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Inflammation > Kidneys > Flashcards

Kidneys Flashcards

1
Q

What is glomerulonephritis

A

Glomerular inflammation, generally caused by immunological mediated injury to the glomeruli
Pathogenic mechanism: deposition of circulating or in situ formation of immune complexes or deposition of antiglomerular basement membrane antibodies

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2
Q

What are the symptoms of glomerulonephritis

A

hypertension, incidental finding of microscopic haematuria, incidental finding of proteinuria, nephrotic syndrome (protein in the urine), progressive renal impairment, acute kidney injury

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3
Q

What are non glomerular causes of microscopic haematuria

A

bladder tumours, renal stones, renal tumours, BPH, UTI, renal injury

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4
Q

What are glomerular causes of microscopic haematuria

A

IgA nephropathy, Alports (genetic condition affecting the basement membrane), thin basement membrane disease, post infectious GN, membranoproliferative PN

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5
Q

What is IgA nephropathy

A

Glomerular deposition of IgA causing inflammation due to abnormalities in IgA
Variable clinical presentation: microscopic haematuria, hypertension, slow progressive renal impairment, rapidly progressive renal impairment, nephrotic range proteinuria

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6
Q

What are the tests and management of IgA nephropathy

A

Lab tests: raised serum IgA, renal biopsy shows mesangial proliferation with IgA deposition
Management: control of BP

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7
Q

What is Henoch Schonelin Purpura

A

most often self-limiting, but some may progress to ESKD
Inflammation of the small blood vessels, esp in kidney, skin and gut
Most common in young children
IgA deposition in the kidney in a similar pattern to IgA nephropathy
Associated with leucocytoclasic vasculitic rash

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8
Q

What is nephrotic syndrome

A

Heavy proteinuria >3.5g
Hypalbuminaemia
Oedema: periorbital in children, peripheral in adults
Hyperlipidaemia (decrease in oncotic pressure stimulates hepatic lipoprotein synthesis resulting in a high cholesterol)

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9
Q

What are the primary causes of nephrotic syndrome

A

membranous nephropathy, FSGS, MCGN, minimal change disease

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10
Q

What are the secondary causes of nephrotic syndrome

A

diabetic nephropathy, SLE, amyloidosis, malignancy, drugs

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11
Q

What is minimal change disease

A

the most common cause of nephrotic syndrome in children.

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12
Q

What are the signs of minimal change disease

A

Proteinuria (abnormal excretion of proteins, mainly albumin, into the urine), oedema (swelling of soft tissues as a consequence of water retention), and hypoalbuminaemia (low serum albumin). Normal light microscopy

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13
Q

What are the causes of minimal change disease

A

Idiopathic esp. in children
NSAIDS
Lithium, pecillicinamine, pamidronate, sulfazalizine, immunisations
Paraneoplastic (Hodgkin’s lymphoma)
Infections (syphilis, TB, mycoplasma, Hep C)
Allergy

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14
Q

What is Focal segmental glomerulosclerosis

A

is the most common cause of nephrotic syndrome in adults. It is characterized by the appearance of tissue scarring in the glomeruli. The term focal is used as some of the glomeruli have scars, while others appear intact; the term segmental refers to the fact that only part of the glomerulus suffers the damage

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15
Q

What are the signs of symptoms of FSGS

A

In children and some adults, FSGS presents as a nephrotic syndrome, which is characterized by edema (associated with weight gain), hypoalbuminemia (low serum albumin, a protein in the blood), hyperlipidemia and hypertension (high blood pressure). In adults, it may also present as kidney failure and proteinuria, without a full-blown nephrotic syndrome.

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16
Q

What is the management for nephrotic syndrome

A

Diuretics
ACE
Anticoagulation (increase risk of VTE if albumin is less than 25 in membranous, less than 20 in other causes)
Statin for high cholesterol
Renal biopsy - children minimal change disease common, so steroids given before biopsy

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17
Q

What is membranous glomerulonephritis

A

Slowly progressive disease of the kidney affecting mostly people between ages of 30 and 50 years, usually Caucasian.

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18
Q

What is GPA

A

a long-term systemic disorder that involves both granulomatosis and polyangiitis.

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19
Q

WHat is ANCA

A

anti neutrophil cytoplasmic antibodies and these have been shown to be pathogenic

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20
Q

What is anti GBM disease

A

Auto antibodies to the glomerular basement membrane causing an RPGN (rapidly progressing glomerular nephritis) with crescent formation
Previously known as goodpastures syndrome
Associated with anti-GBM antibodies and alveolar basement membrane antibodies
An cause absolute anuria with pulmonary haemorrhage
Very short time period
Can die from pulmonary embolism

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21
Q

What does haemturia on urine dipstick indicate

A

malignancy, renal stone, prostatitis, trauma, menstruation, active inflammation in the glomerulus for any reason, rhabdomyolysis

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22
Q

What does proteinuria on urine dipstick indicate

A

diabetes, hypertension, obesity, UTI, GN, APKD, myeloma and amyloidosis, SLE

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23
Q

What does gravity indicate on urine dipstick

A

Gravity: if high glucose in diabetes or dehydration. If low can suggest GN or diabetes insipidus

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24
Q

What is the ideal GFR

A

A GFR below 60 for 3 months or more or a GFR above 60 with kidney damage indicates chronic kidney disease

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25
Q

What are pre renal causes of renal disease

A

due to problems with arterial supply and venous drainage
Single blood supply and drainage, therefore susceptible to :
Hypovolaemia, heart failure, vasodilation, arterial dissection
Susceptible renal artery stenosis:
Atherosclerosis and fibromuscular dysplasia

26
Q

What are instrinsic causes of renal disease

A

due to problems within the renal interstitium/tubules

27
Q

What are post renal causes of renal disease

A

due to problems with outflow tract of the kidney

28
Q

Where is renal biopsy performed

A

usually left kidney, main complication is bleeding, day case. Samples for light, immune, EM

29
Q

What are indicators for renal biopsy

A

Progressive or unexplained renal impairment regardless of urine sediment. Nephrotic and diffuse nephritic syndrome. Significant proteinuria with normal blood pressure

30
Q

What are the effects of prostaglandins in kidneys

A

Cause vasodilatation of afferent arteriole -> increased GFR

31
Q

What are the effects of NSIADS in kidneys

A

Vasoconstriction of afferent -> decreased GFR

32
Q

What are the effects of ACE inhibitors in kidneys

A

Vasodilatation of efferent -> decreased GFR

33
Q

What are the effects of angiotensin II in kidneys

A

Vasoconstriction of efferent -> increased GFR

34
Q

Describe glomerular pathology

A

Severe injury leads to rupture and thrombosis in the Bowman’s capsule i.e. crescent formation. Clinical pattern is usually a loss of function and heavy proteinuria
If insidious, then proteinuria may be the only feature

35
Q

What are the PCT an DCT susceptible to

A

Susceptible to precipitation of solute and luminal obstruction: light chain disease, uric acid, myoglobin (rhabdomyolysis)

36
Q

What causes acute tubular necrosis

A

hypoperfusion, tubular toxins (aminoglycosides, cisplatin, ethylene glycol, IV contrast)

37
Q

What is the interstitium susceptible to

A

Drugs - antibiotics like penicillin, NSIADs, herbal medicine, proton pump inhibitors that reduce acid secretion
Infections - pyelonephritis, viral (e.g. CMV, HIV), fungal/parasitic
Autoimmune - SLE, Sjogren (affects parts of the body that produce fluids like tears and saliva), sarcoid
Alloimmune (transplant rejection)

38
Q

What is chronic interstitial nephritis

A

insidious in onset. Less inflammation, more scarring. Important to establish cause. Steroids unhelpful Less capacity for recovery

39
Q

What is the outflow tract susceptible to

A

single draining pathway
Susceptible to obstruction:
Ureteric: stones, retroperitoneal fibrosis (stops peristalsis), gyane malignancy
Bladder flow: stones, bladder cancer, prostatic (BPH/cancer)
Urethral: stones, urethral stricture

40
Q

What is hydronehprosis

A

swelling of a kidney due to a build-up of urine. Happens when urine cannot drain out from the kidney to the bladder.

41
Q

Where does creatinine come from

A

Nonenzymatic hydrolysis of creation released from skeletal muscle

42
Q

Where does urea come from

A

Hepatic breakdown of protein: endogenous or exogenous

43
Q

What is the renal handing of urea

A

Completely filtered, significant tubular reabsorption

44
Q

What is the renal handling of creatinine

A

Completely filtered, some tubular secretion (up to 20% of clearance)

45
Q

What are the stages and testing of CKD

A

1: normal GFR with other evidence of chronic kidney damage. Test every year
2: GFR 60-89 with other evidence of chronic kdieny damage. Test every year
3: 30-59. 6 months. Split into 3A and 3B.
4: 15-29. 3 months
5: under 15. See every 3 months

46
Q

What are Vander’s 7 renal functions

A

Regulation of water and electrolyte balance
Excretion of metabolic waste
Excretion of bioactive substances that affect body function
Regulation of arterial blood pressure
Regulation of rbc production
Regulation of vitamin D production
Gluconeogenesis

47
Q

How is prostatic disease managed

A

Alpha blocker

48
Q

How are blood pressure and volume managed in kidney disease

A

assess fluid status (weight, JVP and oedema), correct volume then BP (i.e. if overloaded start with diuretic), use ACEI or A2B in almost all cases for BP control (relaxes kidneys by reducing proteinuria), targets (130/80 probably consensus in CKD)

49
Q

Where is erthyropoetin synthesised

A

Synthesised by interstitial fibroblasts in the kidney
Stimulated by low oxygen tension
HIF1alpha protein degraded in normoxia
HIF complex stimulates transcription of epo genes
Epo binds to receptors on erythroid precursors

50
Q

How is anaemia managed in kidney disease

A

Check Hb and ferritin regularly
Check B12 over 187 and folate over 3.1
Iron stores need to be super-normal - Tsats over 30% (18-71) and ferritin over 500 (22-275)
Use epo (often earlier in diabetic) as an injection
Target Hb 100-115g/l

51
Q

How does kidney affect PTH

A

Renal diseases results in high PTH, which would normally would increase tubular excretion of phosphate but due to kidney disease it can’t.
Calciphylaxis: result of high calcium and phosphate. Very pain and high mortality.

52
Q

What does FGF23 drive

A

Kidney’s ability to activate vit D and get rid of phosphate

53
Q

What is calciphylaxis

A

result of high calcium and phosphate. Very pain and high mortality.

54
Q

What is normal range for phosphate

A

0.9 to 1.4 mmol/l

55
Q

What is normal range for calcium

A

2.15-2.55 mmol/l

56
Q

How to maintain mineral bone density in CKD

A

If px not on dialysis and with raised PTH treat vit D deficiency (250OH <50)
If px not on dialysis reserve vit D analogues to those with severe progressive rise in PTH
In px on dialysis aim to keep PTH 2-9x upper limit normal (20-600ng/l)

57
Q

What are the indicates for dialysis

A

Hyperkalaemia resistant to medical treatment
Pulmonary oedema/fluid overload resistant to diuretics
Symptoms of uraemia (above 35/40)- poor appetite, vomiting, weight loss, lethargy and fatigue, itching. Symptoms arises insidiously.
Acidosis

58
Q

What is haemodialysis

A

hospital, satellite unit (nurse led) or home (daily). Taking blood from px body, putting it thought filter that acts as the kidney. In hospital, will need 4-5 hours of treatment 3 days a week. Gives equivalent eGFR to 15-20%

59
Q

What is the water requirement for haemo

A

Water requirement: dialysate flow rate 500-600 ml/min. 30,000ml/hr *4=120 000ml (120 litres per session.

60
Q

What is an AV fistula

A 
Arteriovenous fistula (swings vein around into artery): native artery and vein. Radiocephalic, brachiocephalic, brachiobasilic. Matures in 4-8 weeks. 2 needles usual. Do not stick cannula above fistula.
Complications: clotting. Stenoses. Thrombosis
61
Q

What are the complications of haemo

A

hypotension (if rate of removal is quicker, then there is less fluid in the blood compartment), septicaemia (plastic in body, also line may site in the left atrium), bleeding (uraemia affects platelet function + heparin), clotting of fistula, dialyser reaction, air embolus

62
Q

What is peritoneal dialysis

A

Peritoneal: home based - CAPD or APD

Benefits: done by px at home. No need to attend hospital.
Requirements: physical as px has to lift 2kg bags. Storage space. Hygiene. Some residual kidney function.

Inflammation (12 decks)

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