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Nephrology > General nephrology - COPIED > Flashcards

General nephrology - COPIED Flashcards

1
Q

What four signs makes up nephrotic syndrome?

A

proteinuria >> 4.5 g/ 24hr

dyslipidemia (hypercholesteraemia specifically)

hypoalbuminaemia

peripheral oedema

*** rem. haematuria is rare, and BP may be normal or slighly elevated ***

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2
Q

what usually prevents protein loss in the urine?

A

podocytes

fenestrated membrane

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3
Q

Do you get haematuria with nephrotic syndome?

A

Possibly. It depends on the damage to the glomerulus.

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4
Q

Why can you get sepsis with nephrotic syndrome?

A

Loss of immunoglobulins (proteins) in the urine will compromise the immune system.

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5
Q

Why do you get peripheral oedema with nephrotic syndrome?

A

Due to loss of protein in urine, therefore hypoalbuminemia.

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6
Q

Loss of proteins in the urine. The liver tries to compensate by….

A

producing more albumin

It also produces more cholesterol (hypercholesterolemia)

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7
Q

What is the consequence to the heart of the increase in peripheral oedema with nephrotic syndrome?

A

Reduction in venous return, therefore a reduction in stroke volume.

This reduction in blood flow reduces the GFR.

In addition there is inflammation in the Kidneys that also reduce GFR. THIS STIMULATES RENIN.

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8
Q

What is the consequene of an increase in RENIN production with nephrotic syndrome?

A

In response to low renal BP, Renin is released.

Renin-Angiotensin-aldersterone causes Na2+ to be retained and thus increase in BP.

This will result in more oedema because of the hypoalbuminuria.

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9
Q

What types of oedema can you get with nephrotic syndome?

A

periorbital oedema

ascites

peripheral oedema

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10
Q

Oedema in nephrotic syndrome also causes what problems in the thoracic region?

A

breathlessness

pulmonary oedema

pleural effusion

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11
Q

what does the urine look like in nephrotic syndrome?

A

frothy

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12
Q

What investigations?

A

urine dip stick

MSU, FBC

EUC, LFT, Calcium levels

serum (and urine) immunoglobulins to screen for autoimmune diseases.

CXR - pleural effusion/ oedema

ultrasound, biopsy.

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13
Q

What conditions can lead to nephrotic syndrome?

A

Glomerular disease (e.g. minimal change disease in childhood), focal segmental glomerulosclerosis, membranous nephropathy.

Diabetes

SLE

Amyloidosis

(Hep B and C, HIV) - check this

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14
Q

BUN

A

Bloode urea nitrogen; medical test.

NB. Liver produces urea as a waste product of protein digestion.

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15
Q
A
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16
Q

What benign things can increase urinary protein output?

A

Pyrexia

exercise

adoption of upright posture(postural proteinuria)

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17
Q

What do red cell casts always indicate?

A

renal disease

WC casts may indicate acute pyelonephritis

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18
Q

What are the three big causes of ESKD?

A

Diabetes (number ONE)

Hypertension

Glomerulopathy

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19
Q

What is Glomerulopathy?

A

immunologically mediated disorders with involvement of:

cellular immunity

humoral immunity

inflammatory mediators

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20
Q

Why do you get hypoalbuminemia with nephrotic syndrome?

A

Which protein is lost in the urine due to kidney damage

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21
Q

Why do you get lipiduria with nephrotic syndrome?

A

Passing of lipoproteins in the urine due to kidney damage (thus also hypoalbuminaemia)

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22
Q

What is acute glomerulonephritis?

– acute nephritic syndrome

A

Abrupt onset of glomerular haematuria (RBC casts or dysmorphic RBC),

non-nephrotic range proteinuria, oedema (periorbital, leg or sacral), hypertension and

transient renal impairment.

- OFTEN inflammation of glomeruli/ small b. vessels.

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23
Q

What is nephrotic syndrome?

A

Massive proteinuria (>3.5 g/day),

hypoalbuminaemia, oedema,

lipuria and hyperlipidaemia

NO RBCs in the urine

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25
Q

Why are ACE inhibitors used to treat nephrotic syndrome?

A

to reduce urinary albumin excretion when px ingests > protein.

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26
Q

How do you treat nephrotic syndrome?

A

Restrict sodium and use a thiazide diuretic.

(May have to be parenteral administration because of gut mucosal oedema)

Normal protein diet

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27
Q

Why is prophylactic anticoagulation desirable with nephrotic syndrome?

A

Due to loss of clotting factors (eg. antithrombin) in the urine and an increase in hepatic production of fibrinogen.

Avoid bed rest. Thromboembolism is very common in nephrotic syndrome.

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28
Q

Why use ACE inhibitors or ARBs for nephrotic syndrome?

A

reduce proteinuria by lowering pressure in glomerulus.

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29
Q

Loss of proteins with nephrotic syndrome predisposes patient to what?

A

Thromboembolisms (due to loss of clotting proteins)

Sepsis/ infections (due to loss of immunoglobulins)

Lipid abnormalities - can accelerate atheromas

Anaemia (loss of transferrin)

Oedema (lower limbs, sacrum) + can be periorbital & hands

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31
Q

What class of group for lowering nephrotic associated hyperlipidaemia?

A

HMG-CoA reductase inhibitor

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32
Q

Diagram of mesengial cells between arterioles and bowman’s capsule.

A
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33
Q

What is amyloidosis?

A

group of diseases in which abnormal protein, known as amyloid fibrils (insoluble), is deposited extracellularly. Acquired or inherited disorder of protein folding.

In the kidneys the amyloid deposition reduces the kidney’s ability to filter and hold on to proteins (nephrotic syndrome). Heart also affected (and Liver).

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34
Q

What is azotemia?

A

azot = “nitrogen”, -emia=”blood”

>> nitrogen-rich compounds in the blood (urea, creatinine), due to << kidney filtering.

Can cause uremia and AKI

ATI - acute tubular injury (acute tubular necrosis ATN) is most common cause of intrinsic renal azotemia

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36
Q

What are marked histological changes with diabetic renal disease?

A

glomerular basement membrane thickening

mesangial expansion

progressive depletion of podocytes

later … glomerulosclerosis

IMP> renal injury in diabetes is clinically silent.

37
Q

What lifestyle would you give a diabetic px to reduce risk of developing ESKD?

A

Stop smoking, do exercise, control BP, address hyperlipidaemia.

If microalbuminuria then start ACE inhibitors or ARBs regardless of BP elevation.

38
Q

What’s the relationship of SLE and renal disease?

A

Renal disease occurs in 1/3 of SLE patients,

25% of these reach end-stage CKD within 10 years.

SLE is an autoimmune disorder creating immune deposits in the glomeruli and mesangium.

Systemic lupus erythematosus (SLE) that affects the kidneys is called lupus nephritis.

39
Q

acute glomerulonephritis – acute nephritic syndrome.

A

Abrupt onset of glomerular haematuria (RBC casts or dysmorphic RBC),

non-nephrotic range proteinuria,

oedema,

hypertension and

transient renal impairment (temporarily oliguria and uraemia)

40
Q

PSGN stands for?

A

Post streptococcal GlomeruloNephritis

41
Q

Why is there a delay between Streptococcal infection (maybe throat) and onset of nephritic disorders?

And what’s the outcome? Lifestyle advice?

A

it takes time for immune complex formation & deposition,

and for glomerular injury to occur.

Usually spontaneously resolves.

Strongly limit Sodium and Potassium.

Restrict protein

Loop diuretics usually very useful.

42
Q

What does RPGN stand for?

A

Rapidly Progressive GlomeruloNephritis

43
Q

RPGN features

A

focal necrosis with or without crescents and rapidly progressive renal failure over weeks.

NB> crescents are aggregations of macrophages and epithelial cells in Bowman’s space.

44
Q

What are the main features of Pre-renal AKI?

A

A decrease in blood perfusion and thus << GFR.

Both Kidneys need to be affected (why? remember?)

common causes; hypovolemia, hypotension, <

45
Q

What drugs impair kidney autoregulation?

A

ACE inhibitors

NSAIDs

46
Q

What other things can cause >> creatinine?

A

>> muscle mass

>> red meat ingestion

muscle damage (rhabdomyolysis)

decreased tubular secretion (eg. cimetidine, trimethoprim tx)

47
Q

What must you check when giving hypovolaemic px fluids?

A

BP

signs of jugular venous pressure >>

signs of pulmonary oedema

48
Q

Why do you often see scratch marks with CKD?

A

Uremic pruritus

49
Q

What do red cell casts suggest?

A

glomerulonephritis

50
Q
A
51
Q

What is acute tubular necrosis (ATN)? - acute tubular injury (ATI)

A
52
Q

Lesser known functions of the kidneys

A
  • activation of Vit D
  • metabolism of insulin
    *
53
Q

What are the causes of CKD?

A

could be systemic; diabetes mellitus, hypertension, hyperlipidaemia

chronic damage following renal diseases

autoimmune, e.g. SLE, Goodpasture’s

genetic; polycystic kidney disease

54
Q

What is the goal of CKD care?

A
  • prevent cardiovascular problems
  • prevent ESKD
  • prevent complications of CKD
  • prevent dialysis
55
Q

When to refer to a specialist? Re GFR

A

if GFR <30ml/min/1.73 m2

Sustained decrease of GFR of 25% or more

56
Q

What does the Cockcroft-Gault formula measure, and when is it used?

A
  • Preferred method for estimating renal function or calculating drug dosages in patients with renal impairment e.g. elderly or extremes of muscle mass.
  • Estimate of CrCl

(NB> use ideal weights for obese px)

57
Q

Name some potentially damaging Kidney drug groups

A
  • ACEIs, ARBs,
  • PPIs
  • diuretics
  • antibiotics
  • NSAIDs
  • Lithium
58
Q

What’s the relationship between Metformin and CKD?

A

Metformin should be
avoided if eGFR
below
30ml/min/1.73m2

59
Q

Which drugs might need dose reduced with CKD?

A
  • beta blockers
  • digoxin
  • allopurinol
  • opioids
60
Q

What are the first line antihypertensives for CKD?

A

ACEI, ARBs, and direct renin inhibitors

61
Q

Managing BP with CKD

NICE BP targets

A

CKD + NO diabetes

120-139/ <90mmHg

CKD + diabetes and people with ACR >70mg/n/mmol

120-129<80mmHg

62
Q

If uncontrolled hypertension in CKD then add:

A

non-dihydropyridine CCB
e.g. diltiazem

  • If oedema consider loop diuretic
63
Q

What diuretics can you use in severe CKD?

A

Loops

(Thiazides only effective to GFR 20-25 ml/min)

+ remember can be used with Kidney stones

64
Q

Why do you get metabolic acidosis with CKD? And what’s the treatment?

A

Due to increasing inability of distal convoluted tubule to excrete hydrogen ions

Tx: Oral Sodium Bicarbonate

65
Q

What do you get atherosclerosis with CKD?

A

Associated with
abnormal lipid and
carbohydrate
metabolism, especially
in diabetics.

tx: Consider statins,
antiplatelets/
anticoagulants

66
Q

What is renal mineral bone disorder?

aka Renal Bone Disease

aka Renal Osteodystrophy

A

This involves softening of the bones due
to decalcification and deposition of
calcium at various sites around the body.

The mechanisms involved are complex.

67
Q

What level of Hb is anaemia?

A

Hb < 11 g/dL

68
Q

Symptoms of uraemia?

A

Dermatological – itching, skin pigmentation

Gastrointestinal – nausea, anorexia (ondansetron,
metoclopramide)

Neurological – peripheral neuropathy, restless
legs (clonazepam, pramipexole, gabapentin),

cramps (quinine).

(antihistamines, emollients, Eurax, ondansetron, etc)

69
Q

Which coexisting illnesses increase risk of CKD?

A

Diabetes,

Hypertension

CVD,

structural renal tract disease

multisystem diseases that affect the kidneys, eg. SLE

70
Q

Albuminuria; role in CKD diagnosis?

A

Persistent increased protein in the urine (two positive tests over 3 or more months) is the principal marker of kidney damage, acting as an early and sensitive marker in many types of kidney disease.

71
Q

What is ACR?

A

albumin concentration (mg) / creatinine concentration (g)

Albumin-to-creatinine ratio (ACR) first method of preference to detect elevated protein

72
Q

What ACR level would indicate CKD?

A

30-300 mg/g for >3 months

(relative to young adult level)

73
Q

Tips for diagnosing CKD

A
  • if GFR >60 ml/min/1.73m2, then not CKD unless evidence of kidney damage.
  • features must be present on at least two occasions and for more than three months.
74
Q

Investigations for CKD

A

U & E, glucose

24-hr creatinine clearance; determine level of renal failure

Casts; glomerulonephritis

Red Cells; can come from anywhere

Check < Calcium, phosphates

75
Q

CKD definition (albumin level, GFR)

A

albumin excretion of > 30mg/ day

or

GFR <60 ml/min/1.73 m2

for >3 mtns

** damage needs to be >3mtn to distinguish CKD from acute kidney disease.

76
Q

Definition of CKD

A

Abnormalities of kidney function or structure present for more than 3 months.

Includes all individuals with markers of kidney damage or those with an eGFR of less than 60 ml/min/1.73m2 on at least 2 occasions 90 days apart

(with or without markers of kidney damage).

77
Q

What’s another name for Post streptococcal GlomeruloNephritis?

A

acute proliferative glomerulonephritis

78
Q

Periorbital puffiness and difficulty in putting on rings is a sign of what?

A

nephrotic syndrome

79
Q

What drugs commonly damage the kidneys?

A

NSAIDs,

lithium,

some antibiotics,

bisphophonates

80
Q

Minimal Change Disease - what’s the story

A

podocytes damaged, most common cause of nephrotic syndrome with children.

Proteinura and oedema of MCD can develop very rapidly- almost overnight

81
Q

Glomerulonephritis (GN) accounts for up to 1/3 of patients requiring dialysis.

What are the cardinal symptoms?

A
  • proteinuria
  • haematuria
  • urinary casts
82
Q

Diabetes; what is the initial sign of renal involvement?

A

microalbuminuria

.. progressing to >> proteinuria or even nephrotic syndrome.

*** Note: diabetic nephropathy usually suffer from diabetic retinopathy or neuropathy. Look for this! ***

83
Q

Most important management of diabetes

A

very aggressively lower blood pressure (ACE inhibitors, ARBs)

Excellent glycaemic control

stop smoking

84
Q

APKD - Adult polycystic kidney disease

General info

(picture needed)

A

Most common inherited condition to affect the kidneys, usually presenting in adult life.

Renal cysts can bleed, create haematuria, loin pain and become infected. Cysts enlarge and renal function declines.

Dx: FH, clinical features, CT, ultrasonography.

Tx:control BP, antibiotics, painkillers, dialysis, transplant

Nephrology (3 decks)

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