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Nephrology Flashcards

1
Q

Visible haematuria following recent URTI?

A

IgA Nephropathy

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2
Q

Commonest causes of glomerulonephritis worldwide?

A

IgA Nephropathy (Berger’s disease)

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3
Q

IgA nephropathy associations?

A
  1. Alcoholic cirrhosis
  2. Coeliac disease/dermatitis herpetiformis
  3. Henoch-Schonlein puurpura
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4
Q

IgA nephropathy pathophysiology?

A
  1. Mesangial deposition of IgA immune complexes
  2. Considerable pathological overlap with Henoch-Schonlein purpura (HSP)
  3. Histology = mesangial hypercellularity, positive immunofluorescence for IgA & C3
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5
Q

IgA nephropathy presentation?

A
  1. Young male, recurrent episodes of macroscopic haematuria
  2. Typically associated with a recent respiratory tract infection
  3. Nephrotic range proteinuria is rare
  4. Renal failure unusual
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6
Q

Differentiating between IgA nepropathy and Post-streptococcal glomerulonephropathy?

A

PSG = low complement levels, proteinuria, interval between URTI and symptom onset

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7
Q

PSG vs. IgAN time after URTI?

A
  1. IgAN = 1-2 days
  2. PSG = 1-2 weeks
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8
Q

IgA nephropathy?

A
  1. No treatment, just renal function f/up = Isolated haematuria, no/minimal proteinuria, and normal GFR
  2. ACEi = persistent proteinuria >500, normal/slightly reduced GFR
  3. Steroids = active disease (falling GFR) or failure to respond to ACEi
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9
Q

IgA nephropathy prognosis?

A
  1. 25% ESRF
  2. Marker of good prognosis = frank haematuria
  3. Markers of poor prognosis = male, proteinuria >2, HTN, smoking, hyperlipidaemia, ACE genotype DD
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10
Q

CKD diet?

A

Low sodium, phosphate, potassium, protein (to reduce renal strain as is excreted by kidneys)

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11
Q

Prevention of contrast-induced nephropathy?

A

Volume expansion with 0.9% NaCl

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12
Q

Contrast media nephrotoxicity definition?

A

25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media

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13
Q

When dose contrast-induced nephropathy occur?

A

2-5 days after administration

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14
Q

Contrast nephrotoxocity RFs?

A
  1. Known renal impairment
  2. Age > 70 years
  3. Dehydration
  4. Cardiac failure
  5. Nephrotoxics e.g. NSAIDs
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15
Q

High risk for contrast-induced nephropathy and metformin?

A

Hold metformin for 48 hours until renal function shown to be normal

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16
Q

Minimal change disease presentation?

A

Nearly always as nephrotic syndrome, accounting for 75% of cases in children and 25% in adults

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17
Q

Minimal change disease cause?

A

Majority are idiopathic, in 10-20% a cause is found:
1. Drugs: NSAIDs, rifampicin
2. Hodgkin’s lymphoma, thymoma
3. Infectious mononucelosis

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18
Q

Minimal change disease pathophysiology?

A
  1. T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
  2. Resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin
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19
Q

Minimal change disease features?

A
  1. Nephrotic syndrome
  2. Normotension (HTN is rare)
  3. High selective proteinuria = Only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus
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20
Q

Minimal change disease biopsy?

A
  1. Normal glomeruli on light microscopy
  2. EM shows fusion of podocytes and effacement of foot processes
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21
Q

Minimal change disease Rx?

A
  1. Oral corticosteroids = 80% responsive
  2. Cyclophosphamide = if steroid resitant
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22
Q

Minimal change disease prognosis?

A
  1. 1/3 have one episode
  2. 1/3 have infrequent relapses
  3. 1/3 have frequent relapses which stop before adulthood
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23
Q

Most common inherited cause of kidney disease?

A

ADPKD

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24
Q

ADPKD Type 1?

A
  1. 85% cases
  2. Chromosome 16
  3. Presents with renal failure earlier
  4. Polycystin-1
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25
Q

ADPDK Type 2?

A
  1. 15% cases
  2. Chromosome 4
  3. Polycystin-2
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26
Q

Screening for ADPKD?

A

Abdominal US

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27
Q

US diagnostic criteria for ADPKD in pts with positive family history?

A
  1. 2 cysts, uni or bilateral, if < 30 y/o
  2. 2 cysts in both kidneys if 30-59 y/o
  3. 4 cysts in both kidneys if > 60 y/o
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28
Q

ADPKD Rx?

A

Tolvaptan (VP receptor 2 antagonist) if:
1. CKD 2/3 at start of treatment
2. Evidence of rapidly progressing disease
3. Company provides it with the discount agreed in the patient access scheme

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29
Q

Non-visible haematuria found in what % of population?

A

2.5%

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30
Q

Causes of transient non-visible haematuria?

A
  1. UTI
  2. Menstruation
  3. Vigorous exercise
  4. Sexual intercourse
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31
Q

Causes of persistent non-visible haematuria?

A
  1. Cancer (bladder, renal, prostate)
  2. Stones
  3. BPH
  4. Prostatitis
  5. Urethritis e.g. Chlamydia
  6. Renal causes = IgA nephropathy, thin basement membrane disease
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32
Q

Spurious causes of red/orange urine?

A
  1. Foods = beetroot, rhubarb
  2. Drugs = rifampicin, doxorubicin
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33
Q

Haematuria Ix?

A
  1. Urine dipstick
  2. Persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart
  3. Renal function, ACR, PCR and BP should be checked
  4. Urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected
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34
Q

Haematuria 2ww criteria?

A
  1. > =45 y/o AND = Unexplained visible haematuria without UTI OR visible haematuria that persists or recurs after successful treatment of urinary tract infection
  2. Aged >/60 y/o AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
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35
Q

Haematuria non-urgent referal criteria?

A

Aged >= 60 years with recurrent or persistent unexplained urinary tract infection

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36
Q

Hyperkalaemia classification?

A
  1. Mild = 5.5 - 5.9
  2. Moderate 6.0 - 6.4
  3. Severe = >=6.5
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37
Q

Hyperkalaemia ECG changes?

A
  1. Tented T waves (first)
  2. Loss of P waves
  3. Broad QRS complexes
  4. Sinusoidal wave pattern
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38
Q

Principles of hyperkalaemia treatment?

A
  1. Stabilisation of cardiac membrane = IV calcium gluconate
  2. Short term shift in potassium from ECF to ICF = combined insulin/dextrose and nebulised salbutamol
  3. Removal of potassium from body = calcium resonium (enema more effective than oral), loop diuretics, hyperkalaemia
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39
Q

Indication that kidney disease is chronic and not acute?

A
  1. US (CKD have bilateral small kidneys, except for ADPKD, DN early stages, amyloidosis and HIV-associated nephropathy)
  2. Hypocalcaemia (due to lack of Vitamin D)
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40
Q

MDRD equation for measuring GFR?

A

CAGE
1. Serum creatinine
2. Age
3. Gender
4. Ethnicity

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41
Q

Features which may affect GFR?

A
  1. Pregnancy
  2. Muscle mass (e.g. amputees, body-builders)
  3. Eating red meat 12 hours prior to sample being taken
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42
Q

CKD1?

A

GFR > 90 with some sign of kidney damage on other tests, (if all the kidney tests are normal, there is no CKD)

43
Q

CKD 2?

A

GFR 60-90 (if all the kidney tests are normal, there is no CKD)

44
Q

CKD 3a?

45
Q

CKD 3B?

46
Q

CKD4?

47
Q

CKD5?

48
Q

CKD on haemodialysis most likely cause of death?

49
Q

CKD causes?

A
  1. DN
  2. GN
  3. PN
  4. HTN
  5. ADPKD
50
Q

What is HLA?

A

Name given to MHC in humans

51
Q

HLA chromosome?

A

CHromosome 6

52
Q

HLA system mushkies?

A
  1. Class 1 = A, B, C. Class 2 = DP, DQ, DR
  2. When HLA matching for renal transplant, importance DR > B > A
53
Q

Renal graft survival?

A
  1. Cadaveric transplant = 1 year 90%, 10 year 60%
  2. Living-donor transplant = 1 year 95%, 10 year 70%
54
Q

Renal transplant post-op problems?

A
  1. ATN of graft
  2. Vascular thrombosis
  3. Urine leakage
  4. UTI
55
Q

Renal transplant rejection/failure types?

A
  1. Hyperacute rejection (mins to hrs)
  2. Acute graft failure (<6m)
  3. Chronic graft failure (>6m)
56
Q

Hyperacute renal graft rejection mushkies?

A
  1. Pre-existing antibodies against ABO or HLA antigens
  2. Type II hypersensitivity reaction
  3. Leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
  4. No treatment is possible and the graft must be removed
57
Q

Acute graft failure (<6m) mushkies?

A
  1. Usually due to mismatched HLA, cell mediated (cytotoxic T cells)
  2. Usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
  3. Can be caused by CMV
  4. May be reversible with steroids and immunosuppressants
58
Q

Chronic graft failure (>6m) mushkies?

A
  1. Both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
  2. Recurrence of original renal disease (MCGN > IgA > FSGS)
59
Q

Hypokalaemia ECG?

A
  1. U waves
  2. Small or absent T waves
  3. Prolonged PR interval
  4. ST depression
60
Q

Hypokalaemia predisposes to what drug toxicity?

61
Q

Severe hypokalaemia?

62
Q

Treatment of severe hypokalaemia?

A

KCl replacement should not exceed 20mmol/hr

63
Q

Diagnostic criteria for AKI?

A
  1. Rise in creatinine of 26µmol/L or more in 48 hours OR
  2. > = 50% rise in creatinine over 7 days OR
  3. Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR
  4. > = 25% fall in eGFR in children / young adults in 7 days
64
Q

AKI stages?

A

Stages 1, 2, 3

65
Q

AKI Stage 1?

A
  1. Increase in creatinine to 1.5-1.9 times baseline, or
  2. Increase in creatinine by ≥26.5 µmol/L, or
  3. Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
66
Q

AKI Stage 2?

A
  1. Increase in creatinine to 2.0 to 2.9 times baseline, or
  2. Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
67
Q

AKI Stage 3?

A
  1. Increase in creatinine to ≥ 3.0 times baseline, or
  2. Increase in creatinine to ≥353.6 µmol/L or
  3. Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
  4. The initiation of kidney replacement therapy, or,
  5. In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
68
Q

Renal transplant immunosuppresion regime?

A
  1. Initial = ciclosporin/tacrolimus with a mAb
  2. Maintenance = ciclosporin/tacrolimus with MMF/sirolimus
  3. Add steroids if more than one steroid responsive acute rejection episode
69
Q

Ciclosporin MOA?

A

Calcineurin inhibitor, a phosphatase involved in T cell activation

70
Q

Tacrolimus mushkies?

A
  1. Lower incidence of acute rejection compared to ciclosporin
  2. Also less HTN and hyperlipidaemia
  3. However, high incidence of impaired glucose tolerance and DM
71
Q

MMF MOA and S/E?

A
  1. Blocks purine synthesis by inhibition of IMPDH
  2. Therefore inhibits proliferation of B and T cells
  3. S/e = GI and marrow suppression
72
Q

Sirolimus MOA and S/E?

A
  1. Blocks T cell prolifeation by blocking the IL-2 receptor
  2. Can cause hyperlipidaemia
73
Q

Renal transplant immunosuppression monitoring?

A
  1. CVS = monitor HTN, hyperglycaemia and hyperlipidaemia due to tacrolimus and ciclosporin
  2. Renal failure = due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney
  3. Malignancy = patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinomas
74
Q

What malignancy associated with renal transplant immunosuppression?

A

SCC of skin

75
Q

HUS triad?

A

Generally seen in younger children:
1. AKI
2. MAHA
3. Thrombocytopenia

76
Q

Causes of Secondary/Typical HUS?

A
  1. Classically toxin-producing Escherichia coli (STEC) 0157:H7 (‘verotoxigenic’, ‘enterohaemorrhagic’, most common cause in children, accounting for over 90% of cases
  2. Pneumococcal infection
  3. HIV
  4. Rare = SLE, Drugs, cancer
77
Q

Primary/atypical HUS causes?

A

Complement dysregulation

78
Q

HUS Ix?

A
  1. FBC = Hb < 8, negative Coombs test, thrombocytopenia
  2. Blood film = schistocytes and helmet cells
  3. U&E = AKI
  4. Stool culture = PCR for Shiga toxin
79
Q

HUS Rx?

A
  1. Supportive = IVF, blood transfusion, dialysis if required
  2. No role for ABx
  3. Indication for PLEX = severe cases of HUS not associated with diarrhoea
  4. Eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
80
Q

HTN in CKD Rx?

A

ACEi first line (decrease in eGFR up to 25% or rise in creatinine up to 30% acceptable)

81
Q

HSP definition?

A

IgA mediated small vessel vasculitis

82
Q

HSP features?

A
  1. Palpable purpuric rash with localised oedema over buttocks and extensor surfaces of arms and legs
  2. Abdominal pain
  3. Polyarthritis
  4. Features of IgA nephropathy may occur e.g. haematuria, renal failure
83
Q

HSP Rx?

A
  1. Analgesia for arthralgia
  2. Treatment of nephropathy generally supportive, inconsistent evidence for the use of steroids and immunosuppressants
84
Q

HSP Prognosis?

A
  1. Usually excellent, HSP is a self-limiting condition, especially in children without renal involvement
  2. BP and urinalysis should be monitore to detect progressive renal involvement
  3. Around 1/3rd of pts have a relapse
85
Q

Most common renal cause of AKI?

86
Q

ATN AKI features?

A

Urine osmolality low, urine sodium high

87
Q

Brown casts in urine?

88
Q

Prerenal hypernatraemia cause?

A

Kidneys hold on to sodium to preserve volume

89
Q

Rhabdomyolysis features?

A
  1. AKI with disproportionately raised creatinine
  2. Elevated CK, K
  3. Metabolic acidosis
  4. Myoglobinuria
  5. Hypocalcaemia (myoglobin binds calcium)
  6. Elevated phosphate (released from myocytes)
90
Q

Genetic cause of rhabdomyolysis?

A

McArdle’s syndrome

91
Q

Rhabdomyolysis Rx?

A
  1. IV fluids to maintain good UO
  2. Urinary alkalinisation sometimes used
92
Q

Spironolactone INdications?

A
  1. Ascites (pts with cirrhosis develop a secondary hyperaldosteronism)
  2. HTN
  3. HF
  4. Nephrotic syndrome
  5. Conn’s syndrome
93
Q

Spironolactone s/e?

A
  1. Hyperkalaemis
  2. Gynaecomastia: less common with eplerenone
94
Q

RALES trial?

A

NYHA III + IV, patients already taking ACEi, low dose spironolactone reduces all cause mortality

95
Q

Metabolic acidosis classification?

96
Q

Anion gap calculation?

A
  1. (Na + K) - (Cl + HCO3)
  2. Normally 8-14
  3. If question supplies a chloride level, often a clue to calculate
97
Q

Normal anion gap metabolic acidosis causes?

A
  1. GI bicarb loss = diarrhoea, fistula
  2. RTA
  3. Drugs e.g. acetozolamide
  4. Addison’s
98
Q

Raised anion gap metabolic acidosis causes?

A
  1. Lactate = shock, sepsis, hypoxia
  2. Ketones = DKA, alcohol
  3. Urate = renal failure
  4. Acid poisoning = salicylates, methanol
99
Q

Lactic acidosis types?

A
  1. Type A = sepsis, shock, hypoxia, burns
  2. Type B = metformin
100
Q

Renal cell carcinoma triad?

A
  1. Haematuria
  2. Loin pain
  3. Abdominal mass
101
Q

Left varicocoele what malignancy?

A

Renal cell carcinoma due to occlusion of left testicular vein

102
Q

RCC endocrine effects?

A
  1. EPO –> polycythaemia
  2. PTH –> hypercalcaemia
  3. Renin
  4. ACTH
103
Q

What % of RCC have metastases at presentation?

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