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Phase 2a > Renal Diseases > Flashcards

Renal Diseases Flashcards

1
Q

What is acute kidney injury?

A

Rapid deterioration of renal function

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2
Q

What are the clinical features of acute kidney injury?

A 
Nausea or vomitting
Diarrhoea
Dehydration
Oliguria (Less urine output)
Confusion
Drowsiness
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3
Q

What are the types of acute kidney injury?

A

Pre-renal= Impaired perfusion of the kidneys
Renal= Damage to the kidney apparatus
Post renal= Urinary outflow obstructed

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4
Q

Which type of AKI is the most common?

A

Pre-renal

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5
Q

What causes pre-renal AKI?

A

Volume depletion by vomitting or diarrhoea, hypotension, cardiac failure, sepsis, some medications

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6
Q

What causes renal AKI?

A

Glomerular disease like glomerulonephritis, tubular injury, nephritis

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7
Q

What causes post-renal AKI?

A

A blockage from something such as an enlarged prostate or kidney stones

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8
Q

What is the epidemiology of AKI?

A

15% of adults admitted to hospital develop AKI, more common in the elderly

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9
Q

What are the risk factors for AKI?

A

Over 65
Being dehydrated
Severe infection or sepsis
Blockage in the urinary tract
Pre-existing kidney problems
Long-term disease such as heart failure, diabetes, liver disease
Certain medications such as NSAIDs, blood pressure medications, aminoglycosides

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10
Q

How is AKI diagnosed?

A

Usually diagnosed with GFR test for creatinine levels. Serial creatinine readings= Acute rise

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11
Q

How is AKI treated?

A

Treat underlying cause

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12
Q

What are some possible complications of AKI?

A

Volume overload

Metabolic acidosis

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13
Q

What is chronic kidney disease?

A

An overall term for loss of kidney functions

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14
Q

What is stage G1 CKD?

A

A normal GFR but other tests have detected kidney damage

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15
Q

What is stage G2 of CKD?

A

GFR of 60-89 ml/min, with other signs of kidney damage

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16
Q

What is stage G3a of CKD?

A

GFR of 45-59 ml/min

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17
Q

What is stage G3b of CKD?

A

GFR of 30-44 ml/min

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18
Q

What is stage G4 of CKD?

A

GFR of 15-29 ml/min

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19
Q

What is stage G5 of CKD?

A

GFR below 15ml/min, almost complete loss of function

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20
Q

What is stage A1 of CKD?

A

ACR of <3mg/mmol

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21
Q

What is stage A2 of CKD?

A

ACR of 3-30 mg/mmol

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22
Q

What is stage A3 of CKD?

A

ACR of >30 mg/mmol

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23
Q

Why is there anaemia in CKD?

A

Reduce erythropoietin and increased blood loss

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24
Q

Why is there bone disease in CKD?

A

Renal phosphate retention and impaired 1,25-Vit D production, leads to a fall in serum calcium, so release of PTH, so skeletal decalcification

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25
Q

What are the clinical features of CKD?

A
  • Oedema of ankles, feet and hand
  • Shortness of breath
  • Nausea, vomitting, diarrhoea
  • Anaemia- pallor lethargy
  • Confusion, Coma
  • Hypertension
  • Nocturia, polyuria, haematuria
  • Osteomalacia, bone pain, hyperparathyroidis
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26
Q

What is the aetiology of CKD?

A

Polycystic kidney disease, tuberous sclerosis, glomerular disease, urinary tract obstruction, diabetes, kidney infections, NSAIDs

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27
Q

What is the epidemiology of CKD?

A

Common. Increases with age

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28
Q

What are the main treatments for CKD?

A
  • Lifestyle changes
  • Antihypertensives
  • Dialysis
  • Kidney transplant
  • Vit D supplements and bisphosphonates
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29
Q

How is CKD diagnosed?

A
  • Abnormalities on scans and histology
  • History
  • Blood tests: Serum calcium, phosphate and uric acid, anaemia
  • GFR: Assess renal function
  • ACR
  • Dipstick: Haematuria, albuminuria
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30
Q

What are some possible complications of CKD?

A

Hypertension, renal osteodystrophy, uraemic encaphalopathy, dialysis amyloid deposition

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31
Q

What is the epidemiology of ADPKD?

A

Commonest inherited kidney disease
Autosomal dominant with high penetrance
Usually presents in adulthood
More common in males

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32
Q

What causes ADPKD?

A

Mutations in PKD1 (85%) on chromosome 16

Mutations in PKD2 (15%) on chromosome 4

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33
Q

What are the risk factors for ADPKD?

A

Family history, ESRF, or hypertension

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34
Q

Briefly explain the pathophysiology of ADPKD

A

PKD1 encodes polycystin 1 which regulates tubular and vascular renal development. PKD2 encodes polycystin 2 which functions as a calcium channel. The polycystin complex occurs in cilia that are responsible for sensing tubular flow. Disruption of the polycystin pathway results in reduced cytoplasmic calcium, which in principle cells causes defective ciliary signalling, and disorientated cell division, leading to cyst formation. This then leaves to apoptosis of healthy tissue and fibrosis.

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35
Q

What is the clinical presentation of ADPKD?

A

Can be clinically silent for many years.
Loin pain, haematuria, excessive water and salt loss, nocturia, renal enlargement, hypertension, kidney stones
Polycystic liver disease, Pancreatitis, haemorrhage

36
Q

How is ADPKD diagnosed?

A

Personal history
Family history
Raised blood pressure
Ultrasound= More than 4 cysts per kidney if over 60, more than 2 cysts per kidney if over 40, more than 3 cysts overall if over 15
Genetic testing for PKD1 however this is difficult to do

37
Q

How is ADPKD treated?

A

No treatment to slow cysts
BP control with ACE inhibitor
Treat stones and give analgesia
Laparoscopic removal of cysts or full nephrectomy
Monitoring of condition with serum creatinine
Screening of family
Counselling

38
Q

What is the epidemiology of ARPKD?

A

Rarer that ADPKD
Autosomal recessive inheritance
Disease in infancy

39
Q

What is the aetiology of ARPKD?

A

PKHD1 mutation on long arm (q) of chromosome 6

40
Q

What are the risk factors for ARPKD?

A

Family history

41
Q

What is the differential diagnosis of ARPKD?

A

ADPKD, Multicystic dysplasia, renal vein thrombosis, hydronephrosis

42
Q

What is the clinical presentation of ARPKD?

A

Variable
Many present in infancy with renal cysts and congenital hepatic fibrosis
Enlarged polycystic kidneys
30% Develop kidney failure

43
Q

How is ARPKD treated?

A
  • Laproscopic removal of cysts/ full nephrectomy
  • BP control w ACE inhibitor
  • Treat stones and analgesia
  • Renal replacement therapy for ESRF
  • Counselling and support
44
Q

How is ARPKD diagnosed?

A
  • Diagnosed antenatally or neonatally
  • Ultrasound- to view cysts
  • CT and MRI to monitor liver disease
  • Genetic testing
45
Q

What is the epidemiology of minimal change disease?

A
  • Commonest cause of nephrotic syndrome in children
  • Most common in boys under 5
  • Accounts for 20% of adult nephrotic syndrome
46
Q

What are the clinical features of minimal change disease?

A
  • Proteinuria
  • Oedema (Often in face)
  • Fatigue
  • Frothy urine
47
Q

What are the risk factors/aetiology of minimal change disease?

A
  • Can be idiopathic
  • Atopy is present in 30% of cases and allergic reactions can trigger nephrotic’s syndrome
  • Drugs: NSAIDs, lithium, antibiotics, bisphosphonates, sulfasalazine
  • Hep C, HIV, and TB
  • Associated with Hodgkins lymphoma
48
Q

Briefly explain the pathophysiology of minimal change disease?

A

Glomeruli appear normal on light microscopy but on electron microscopy, fusion of foot processes of podocytes seen, which is consistent with a disrupted podocyte actin cytoskeleton. Immature differentiated CD35 stem cells appear to be responsible

49
Q

How is minimal change disease diagnosed?

A

Biopsy: Normal under light microscopy, electron microscopy shows fused podocyte foot processes

50
Q

How is minimal change disease treated?

A
  • High dose corticosteroids e.g. prednisolone

- Frequent relapse is treated with cyclophosphamide or cyclosporin/tacrolimus

51
Q

What is nephrotic syndrome?

A

Triad of

  • Proteinuria >3.5g/day
  • Hypoalbuminaemia
  • Oedema
52
Q

What is the epidemiology of nephrotic syndrome?

A
  • Relatively rare
  • Diabetes is most common secondary cause
  • Minimal change disease is the most common cause in children and can also cause it in adults
53
Q

What is the aetiology of nephrotic syndrome?

A

Primary causes= Minimal change disease, focal segmental glomerulosclerosis, membranous neuropathy
Secondary causes= Diabetes mellitus, amyloid, infections, SLE, RA, Malignancy, Drugs (NSAIDs, gold)

54
Q

Briefly explain the pathophysiology of nephrotic syndrome

A

Injury to the podocytes= Proteinuria. Severe hyperlipidaemia is often present: liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots

55
Q

What are the risk factors of nephrotic syndrome?

A

Diabetes mellitus, minimal change disease in children

56
Q

What are the differentials for nephrotic syndrome?

A

Congestive heart failure, cirrhosis

57
Q

What is the clinical presentation of nephrotic syndrome?

A
  • Normal-mild increase in BP
  • Proteinuria >3.5g/day
  • Normal-mild decrease in GFR
  • Hypoalbuminaemia
  • Frothy urine
  • Pitting oedema of ankles, genitals, abdomen and face
58
Q

How is nephrotic syndrome diagnosed?

A
  • Establish cause= Renal biopsy
  • Urine dipstick= High protein
  • CXR/Renal ultrasound= Pleural effusion
  • Serum albumin= Low
  • BP is normal or mildly increased
  • Renal function= Normal or mildly impaired
  • Serum creatinine, eGFR, lipids and glucose
  • Differential diagnosis testing
59
Q

How is nephrotic syndrome treated?

A
  • Reduced oedema: loop diuretics, thiazide diuretics. Fluid and salt retention
  • Reduce proteinuria: ACE inhibitors, ARBS
  • Reduce risk of complications: prophylactics’ anticoagulation with warfarin, reduce cholesterol with statins, treat infections
  • Treat underlying cause
60
Q

What are the complications of nephrotic syndrome?

A
  • Susceptible to infections
  • Thromboembolism
  • Hyperlipidaemia
61
Q

What is pyelonephritis?

A
  • Infection of the renal parenchyma and soft tissues of renal pelvis and upper ureter
  • Majority caused by UPEC= Uropathogenic E coli
62
Q

What are the main organisms that cause pyelonephritis?

A 
Klebsiella spp.
Ecoli (majority)
Enterococcus spp.
Proteus spp.
Staph spp.
63
Q

What are the risk factors for pyelonephritis?

A
  • Structural renal abnormalities
  • Calculi (Stones)
  • Catheterisation
  • Pregnancy
  • Diabetes
  • Immunocompromised
64
Q

How is pyelonephritis diagnosed?

A
  • Tender loin on examination
  • Urine dipstick= Nitrates, leucocyte elactase, protein, and foul smelling urine
  • Midstream urine microscopy, culture and sensitivity= Gold standard
  • Bloods= FBC for increased WCC, or Increased CRP/ESR
  • Urgent ultrasound= detects calculi, obstruction, abnormal anatomy
65
Q

What is the epidemiology of pyelonephritis?

A
  • Predominantly affects females under 35
  • Associated with sepsis and systemic upset
  • Mainly caused by UPEC
66
Q

What are the differentials of pyelonephritis?

A

Diverticulitis, abdominal aortic aneurysm, kidney stones, cystitis, prostatitis

67
Q

What are the clinical features of pyelonephritis?

A
  • Triad of loin pain, fever and pyuria
  • May have severe headache
  • Rigors
  • Significant bacteruria
  • Malaise, nausea, vomitting
  • Oliguria if cause is AKI
68
Q

How is pyelonephritis treated?

A
  • Rest
  • Cranberry juice and lots of fluids
  • Analgesia
  • Antibiotics= Oral ciprofloxacillin or oral co-amoxiclav. If severe, IV gentamicin or IV co-amoxiclav
  • Surgery to drain abcesses or relieve calculi that are causing infection
69
Q

What are the characteristic features of acute nephritis syndrome?

A

Haematuria, proteinuria, hypertension and oedema

70
Q

What are the possible causes of acute nephritis syndrome?

A
  • Post strep infection
  • SLE
  • Systemic sclerosis
  • ANCA associated vasculitis
  • Goodpasture syndrome
  • IgA nephropathy (Commonest)
71
Q

How is acute nephritis syndrome diagnosed?

A
  • Take history to determine cause
  • Measure eGFR, Proteinuria, serum U&E, Albumin
  • Culture= throat/skin swab
  • Urine dipstick= Proteinuria, and haematuria
  • Renal biopsy if needed
72
Q

What is the epidemiology of renal cell carcinoma?

A
  • Most common renal tumour in adults
  • Accounts for 2-3% of all malignancies
  • More common in males
  • Usually presents after 50 yrs
  • Highest incidence is in Czechia
73
Q

What are the risk factors for renal cell carcinoma?

A
  • Smoking
  • Obesity
  • Hypertension
  • Polycystic kidney disease
  • Renal failure and haemodialysis
  • Von hippel lindau syndrome
74
Q

What are the clinical features of renal cell carcinoma?

A
  • Often asymptomatic
  • Haematuria, loin/flank pain, abdominal mass
  • Anorexia, malaise and weight loss
  • Rarely, invasion of left renal vein causes compression of left testicular vein causing varicocele
  • Polycythaemia in 5%
  • Hypertension in 30%
  • Anaemia due to low EPO
  • Fever in 20%
75
Q

How is renal cell carcinoma diagnosed?

A
  • Ultrasound to distinguish cyst from tumour
  • CT of chest and abdomen with contrast to show renal mass, renal vein involvement and kidney function
  • MRI for staging
  • Blood pressure
  • Bloods= FBC for polycythamia and anaemia, increased ESR, Abnormal liver biochemistry
  • Renal biopsy and bone scan if needed
76
Q

How is renal cell carcinoma treated?

A
  • Localised disease is treated with surgery
  • Ablative techniques such as cryoablation and radiotherapy
  • Interleukin-2 and interferon alpha
77
Q

What is renal cell carcinoma?

A
  • Malignant cancer of the proximal convoluted tubules epithelium
  • Spread may be direct (Via renal vein), via lymph or haematogenous
78
Q

What is Wilm’s tumour?

A
  • Childhood tumour of the primitive renal tubules and mesenchymal cells
79
Q

What are the clinical features of Wilm’s tumour?

A
  • Abdominal mass

- Haematuria

80
Q

How is Wilm’s tumour diagnosed?

A
  • Ultrasound, CT and MRI
81
Q

How is Wilm’s tumour treated?

A
  • Nephrectomy
  • Radiotherapy
  • Chemotherapy
82
Q

Where are the classical places that renal stones form?

A
  • Pelviureteric junction
  • Pelvic brim
  • Vesicoureteric junction
83
Q

What are the risk factors for renal stones?

A
  • Anatomical abnormalities
  • Chemical composition of urine
  • Dehydration
  • Infection
  • Hypercalcaemia, hyperoxaluria, hyperuricaemia
  • Primary renal disease
  • Diet
  • Family history
84
Q

What are the clinical features of renal stones?

A
  • Many asymptomatic
  • Haematuria
  • Renal colic; sudden severe pain in the loin which travels to the groin. More painful is the stone is moving. Nausea and vomitting
  • Dysuria, strangury, frequency
  • Recurrent UTIs
85
Q

What are the causes of renal stones?

A
  • Calcium; excessive dietary calcium. Excessive bone resorption
  • Uric acid; Hyperuricaemia (gout)
  • Cystine stones; Cystinuria (family history)
86
Q

How are renal stones diagnosed?

A
  • First line; Kidney ureter bladder X ray
  • Gold standard; Non contrast CT of kidney, ureter and bladder
  • Chemical analysis of stones
  • Bloods
  • Dipstick for haematuria
87
Q

How are renal stones treated?

A
  • Diclofenac for pain
  • If less than 5mm, spontaneous passage
  • Oral nifedipine or alpha blocker (Tamsulosin) to promote expulsion
  • Extracorporeal shockwave lithotripsy for larger stones

Phase 2a (31 decks)

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