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Y3M - Renal > CKD > Flashcards

CKD Flashcards

1
Q

Definition of CKD.

A

Abnormal kidney structure or function present for >3 months with implications for health.

Manifested by abnormal albumin excretion or decreased kidney function.

The patient does not have CKD if they have a score of A1 combined with G1 or G2. They need at least an eGFR of < 60 or proteinuria for a diagnosis of CKD.

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2
Q

What are the stages of CKD by GFR?

A

G1 - > 90

G2 - 89-60

G3a - 59-45

G3b - 44-30

G4 - 29-15

G5 - < 15

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3
Q

What is the other KDIGO staging of kidney disease?

A

Albumin excretion (mg/24h) and albumin to creatinine ratio (ACR)

A1 = < 30 and ratio < 3

A2 = 30-300 and ratio 3-30

A3 = >300 and ratio >30

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4
Q

When might reversal of CKD be likely?

A

Relief of UTO

Immunosuppressive therapy for GN or systemic vasculitis

Treatment of accelerated hypertension

Correction of critical narrowing arteries

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5
Q

Give congenital and inherited causes of CKD.

A

APCKD

Medullary cystic disease

Tuberous sclerosis

Oxalosis

Cystinosis

Congenital obstructive uropathy

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6
Q

Give glomerular disease causes of CKD.

A

Primary glumerulonephritides like focal glomerulosclerosis

2ndary:

SLE

Polyangiitis

Amyloidosis

Diabetic glomerulosclerosis

Accelerated hypertension

HUS

TTP

Systemic sclerosis

Sickle cell disease

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7
Q

Give vascular disease causes of CKD.

A

Hypertensive nephrosclerosis

Renovascular disease

Small and medium sized vessel vasculitis

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8
Q

Give examples of tubulointerstitial disease causing CKD.

A

Tubulointerstitial nephritis

Reflux nephropathy

TB

Schistosomiasis

Nephrocalcinosis

Multiple myeloma

Renal papillary necrosis

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9
Q

Give examples of UTOs causing CKD.

A

Calculus disease

Prostatic disease

Retroperitoneal fibrosis

Pelvic tumours

Schistosomiasis

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10
Q

Common causes of CKD.

A

Diabetes

Hypertension

GN

Renovascular disease

Polycystic kidney disease

Obstructive nephropathy

Chronic/recurrent pyelonephritis

Age-related decline

NSAIDs/PPis/lithium

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11
Q

Do patients with stage G2 CKD have disease?

A

Not if they don’t have other evidence of kidney damage.

Such as haematuria, proteinuria, structurally abnormal kidneys, inherited kidney disease or biopsy changes.

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12
Q

Most common cause of GN in sub-saharan Africa.

A

Malaria

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13
Q

A common cause of CKD in middle east and southern Iraq that is not common in western countries.

A

Schistosomiasis

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14
Q

Prognosis of CKD correlates with…

A

Hypertension particularly if poorly controlled.

Proteinuria

Degree of scarring on histology

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15
Q

Clinical approach of CKD.

A

History

Examination

Investigation

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16
Q

History of CKD.

A

Does the patient really have CKD? - eGFR is not always an accurate tool as it can vary due to several factors.

Possible causes such as UTI, LUTS, systemic disorders and renal colic.

Check drug history.

Check FH for renal disease and subarachnoid haemorrhage (APCKD)

Current state/symptoms

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17
Q

Possible signs and symptoms of CKD.

A

Fluid overload

Anorexia

N+V

Restless legs

Fatigue

Weakness

Pruritus

Bone pain

Amenorrhoea

Muscle cramps

Peripheral neuropathy

Pallor

HTN

Impotence.

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18
Q

Examination of CKD.

A

Periphery - Oedema, vascular disease, neuropathy, rash, gouty tophi, joint disease, arteriovenous fistula, immunosuppression, asterixis.

Face - anaemia, xanthelasma, yellow tinge, jaundice, gum hypertrophy, cushingoid, periorbital oedema, telangiectasia

Neck - JVP, tunnelled line

CVS - BP, cardiomegaly, endocarditis

Resp - Pulmonary oedema or effusion

Abdomen - catheter or scars from previous cathether, signs of previous transplant, palpable kidney/liver

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19
Q

Investigations of CKD.

A

U&Es, Hb, glucose, Ca2+, PO43-, PTH, ANA, ANCA, APA, complement, anti-GBM etc…

Urine - dipstick, MC&S, A:CR or P:CR

Imaging - USS, CT etc…

Histology - Consider renal biopsy

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20
Q

How is renal function monitored in CKD.

A

GFR and albuminuria should be monitored according to risk.

Annually if not…

High risk = 6 months

Very high risk = 3 - 4 months

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21
Q

Risk factors for CKD decline.

A

BP

DM

Metabolic distburances

Volume depletion

INfection

NSAIDs

Smoking

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22
Q

What is the multidisciplinary management team of CKD?

A

Renal physicians

GPs

Renal specialist nurses

Dieticians

Pharmacists

Vascular/Transplant surgeons

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23
Q

What are the main aims of CKD management.

A

Appropriate referral to nephrology

Treatment to slow renal disease progression

Treatment of renal complications of CKD

Treatment of other complications of CKD

Preparation for renal replacement therapy.

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24
Q

What are general treatment of underlying disease of CKD?

A

Diabetic monitoring

Treat hypertension

Treat infections

Tolvaptan for APCKD

Immunosuppression for GN

Quit smoking

Maintain a healthy weight and exercise

Offer atorvastatin 20mg for primary prevention against and any cardiovascular disease.

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25
Q

Reduction of cardiovascular disease in CKD.

A

Statin

Control BP

Improve diabetes control

Advise weight loss

Advise exercise

Stop smoking

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26
Q

Aims for treatment of hypertension to slow renal disease progression.

A

Target systolic BP is < 140 mmHg and diastolic < 90 mmHg.

If DM or A:CR is > 70 then systolic target is < 130 and diastolic < 80.

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27
Q

When should renin-angiotensin treatment be given?

A

DM and A:CR > 3mg/mmol

Hypertension and A:CR > 30 mg/mmol

Any CKD with A:CR > 70 mg/mmol

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28
Q

What BP medication can you give?

A

ACEi and ARBs, do not combine due to risk of hyperkalaemia or hypotension.

You need to check K+ and renal funciton prior to giving.

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29
Q

When should you stop ACEi/ARB treatment?

A

If K+ > 6mmol, eGFR drop > 25%, creatinine drop > 30%

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30
Q

Glycaemic control aims of CKD.

A

HbA1c of 53 mmol/mol (7.0%)

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31
Q

Give examples of complications of CKD.

A

Anaemia

CKD mineral and bone disorder (CKD-MBD)

Calciphylaxis

Cardiovascular disease

Pericarditis

Skin disease

Gastrointestinal

Metabolic abnormalities

Endocrine abnormalities

Nervous system abnormalities

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32
Q

What type of anaemia do you usually see in CKD?

A

Normochromic normocytic anaemia

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33
Q

Give reasons why anaemia might develop in CKD.

A

EPO deficiency

Increased blood loss from GI bleed, repeated blood sampling and blood loss during dialysis.

Bone marrow toxins are retained in CKD

Haematinic deficiency (decreased iron, vitamin B12 or folate)

Increased red cell destruction due to having a lower life span as uraemia and haemodialysis causes degrees of haemolysis.

ACEi can cause anaemia

Functional iron deficiency from inflammation and infection

Bone marrow suppression from uraemia

34
Q

Explain the treatment course of anaemia in CKD.

A

Check Hb when eGFR < 60.

Investigate and rule out/treat other deficiencies such as iron, B12 and folate. Iron treatment should be IV.

Rule out chronic blood loss.

Consider giving EPO if Hb < 110

35
Q

Give 3 side-effects that might occur due to EPO.

A

Hypertension

Functional iron deficiency

Anti-erythropoietin antibody-mediated pure red cell aplasia.

36
Q

Explain the hypertension in EPO treatment of CKD.

A

Happens in about 30%.

This means that the blood pressure should be monitored in the first 6 months continously to avoid significant side-effects of hypertension

37
Q

Treatment of functional iron deficiency in EPO treatment.

A

Give IV iron supplements

38
Q

Explain anti-erythropoietin antibody mediated pure red cell aplasia.

A

Stimulation of antibodies towards EPO in host leading to severe anaemia with a Hb typically of < 60 g/L

39
Q

Hb concentration goal in treatment of anaemia in CKD.

A

Aim for an Hb of 100-120

40
Q

General causes of CKD-MBD.

A

Changes in calcium, phosphorus, PTH, FGF23 and vit D metabolism.

Hyperparathyroid bone disease

Osteomalacaia

Osteoporosis

Osteosclerosis

Adynamic bone disease.

41
Q

Explain the pathogenesis of early CKD-MBD.

A

Phosphate excretion falls early in CKD.
The phosphate that is left -> FGF23 release.
FGF23 causes phosphaturia to lower phosphate levels again.

FGF23 also downregulates renal 1alpha-hydroxylase. This leads to reduced action of activated vitamin D.

Despite the FGF23, phosphate levels will rise in blood again.

42
Q

What happens in CKD-MBD as the CKD progresses?

A

Less 1alpha-hydroxylase production in kidneys leads to less conversion of 25-D3 into the active 1,25-dihydroxycholecalciferol.

This deficiency leads to reduced gut calcium absorption -> fall in calcium.

The reduced activation of vitamin D receptors in parathyroid, as well as the falling levels of calcium leads to an increase in PTH.

Secondary hyperparathyroidism ensues.

PTH promotes reabsorption of calcium from bone and from kidneys.

43
Q

What does the secondary hyperparathyroidism in CKD-MBD cause in terms of bone disease?

A

Increased osteoclastic activity

Cyst formation

Bone fibrosis (osteitis fibrosa cystica)

44
Q

What are the biochemical markers for secondary hyperparathyroidism in CKD-MBD?

A

Low Ca2+

High PTH

High phosphate

High ALP

45
Q

Radiological findings of secondary hyperparathyroidism in CKD-MBD.

A

Digital subperiosteal erosions

Pepperpot skull (not the same as raindrop skull!)

46
Q

Complication of longstanding secondary hyperparathyroidism in CKD-MBD.

A

Hyperplasia of the glands with autonomous or tertiary hyperparathyroidism.

This means that pTH now occurs independently of calcium or 1,25-D3 control.

The high bone turnover leads to hypercalcaemia

47
Q

Give bone diseases due to low turnover in CKD-MBD.

A

Adynamic bone disease

Osteomalacia

48
Q

Explain adynamic bone disease.

A

Both bone formation and resportion are depressed.

Skeleton becomes inert.

The bone turnover is redcued usually due to over-treatment with active vitamin D, low PTH, accumulation of aluminium used as a phosphate binder or diabetes.

This means that there might be hypercalcaemia as well due to calcium supplements.

49
Q

What causes osteomalacia in CKD-MBD?

A

Def. of 1,25-D3 and hypocalcaemia -> impaired mineralisation of osteoid.

50
Q

What causes osteosclerosis in CKD-MBD?

A

Longstanding hyperparathyroidism causes increased bone density particularly in the spine.

Bans of sclerotic and porotic bone gives rise to what is called a rugger jersey on X-ray.

51
Q

Radiological findings in CKD-MBD.

A

Pseudofractures called Looser’s zones

Subperiosteal erosions

Pepperpot skull

Rugger jersey spine

Adenomas (brown tumours)

52
Q

Treatment of CKD-MBD.

A

Treat if phopshate > 1.5 mmol/ or > 1.7 mmol/l on RRT with dietary restriction +/- phosphate binders.

Give vitamin D supplements such as colecalciferol if there is deficiency.

If PTH is still high treat with an activated vit D analogue.

Exclude iron def.

Dietary advice of restricting protein, K+ and phosphate.

53
Q

Aims of treatment of CKD-MBD.

A

Normal phosphate and calcium

Control PTH withing 2- to 3- fold the upper limit of normal to prevent adynamic bone disease to develop.

54
Q

Give examples of types of drugs used in CKD-MBD.

A

Gut phosphate binders (sevelamer attenuates vascular calcification and lowers cholesterol as well!)

Aluminium-containing gut phosphate binders (can lead to aluminium bone disease and cognitive impairment)

Tenapanor (indirectly inhibits paracellular absorption of phosphate)

Calcitriol

Calcimimetic agents

55
Q

Diagram of CKD-MBD.

A
56
Q

Screening of diabetic patients for nephropathy.

A

Raised urine Albumin:Creatinine ratio and P:CR

Evidence of long-standing/poorly controlled DM

Evidence of other microvascular disease

57
Q

Treatment of diabetic nephropathy

A

ACEi/ARBs to reduce proteinuria

Anti-hypertensives

CVS risk modification

Continue other screens

58
Q

What can chronic raised BP cause?

A

Nephrosclerosis

It is usually hard to tell if HTN caused CKD or CKD caused HTN

59
Q

Investigations to identify whether HTN is primary or secondary to CKD.

A

Clinical findings

24 hour urinary metanephrines (phaeo)

Aldosterone:Renin ratio

Cortisol and Dexa supp test

TSH

MRA (renal artery stenosis)

60
Q

Types of polycystic kidney disease.

A

Type 1 (85%; PKD1 mutation autosomal dominant)

Type 2 (15%; PKD2 mutation autosomal dominant)

61
Q

Symptoms of Polycystic kidney disease.

A

Size of kidneys

Infection

Flank pain

Haematuria

Fever

Asymptomatic

62
Q

Diagnosis of PCKD

A

Family history is key (renal disease and subarachnoid haemorrhages)

USS

63
Q

Treatment of PCKD.

A

Control BP

Tolvaptan

Genetic counselling and testing

64
Q

What is calciphylaxis?

A

Calcific uraemic arteriolopathy - rare but life-threatening.

65
Q

Clinical presentation of calciphylaxis.

A

Painful skin patches

Plaques

Ulcers

Non-healing eschars

Panniculitis

Dermal necrosis

66
Q

Histological features of calciphylaxis.

A

Vascular calcification

Superimposed small-vessel thrombosis

67
Q

Risk factors of calciphylaxis.

A

Hyperparathyroidism

Elevated serum phosphate

Morbid obesity

Warfarin use

Many die within a year of diagnosis

68
Q

Risk factors of cardiovascular disease in CKD.

A

HTN

DM

Dyslipidaemia

Smoking

Male gender

69
Q

What is the main cardiovascular complication of CKD?

A

Coronary artery and generalised vascular calcification.

70
Q

How dooes peripheral vessel calcification present?

A

Increased vascular stiffness with increased pulse pressure, increased pulse wave velocity, increased afterload -> LV hypertrophy.

71
Q

Risk factors of calcification

A

Raised calcium and phosphate product

Hyperparathyroidism

Uraemia

Inflammation

72
Q

Investiations of vascular calcification in CKD.

A

Abdo X-ray (pipe-stem calcifications)

Electron beam or multislice CT

Vascular Doppler

73
Q

Treatment of cardiovascular disease in CKD.

A

Antiplatelets (low dose aspirin)

Atorvastatin

74
Q

Types of pericarditis that can occur in CKD.

A

Uraemic pericarditis

Dialysis pericarditis

75
Q

What is pruritus caused by in CKD?

A

Accumulation of nitrogenous waste products of protein catabolism

Hypercalcaemia and high phosphate

Hyperparathyroidism

Iron deficiency

76
Q

What is nephrogenic systemic fibrosis?

A

Systemic fibrosing skin disorder.

Gadolinium-containing contrast account for over 95% of cases.

Diagnosis is based on biopsy of an involved site,

Prevention is key, gadolinium based contrast should be avoided.

77
Q

GI complications of CKD.

A

Reflux oesophagitis

Gastritis

Peptic ulcers

Constipation in CAPD

Acute pancreatitis

78
Q

Metabolic abnormalities in CKD.

A

Gout

Lipids -> hypercholesterolaemia

79
Q

Endocrine abnormalities in CKD.

A

Hyperprolactinaemia

Decreased serum testosterone

Menstrual irregularities

GH def.

Altered protein binding

80
Q

Nervous systems effects of CKD.

A

Uraemia affects CNS -> decreased seizure threshold, asterixis, treamor and myoclonus.

Anxiety, depression and impaired cognition can also occur.

81
Q

Reasons of referral to specialist in CKD

A

eGFR < 30

ACR ≥ 70 mg/mmol

Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year

Uncontrolled hypertension despite ≥ 4 antihypertensives

Y3M - Renal (11 decks)

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