Renal Flashcards

1
Q

How do thiazide diuretics work

A

Block the sodium chloride renal symporter

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2
Q

Another name for necrotising glomerulonephritisi

A

Eosinophilic granulomatosis with polyangitis

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3
Q

Pathology IgA nephropathy

A

IgA deposits build up in the kidneys, causing inflammation and damage in the kidneys
Triggers glomerular inflammation and scarring

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4
Q

Most common cause of GN

A

IgA nephropathy

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5
Q

Presentation IgA nephropathy

A

Haematuria
URTI
Gastroenteritis
Acute or chronic renal failure may develop
HTN (rare)
Oedema (rare)

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6
Q

Diagnosis of IgA nephropathy

A

Renal biopsy; Focal or diffuse mesangial proliferation as well as extracellular matrix expansion
Immunofluorescent tests; diffuse mesangial IgA deposition

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7
Q

Treatment of IgA neprhopathy

A

ACEI if HTN/Proteinuria present
Steriods

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8
Q

What is assosiated with poorer prognosis in IgA neprhopathy

A

HTN

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9
Q

Granulomastosis with polyangitis (GPA) affects what sized vessels

A

small to medium

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10
Q

What does GPA most commonly affect

A

Kidneys
Lungs

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11
Q

Symptoms of GPA

A

Cough
Haemoptysis
Haematuria
Proteinuria
Nasal obstruction
Epistaxis
Rhinitis
Saddle nose deformity
Subglottic stenosis
Fever
Weight loss
Myalgia
Skin involvement
Eye involvement
GI Sx
Neurological Sx

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12
Q

Diagnosis of GPA

A

c-ANCAs
Biopsy showing necrotising granulomas and vasculitis

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13
Q

Treatment of GPA

A

Steriods
Cyclophosphamide

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14
Q

Features of nephrotic syndrome

A

Massive proteinuria >3/5g/day
Oedema
Hypoalbuminuria
Increased tendency for hyperlipidaemia, thrombosis and infection

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15
Q

Features of nephritic syndrome

A

Haematuria
Oliguria
Oedema
Proteinuria < 3.5g/day
HTN
Uraemic symptoms

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16
Q

Uraemic symptoms

A

Anorexia
Puritius
Lethargy
Nausea

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17
Q

What is the way to determine protein excretion

A

early morning albumin creatinine ACR ratio

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18
Q

Feautres of type 1 mesangiocapillary glomerulonephritis (MCGN)

A

Tramline appearance on biopsy
Haematuria
Proteinuria
Nephrotic syndrome
Frank kidney disease
Reduced plasma levels of C3, C4
Can be assosiated with Hep B / C

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19
Q

Features of type 2 mesangiocapillary glomerulonephritis (MCGN)

A

Can occur idiopathically or after measles infection
Cells stain positive for C3
Partial lipodystrophy

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20
Q

Urine findings of FSGS

A

Protein
Hyaline
Broad, waxy casts

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21
Q

Renal biopsy findings of crescentric GN

A

Extensive crescents

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22
Q

Features of eosinophilic granulomatosis with polyangitis

A

Asthma
Blood eosinophilia >10%
Vasculitic neuropathy
Pulmonary infiltrates
Sinus disease
Extravasculareosoinophils on biopsy findings

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23
Q

WHat is goodpasture syndrome

A

An autoimmune disease where antibodies are produced against the glomerular basement membrane and the alveolar basement membrane

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24
Q

Goodpastures involves

A

GN
Pulomonary renal syndrome
Pulmonary invovlement more common when environmental triggers
- smoking
- inhalation of cocaine
- respiratory ifnection
- exposure to hydrocarbons

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25
Q

Assosiations of goodpastures

A

HLA-DR15
HLA-DRB1

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26
Q

Presentation of goodpastures

A

Haematuria
Frothy urine/proteinuria
Decreased UO
Peripheral oedema
Haemoptysis
Dyspnoea

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27
Q

What differentiates goodpastures from other diseases that cause both pulmonary and renal invovlement

A

anti-GBM antibodies

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28
Q

Treatment of goodpastures

A

Plasma exchange
Prednisolone
Cyclophosphamide

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29
Q

ESR in goodpastures

A

Normal

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30
Q

Renal biopsy in goodpastures

A

Crescenteric glomerulonephritis
Linear deposition of complement (C3) and IgG along the basement membrane

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31
Q

Features of HIV assosiated nephropathy

A

Focal segemental glomeruloneprhtisi with a collapsed glomerular tuft
Microcystic tubular dilatation

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32
Q

Treatment of minimal change disease with frequent relapses

A

High dose steriods
Cyclophosphamide

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33
Q

What do recurrent UTIs, including in childhood, may indicate ?

A

Chronic reflux nephropathy

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34
Q

What may chronic reflux nephropathy lead to?

A

Difficult to treat HTN

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35
Q

Investigation for chronic reflux nephropathy

A

Excretion urography testing

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36
Q

Blood and urinary findings of acute tubular necrosis

A

Na > 40
Urinary osmolality <350

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37
Q

Causes of acute tubular necrosis

A

Hypotension
Nephrotoxins
Renal hypoperfusion

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38
Q

Pathophysiology of ATN

A

Ischaemia
Results in injury of tubular cells, most prominently in the straight position of the proximal tubules and the thick ascending loop of Henle
Cell death results in cast formation
Casts and debris obstruct tubules in multiple nephrons further reducing renal function due to reduced filtration
Ischaemia also reduces the production of vasodilators (NO and prostacyclin) causing vasoconstriction and hypoperfusion

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39
Q

Treatment of AVN

A

Supportive

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40
Q

Genetics of ADPKD

A

Mutation in PKD1 gene (85%)
(abscence of functioning of polycystin)
Others defect in PKD2

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41
Q

What antibodies are seen in sjrogrens syndrome

A

Ro and La autoantibodies

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42
Q

Investigation of renal artery stenosis

A

Magnetic resonance angiography

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43
Q

What can happen if you have an untreated UTI in patients with diabetes

A

Renal papillary necrosis, which results in linear breaks at the papillary base, and ureteric obstruction may reults if the papillae have sloguhed off

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44
Q

Features of alport syndrome

A

Chronic renal failure
- gross haematuria
- proteinuria
- peripheral oedema
Sensorineural hearing loss
Lenticonus
Fatigue
SOB
HTN

INHERITED
- FH of microscopic haematuria in a first degree relative

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45
Q

Features of allergic interstitial nephritis

A

Eosinophillia
Haematuria
Pyuria
Diffuse maculopapular rash
Fever

Can occur 2 weeks after causative drug

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46
Q

Treatment of allergic interstitial nephritis

A

Discontinue causative agent
IVF

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47
Q

What is adynamic bone disease and what is it caused by

A

Can be caused by overtreatment with alfacalcidol
Most prevalent in diabetic patients and those on peritoneal dialysis
Assosiated with increased risk of hip fractures
Tendency towards hypercalcaemia as the bone loses its capacity to buffer serum calcium

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48
Q

Histology of adynamic bone disease

A

Reduction in both bone formation and resorption
Thin osteoid seams
Little active mineralisation
Few osteoclasts

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49
Q

Calcium, phosphate and PTH levels in osteoporosis

A

Normal

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50
Q

What is osteitits fibrosa cystica assosiated with

A

Hyperparathyroidism

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51
Q

What points towards nephrotic syndroem

A

Low albumin
Abnormal cholesterol
Increased urinary albumin excretion

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52
Q

What is the most common cause of nephrotic syndrome in the older age group

A

Membranous nephropathy

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53
Q

What symptom needs to be present for a diagnosis of nephrtitc syndrome

A

Haematuria

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54
Q

What is buergers disease

A

Accelerated thrombosis of medium and small vessles
Predominately in the lower limbs
Presents with rapidly worsening claudication in heavy smokers

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55
Q

What would make you think of a cholesterol embolism

A

Recent arterial instrumentation
Marked eosinophilia
Increasing creatinine

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56
Q

WHen would CMV reactivation after transplabntation from a previously infected donor occur and treatment

A

4-6 weeks after surgery
Minor infection - valaciclovir or valganciclovir
Severe infection - ganciclovir

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57
Q

WHat are bartter and Gitelam syndromes

A

Renal tubular salt wasting disorders in which the kidneys cannot reabsorb chloride in the thick ascending limb of the loop of Henle, or the distal convoluted tubule, depending on the mutation

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58
Q

Time frame of acute graft rejection

A

First 4 weeks

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59
Q

Time frame of delayed graft reaction

A

> 3 months

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60
Q

Most common causes of acute interstitial nephritis

A

NSAIDs
Penicillin
Sulfa containing drugs

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61
Q

What is the most common cause of acute interstitial nephritis (in broad terms)

A

Immunologically induced hypersensitivity reaction to an antigen, usually a drug or infectious agent

62
Q

What would cast nephropathy indicate

A

Myeloma

63
Q

What does IgA nephropathy have a close relationship to

A

URTIs

64
Q

Pathology of type I RTA

A

DISTAL RTA
A-intercalated cells in the distal and collecting tubules fail to secrete H and absorb K

65
Q

Features of type I RTA

A

Can be assosiated with DI and salt wasting states
Severe metabolic acidosis and hypokalaemia
Urinary tract calculi (2ndry to the severe acidosis)
GFR often unaffected

COMMON

66
Q

Pathology of type II RTA

A

PROXIMAL RTA
Proximal tubule cells fail to reabsorb bicarbonate

67
Q

Features of type II RTA

A

Potassium normal or low
Metabolic acidosis (less severe)
GFR often unaffected
assosiated with osteomalacia and rickets

RELATIVELY UNCOMMON

68
Q

Pathology of Type III RTA

A

Shares features of both type I and II
- impaired proximal bicarbonate resorption and impaired distal acidification

69
Q

Features of type III RTA

A

Rare variant

Acidosis
Biochemical abnormalities will depend on whether the distal or proximal tubule is predominant

70
Q

Pathology of Type 4 RTA

A

Kidney either resistant to aldosterone or the plasma aldosterone levels are low

71
Q

Features of type 4 RTA

A

Hyperkalaemia
CKD usually present

Commonly due to mineralocorticoid deficiency

72
Q

Management of renal tubular diseases

A

Correction of electrolyte disturbances and pathological sequalae
Usually oral bicarbonate and potassium replacement therapy

73
Q

What is liddles syndrome

A

Pseudohyperaldosteronism - hypokalaemic metabolic alkalosis with HTN and volume overload, despite normal or low aldosterone level

74
Q

Lung biopsy of goodpastures

A

Disruption of alveolar septa
Haemosiderin laden macrophages

75
Q

Assosiations of membranous nephropathy

A

SLE
Bowel and lung malignancies
Penicillamine therapy
Hep B infection
Plasmodium malariae

Assosiation with HLA DR3

76
Q

What is common in 40% of patients with nephrotic syndrome

A

Renal vein thrombosis

77
Q

Most common causative organism of peritoneal dialysis peritonitis

A

Staph A or epidermis

78
Q

Treatment of common cause of peritoneal dialysis peritonitis

A

Vancomycin

79
Q

Blood findings of minimal change nephropathy

A

Normal high density lipoprotein cholesterol levels
Elevated low density lipoprotein cholesterol concentrations

80
Q

Commonest cause of death in renal dialysis patients

A

CV disease

81
Q

Causes of amyloid

A

Myeloma
Hereditary forms of amyloidosis
Chronic disease e.g. RA

82
Q

What can renal amyloidosis precipitate

A

Nephrotic syndrome

83
Q

Which diuretic causes the greatest retention of lithium

A

Thiazide diuretics

84
Q

Inheritance of fabry disease

A

X linked

85
Q

Features of fabry disease

A

Corneal microscopic lipid deposits
Maltese cross lipid globules in urine microscopy
Skin angiokeratomas
Decreased sweating
Leg lymphodema
Peripheral neuropathy
Cardiac conduction defects
Premature CV disease

86
Q

Pathology of fabry disease

A

X linked lysosomal storage disorder
Characterised by myelin deposits in the tubular and vascular epithelium, resulting in ischaemic nephropathy

87
Q

IgA nephropathy vs post strep glomerulonephritis

A

IGA nephropathy - frank haematuria 24-48 hours following onset of symptoms of resp tract infection. Normotensive, only a trace of proteinuria. Can also be triggered by UTI and gastroenteritis
Post strep glomerulonephritis - following group A strep infections, symptoms begin around 10 days post strep infection and frank haematuria can be seen

88
Q

Different types of lupus related renal disease

A

Class I - Minimal mesangial lupus nephritis - normal crt and urinarylysis, minimal or no proteinuria. Mildest and earlier form
Class II - Mesangial proliferative lupus nephritis - microscopic haematuria and proteinuria. BP normal
Class III - Focal lupus nephritis
Class IV - Diffuse lupus nephritis - symptoms of nephrotic syndrome, but burden of renal disease leads to reduction in GFR and raised crt
Class V - Membraneous lupus nephritis - siginificant proteinuria and peripheral oedema. Crt normal. Hamaturia and HTN seen but not essential. May occur in abscence of other symptoms of lupus !!
Class VI - Advanced sclerosing lupus nephritis - damage to > 90% of glomeruli, leading to slowly progressive renal failure

89
Q

Light microscopy findings of membranous lupus nephritis

A

Diffuse thickening of the glomerular capillary wall on light microscopy

90
Q

Treatment of pagets disease

A

Zoledronate

91
Q

What can long term nitrofurantoin treatment result in

A

Pulmonary fibrosis

92
Q

Serum electrophoresis in patients with nephrotic syndrome

A

Increased a1 and a2 globulin fractions
Decreased serum albumin

93
Q

What kind of stones are always radiopaque and therefore can be seen on X ray

A

Calcium stones

94
Q

What is recent urolithiasis in a young adult with negative x ray findings suspicious of

A

cystinuria (cystine stones)

95
Q

Test for cystinuria

A

Positive urine analysis for hexagon shaped crystals on urine analysis
CT
Poorly radioopaque - cannot see on xray

96
Q

What causes effacement of foot processes seen on electron microscopy

A

minimal change disease

97
Q

Kidney biopsy of post strep glomerulonephritis

A

Granular deposits of IgG, IgM and C3 complement

98
Q

Thyroxine levels in nephrotic syndrome

A

Reduced
Due to enhanced urinary excretion of thyroxine binding globulin

99
Q

Most important function of the proximal convoluted tubule

A

Sodium reabsorption

100
Q

IgA nephropathy disease course

A

Symptoms tend to recur with subsequent RTIs
Long term renal impairement relatively uncommon
Non visible haematuria can be noted between visible episodes

101
Q

Renal biopsy for lupus nephritis

A

“Full house” immunology on immunostaining
Mesangial deposition of IgA, IgG, IgM, C3 and C4

102
Q

Pneumonic for high anion gap metabolic acidosis

A

CAT MUDPILES
C - Cyanide poisoning
A - aminoglycosides
T - toluene
M - methanol
U - uraemia
D - DKA
P - Paracetomal
I - Isoniazid
L - Lactic acid
E - ethanol
S - salicylates

103
Q

Causes of normal ion gap metabolic acidosis

A

Hypercalcaemia
Type I RTAA

104
Q

Pathology of medullary sponge kidney

A

Dilatation of the collecting ducts in the papillae with accompanying cystic changes
One or both, or part of one kidney, may be affected
In severe cases the medually area has a sponge like appreance
Cyst formation commonly assosiated with small calculi within the cysts

105
Q

Diagnosis of meduallry sponge kidney

A

Excretion urography

106
Q

Investigation of chronic reflux nephropahty

A

TC-DMSA scintigraphy - renal scars, as areas of reduced uptake
IV urography - localised scarring as parenchymal loss and clubbed calycyes

107
Q

What does adult PCKD often present with

A

Young adult with HTN

108
Q

Features of meduallry cystic disease

A

Autosomally inherited
Presents in early adulthood with progressive renal impariment
Smallcysts at the cortico-meduallry junctions with assosiated tubule-interstitation inflammation and scarring
glomeruli unaffected

109
Q

What is nephrocalcinosis

A

deposition of calcium in the renal parencyhma

110
Q

causes of nephrocalcinosis

A

Hypercalcaemia
Hyperparathyroidism
TB

111
Q

Presentation of meduallry sponge kidney

A

Recurrent UTIs
Haematuria on urine dip in the absence of recent infection
Excretion urography - small calculi in papillary zones, increase in radiodensity after contrast medium is injected

112
Q

Urinary calcium excretion in familial hypocalciuric hypercalcaemia

A

Low

113
Q

Most common presentation of familial hypocalcuric hypercalcaemia

A

Renal stone disease

114
Q

What mechanism does solute removal occur on haemodiaylsis

A

Diffusion

115
Q

What chronic upper respiratory tract changes are seen in granulomatosis with polyangitis

A

Sinusitis
Otitis
Mastoiditis
Nasal crusting
Epistaxis
Saddle nose deformity

116
Q

Lung changes in granulomatosis with polyangitis

A

Multiple nodules
Cavitating lesions
Diffuse alvolar changes

117
Q

What is the confirmatory test for granulomatosis with polyangitis

A

c-ANCA

118
Q

S/E of finasteride and why

A

Gynaecomastia and breast tenderness
Leads to increased conversion of testosterone to estradiol and androstenediol

119
Q

S/E of finasteride

A

Gynaecomastia
Breast tenderness
Impotence
Decreased libido
Decreased ejaculate volume
Depression
Anxiety

120
Q

What can chemotherapy involving rapid lysis of malignant cells lead to

A

Release of large amounts of nucleoprotein and increased uric acid production

121
Q

How many men with BPH have prostatic carcinoma

A

10-30%

122
Q

Treatment for rapid symptom relief of BPH

A

Alpha blockade

123
Q

What is kawasaki disease and who does it mainly affect

A

Acute systemic vasculitis
Children < 5 y/o

Fever lasting >5 days
Bilateral conjunctival congestion
Dryness and redness of lips and oral cavity 3 days after onset
Acute cervical lymphadenopathy
Polymorphic rash
Redness and oedema of palms and soles of feet 2-5 days after onset

124
Q

What is spared in polyarteritis nodosa

A

Pulmonary circulation

125
Q

What is characteristic of polyarteritis nodosa

A

Small aneurysms strung like beads of a rosary

126
Q

WHat is polyarteritis nodosa assosiated with

A

Chronic Hep B

127
Q

Incidence of contrast induced nephropathy in the general population

A

low, 1-6%

128
Q

Renal assosiations of turners syndrome

A

Renal artery stenosis
Increased renal cyst formation S
Single horse shoe kidney

129
Q

HOw to calculate the anion gap

A

(SODIUM + POTASSIUM) MINUS (BICARB + CHLORIDE)

130
Q

Normal anion gap

A

10-16

131
Q

Bone profile findings of a patient with CKD5

A

Low calcium
High phosphate
High PTH
High ALP

132
Q

What does ATN usualy arise following

A

An acute ischaemic or nephrotoxic event

133
Q

What is helpful in distingushing between pre kidney disease and ATN

A

Urine osmolality
- decreased in ATN, reflecting reduced tubal function and filtration rate. Urinary sodium > 40
- osmolality typically high in pre kidney disease in the context of poor UO and high creatinine. Urinary sodium <20

134
Q

Urine dipstick of ATN

A

Typically bland

135
Q

What do myoglobin casts indicate

A

Rhabdomyolysis

136
Q

Presentation of goodpastures disease

A

Rapidly progressive glomerulonephritis
Pulmonary haemorrhage

137
Q

What is the pathology of hypocalcaemia and secondary hyperparathyroidism in CKD

A

Diminished activity of renal 1-a-hydroxylase

138
Q

WHat will be present in 10% of membranous glomerulonephritis

A

Malignancy

139
Q

Causes of membranous nephropathy

A

Malignancy
Drugs (gold, penicillamine)
Autoimmune diseases (SLE)
Infections (hepatitis)

140
Q

Pathology of acute organ rejection

A

Mediated via T cell response

141
Q

Treatment of acute organ rejection

A

Anti-T cell monoclonal antibodies
Corticosteriods

142
Q

What is a common cause of renal impairment in a patient with gouty arthritis

A

Uric acid stones

143
Q

What is a common complication seen in up to 50% of CKD patients on haemodialysis

A

Protein-calorie malnutrition

144
Q

Features of gietleman syndrome

A

Hypochloraemia
Hypokalaemia
Hypomagnesia

Increased urinary sodium and potassium loss
NO HTN

Due to defects in the thiazide sensitive sodium chloride symporter

145
Q

Wat is released after tissue destruction/breakdown

A

Intracellular potassium

146
Q

Tubular dysfunction / ATN is assosiated with the presence of what within the urine

A

Casts

147
Q

What is suggestive of microscopic polyangitis

A

Neurological decline
Mononeuritis
Glomerulonephritis

148
Q

Antibody assosiation of microscopic polyangitis

A

p-ANCA

149
Q

How much IVF is likely to increase the intravascular volume

A

200ml

150
Q

Anion gap in RTA

A

NORMAL anion gap

151
Q
A