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Clincal - Renal > Renal Conditions > Flashcards

Renal Conditions Flashcards

1
Q

What is glomerulonephritis?

A

Term encompasses a number of conditions which:

  • are caused by pathology in the glomerulus
  • present with proteinuria, haematuria or both
  • are diagnosed on renal biopsy
  • cause CKD
  • can progress to kidney failure
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2
Q

What is the difference between nephrotic or nephritic glomerular disease?

A

Nephrotic - proteinuria due to podocyte pathology

Nephritic - haematuria due to inflammatory damage

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3
Q

What are the three causes of nephrotic syndrome?

A

Minimal change glomerulonephritis

Minimal change focal segmental glomerulosclerosis

Membranous glomerulonephritis

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4
Q

What is minimal change glomerulonephritis?

How is it diagnosed?

How is it treated?

A

Presents in childhood/adolescence - most is idiopathic or drugs (NSAIDS, lithium)

Heavy proteinuria
No progression to renal failure

Light microscope = normal
Electron microscope = effacement of podocyte foot processes

Treatment - prednisolone 1mg/kg for 4-16 weeks
75% of adults will respond
Frequent relapses require longer term immunosuppression

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5
Q

What is focal segmental glomerulosclerosis?

How is it diagnosed?

How is it treated?

A

Commonest glomerulonephritis seen on renal biopsy

Primary (idiopathic) or secondary (HIV, heroin, lithium, lymphoma)

At risk of progressive CKD and kidney disease

Diagnosis - glomeruli have scarring of certain segments

Treatment = ACEi/ARB and BP control. Corticosteroids only in primary disease

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6
Q

What is membranous nephropathy?

How is it diagnosed?

How is it treated?

A

Primary (idiopathic) or secondary to malignancy, infection, immunological disease or drugs

Diagnosis = Anti-phospholipase A2 receptor antibody in 70-80% of idiopathic disease. Diffusely thickened GBM due to sub epithelial deposits

Treatment = ACEi/ARB and BP control. Immunosuppression only in those at high risk of progression

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7
Q

What is membranoproliferative glomerulonephritis?

How is it diagnosed?

How it is treated?

A

Can be immune complex associated - driven by increased or abnormal immune complex deposits in kidney which activate complement

C3 glomerulopathy - due to genetic or acquired defect in complement pathway

Diagnosis = proliferative glomerulonephritis with electron dense deposits. Immunoglobulin deposition distinguishes immune complex associated disease from C3 glomerulopathy

Treatment = ACEi and ARB. Trial of immunosuppression if no underlying cause found and progressive decline in renal function

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8
Q

Define nephrotic syndrome

A

Proteinuria

Hypoalbuminaemia (usually <30g/L)

Peripheral oedema

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9
Q

What is the presentation of nephrotic syndrome?

A

Generalised pitting oedema which can be rapid and severe

Ask about systemic symptoms e.g joint, skin

Consider malignancy and chronic infection

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10
Q

What is the management of nephrotic syndrome?

A

Reduce oedema - fluid and salt restriction. Loop diuretics and thiazide can be added if oedema remains resistant

Treat underlying cause - adults need renal biopsy

Reduce proteinuria - ACEi or ARB

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11
Q

What are the three complications of nephrotic sydrome?

A

Thromboembolism - hypercoaguable due to clotting factors, decrease anti-thrombin III

Infection - urine losses of immunoglobulins and immune mediators lead to increase risk of urinary, respiratory and CNS infection.

Hyperlipidaemia - increased cholesterol. Thought to be due to hepatic synthesis in response to decreased oncotic pressure and defective lipid breakdown

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12
Q

What is IgA nephropathy?

How does it present?

How is it diagnosed?

How is it treated?

A

Nephritic Syndrome - commonest
Occurs at any age

Deposition of IgA in the glomerulus

Presentation = asymptomatic non-visible or episodic visible haematuria, increased BP, proteinuria

Diagnosis = renal biopsy - IgA in mesangium

Treatment = ACEi/ARB reduce proteinuria and protect renal function. Corticosteroids and fish oil if persistent proteinuria

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13
Q

What is rapidly progressing glomerulonephritis?

A

An aggressive glomerulonephritis, progressing to renal failure over days or weeks

Causes - small vessel/ANCA vasculitis, lupus nephritis, anti GBM disease

Diagnosis - breaks in the GBM allow an influx of inflammatory cells so crescents are seen on renal biopsy

Treatment - corticosteroids and cyclophosphamide

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14
Q

How do you investigate nephrotic syndrome?

A

Bloods - FBC/ U&Es, CRP, immunoglobulins, complement, autoantibodies (ANCA), blood culture

Urine - M, C &S

Imaging - CXR pulmonary haemorrhage, renal USS

Renal biopsy - required for diagnosis

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15
Q

Is IgA nephropathy nephrotic or nephritic?

Is IgG nephropathy nephrotic or nephritic?

A

Nephritic - deposition of IgA in glomerulus

Nephritic - deposition of IgG - good pasture syndrome

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16
Q

What is diabetic nephropathy?

A

Commonest cause of end stage renal failure

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17
Q

What is the effect on the kidney?

A

Hyperglycaemia leads to increased growth factors

RAAS activation

Production of advanced glycosylation end products

Oxidative stress

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18
Q

What can diabetic nephropathy cause to the kidney?

A

Increased glomerular capillary pressure

Podocyte damage

Endothelial dysfunction

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19
Q

What is the first clinical sign of diabetic nephropathy effect on the kidney?

A

Albuminuria

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20
Q

What is the treatment for diabetic nephropathy?

A

Intensive DM control prevents microalbuminaemia and reduces risk of progression of macroalbuminaemia

BP 130/80mmHg - use ACEi or ARB for cardio and renal protection

Sodium restriction to less than 2g/day

Statins to reduce CV risk

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21
Q

What is lupus nephritis?

A

SLE is a systemic autoimmune disease with antibodies against nuclear components

Deposition of antibody complexes causes inflammation and tissue damage

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22
Q

How does lupus nephritis present?

A

Rash

Photosensitivity

Ulcers

Arthritis

Serositis

CNS effects

Cytopenias

Renal disease

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23
Q

How is lupus nephritis diagnosed?

A

Clinical diagnosis

Antibody profile - ANA is sensitive but not specific

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24
Q

How is lupus nephritis treated?

A

Depends on the histological class

Class 1 and II - ACEi and ARB for renal protection

Class III-V requires immunosuppression

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25
Q

How do you treat small vessel vasculitis?

A

High dose glucocorticoids

Plasma exchange if it presents with renal failure or pulmonary haemorrhage

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26
Q

How is small vessel vasculitis diagnosed?

A

Clinical

ANCA

And biopsy

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27
Q

How can myeloma cause renal disease?

A

Tubular obstruction due to light chain casts

Deposition of light chain in glomerulus

Hypercalaemia

Renal tract infection due to immunoparesis

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28
Q

How does atherosclerotic renovascular disease cause problems?

How is it diagnosed?

A

RAAS activation which causes treatment resistant BP and/or deterioration in renal function on ACEi or ARB

Diagnosis = >1.5cm asymmetry in renal size

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29
Q

How is atherosclerotic renal disease treated?

A

Modification of CV risk factors - statins, aspirin, antihypertensives

ACEi and ARB - Used to be contraindicated due to concern about renin dependent renal perfusion and deterioration in function

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30
Q

How does sickle cell nephropathy cause renal problems?

How is it diagnosed?

How is it treated?

A

Hbss is associated with hyperfiltration (lower than expected creatinine) and albuminuria

Diagnosis - clinical, biopsy only if looking for another diagnosis

Treatment - ACEi or ARB

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31
Q

What does the PCT reabsorb?

A

Na+ (70%)

Glucose (100%)

Bicarbonate

Phosphate

Amino acids

Uric acid

32
Q

What syndrome can be found in the PCT?

How is it treated?

A

Fanconi Syndrome - generalised impairment of PCT function

Treatment - replace phosphate

33
Q

What type of acidosis can occur if there is a problem with the PCT?

What causes it?

How is it treated?

A

Proximal (type 2) renal tubular acidosis

Due to failure of bicarbonate reabsorption

Distal reabsorption of bicarbonate intact so serum bicarbonate usually >12mmol/L

Treatment = bicarbonate and potassium replacement

34
Q

What two diuretics act on the PCT?

A

Osmotic diuretic - Mannitol - used for cerebral oedema to decrease ICP

Carbonic anhydrase inhibitor - acetazolamide - used in glaucoma and altitude sickness. Can lead to metabolic acidosis due to increased bicarbonate excretion

35
Q

What is the function of the thick ascending limb?

What transporter is found here?

A

Reabsorbs Na+ and other electrolytes

NKCC2 transporter

36
Q

What syndrome can occur in the thick ascending limb?

What can it lead to?

What age does it tend to occur?

A

Bartter syndromes - due to impaired salt transport in thick ascending loop

Can cause a hypokalaemia, hypochloraemic, metabolic alkalosis

Usually presents in childhood

37
Q

What diuretics are used on the thick ascending loop of henle?

What is the mechanism of action?

What are they used to treat?

What are the side effects?

A

Loop diuretics - furosemide

Block NKCC2 transport - increase solute load of filtrate and reduce water absorption

Increase excretion of water

Readily absorbed from GI tract

Uses - peripheral oedema (Heart failure, ascities)
Can be used to treat Hypercalcaemia

Side effects = hypokalaemia, metabolic alkalosis, hypovolaemia

38
Q

What are loop diuretics used to treat?

When can they be useful?

A

Uses - peripheral oedema (Heart failure, ascities)

Can be used to treat Hypercalcaemia

39
Q

What is the function of the DCT?

What transporter is found in the DCT?

A

Reabsorbs Na+ and other electrolytes

NaCl transporter

40
Q

What syndrome can occur in the DCT?

When does it present?

How is it treated?

A

Gitelman syndrome - loss of function of NaCl transporter

Milder than bartter syndrome

Presents in adolescence/adulthood with incidental finding of electrolyte abnormalities

Treatment = electrolyte supplementation

41
Q

What diuretics can be used in the DCT?

What is the mechanism of action?

What can they be used to treat?

A

Thiazide - bendroflumethiazide

Inhibit NaCl transporter - decrease NaCl reabsorption and increase water loss

Used to treat raised BP

Side effect = hyponatraemia, hypokalaemia

Reduces Ca2+ excretion
Reduces uric acid excretion
Glucose intolerance can occur

42
Q

What is the function of the cortical collecting duct?

A

Acid-base and K+ homeostasis

Aldosterone acts to retain Na+ and excrete K+

43
Q

What problem can occur in the DCT?

What causes it?

How is it diagnosed?

What is the treatment for it?

A

Distal (type 1) renal tubular acidosis - failure of H+ excretion

Primary genetic disease or secondary autoimmune disease (SLE) or toxins (lithium)

Diagnosis - urine fails to acidify pH >5.3 despite metabolic acidosis

Treatment - bicarbonate replacement and management of underlying disease

44
Q

What is the treatment for distal (type 1) renal tubular acidosis?

Where does it occur?

A

Bicarbonate replacement and management of underlying disease

Occurs in DCT

45
Q

What diuretics can be used in the DCT?

What are they used for?

What can they cause?

A

K+ sparing - aldosterone antagonists e.g. spironolactone, amiloride

Uses - aldosteronism, heart failure, cirrhosis, K+ wasting states

Decrease Na+ and K+ excretion

Can cause hyperkalaemia and acidosis

46
Q

What is acute tubulointerstitial nephritis?

How does it present?

What would the biopsy show?

A

Damage to renal tubules and interstitium

Presents with AKI

Inflammatory cell infiltrate in the interstitium and/or tubule

47
Q

What are the three causes of acute tubulointerstitial nephritis?

A

Drugs - antibiotics, NSADIs, PPIs, diuretics, ranitidine, anticonvulsants and warfarin

Infections - Streptococcus, pneumococcus, staphylococcus, campylobacter, E.coli

Autoimmune disease - SLE, sarcoid, Sjögren’s syndrome, ANCA

48
Q

What drugs can cause acute tubulointerstitial nephritis?

A

Antibiotics

NSADIs

PPIs

Diuretics

Ranitidine

Anticonvulsants

Warfarin

49
Q

What infections can cause acute tubulointerstitial nephritis?

A

Streptococcus

Pneumococcus

Staphylococcus

Campylobacter

E.coli

50
Q

What autoimmune conditions can cause acute tubulointerstitial nephritis?

A

SLE

Sarcoid

Sjogrens

ANCA

51
Q

What is the treatment for acute tubulointerstitial nephritis?

A

Stop causative agent or treat underling cause

Steroids are used

52
Q

What is chronic tubulointerstitial nephritis?

What does the biopsy show?

What commonly causes it?

A

Insidious onset and slowly progressive renal impairment

Biopsy = shows interstitial fibrosis and tubular atrophy

Commonly - due to drugs or infection

53
Q

What drugs can cause chronic tubulointerstitial nephritis?

A

NSAIDs

Lithium

Calcineurin inhibitors

Aminosalicylates

54
Q

What infections can cause chronic tubulointerstitial nephritis?

A

TB

Pyelonephritis

Leptospirosis

HIV

55
Q

What immune diseases can cause chronic tubulointerstitial nephritis?

A

Sarcoid

Sjögren’s syndrome

56
Q

What specific nephrotoxins can cause chronic tubulointerstitial nephritis?

A

Lead

Cadmium

Mercury

Artistolochic acid

57
Q

What haematological disorder can cause chronic tubulointerstitial nephritis?

A

Myeloma

58
Q

What is the treatment for chronic tubulointerstitial nephritis?

A

Stop causative agent or treat underlying cause

Reduce risk of progression as per CKD management - ACEi/ARB, BP control, glucose, lipids

59
Q

Name some nephrotoxins

A

Analgesics - NSAIDs

Antimicrobials - aminoglycosides, penicillin, rifampicin, acyclovir

Other drugs - PPIs, cimetidine, furosemide, thiazide, lithium, ACEi/ARB, iron, calcineurin inhibitors

Crystals - urate

Proteins - IgS in myeloma, light chain disease

Bacteria - streptococci, legionella, brucellosis, mycoplasma, chlamydia

Virus. EBV, CMV, HIV, adenovirus

Parasites - toxoplasma

Radiocontrast material

60
Q

What is rhabdomyolysis?

How can this cause renal impairment?

A

Results from skeletal muscle breakdown with release of intracellular contents (K+ and myoglobin) into the extracellular space

Increased cytokines and decrease nitric oxide cause renal vasoconstriction

Myoglobin is filtered by the glomeruli causing obstruction and inflammation

61
Q

How does rhabdomyolysis present?

A

History of trauma, surgery, immobility, hyperthermia, seizures

Muscle pain, tenderness, swelling, AKI = red/brown urine

62
Q

How is rhabdomyolysis diagnosed?

A

Serum myoglobin

Plasma creatinine 5 times upper limit

63
Q

What is the treatment for rhabdomyolysis?

A

Supportive

Urgent treatment for hyperkalaemia

IV fluid rehydration - maintain urine output 300mL/hour until myoglobin has ceased

64
Q

What is the treatment for urate neprhopathy?

A

Tumour lysis - aggressive hydration

Allopurinol to decrease synthesis of uric acid

65
Q

What is urate nephropathy?

A

Uric acid crystals precipitate within the tubulointerstitium causing decreased GFR and secondary inflammation

Seen in tumour lysis syndrome when a high tumour burden and sensitivity to chemotherapy cause uric acid which precipitates in association with increased phosphate

66
Q

What is autosomal dominant polycystic kidney disease?

A

85% have mutations in PKD1 (chromosome 16) and reach end stage renal failure by 50s

Mutation in PKD2 (chromosome 4) has slower course, reaching end stage renal failure by 70s

67
Q

How does autosomal dominant polycystic kidney disease present?

A

May be clinically silent unless cysts become symptomatic due to size/haemorrhage

Loin pain

Visible haematuria

Cyst infection

Renal calculi

Increased BP

Progressive renal failure

68
Q

What extrarenal symptoms may autosomal dominant polycystic kidney disease present as?

A

Liver cysts

Intracranial aneurysm

Mitral valve prolapse

Ovarian cyst

Diverticula disease

69
Q

How is autosomal dominant polycystic kidney disease diagnosed?

A

USS

Renal cysts are common and increases prevalence with age so diagnostic criteria are age related
E.g. 15 - 39 >3 cysts, 40-59 >2 cysts in each kidney

70
Q

What is the treatment for autosomal dominant polycystic kidney disease?

A

Water intake 3 - 4 L/day may suppress cyst growth

Increased BP should be treated to target <130/80 mmHg
1st line = ACEi/ARB
2nd line = thiazide like
3rd line = B-blocker

Treat infection

Haematuria managed conservatively

Persistent/severe pain may require cyst decompression

Plan - for RRT including pre-emptive transplantation

71
Q

How common is autosomal recessive polycystic kidney disease?

Where is the mutation?

How does it present?

How is it treated?

A

1 in 20,000

Mutation on chromosome 6

Presentation - ante/perinatal with renal cysts (salt and pepper on USS), congenital hepatic fibrosis which leads to portal hypertension

Poor prognosis if neonatal respiratory distress

Treatment - no specific therapy

72
Q

What is Alport Syndrome?

How common is it?

A

X-linked recessive, affects 1/5000 people

Due to mutations in the COL4A5 gene which encodes the alpaca chain of type 4 collagen

73
Q

How does Alport syndrome present?

A

Haematuria

Proteinuria

Progressive renal insufficiency

High-tone sensorineural hearing loss

74
Q

What does Alport syndrome transplantation increase the risk of?

A

Anti-GBM Disease

As type 4 collagen is the antigen in anti-GBM disease as the graft type 4 collagen is recognised as foreign

75
Q

What is cystinuria?

How is it inherited?

How it is treated?

A

Autosomal recessive defect prevents reabsorption of cystine and dibasic amino acids in PCT

Leads to cystinuria and cystine stone formation

Treatment - diet, increase fluid intake and urine alkalisation

76
Q

Name two lysosomal storage disorders

A

Fabry disease - due to deficiency of the enzyme alpha-glucosidase

Cystinosis - storage disorder with accumulation of cystine

Clincal - Renal (5 decks)

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