is usually reabsorbed in the proximal tubule?

Why does reabsorption plateau as the amount of plasma glucose increases?

A

Usually, 100% of glucose is reabsorbed in the proximal tubule

This rate of reabsorption plateaus because the transport mechanisms driving this reabsorption can become saturated

Excess glucose that isn’t reabsorbed is then excreted in the urine (as is the case in DM)

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32
Q

What marker can be used instead of Inulin and why? What is it’s downside?

A

Creatinine can be used as an endogenous replacement to inulin, and is also easy to measure

However, creatinine is excreted into the renal tubule

Also, creatinine exhibits a lag phase in which a steep fall in GFR is only represented by a small rise in creatinine. A frankly elevated creatinine would demonstrate obvious kidney disease

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33
Q

What cells release renin?

What cells sense the amount of NaCl in the distal tubule?

What happens to renin secretion if NaCl is reduced, or if afferent arteriole pressure drops?

A

Renin is released from granular cells

Macula densa cells sense NaCl levels

If NaCl is reduced or if pressure in the afferent arteriole drops then more renin is released, more Na+ is reabsorbed and blood volume and pressure rises

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34
Q

What enzyme is deficient in Anderson Fabrys disease?

How is this condition inherited?

A

alpha-galactosidase A is deficient

Condition is inherited in an X-linked manner

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35
Q

How common are the various stages of CKD? Why is it important to monitor?

A

Stage 1 and 2 - ~7%

Stage 3 - 5%

Stage 4 and 5 - 0.1-.02%

CKD increases cardiovascular risk

Patients with proteinuria are more likely to progress to more severe stages of CKD. Higher the proteinuria, the faster the progression

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36
Q

On diagnosis of a patient with Alport’s Syndrome, what is typically seen on renal biopsy?

A

Variable thickness of the GBM, shows lots of splitting

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37
Q

When performing an examination of a patient, what are some classical clinical signs that could point in the direction of kidney disease?

A

Retinopathy

Leukonychia (due to loss of protein)

Gouty tophi

Splinter haemorrhages (NB - also associated with bacterial endocarditis)

Vasculitic skin rashes e.g. Henoch-Schonlein Purpura (HSP)

Malar rash in patients with SLE

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38
Q

What other extra-renal clinical features may be seen in a patient with ADPKD?

A

Cardiac disease

Diverticular disease

Increased incidence of hernias

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39
Q

What does “microalbuminuria” mean (hint: it doesn’t mean a small amount of albumin!)

What is it an early indicator of?

A

Refers to excretion of albumin at abnormal quantities, but still below the limit of protein detection with a urine dipstick

It is the earliest expression of diabetic nephropathy, and is a standard part of routine diabetic assessment

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40
Q

What drugs would you avoid in a patient with an AKI?

A

NSAIDs

ACE inhibitors/ARBs

Diuretics

Gentamicin

Contrast

Trimethoprim

Potassium-sparing diuretics

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41
Q

What are some of the predisposing risk factors for developing an AKI?

A

Increasing age

Diabetes

Previous AKI

CKD

Cardiac failure

Liver disease

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42
Q

How is CKD-MBD managed (via medication and dietary changes)?

A

Medication

  • Alfacalcidol (active Vitamin D)
  • Phosphate binders
    • Calcium-based
    • Aluminium
    • Non-calcium based
  • Calcimimetics

Dietary

  • Phosphate restriction
  • Salt reduction
  • Potassium restriction (if persistently elevated)
  • Fluid restriction
  • Correct metabolic acidosis
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43
Q

Is the likelihood of developing CKD increased with advancing age?

A

Yes! As age increases, so does the likelihood of developing CKD

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44
Q

What membrane is the Na+/K+ pump exclusively presented on?

A

The basolateral membrane - essential for reabsorption of Na+

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45
Q

What markers are involved in development of Mineral and Bone Disease (as a consequence of CKD)?

A

Calcium

Phosphate

PTH

Vitamin D

FGF-23

and they’re all interconnected

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46
Q

What staging criteria is used to grade AKI?

A

KDIGO staging

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47
Q

A strong acid dissociates partially/completely in solution

A weak acid dissociates partially/completely in solution

A

Strong - dissociates completely

Weak - dissociates partially

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48
Q

What 4 factors is eGFR based on?

A

Serum creatinine levels

Age

Sex

Ethnicity

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49
Q

Henoch-Schonlein Purpura (HSP) - what symptoms might it present with? In particular, where might you see rash development?

A

Abdominal pain

Joint pain

Acute Kidney Injury

Characteristic rash is seen over the buttocks, backs of legs and feet

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50
Q

What traits would an ideal marker for GFR possess?

A
  • Appear at a constant rate
  • Be freely filtered at the glomerulus
  • Not be reabsorbed from the renal tubule
  • Not be secreted by the renal tubule
  • Not undergo extra-renal elimination
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51
Q

NephrOTIC syndrome - treatment

A

General

  • fluid restriction
  • salt restriction
  • diuretics
  • ACE inhibitors/ARBs
  • Maybe anticoagulation, and IV albumin if the patient is volume depleted

Immunosuppression

The aim of treatment is to induce sustained remission

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52
Q

Describe the reabsorption of NaCl in the thick ascending limb of the Loop of Henle. How many ions are transported out in each passage, and what is the net charge change?

What class of drug interferes with this?

A

Triple co-transporter (Na+, K+ and Cl-) on the apical membrane allows reabsorption of NaCl.

For each turn, there is 1 Na+, 1 K+ and 2 Cl-, giving a neutral change in charge

(Reminder - H2O cannot be reabsorbed here as the thick ascending limb is impermeable to water)

Loop diuretics target the triple co-transporter and prevent reabsorption of NaCl

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53
Q

What are the blood pressure targets when treating someone with CKD?

How is this affected by diabetes/those with an ACR >70 mg/mmol?

A

Systolic below 140 mmHg and diastolic below 90 mmHg

If diabetic/high ACR - systolic below 130 mmHg and diastolic below 80 mmHg

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54
Q

What does the appearance of red cell casts in the urine tell us?

A

Tell us there is an active inflammatory process

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55
Q

How might haematuria present?

How might proteinuria present? What are the classifications?

A

Haematuria

  • asymptomatic, microscopic haematuria
  • episodes of painless macroscopic haematuria, usually in the context of an infection

Proteinuria

  • microalbuminuria (30-300 mg/day)
  • asymptomatic proteinuria (< 1g/day)
  • heavy proteinuria (1-3g/day)
  • nephrotic syndrome (>3g/day)
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56
Q

Focal Segmental GlomeruloSclerosis (FSGS) is the most common cause of nephrotic syndrome in children/adults

What are the investigations and treatment?

Does this condition cause progressive renal failure?

A

FSGS is the most common cause of nephrotic syndrome in adults (35% of cases)

Investigations - Renal biopsy shows minimal Ig/Complement deposition on light microscopy and focal scar tissue may be seen

Treatment - remission with prolonged use of steroids in 60% of patients (much more resistant than minimal change)

50% of patients progress to end stage renal failure after 10 years

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57
Q

Damage to what structures results in a proliferative lesion? What is present in the urine?

Damage to what structures results in a non-proliferative lesion? What is present in the urine?

A

Damage to endothelial or mesangial cells leads to a proliferative lesion, and the presence of red cells in the urine

Damage to podocytes leads to a non-proliferative lesion, and the presence of protein in the urine.

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58
Q

ADPKD is more likely to be symmetrical/asymmetrical

ARPKD is more likely to be symmetrical/asymmetrical

Where do cysts seen to be appearing from in ARPKD?

A

Autosomal dominant is more likely to be unilateral and asymmetrical

Autosomal recessive is more likely to be bilateral and symmetrical

In autosomal recessive, cysts are seen to appear from the collecting duct system

59
Q

Describe the reabsoprtion of Na+, Cl- and H2O in a) the Descending limb and b) the Ascending limb of the Loop of Henle

How does this affect osmolarity?

A

Descending limb

  • NaCl is not reabsorbed
  • highly permeable to H2O

Ascending limb

  • NaCl is reabsorbed
  • highly impermeable to H2O

Selective permeabilities enable an osmotic gradient to be established in the medulla

60
Q

What is the Henderson-Hasselbach equation?

A

pH = pK + log[A-]/[HA]

A- = base

HA = acid

61
Q

What is the (expensive) treatment for Anderson Fabrys disease?

A

enzyme replacement of alpha-galactosidase A, using Fabryzyme

62
Q

Which of the following drugs does NOT cause hyperkalaemia?

  • Spironolactone
  • Ramipril
  • Amiloride
  • Furosemide
  • Atenolol
A

Furosemide

63
Q

Alport’s Syndrome - treatment

A

No specific treatment

Standard aggressive management of BP and proteinuria, but ultimately the mainstay of treatment is dialysis/transplantation

64
Q

Kidney disease - signs on presentation (both systemic and local/renal)

A

Systemic Signs

  • related to disease
    • pyrexia, skin rash, heart murmurs, consolidation, ENT signs, retinopathy, neuropathy
  • related to loss of kidney function
    • pallor, arrythmia, pericardial rub, raised JVP, lung crepitations, oedema, gout

Local/Renal signs

  • tenderness in loins or upper abdomen
  • arterial bruits
  • palpable kidneys
65
Q

If a patient presented with a vasculitis and also had asthma and eosinophilia, what would be the likely type of vasculitis?

What about if they presented with inflammation within the respiratory tract?

A

eGPA

If presenting with resp symptoms, more likely GPA

66
Q

What measurement is widely accepted as the best overall measure of kidney function?

How is it used to stage chronic kidney disease?

A

GFR - basically anything below 60 mL/min is concerning

Stages of CKD

  • Stage 1 - evidence of kindey damage with normal or raised GFR (>90 mL/min/1.73m2)
  • Stage 2 - evidence of kidney damage with normal or mildly reduced GFR (60-89 mL/min/1.73m2)
  • Stage 3 - moderately reduced GFR (30-59 mL/min/1.73m2)​
  • Stage 4 - severely reduced GFR (15-29 mL/min/1.73m2)
  • Stage 5 - kidney failure (<15 or dialysis
67
Q

What is the difference between central and nephrogenic diabetes insipidus?

A

Central - inability to produce/secrete ADH

Nephrogenic - ADH doesn’t have an effect on the tubules in the kidney and

68
Q

Briefly describe the cycle in cardio-renal syndrome

A

Reduced cardiac output > decreased bloodflow > decreased perfusion of kidneys > impaired renal function, meaning increased Na+ and water retention > decreased cardiac input

69
Q

What’s the diagnosis?

Who gets this condition most commonly?

A

Fibromuscular dysplasia

Prevalence of 4/1000

Most common in women aged 15-50

Familial in 10% of cases and tends to involve both renal arteries. Also has associations with other hereditary conditions

70
Q

What amount of all salt and water is reabsorbed in the proximal tubule?

The reabsorption of Na+ drives the reabsorption of what anion? By what reabsorption pathway is this done?

A

67% of all salt and water is reabsorbed in the PT

Na+ reabsorption drives the reabsorption of Cl- via the paracellular pathway

71
Q

Briefly describe the pathogenesis of diabetic nephropathy

A

Renal Hypertrophy - Plasma glucose stimulates growth factors within the kidney, which causes expansion of mesangial cells. This results in nodule lesion formation and glomerulosclerosis

This then goes on to cause inflammation, proteinuria (due to GBM thickening and dysfunction of podocytes) and a resulting tubulointerstitial fibrosis

72
Q

What two processes govern micturation?

A

Micturation reflex - initiated by stretch receptors in the wall of the bladder. Causes simultaneous bladder contraction and opening of both the internal and external urethral sphincters

Voluntary control - deliberate tightening of the external sphincter and surrounding pelvic diaphragm

73
Q

What is the definition of AKI?

A

An abrupt (<48 hours) decline in kidney function defined as…

  • an absolute increase in serum creatinine by 26.4 micromol/l

OR

  • an increase in creatinine by >50%

OR

  • a reduction in urinary output
74
Q

How is ADPKD managed?

What new treatment has recently been approved by NICE to reduce cyst volume and progression?

A

Rigorous control of hypertension

Ensuring adequate hydration

Aim to reduce amounts of proteinuria

Monitor closely for cyst haemorrhage/infection

Tolvaptan is the new drug approved by NICE

75
Q

Can eGFR be used for both CKD and AKI?

A

No! eGFR is of no use in an acute setting

76
Q

Stretching of what structure also has an effect on ADH release?

What effects do nicotine and alcohol have on ADH release?

A

Activation of left atrial stretch receptors affects ADH release

A decrease in atrial pressure results in an increase in ADH release (the body is signalling that there is a need for a large change in plasma volume)

Nicotine - stimulates ADH release

Alcohol - inhibits ADH release

77
Q

Give a general definition of glomerulonephritis

A

Immune-mediated disease of the kidneys affecting the glomeruli, with secondary tubulointerstitial damage

Disruption of the glomerular basement membrane between the glomerular capillary and Bowman’s space leads to haematuria and/or proteinuria

There are numerous types of glomerulonephritis! Site and type of injury determines the clinical presentation

78
Q

How is glomerulonephritis diagnosed?

A

Clinical presentation

Blood tests

Urine examination

  • urinalysis - haematuria, proteinuria
  • urine microscopy - RBC (dysmorphic), RBCs and granular casts, lipiduria
  • urine protein:creatinine ratio - used to quantify proteinuria

Kidney biopsy - uncomfortable and considerable risk of bleeding, so rarely done

79
Q

Above what level is considered hyperkalaemia? What can it cause?

A

Normal K = 3.5-5

Hyperkalaemia = anything above 5 (life-threatening if above 6.5)

Associated with arrhythmias

Need to assess ECG and muscle weakness

80
Q

What is the normal GFR?

How much of this is absorbed in the proximal tubule?

A

125 ml/min, or 180 litres/day

80 ml/min is absorbed in the proximal tubule i..e the majority of reabsoprtion occurs at the beginning of the nephron

81
Q

What hormones does the kidney produce?

What hormones act on the kidney

A

Produced

  • Renin - forms part of the RAAS
  • Erythropoetin - stimulates RBC production in the bone marrow
  • 1,25-dihydroxycholicalciferol

Acting on

  • ADH
  • PTH
  • Aldosterone
82
Q

What is the triad of kidney-related symptoms that is seen in NephrOTIC syndrome?

What cells in the glomerulus are affected? Is this proliferative or non-proliferative?

How will patients typically present?

A

Proteinuria >3g/day (mostly albumin, also globulins)

Hypoalbuminaemia (<30)

Oedema/fluid retention

(also hypercholesterolaemia)

NB - renal function is usually normal!

Podocytes are affected, and indicates a non-proliferative process

Presentation - patients swell up! May also have periorbital oedema

83
Q

How would the kidneys appear on imaging if a patient had ischaemic nephropathy?

A

They would appear smaller - compromised blood supply causes atrophy and a reduction in size, eventually resulting in CKD

84
Q

In the event of overhydration, what happens to the aquaporins present on the luminal membrane?

A

ADH is turned off in an overhydrated state, resulting in internalisation of aquaporins back into the cytoplasm of the distal tubular cell

85
Q

Tubular fluid leaving the Ascending Loop of Henle and entering into the Distal tubule is hypo/hyper-osmotic to plasma

A

Hypo-osmotic (100 mosmol/l), while the surrounding interstitial fluid of the cortex is 300 mosmol/l

86
Q

What is the pH of the following…

  • arterial blood
  • venous blood
  • average pH of blood
A

arterial - 7.45

venous - 7.35

average - 7.4

87
Q

How does osmolarity vary through the Loop of Henle?

A

Comes from PT as 300 mosmol/l

Water leaves descending limb by osmosis > 400 mosmol/l

NaCl is removed from the ascending limb, increasing the osmolarity of the interstitial fluid and diluting the tubular fluid > 200 mosmol/l

This is process continues and a steady state is reached

Fluid then leaves the Loop of Henle and passes into the DT as hypo osmotic

88
Q

What clinical features might you see in a patient with Anderson Fabrys disease?

A

Renal failure

Angiokeratomas e.g. telangiectasia around the umbilicus

Cardiomyopathy/valvular disease

Neurological and psychiatric manifestations as well

89
Q

What two hormones are in opposition with regards to Na+ levels?

A

Aldosterone (increases sodium reabsorption) and Atrial Natriuretic Hormone (decreases sodium reabsorption)

90
Q

How long should patients that have suffered an AKI be monitored for to investigate the possible progression to CKD?

A

Following AKI, patients need to be monitored for at least 2-3 years, even if serum creatinine has returned to normal

91
Q

What antibody test can be used to detect Goodpasture’s Syndrome?

A

Anti-GBM antibody

92
Q

The distal tubule can be thought of as two segments: “early” and “late”

What ions are reabsorbed/secreted in each segment?

A

Early segment

  • Na+-K+-Cl- triple co-transporter (NaCl reabsoprtion)

Late segment

  • Ca2+ reabsorption
  • H+ secretion
  • Na+ reabsorption
  • K+ reabsorption
93
Q

How can myelomas potentially cause renal dysfunction?

A

Myeloma = cancer of plasma cells

A collection of abnormal plasma cells aggregate in bone marrow and cause impairment of production of normal red cells

There is also abnormal production of a paraprotein (abnormal antibody), which can result in renal dysfunction

94
Q

What blood tests must be requested when dealing with a patient with a suspected AKI?

What other easy clinic-based test needs to be performed? What further testing might this lead to?

A

Haemoglobin

Bicarbonate

Phosphate

Calcium

If suspecting sepsis - CRP, lactate and cultures

Patients also need urine dipstick testing - if evidence of haematuria/proteinuria, then test immunology (ANCA, ANA, immunoglobulins and complement)

95
Q

How is ADPKD diagnosed?

A

USS of kidneys - appearance on multiple bilateral cysts

Renal enlargement - may be up to 14/15cm in size

CT/MRI if unclear on USS

Genetic analysis (linkage, mutation analysis)

96
Q

What is the purpose of “countercurrent multiplication”?

A

To concentrate the medullary interstitial fluid

This allows the kidneys to produce different volumes and concentrations of urine in accordance to the amount of circulating ADH

97
Q

The majority of cases of GN are primary/secondary

Give some causes of secondary GN

A

Majority are primary (idiopathic)

Secondary causes include infections, drugs, malignancies or systemic diseases e.g. systemic vasculitides, lupus, Goodpastures, HSP etc.

98
Q

What would the following crystals indicate when viewed on urine microscopy?

  • Calcium oxalate
  • Uric acid
  • Phosphate
  • Cysteine
A

Calcium oxalate - kidney stones

Uric acid - gout

Phosphate - UTIs/pseudogout

Cysteine - cystinuria

99
Q

What are the principles of treatment for glomerulonephritis?

A

Reduce the degree of proteinuria

Induce remission of nephrotic syndrome

Preservation of long term renal function

100
Q

CKD progression - risk factors

A

CVD

Proteinuria

AKI

Hypertension

Diabetes

Smoking

Afro-caribbean/Asian ancestry

Chronic use of NSAIDs

Untreated urinary tract outflow obstruction

101
Q

What is Renal AKI, and what are some of the causes?

A

Diseases causing inflammation/damage to kidney cells

Vascular causes - vasculitis, renovascular disease

Glomerular causes - GN

Interstitial nephritis - drugs (most common cause), infection (e.g. TB), systemic (e.g. sarcoid)

Tubular injury - ischaemia, drugs (e.g. gentamicin), contrast, rhabdomyolysis

102
Q

What are some of the clinical features of ADPKD?

A

Reduced ability to concentrate urine

Chronic pain

Hypertension in younger patients - most common feature

Haematuria - if the cyst ruptures

Cyst infection

Renal failure

NB - be suspicious of young people with high blood pressure and no family history

103
Q

Membranous nephropathy is the second commonest cause of nephrotic syndrome in adults, and can have primary or secondary causes. Name some of the common secondary causes

What might be seen on renal biopsy, and what is the treatment?

A

Secondary causes

  • infection
  • connective tissue diseases
  • malignancies
  • drugs

Biopsy shows subepithelial immune complex deposition in the basement membrane

Treatment - Steroids/alkylating agents/B cell monoclonal antibodies

104
Q

What are the chances of an affected individual having children with ADPKD? How does this affect management?

A

50% chance that children will also have the disease. This means that genetic counselling is required both pre- and post-testing

105
Q

How is AKI managed?

A

If hypovolaemic, prescribe fluids and carefully manage. Recommend a series of 250ml boluses for resusc. and reassess after each

Stop high risk medicines and contrast

Treat the underlying cause

106
Q

GN treatment - what are some of the immunosuppressive options?

A

Drugs

  • corticosteroids (prednisolone po, MethylPred IV)
  • azathioprine
  • alkylating agents (cyclophosphamide/chlorambucil)
  • calcineurin inhibitors (cyclosporin/tacrolimus)
  • mycophenolate mofetil (MMF)

Plasmapharesis (therapeutic plasma exchange, used if e.g the patient has vasculitis and you want to rapidly remove the circulating antibodies

Antibodies

  • IV immunoglobulin
  • Monolonal T or B cell antibodies
107
Q

If it was essential to get an accurate assessment of GFR, what measurement would be used?

A

51Cr-EDTA clearance

eGFR is useful but not entirely accurate, especially at higher GFR (hence reports using “above 60 ml/min”)

108
Q

In a patient with ADPKD, where else might cysts be seen? How does this affect the organ in question’s function?

A

Hepatic cysts are the most common extra renal manifestation

Liver function is typically preserved, however cysts can result in SoB, pain, ankle swelling and ascites

Cysts may also present in the brain and lead to intra-cranial aneurysms

109
Q

How is myeloma with renal dysfunction diagnosed? In particular, what is looked for in bloods and urine?

A

Have a high index of

Bloods - serum protein electrophoresis and serum free light chains

Urine - Bence Jones protein

Other tests - bone marrow biopsy, skeletal survey, renal biopsy

110
Q

Reminder - what are the classification of CKD based on eGFR?

A

Stages 1-5

Anything sub 60 GFR is stage 3-5

111
Q

Hyperkalaemia - medical treatment

A

Protect the myocardium

  • 10mls 10% calcium gluconate (2-3 mins) - FIRST THING!!!

Move K+ back into cells

  • Insulin (10 units of actrapid) with 50mls 50% dextrose
  • Salbutamol nebuliser

Prevent absorption from GI tract

  • Calcium resonium (NB - this is not done in the acute setting)
112
Q

Which of the following is NOT an indicator for emergency dialysis?

  • Pulmonary oedema (in the context of AKI)
  • Life threatening hyperkalaemia
  • Uraemic pericarditis
  • Elevated creatinine >500
  • Severe acidosis
A

Elevated creatinine >500

113
Q

Where is atrial natriuretic peptide/hormone (ANP or ANH) produced and stored?

When is it released?

A

Produced by the heart and stored in atrial muscle cells

ANP is released when these cells are mechanically stretched due to increased circulating plasma volume

114
Q

Why is blood pressure important in the context of kidney disease? What complications could develop?

A

Kidney disease could result in hypo OR hypertension

This could result in the development of accelerated hypertension (recent significant increase in BP over baseline, associated with end organ damage). Accelerated hypertension is a medical emergency, features a diastolic BP >120 mmHg, and may cause papilloedema, encephalopathy, fits, cardiac failure and acute renal failure

115
Q

What is Alport’s Syndrome?

What mutation is involved and how is the disease inherited?

A

Hereditary nephritis due to a disorder of Type IV collagen matrix

Mutation on the COL4A5 gene leads to a deficient collagenous matrix (nb - COL4A3 and A4 also cause Alport syndrome, but these are on autosomes, whereas A5 is on the X chromosome)

Inheritance pattern for COL4A5 mutation is X-linked

116
Q

Describe the following in a) dehydration and b) overhydration

  • ADH levels
  • water permeability
  • tonicity of urine
A

Dehydration

  • High ADH
  • High water permeability (aquaporins expressed)
  • Hypertonic urine (up to 1400 mosmol/l)

Overhydration

  • Low ADH
  • Low water permeability (aquaporins internalised)
  • Hypotonic urine (<50 mosmol/l)
117
Q

What are some of the causes of Pre-Renal AKI?

What drug needs to be avoided in this context?

What complication may develop if a Pre-Renal AKI isn’t treated?

A

Hypovolaemia and Hypotension. Also renal hypotension as a result of e.g. NSAIDs/COX-2 inhibitors, ACEi/ARBs or Hepatorenal syndrome.

ACE inhibitors cause a slight reduction in the GFR, if there is a major drop in renal perfusion there will then be a major drop in GFR. (Also the other drugs listed above)

If left untreated, a pre-renal AKI may develop into Acute Tubular Necrosis

118
Q

What are some of the causes of Post-Renal AKI?

A

Post-renal is obstructive, leading to hydronephrosis and a resulting loss in concentrating ability

  • Stones
  • Malignancy
  • Strictures
  • Extrinsic pressure
119
Q

As a result of the variance in osmolarity through the loop of Henle, where in the kidney is the osmolarity of the tubular fluid highest?

A

In the medulla (as this is where the Loop of Henle is found), osmolarity then decreases again as the nephron passes back into the cortex

120
Q

What are urinary casts? When is their formation pronounced and what can the different types of cast tell us?

A

Microscopic cylindrical structures that present in the urine in certain disease states. Formation is pronounced in environements favouring protein denaturation and precipitation (e.g. low urine flow, low pH etc.)

Types of Cast

  • Hyaline casts - usually benign
  • Red cell casts - always pathological, usually associated with nephritic syndrome
  • Leucocyte casts - signals infection or inflammation
  • Granular casts - indicative of chronic disease
121
Q

Alport’s syndrome - clinical presentation

A

Haematuria (also proteinuria at a later stage, but this confers a bad prognosis)

Sensorineural deafness

Ocular defects

Leiomyomatosis of oesophagus/genitalia

122
Q

Describe the following with regards to increasing ADH levels

  • urine osmolarity
  • urine volume
  • NaCl excretion
A

As ADH levels increase, osmolarity increases and volume decreases

NaCl excretion is completely unaffected by ADH!!

123
Q

What is seen on renal biopsy on a patient with IgA nephropathy?

How is this condition treated, and what % will progress on to ESRF?

A

Renal biopsy shows mesangial cell proliferation and expansion with IgA deposits in the mesangium (mesangial cells prolierate and expand in repsonse to IgA complexes being deposited in the kidneys)

Treatment is with BP control/ACE inhibitors and ARBs/Fish oil

25% progress to end stage renal failure within 10-30 years

124
Q

What are the two types of proteinuria to be familiar with? How do they differ?

A

Overflow proteinuria - excessive amounts of protein in the blood is passed into glomerulus, meaning not all protein can be reabsorbed e.g. Bence Jones proteinuria

Glomerular proteinuria (MOST COMMON)- excessive amounts of protein is passed from the glomerulus into the tubule, despite normal amounts of protein in the blood e.g. albuminuria

125
Q

What is the timescale for

  • Acute Kidney Injury
  • Chronic Kidney Disease?
A

Acute - decline in GFR over hours/days/weeks

Chronic - at least 90 days

126
Q

What are some of the signs and symptoms of Renal AKI?

A

Non-specific symptoms

  • Constitutional - weight loss, anorexia, fatigue etc.
  • N and V
  • Itch
  • Fluid overload - oedema, SoB

Signs

  • Fluid overload
  • Uraemia > itch and pericarditis
  • Oliguria
127
Q

What simple test can be used to establish whether a patient is presenting with glomerulonephritis vs a non-glomerular disease like interstitial nephritis?

A

Urine dipstick - non-glomerular conditions will have no protein/red cell leakage

If blood and protein are present in the urine, then the condition is likely GN

128
Q

What drug is prescribed to patients with CKD to prevent the development of primary and secondary CVD?

A

Statins e.g. atorvastatin

129
Q

What effect does the release of ANP have?

A

Promotes the excretion of Na+ and diuresis, thus decreasing plasma volume

130
Q

Give some examples of drugs that should be avoided in patients with kidney disease?

A
  • NSAIDs
  • ACE inhibitors/ARBs/diuretics
  • Antibiotics - gentamicin, trimethoprim, penicillins
  • PPIs
  • Radiology contrast
131
Q

When would you alter the dose of ACE inhibitors/ARBs in a patient with CKD?

A

If the GFR decrease from pre-treatment baseline exceeds 25%

or

The serum creatinine increase from baseline exceeds 30%

132
Q

What is the main treatment for myeloma with renal dysfunction?

A

Stem cell transplant and chemotherapy

Also need to stop nephrotoxic drugs and manage hypercalcaemia

Can also perform plasma exchange to remove free light chains

Dialysis can be performed as supportive treatment

133
Q

What are some of the signs of NephRITIC syndrome?

What cells in the glomerulus are affected? Is this proliferative or non-proliferative?

A

Acute kidney injury and haematuria

Oliguria (reduced urine output)

Oedema/fluid retention

Hypertension

Active urinary sediment - RBCs, granular casts, proteinuria etc.

Endothelial cells are affected, and is indicative of a proliferative process

134
Q

What new measurement was incorporated alongside eGFR in 2014?

What are the categories?

A

Albumin Creatinine Ratio (ACR)

A1 - <3 mg/mmol

A2 - 3-30 mg/mmol

A3 - >30 mg/mmol

Has a big clinical effect on patient’s outcome

135
Q

What are some of the common causes of chronic kidney disease?

A

Diabetes and Hypertension - make up 66% of all CKD causes

Glomerularnephritis - primary and secondary

Vascular causes - mainly renal artery stenosis and small vessel vasculitis (GPA, microscopic polyangiitis)

Reflux nephropathy and polysystic kidneys

136
Q

What are the main two chromosomal mutations associated with Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

Which is more common? Which develop ESRF at an earlier stage?

A

PKD gene 1, located on chromosome 16 (85% of cases)

PKD gene 2, located on chromosome 4 (15% of cases)

PKD gene 1 is the more common of the two, and PKD1 patients develop End-Stage Renal Failure earlier on

137
Q

Describe the secretion of ADH from the posterior pituitary

A

Octapeptide is synthesised by the supraoptic and paraventricular nuclei in the hypothalamus

This is then transported down nerve terminals and stored in granules in the posterior pituitary

Primary stimulus e.g. dehydration > drop in plasma osmolarity resulting in Ca2+-dependent exocytosis > release of ADH

138
Q

What marker satisfies all of these criteria?

What are its downsides?

A

Inulin satisfies these criteria. However, it is not endogenous and it is not easy to measure

139
Q

When diagnosing an ANCA-associated vasculitis, what antibodies might be detected on immunology? Give a condition associated with elevated levels of each

A

Anti-MPO (more commonly raised in microscopic polyangiitis)

Anti-PR3 (more commonly raised in GPA

140
Q

Diabetic nephropathy - prevention and management. In particular, doing what slows progression?

A

Glycaemic control (as per usual with DM)

Anti-hypertensive therapy - keep BP <130/80 and give ACE inhibitors/ARBs

Lipid control

Reducing proteinuria slows progression (done through ACEIs/ARBs)

Renal replacement therapies are also an option - simultaneous kidney-transplant (type I DM only), kidney transplants, haemodialysis and preitondeal dialysis

141
Q

What is the average age of patients with ADPKD? How early might this condition present?

A

Mean age of presentation is 31

Early onset may be seen in utero, or first year of life

142
Q

What antibody is seen in 70% of patients with primary membranous nephropathy?

A

Anti PLA2r antibody

143
Q

Which parts of the nephron are found in…

  • the cortex
  • the medulla?
A

Cortex

  • proximal tubule
  • distal tubule

Medulla

  • Descening and Ascending limbs of Loop of Henle
144
Q

Name some of the common causes of primary (idiopathic) glomerulonephritis

A

Minimal change

Focal Segmental GlomeruloSclerosis (FSGS)

Membranous GN

Membranoproliferative GN

IgA Nephropathy

Year 2 - Renal (6 decks)

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