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MRCP > Renal > Flashcards

Renal Flashcards

1
Q

Genetics of Alport’s syndrome?

A

X linked dominant

  • defect in gene which codes for type IV collagen -> abnormal glomerular BM
  • more severe disease in males
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2
Q

Cause (most common) of Alport’s patient with failing renal transplant?

A

Presence of anti-GBM antibodies leading to Goodpasture’s syndrome-like picture

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3
Q

Features of Alport’s syndrome?

A
  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • lenticonus: protrusion of the lens surface into the anterior chamber
  • retinitis pigmentosa
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4
Q

Renal biopsy features of Alport’s syndrome?

A

splitting of lamina densa seen on electron microscopy

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5
Q

Diagnosis of Alport’s syndrome?

A
  • molecular genetic testing.
  • renal biopsy: electron microscopy showing characteristic finding of longitudinal splitting of lamina dense of the glomerular BM, resulting in a “basket-weave” appearance
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6
Q

Management of cranial DI?

A

tx underlying cause. desmopressin

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7
Q

Management of nephrogenic DI?

A

thiazides , low salt/protein diet

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8
Q

what systemic conditions cause cranial DI?

A
  • histiocytosis X
  • DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
  • haemochromatosis
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9
Q

what antibodies are assoc with primary membranous nephropathy?

A

anti-phospholipase A2 receptor antibodies

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10
Q

common causes of secondary membranous nephropathy?

A
  • malignancies: solid tumours (lung/ colon etc)
  • infections: hep B/C, HiB, malaria, syphilis, schistosomiasis
  • autoimmune diseases: SLE, sarcoid, IBD
  • drugs: NSAIDs, captopril, gold, penicillamine, lithium, clopidogrel
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11
Q

Causes of renal artery stenosis?

A

90%: atherosclerosis

10%: fibromuscular dysplasia (‘string of beads’ appearance of renal arteries)

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12
Q

Features of fibromuscular dysplasia??

A
  • HTN
  • CKD/ AKI secondary to ACEi initiation
  • flash pulmonary oedema
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13
Q

Causes of rapidly progressive GN?

A

aka crescentic glomerulonephritis

- Goodpastures, ANCA positive vasculitis

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14
Q

Common causes of polyuria?

A

diuretics, caffeine & alcohol
diabetes mellitus
lithium
heart failure

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15
Q

What antibody could be used in treatment of haemolytic uraemic syndrome?

A

Eculizumab (C5 inhibitor monoclonal antibody)

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16
Q

MOA of tolvaptan?

A

vasopressin receptor 2 antagonist

- reduces water absorption and increases water loss without sodium loss

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17
Q

CKD: if albumin: creatinine ratio is between 3-70mg/mmol, what to do?

A

repeat sample with a subsequent early morning sample.

  • > 3 is considered clinically important proteinuria
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18
Q

CKD: if albumin: creatinine ratio is >70mg/mmol, what to do?

A

refer to nephrologist

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19
Q

Management of proteinuria in CKD?

A

1st line: ACEi (ARB)

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20
Q

features of rhabdomyolysis?

A
  • AKI with disproportionately raised Cr
  • High CK
  • Myoglobinuria
  • HypoCa (Myoglobin binds calcium)
  • High phosphate (released from mycocytes)
  • HyperK
  • met acidosis
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21
Q

Fractional urea excretion in urine in pre-renal uraemia vs ATN?

A

pre-renal: <35% fractional urea excretion

acute tubular necrosis: >35%

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

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22
Q

Reason for hyper acute organ rejection?

A

presence of pre formed antibody e.g. HLA mismatch/ ABO incompatibility

tx: removal of graft, if left in situ -> abscess

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23
Q

Reason for acute organ rejection? usually during first 6 months

A

usually T cell mediated
- tissue infiltrates and vascular lesions

tx: medical management

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24
Q

Main reason for chronic organ rejection? occurs after first 6 months

A

vascular changes predominate

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25
Q

Most common and severe from of glomerulonephritis secondary to SLE?

A

Class IV: Diffuse proliferative GN

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26
Q

what are stag horn calculi composed of?

A

struvite (ammonium, magnesium phosphate, triple phosphate)

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27
Q

What bacteria predispose to stag horn calculi?

A

ammonia producing bacteria.

e.g. ureaplasma urealyticum, proteus infections

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28
Q

what stones are radio-lucent?

A

urate stones, xanthine stones

*cystine stones are semi-opaque, with a ground glass appearance.

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29
Q

extra renal manifestations of PCKD?

A
  • liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
  • berry aneurysms (8%): -> subarachnoid haemorrhage
  • CVS: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
  • cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
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30
Q

Triad of features in haemolytic uraemic syndrome?

A

AKI, MAHA, Thrombocytopenia

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31
Q

Causes of transient or spurious non-visible haematuria?

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

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32
Q

most common histological sybtype or renal cell cancer?

A

clear cell (75-85%)

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33
Q

Paraneoplastic hepatic dysfunction syndrome?

A

seen in renal cell carcinoma

  • aka Stauffer syndrome
  • presents as cholestasis/ hepatosplenomegaly
  • secondary to increased IL-6
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34
Q

management of renal cell carcinoma?

A
  • partial/ total nephrectomy
  • IFN-alpha, IL-2 can reduce tumour size
  • tyrosine kinase inhibitors! e.g. sorafenib, sunitinib
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35
Q

causes of nephrogenic DI?

A
  • genetic: more common- defective ADH receptor, less common- defective aquaporin 2 channel
  • electrolytes: hypercalcaemia, hypokalaemia
  • lithium: desensitizes the kidney’s ability to respond to ADH in the collecting ducts
  • demeclocycline
  • tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
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36
Q

Genetics of ADPKD type 1 vs ADPKD type 2?

A

type 1 : chr 16

type 2: chr 4

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37
Q

what antibodies are used in immunosuppression post renal transplant?

A

selective inhibitors of IL-2 receptor: daclizumab, basilximib

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38
Q

commonest cause of glomerulonephritis worldwide?

A

IgA nephropathy aka Berger’s disease

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39
Q

Assoc conditions of IgA nephropathy?

A

alcoholic cirrhosis,
coeliac disease,
henoch-schonlein purpura

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40
Q

Mx of IgA nephropathy?

A

steroids/ immunosuppressants

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41
Q

Poor prognostic markers of IgA nephropathy?

A 
male, 
proteinuria (esp >2g/day),
HTN, hyperlipidaemia
smoking, 
ACE genotype DD
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42
Q

Good prognostic markers of IgA nephropathy?

A

frank haematuria

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43
Q

histology of renal biopsy in IgA nephropathy?

A

mesangial hypercellularity, positive immunofluorescence for IgA & C3

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44
Q

renal biopsy findings in Goodpasture’s syndrome?

A

Linear IgG deposits along the basement membrane

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45
Q

Mx of Minimal change glomerulonephritis?

A

majority 80% are steroid-responsive.

2nd line- cyclophosphamide

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46
Q

reasons why patients may fail to respond to erythropoietin therapy?

A
  • iron deficiency
  • inadequate dose
  • concurrent infection/inflammation
  • hyperparathyroid bone disease
  • aluminium toxicity
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47
Q

How long may finasteride take to work for BPH?

A

6 months

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48
Q

SE of erythropoietin injections?

A
  • accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
  • bone aches
  • flu-like symptoms
  • skin rashes, urticaria
  • pure red cell aplasia* (antibodies against EPO)
  • raised PCV increases risk of thrombosis (e.g. Fistula)
  • iron deficiency 2nd to increased erythropoiesis
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49
Q

Ix of renal vascular disease/ renal artery stenosis?

A

MR angio

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50
Q

Management of renal artery stenosis?

A

balloon angioplasty

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51
Q

most common cause of peritonitis secondary to peritoneal dialysis?

A

Coagulase negative staph e.g. staph epidermidis

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52
Q

Complications of nephrotic syndrome?

A
  • increased risk of clots (loss of antithrombin III and plasminogen in the urine)
  • hyperlipidaemia
  • CKD
  • increased risk of infection due to immunoglobulin loss in urine
  • hypocalcaemia (vitamin D and binding protein lost in urine)
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53
Q

Causes of type 1 membranoproliferative glomerulonephritis?

A
  • 90% of cases are type 1

causes: cryoglobulinaemia, Hep C

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54
Q

electron microscopy showing: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

A

type I membranoproliferative glomerulonephritis

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55
Q

Causes of type 2 membranoproliferative disease?

A

partial lipodystrophy (classically patients have loss of subcut tissue from their face), factor H deficiency

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56
Q

pathophysiology of type 2 membranoproliferative disease?

A
  • persistent activation of alternative complement pathway
  • low circulating levels of C3
  • C3b nephritic factor found in 70%
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57
Q

electron microscopy showing: intramembranous immune complex deposits with ‘dense deposits’

A

type 2 membranoproliferative glomerulonephritis aka ‘dense deposit disease’

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58
Q

causes of type 3 membranoproliferative glomerulonephritis?

A

hep B and C

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59
Q

Management of membranoproliferative glomerulonephritis?

A

steroids

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60
Q

Which HLA matching is most important for renal transplant?

A

HLA DR >B > A

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61
Q

Wilms tumour associations?

A
  • Beckwith-Wiedemann syndrome
  • part of WAGR syndrome with Aniridia, Genitourinary malformations, mental Retardation
  • hemihypertrophy
  • around 1/3 of cases are associated with a loss-of-function mutation in the WT1 gene on chromosome 11
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62
Q

Ix for vesicoureteric reflux?

A

micturating cystourethrogram

  • after this, DMSA scan to look for renal scarring
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63
Q

endocrine effects of renal cell carcinoma?

A

erythropoietin, parathyroid hormone (HyperCa), renin, ACTH

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64
Q

How to calculate anion gap?

A

Na+ + K+ - (Bicarb + Cl-)

*normal anion gap is 8-14 mmol/L

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65
Q

How to calculate anion gap?

A

Na+ + K+ - (Bicarb + Cl-)

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66
Q

Causes of normal anion gap or hyperchloraemic metabolic acidosis?

A
  • GI bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
  • renal tubular acidosis
  • drugs: e.g. acetazolamide
  • ammonium chloride injection
  • Addison’s disease
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67
Q

Causes of high anion gap metabolic acidosis?

A
  • lactate: shock, hypoxia
  • ketones: diabetic ketoacidosis, alcohol
  • urate: renal failure
  • acid poisoning: salicylates, methanol
  • 5-oxoproline: chronic paracetamol use
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68
Q

Which of the following types of renal stones are said to have a semi-opaque appearance on x-ray?

A

cystine stones

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69
Q

Management of oxalate stones?

A
  • cholestyramine - reduces urinary oxalate secretion

- pyridoxine: same

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70
Q

Management of uric acid stones?

A

allopurinol

urinary arlkalinization e.g. oral bicarb

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71
Q

What is seen in stage 1 diabetic nephropathy?

A

hyperfiltration: increase in GFR

- may be reversible

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72
Q

What is seen in stage 2 diabetic nephropathy?

A

silent or latent phase

  • GFR remains elevated
  • most do not develop microalbuminuria for 10 years
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73
Q

What is seen in stage 3 diabetic nephropathy?

A

microalbuminuria

albumin excretion 30-300mg/day

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74
Q

What is seen in stage 4 diabetic nephropathy?

A

persistent proteinuria (dipstick +)
HTN
Histology shows diffuse and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)

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75
Q

What is seen in stage 5 diabetic nephropathy?

A

end stage renal disease, GFR typically <10 mL/min

renal replacement therapy needed

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76
Q

Causes of acute interstitial nephritis?

A
  • drugs: the most common cause, particularly antibiotics
    penicillin, rifampicin, NSAIDs, allopurinol, furosemide
  • systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
  • infection: Hanta virus , staphylococci
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77
Q

Features of acute interstitial nephritis?

A
  • fever, rash, arthralgia
  • eosinophilia
  • mild renal impairment
  • hypertension
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78
Q

Investigations of acute interstitial nephritis?

A

sterile pyuria, white cell casts

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79
Q

High B-HCG + testicular lump?

A

seminoma

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80
Q

Early features of TCA overdose?

A

anticholinergic symptoms: dry mouth, dilated pupils, agitation, sinus tachy, blurred vision

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81
Q

Features of severe TCA overdose?

A

arrhythmias, seizures, met acidosis, coma

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82
Q

ECG changes assoc w TCA overdose?

A

sinus tachy,
QRS widening,
QT prolongation

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83
Q

Management of TCA overdose?

A

1st line for hypotension or arrhythmias: IV bicarb

  • IV lipid emulsion increasingly used to bind free drug and reduce toxicity
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84
Q

Dialysis in TCA overdose?

A

DIALYSIS INEFFECTIVE

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85
Q

Adverse effects of finasteride?

A

impotence
decreased libido
ejaculation disorders
gynaecomastia and breast tenderness

  • also causes decreased levels of PSA
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86
Q

features of ethylene glycol toxicity?

A
  • confusion, slurred speech
  • High anion gap met acidosis
  • AKI
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87
Q

Management of ethylene glycol toxicity?

A
  • 1st Line: fomepizole (inhibitor of alc dehydrogenase)
  • ethanol: works by competing with ethylene glycol for the enzyme alc dehydrogenase, limits formation of toxic metabolites.
  • haemodialysis has a role in refractory cases
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88
Q

what antibiotics inhibit protein synthesis?

A
  • 50S subunit: macrolides, chloramphenicol, clindamycin, linezolid, streptogrammins
  • 30S subunit: aminoglycosides, tetracyclines
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89
Q

what antibiotics inhibit DNA synthesis?

A

quinolone e.g. ciprofloxacin

90
Q

what antibiotics inhibit RNA synthesis?

A

rifampicin

91
Q

What is cetuximab?

A

epidermal growth factor R antagonist

- used in metastatic colorectal ca + H&N ca

92
Q

what is alemtuzumab?

A

anti-CD52, used in CLL

93
Q

What is abciximab?

A

glycoprotein IIb/IIIa receptor antagonist

  • used in patients undergoing PCI
94
Q

What is OKT3?

A

anti-CD3, used to prevent organ rejection

95
Q

Features of methanol poisoning?

A
  • similar to alcohol (intoxication, nausea)
  • visual problems (e.g. blindness)
  • due to accumulation of formic acid
96
Q

Management of methanol poisoning?

A
  • fomepizole (competitive inhibitor of alcohol dehydrogenase) or ethanol
  • haemodialysis
  • cofactor therapy with folinic acid to reduce ophthalmological complications
97
Q

Which clotting factors does LMWH act on vs unfractionated heparin?

A

LMWH: increases ATIII effect on fXa

Unfractionated heparin: activates ATIII, inhibits thrombin, fXa, IXa, XIa, XIIa.

98
Q

Adverse effects of heparins?

A

bleeding,
thrombocytopenia (Heparin induced thrombocytopenia),
osteoporosis (increase risk of #)
hyperK

99
Q

features of heparin-induced thrombocytopenia (HIT)?

A
  • antibodies form against complexes of platelet factor 4 and heparin
  • develops 5-10 days after tx
  • prothrombotic condition
  • 50% reduction in platelets
  • skin allergy
100
Q

Management of nocturia symptoms in overactive bladder?

A
  • moderate fluid intake at night
  • furosemide 40mg in late afternoon may be considered
  • desmopressin may be helpful
101
Q

Management of overactive bladder?

A
  • offer bladder retraining exercises
  • 1st line: antimuscarinics e.g. oxybutynin, tolterodine, darifenacin
  • 2nd line: mirabegron
102
Q

what constitutes AKI?

A
  • Cr rise of >26 in 48h
  • Cr rise of >50% within last 7 days
  • Fall in UO <0.5mL/kg/h for >6h
103
Q

1st line mx of acute epididymo-orchitis?

A

IM ceftriaxone 500mg + Oral doxy for 2 wks

104
Q

Complications of plasma exchange?

A
  • hypocalcaemia
  • metabolic alkalosis
  • removal of systemic medications
  • coagulation factor depletion
  • Ig depletion
105
Q

Management of haemolytic uraemia syndrome?

A
  • supportive e.g. fluids/ bloods
  • if severe and not associated with diarrhoea: plasma exchange
    • eculizumab (C5 inhibitor monoclonal antibody)
106
Q

How to stage CKD?

A

stage 1: eGFR >90, with some sign of kidney damage (if all tests are normal, NO CKD)
stage 2: 60-90, + some sign of kidney damage
stage 3a: 45-49
stage 3b: 30 -44
stage 4: 15-29
stage 5: <15mL/min

107
Q

How does alcohol lead to polyuria?

A

alcohol bingeing can lead to ADH suppression in the posterior pituitary gland -> leading to polyuria

108
Q

Causes of AL Amyloidosis?

A
  • most common
  • L for Ig Light chains
  • Myeloma, Waldenstroms, MGUS
109
Q

Features of AL amyloidosis?

A

nephrotic syndrome, cardia/ neuro involvement, macroglossia, periorbital eccymoses

110
Q

Causes of AA Amyloidosis?

A

A for precursor serum amyloid A protein

  • seen in chronic infection/ inflammation
  • TB, bronchiectasis, rheumatoid arthritis
111
Q

Features of AA Amyloidosis?

A

renal involvement most common feature

112
Q

Causes of Beta-2 microglobulin amyloidosis?

A

assoc w patients on renal dialysis

  • precursor = beta-2 microglobulin, part of the MHC
113
Q

Tolvaptan use in PCKD?

A
  • used to slow progression of disease in some patients
  • V2R antagonist - > reduces cell proliferation, cyst formation and fluid excretion –> reduces kidney growth and protects renal fn
114
Q

normal glomeruli on light microscopy,
+
electron microscopy shows fusion of podocytes and effacement of foot processes

A

Minimal change disease

115
Q

Features of minimal change disease?

A

nephrotic syndrome, normotension, Highly selective proteinuria (increased glomerular permeability to serum albumin)

116
Q

Causes of minimal change disease?

A

majority: idiopathic (80-90%)

other causes:
drugs- NSAIDs, rifampicin
Hodgkins lymphoma, thymoma
Infectious mono

117
Q

Biopsy findings of HIV associated nephropathy?

A

Pathological hallmark: focal segmental glomerulosclerosis (FSGS) with a collapsed glomerular tuft, with evidence of numerous tubuloreticular structures on electron microscopy

118
Q

Key features of HIV-associated nephropathy?

A
  • Massive proteinuria -> nephrotic syndrome
  • large kidneys may be seen
  • focal segmental glomerulosclerosis with focal/ global capillary collapse on renal biopsy
  • high Ur, Cr
  • normotension
119
Q

Features of scleroderma renal crisis?

A
  • presence of RNA polymerase antibodies
  • severe hyper-reninaemic HTN
  • Mild MAHA
  • obliterative vasculopathy, ‘Onion skin lesions’
120
Q

Treatment of choice in scleroderma renal crisis?

A

ACEi

  • to reduce BP, and improves kidney function
121
Q

Cause of primary/ atypical haemolytic uraemic syndrome?

A

complement dysregulation

122
Q

what to co-prescribe when starting goserelin (gonadorelin analogues)?

A

anti-androgen tx such as cyproterone acetate

  • due to risk of tumour flare during initiation of goserelin
  • this phenomenon is secondary to initial stimulation of LH release by pituitary gland -> raised testosterone levels
123
Q

Renal biopsy showing:

  • electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
  • immunofluorescence: granular or ‘starry sky’ appearance
A

post streptococcal glomerulonephritis

124
Q

most common cause of nephrotic syndrome in adults?

A

focal segmental glomerulosclerosis or Membranous glomerulopathy

125
Q

renal biopsy

  • > focal and segmental sclerosis and hyalinosis on light microscopy
  • > effacement of foot processes on electron microscopy
A

focal segmental glomerulosclerosis

126
Q

Renal biopsy showing:
- electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

A

Membranous glomerulonephritis

127
Q

Autoantibodies in idiopathic membranous glomerulonephritis?

A

Anti-phospholipase A2 antibodies

128
Q

typical presentation of membranous glomerulonephritis?

A

nephrotic syndrome

- renal biopsy: spike and dome appearance

129
Q

Causes of membranous glomerulonephritis?

A
  • idiopathic: due to anti-phospholipase A2 antibodies
  • infections: hepatitis B, malaria, syphilis
  • malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
130
Q

What type of SLE renal disease leads to membranous glomerulonephritis/ proteinuria?

131
Q

Good prognostic features of Membranous glomerulonephritis?

A

female, young age at presentation, asymptomatic proteinuria

132
Q

Management of membranous glomerulonephritis?

A

ACEi/ ARB
- improves prognosis, reduces proteinuria

+ immunosuppression if severe/ progressive disease: steroids + cyclophosphamide

anticoagulation for high risk patients

133
Q

when does contrast-induced nephropathy normally present after contrast administration?

134
Q

causes of focal segmental glomerulosclerosis?

A
  • idiopathic
  • secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle-cell
135
Q

Retroperitoneal fibrosis associated with?

A
  • Riedel’s thyroiditis
  • previous radiotherapy
  • sarcoidosis
  • inflammatory abdominal aortic aneurysm
  • drugs: methysergide
136
Q

renal biopsy shows:

  • electron microscopy: characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance
A

Alports syndrome

- X linked dominant

137
Q

how long does it take for an AV fistula to fully mature?

138
Q

features of cystinuria?

A
  • auto recessive
  • recurrent renal stones
  • stones classically yellow, crystalline, semi-opaque on XR
139
Q

Diagnosis of cystinuria?

A

cyanide-nitroprusside test

140
Q

Mx of cystinuria?

A
  • hydration
  • D-penicillamine
  • urinary alkalinization
141
Q

risk factors for urate stones?

A
  • gout

- ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid

142
Q

drug causes of renal stones?

A

drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline

143
Q

risk factors of renal stones?

A
  • dehydration
  • hypercalciuria, hyperparathyroidism, hypercalcaemia
  • cystinuria
  • high dietary oxalate
  • renal tubular acidosis
  • medullary sponge kidney, polycystic kidney disease
  • beryllium or cadmium exposure
144
Q

causes of papillary necrosis?

A
  • chronic analgesia use
  • sickle cell disease
  • TB
    acute pyelonephritis
    diabetes mellitus
145
Q

features of papillary necrosis?

A

fever, loin pain, haematuria

IVU - papillary necrosis with renal scarring - ‘cup & spill’

146
Q

features of goodpasture’s syndrome?

A

pulmonary haemorrhage,

rapidly progressive GN: proteinuria + haematuria

147
Q

Factors which increase likelihood of pulmonary haemorrhage in Goodpasture’s syndrome?

A
  • smoking
  • lower respiratory tract infection
  • pulmonary oedema
  • inhalation of hydrocarbons
  • young males
148
Q

nephrotic syndrome + marked loss of subcutaneous tissue from the face

A

Type II membranoproliferative GN (mesangiocapillary)

  • assoc with partial lipodystrophy
149
Q

Disorders associated with glomerulonephritis and low serum complement levels

A
  • post-streptococcal glomerulonephritis
  • subacute bacterial endocarditis
  • systemic lupus erythematosus
  • mesangiocapillary glomerulonephritis
150
Q

what is calciphylaxis?

A
  • rare complication of ESRF
  • deposition of calcium within arterioles -> microvascular occlusion and necrosis of supplied tissue
  • most commonly affects skin and presents w painful necrotic skin lesions
151
Q

Features of Fanconi Syndrome?

A
  • generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule
  • Type 2 (proximal) renal tubular acidosis
  • polyuria
  • aminoaciduria
  • glycosuria
  • phosphaturia
  • osteomalacia
152
Q

Most common cause of Fanconi syndrome in children?

A

cystinosis

153
Q

most common cause of death in amyloidosis?

A

cardiac involvement

154
Q

Eye abnormality in Alport syndrome?

A

anterior lenticonus

- characterised by protrusion of the anterior aspect of the lens

155
Q

management of reducing urinary calcium if there is only a marginal calciuria (causing recurrent stones)?

A

can give potassium citrate

- urinary citrate forms soluble complexes with calcium ions, and inhibit crystal growth and aggregation

156
Q

Reason why calcium oxalate stones are predisposed in crowns/UC and in bowel resection?

A

Particularly in ileal resection.
With fat malabsorption, unabsorbed long-chain fatty acids bind calcium in the lumen
> less calcium available to bind oxalate
> higher levels of oxalate to ppt into calcium oxalate stones

157
Q

Relapse rates of Membranoproliferative glomerulonephritis in renal transplant pts?

A

80-100% in type II

Lower in type I

158
Q

Relapse rates of IgA nephropathy in renal transplant pts?

159
Q

Relapse rates of focal segmental glomerulonephritis in renal transplant pts?

160
Q

What conditions may reoccur following kidney transplantation

A

IgA nephropathy
Membranoproliferative GN
Focal segmental glomerulosclerosis
Membranous GN

161
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis

A
  1. post-streptococcal GN associated with low complement lvls
  2. main symptom in post-streptococcal GN is proteinuria
  3. there is typically an interval between URTI and the onset of renal problems in post-streptococcal GN
162
Q

Management of focal segmental glomerulonephritis?

A

Steroids +/- immunosuppressants

163
Q

Management of IgA nephropathy if isolated haematuria, no proteinuria, normal Cr?

A

no treatment needed, other than follow-up to check renal function

164
Q

Management of IgA nephropathy if there is persistent proteinuria (>500-1000mg/d), normal or slightly reduced eGFR?

165
Q

Management of IgA nephropathy if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors?

A

Immunosuppression with corticosteroids

166
Q

Why is calcium low in rhabdomyolysis

A

Myoglobin binds calcium

167
Q

Why is calcium low in rhabdomyolysis

A

Myoglobin binds calcium

168
Q

Rhabdoymyolysis electrolyte abnormalities?

A

HypoCa
HyperPO4
HyperK

169
Q

Viral cause of acute kidney transplant graft failure? (Ie within 6 months)

170
Q

Features of papillary necrosis?

A

fever, loin pain, haematuria

IVU - papillary necrosis with renal scarring - ‘cup & spill’

171
Q

Causes of papillary necrosis?

A 
chronic analgesia use
sickle cell disease
TB
acute pyelonephritis
diabetes mellitus
172
Q

Why are patients with nephrotic syndrome in a hypercoagulable state?

A

loss of antithrombin III and plasminogen in urine

173
Q

Complications of nephrotic syndrome?

A
  • DVT/PE
  • renal vein thrombosis (pain + sudden deterioration renal fn)
  • increased risk of infection (urine loss of Ig)
  • hypoCa (vitamin D and binding protein lost in urine)
  • ckd
  • hyperlipidaemia (increasing risk of ACS, stroke)
174
Q

Which HIV medication is associated with kidney damage?

A

Protease inhibitors such as indinavir can precipitate intratubular crystal obstruction

175
Q

What management options for renal cell carcinoma?

A

If size <7cm, confined disease: partial/ total nephrec

Alpha IFN and IL2 can reduce tumour size and help w mets

receptor tyrosine kinase inhibitors (e.g. sorafenib, sunitinib)

176
Q

Diagnosis of amyloidosis?

A

biopsy of skin, rectal mucosa, or abdominal fat
- Congo red staining: apple green birefringence

serum amyloid precursor (SAP) scan

177
Q

Failure of renal transplant in Alport’s syndrome?

A

De novo anti-GBM antibody disease
(In ~5%)
- antibodies against collagen alpha-5(IV) chain

178
Q

virus precipitating post transplant lymphoproliferative disorder?

179
Q

Ultrasound diagnostic criteria of Autosomal Dominant Polycystic kidney disease (in pts with positive family history)?

A
  1. 2 cysts, unilateral or bilateral, if aged < 30 years
  2. 2 cysts in both kidneys if aged 30-59 years
  3. 4 cysts in both kidneys if aged > 60 years
180
Q

What management is offered in ADPCKD (auto dom Polycystic kidney disease) to slow disease progression?

A

tolvaptan (vasopressin receptor 2 antagonist)

if:
> CKD stage 2 or 3 at the start of treatment
> evidence of rapidly progressing disease

181
Q

Most common causes of polyuria? (>1 in 10)

A

diuretics, caffeine & alcohol
diabetes mellitus
lithium
heart failure

182
Q

infrequent causes of polyuria (1 in 100)?

A

HyperCa

Hyperthyroidism

183
Q

Rare causes of polyuria (1 in 1000)?

A

chronic renal failure
primary polydipsia
hypokalaemia

184
Q

Very rare causes of polyuria (<1 in 10000)?

A

Diabetes insipidus

185
Q

why is it important to identify fibromuscular dysplasia as an underlying cause of renal artery stenosis?

A

typically in younger patients
> characteristic ‘string of beads’ appearance on angiography

-> respond well to balloon angioplasty

186
Q

how to make diagnosis of CKD? how many blood tests needed?

A

eGFR < 60 ml / min / 1.73 m2 on at least 2 occasions separated by a period of at least 90 days.

+
kidney damage:
e.g. albuminuria, urine sediment abnormalities, electrolyte abnormalities, histological abnormalities, structural abnormalities and a history of kidney transplantation.

187
Q

management of intraperitoneal sepsis?

A

intraperitoneal vancomycin + ceftazidime

OR IP vancomycin + PO ciprofloxacin

common bugs: staph aureus, psuedomonas, staph epidermidis

188
Q

most common organism causing peritoneal dialysis sepsis?

A

staph epidermidis

189
Q

Diagnosis of calciphylaxis?

A

skin biopsy

190
Q

Treatment of calciphylaxis?

A
  • reducing Ca and PO4 levels
  • controlling hyperparathyroidism
  • avoid contributing drugs such as warfarin and calcium containing compounds
191
Q

Management of cystine renal stone?

A

Urinary alkalinisation (potassium citrate) + hydration

2nd line: chelating agent D-penicillamine

192
Q

In secondary hyperparathyroidism (2’ CKD), at what level of PTH would you begin supplementation with Ca/Vit D?

A

PTH levels > 2x UL of normal
- supplementation with Ca/Vit D commenced to decrease risk of progression to tertiary disease and decrease complications such as bone resorption/ #/ ectopic calcification

  • if replace when PTH lvls too low: risk of adynamic bone disease
193
Q

What is adynamic bone disease?

A

reduced synthesis of bone matrix due to decreased osteoblast/clast activity > can lead to fragility #s

  • most common form of renal osteodystrophy
  • pathophys is unclear, but excessive suppression with PTH plays a major role (hence Vit D/ Ca usually supplemented only when PTH lvls >2 UL of normal)
194
Q

why does anti GBM disease occur after renal transplant in Alport’s syndrome?

A

Alports: genetic disorder of Type IV collagen

  • pts may mount immune response to type IV collagen on graft transplant as it is a novel antigen
  • > leads to anti-GBM antibodies + RPGN
195
Q

Management of severe atypical Haemolytic uraemic syndrome not assoc w diarrhoea?

A

plasma exchange may be indicated
+
eculizumab (C5 inhibitor monoclonal Ab)

196
Q

What stones do indinavir give rise to?

A

pure indinavir stones that are undetectable on plain XR or CT

197
Q

Mx to reduce calcium stones due to hypoercalciuria?

A

Thiazide diuretics

e. g chlorthalidone
- to increase distal tubular calcium resorption

198
Q

Mx to reduce oxalate stones?

A

cholestyramine, pyridoxine

- reduce urinary oxalate secretion

199
Q

Mx to reduce uric acid stones?

A

Allopurinol

Urinary alkalinization e.g. bicarbonate

200
Q

Features of tubulointerstitial nephritis with uveitis?

A
  • usually in young females
  • fever, weight loss, painful/red eyes
  • Urinalysis: Leukocytes + protein +
201
Q

infectious disease that may predispose to minimal change disease?

A

Infectious mononucleosis

202
Q

Absolute contraindications to renal biopsy?

A
  1. Polycystic kidneys,
  2. Urinary tract obstruction or hydronephrosis
  3. uncontrolled HTN
  4. significant renal malignancy
  5. significant bleeding disorders
203
Q

what management should be considered in T1DM pts nearing ESRF?

A

joint pancreas and kidney transplants

  • will need lifelong immunosuppression after this.
  • likely needs MDT discussion
204
Q

Criteria for renal referral in AKI?

A
  • renal transplant
  • ITU patient with unknown cause AKI
  • vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
  • stage 3 AKI
  • CKD stage 4/5
  • need for renal replacement therapy
  • AKI with unknown cause/ inadequate response to tx
205
Q

How does plasma exchange increase the risk of post renal biopsy bleed?

A

depletion of fibrinogen levels + reduction in plt count

- should monitor fibrinogen daily + replace with FFP if deplete

206
Q

Complications of Plasma exchange?

A 
hypocalcaemia - due to presence of citrate used as anticoagulant for the extracorporeal system
metabolic alkalosis
removal of systemic medications
coagulation factor depletion
Immunoglobulin depletion
207
Q

How to give EPO agents? (IV vs sc)

A

Give sc in pre-dialysis patients and IV in patients undergoing HD

208
Q

stones assoc with alkaline urine?

A

Struvite stones

  • formed in the presence of increased urinary ammonia and alkaline urine (>7.2).
  • These occur as a result of urease producing bacteria (and are thus associated with chronic infections).
209
Q

Treatment of dialysis disequilibrium syndrome?

A

Mannitol or hypertonic saline

- increases plasma osmolarity and reduces cerebral oedema

210
Q

Urine microscopy of Indinavir renal stones?

A

Needle shaped crystals

211
Q

General issue in Fanconi syndrome?

A

Disorder of proximal renal tubular function

  • impaired re absorption of filtered solutes
  • > LOW bicarbonate, K, phosphate, glucose, uric acid and amino acids lost in urine

-> development of type 2 (proximal) renal tubular acidosis (high Cl, low bicarb)

212
Q

Causes of Fanconi syndrome?

A 
Cystinosis (most common cause in children)
Sjögren’s syndrome
Multiple myeloma
Nephrotic syndrome
Wilson’s disease
213
Q

Absolute contraindications to donating a kidney?

A 
active malignancy
chronic infection
overt proteinuria
bilateral renal artery atherosclerosis
 sickle cell disease
Uncontrolled hypertension
214
Q

Management of class V lupus nephritis (membranous)?

A

IV methylprednisolone + IV cyclophosphamide

  • endorsed by KDIGO (Kidney Disease Improving Global Outcomes) guidelines
215
Q

Contraindications to starting testosterone replacement?

A 
Prostate cancer
PSA >4ng/ml
male breast cancer
severe sleep apnoea
severe LUTS due to BPH
216
Q

Common causes of bilateral hydronephrosis?

A 
SUPER:
Stenosis of the urethra
Urethral valve
Prostatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis
217
Q

Common causes of unilateral hydronephrosis?

A

Pelvic-ureteric obstruction (congenital or acquired)
Aberrant renal vessels
Calculi
Tumours of renal pelvis

218
Q

indications for plasma exchange in ANCA-associated vasculitis?

A
  • Severe active renal disease (serum Cr > 354 micromol/L or require dialysis)
  • Pulmonary haemorrhage
  • Concurrent anti-GBM autoantibody disease.
219
Q

What kind of GN does post strep GN cause?

A

acute, diffuse proliferative glomerulonephritis

220
Q

Subsequent maintenance therapy in lupus nephritis after inducing remission?

A

mycophenolate

MRCP (21 decks)

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