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MRCP - Passmed > Renal > Flashcards

Renal Flashcards

1
Q

How can you prevent calcium stones?

A

This is caused by hypercalcuria hence you can:

  • High fluid intake
  • Add lemon juice to water
  • Avoid carbonated drinks
  • Limit salt intake
  • K citrate may be useful
  • Thiazide diuretics - increases distal tubular ca resorption ***
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2
Q

How can you prevent oxalate stones?

A

cholestyramine reduces urinary oxalate secretion

pyridoxine reduces urinary oxalate secretion

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3
Q

How can you reduce uric acid stones?

A

allopurinol

urinary alkalinization e.g. oral bicarbonate

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4
Q

podocyte fusion and effacement of the podocyte foot processes on renal biopsy

What diagnosis?
Mx?

A

Minimal change disease

mx- oral corticosteroids (80% of cases) -> cyclophosphamide in steroid resistant cases

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5
Q

What does focal segmental glomerulosclerosis cause?

A

cause of nephrotic syndrome and chronic kidney disease

typically presents in younger adults

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6
Q

What are some 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

Also high recurrence rate in renal transplants

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7
Q

What are the main extra-renal manifestations of ADPKD?

A

Liver cysts - 70% most common feature

Berry aneurysms - can rupture -> SAH

CVS - MV prolapse, M / T valve incompetence, aortic root dilatation, aortic dissection

Cysts in other organs - pancreas, spleen
Rarely - thyroid, oesophagus and ovary

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8
Q

In children presenting suspectingly for minimal change disease what is mx?

A

1st line oral pred

If steroid non-responsive, high suspicion of alternative diagnosis or declining renal func (on calcuerin inhibitor) -> renal biopsy

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9
Q

Which immunosuppression can cause tremor?

A

Tacrolimus

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10
Q

Which renal stones are radio-opaque?

A

Calcium oxalate

Mixed calcium oxalate / phosphate

Triple phosphate

Calcium phosphate

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11
Q

Which renal stones are radio-lucent?

A

Urate stones

Xanthine stones

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12
Q

Which renal stones are semi-opaque? what do they look like?

A

Cystine stones - ground glass appearance

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13
Q

Why do you get mineral bone disease in ckd?

A

Basic problems in chronic kidney disease (CKD):
> 1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low vitamin D
> the kidneys normally excrete phosphate → CKD leads to high phosphate

This, in turn, causes other problems:
> the high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
> low calcium: due to lack of vitamin D, high phosphate
> secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

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14
Q

How is mineral bone disease risk reduced in CKD?

A

The aim is to reduce PO4 and PTH levels.

reduced dietary intake of phosphate is the first-line management

phosphate binders

vitamin D: alfacalcidol, calcitriol

parathyroidectomy may be needed in some cases

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15
Q

MoA of Spironolactone?

A

Aldosterone antagonist: acts on the cortical collecting ducts as a diuretic via inhibition of mineralocorticoid receptor

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16
Q

What is the most common type of glomerulonephritis in adults? how does this present / biopsy

A

Membranous glomerulonephritis - third most common cause of ESRF

Nephrotic syndrome / proteinuria

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17
Q

What are the 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

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18
Q

Young female, hypertension and asymmetric kidneys → what diagnosis?

A

Fibromuscular dysplasia

HTN is secondary to renal artery stenosis (this is the 2nd most common cause after renal vascular disease)

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19
Q

Why does lithium cause DI?

A

Causes nephrogenic DI - densitises kidneys ability to respond to ADH in collecting ducts

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20
Q

Features of Goodpasture syndrome?

A

Goodpastures syndrome = Anti-GBM disease - small vessel vasculitis associated with:

pulmonary haemorrhage

rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria

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21
Q

Ix findings in Goodpastures syndrome?

A

renal biopsy: linear IgG deposits along the basement membrane

raised transfer factor secondary to pulmonary haemorrhages

Anti-GBM antibodies

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22
Q

Main mx for rhabdomyolysis?

A

IV fluids

Urinary alkalinization used sometiems

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23
Q

Which drugs to stop in AKI?

A

DAMN

D diuretics
A ace/ arbs + aminoglycosides (eg gent)
M metformin
N nsaids except aspirin at low dose 75mg

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24
Q

What are some adverse effects associated with aldosterone antagonists? how can you reduce this risk?

A

Hyperkalaemia

Gynaecomastia - less common with eplerenone (more selective with less afinity for androgen receptors)

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25
Q
A
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26
Q

Which medication can be used in ADPKD and when?

A

Tolvaptan (Vasopression receptor 2 antagonist) - slows progression of cyst development + renal insufficiency to be used if:
> CKD 2 /3 at start of tx
> Evidence of rapidly progressive disease
> + company provides it with discount agreed in patient access scheme

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27
Q

In hyperkalaemia which medications can be used to remove K from the body?

A

Calcium resonium (oral / enema) -> enema more effective than oral as K is secreted by rectum

Loop diuretics

Dialysis - considered in patients w AKI and persistent hyperkalaemia

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28
Q

What are the indications for renal replacement therapy in AKI?

A

The following if refractory to medical mx:
1. Hyperkalaemia
2. Met acidosis
3. Sx or complications of uraemia - pericarditis / encephalopathy
4. severe pulmonary oedema

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29
Q

Screening test for ADPKD?

A

USS Urinary system

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30
Q

clinically is characterized by fever, deranged transaminases, leukopenia and thrombocytopenia

Important to consider in those with renal transplant recipients

Diagnosis? Ix? Mx?

A

CMV infection

Ix - Viral PCR
Mx - Ganciclovir

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31
Q

Which condition can cause AKI following initiation of ACEi

Younger females?
Older patients?

A

Younger females - Fibromuscular dysplasia

Older - Atherosclerosis of renal arteries

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32
Q

What are the biopsy findings in Amyloidosis?

A

Congo red stain shows apple-green birefringence under polarised light

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33
Q

What are the features of acute interstitial nephritis?

What is a common cause?

A

Sterile pyuria and white cell casts in the setting of rash and fever is suggestive of acute interstitial nephritis - also eosinophilia

Commonly due to abx therapy (penicillins , rifampicin, NSAIDs, allopurinol, furosemide)

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34
Q

What blood results should have you considering rhabdomyolysis?

A

Lactic acidosis
Hyperkalaemia
+ features of ATN

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35
Q

What are the features of HIV-associated nephropathy (HIVAN)

A

There are five key features of HIVAN:
> massive proteinuria resulting in nephrotic syndrome
> normal or large kidneys
> focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
> elevated urea and creatinine
> normotension

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36
Q

Alport syndrome - inheritance?

A

X-linked dominant

Man like alport is dominant in the air, got that x factor

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37
Q

What is Calciphylaxis? when is it seen? what increases risk of this?

A

Rare complication of ESRF -> deposition of ca in arterioles -> microvascular occlusion + necrosis of tissue hence presenting with painful necrotic skin leisons

Risk is seen with:
Hypercalaemia, hyperphosphataemia + hyperparathyroidism

Warfarin can cause / exacerbate in high risk patients

tx involves reducing levels of this and controlling hyperparathyroidism + avoiding contributing drugs

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38
Q

HLA matching for renal transplants which are the most important HLA antigens?

A

when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A

DR Berry Aneurysm

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39
Q

Indications for use of spironoloactone?

A

ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used

hypertension: used in some patients as a NICE ‘step 4’ treatment

heart failure - NYHA III + IV already on ACEi (reduces all cause mortality)

nephrotic syndrome
Conn’s syndrome

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40
Q

Most common cause of peritonitis secondary to peritoneal dialysis?

A

Coagulase -ve staph eg staph epidermis (also staph aureus)

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41
Q

What murmur is associated with mitral valve prolapse?

A

late systolic murmur accompanied by a mid-systolic click

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42
Q

What are some possible complications of nephrotic syndrome?

A

> Increased VTE risk due to loss of antithrombin III and plasminogen - DVT, PE or renal vein thrombosis -> sudden decline in renal func.
hyperlipidaemia - increased risk of ACS + Strokes
CKD
Increased risk of infection due to Ig loss
Hypocalcaemia secondary to Vit D and binding protein loss

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43
Q

What electrolyte changes cause nephrogenic DI?

A

Hypercalcaemia

Hypokalaemia

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44
Q

RFs for urothelial (transitional cell) caricinoma of bladder?

A

Smoking

Aniline dyes

Rubber manufacturing

Cyclophosphamide

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45
Q

RFs for SCC of bladder?

A

Smoking

Schistosomiasis

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46
Q

History of chronic sinusitis, haemoptysis + microscopic haematuria + raised IFMs

cANCA +ve

What is the diagnosis? what kidney disease does this cause? renal biopsy shows what?

A

Granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis

Causes rapidly progressive glomerulonephritis - cresenteric glomerulonephritis

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47
Q

How can you distinguish between prerenal uraemia and ATN?

A

Urinary sodium:
- Prerenal uraemia -> kidneys respond to reduced perfusion by conserving Na hence low urinary Na
- ATN -> kidneys can’t reabsorb Na hence high urinary Na

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48
Q

When does PSGN and IgA nephropathy develop ?

A

PSGN develops 1-2 weeks after URTI.

IgA nephropathy develops 1-2 days after URTI

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49
Q

What are some 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

50
Q

Glomeruli with epithelial crescents are suggestive of?

A

Rapidly progressive glomerulonephritis

51
Q

Rapidly progressive glomerulonephritis with upper respiratory signs is suggestive of which dx? ab?

A

Granulomatosis with polyangiitis

cANCA ab

52
Q

Mx of choice for HIV associated nephropathy?

A

Anti-retroviral therapy

53
Q

How to distinguish between typical and atypical HUS?

A

typical caused by Ecoli - shiga toxin

atypical isn’t caused by this usually complement dysregulation - can be normal though

54
Q

Definition of AKI?

A

a rise in serum creatinine of 26 micromol/litre or greater within 48 hours

a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days

a fall in urine output to less than 0.5 ml/kg/hour (1/2 their weight) for more than 6 hours in adults and more than

55
Q

How long does it take for AV fistula to develop?

A

6-8 weeks

56
Q

How long before effects of Finasteride for BPH can be seen?

A

6 months

a1 agonists work much faster

57
Q

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

Is suggestive of which type of kidney damage?

A

Acute interstitial nephritis

58
Q

What is Fanconi syndrome? What happens in it?

A

Fanconi syndrome is a reabsorptive defect in PCT

This leads to increased excretion of nearly all amino acids, glucose, bicarbonate and phosphate (T2 Proximal RTA)

59
Q

In a patient with hypercalciuria and renal stones, calcium excretion and stone formation

can be decreased by the use of what? eg?

A

Thiazide diuretics eg indapamide

Potassium citrate can also be useful

60
Q

Prevention of oxalate stones?

A

cholestyramine reduces urinary oxalate secretion

pyridoxine reduces urinary oxalate secretion

61
Q

Prevention of Urate stones?

A

allopurinol

urinary alkalinization e.g. oral bicarbonate

62
Q

Respiratory issues + some / all of: HTN, HyperCa and haematuria is suggestive of what?

A

Renal cell carcinoma

can metastasise to lungs

63
Q

What are the different classess of SLE related renal disease?

A

WHO classification
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis

Class IV - most common and severe version

64
Q

Young, recurrent UTIs and CKD

What is the likely underlying cause? ix?

A

Reflux nephropathy

Ix - Micturating cystography, DMSA scan to check for renal scarring

65
Q

Grading of VUR?

A

I Reflux into the ureter only, no dilatation

II Reflux into the renal pelvis on micturition, no dilatation

III Mild/moderate dilatation of the ureter, renal pelvis and calyces

IV Dilation of the renal pelvis and calyces with moderate ureteral tortuosity

V Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

66
Q

Anion gap in RTA?

A

Normal

67
Q

Epididymo-orchitis abx of choice?

A

IM ceftriaxone stat + oral doxycycline for 2 weeks

68
Q

Causes of raised anion gap met acidosis?

A

lactate:
shock
sepsis
hypoxia

ketones:
diabetic ketoacidosis
alcohol

urate: renal failure

acid poisoning: salicylates, methanol

69
Q

bicalutamide MoA?

A

non-steroidal anti-androgen

blocks the androgen receptor

70
Q

Factors that increase the risk of pulmonary haemorrhage in Goodpastures syndrome (Anti-GBM disease)?

A

smoking

lower respiratory tract infection

pulmonary oedema

inhalation of hydrocarbons

young males

71
Q

Why do patients with chronic kidney disease have a raised phosphate level?

A

Decreased renal excretion

72
Q

What is thin basement membrane disease?

A

Inherited disorder of type IV collagen

Diagnosis based on persistent haematuria, normal kidney function and fhx of haematuria w/out kidney failure

73
Q

haemoptysis + AKI/proteinuria/haematuria

What disorder?

A

Anti-GBM disease

74
Q

Modification of Diet in Renal Disease (MDRD) equation is a widely used formula to estimate the glomerular filtration rate (eGFR) in patients with chronic kidney disease

What variables does it use?

What factors can affect the results?

A

CAGE - Creatinine, Age, Gender, Ethnicity

Factors which may affect the result
> pregnancy
> muscle mass (e.g. amputees, body-builders)
> eating red meat 12 hours prior to the sample being taken

75
Q

ABG abnormality in excess 0.9% NaCL use?

A

Hyperchloraemic metabolic acidosis

76
Q

Contrast-induced nephropathy

time frame?

A

Occurs 2 -5 days after administration

77
Q

Which tumour marker is raised in testicular seminomas?

A

hCG

78
Q

Causes of nephrogenic DI?

A

Genetic

Electrolytes - hypercalcaemia, hypokalaemia

Lithium

Demeclocycline

tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

79
Q

Disorders associated with glomerulonephritis and low serum complement levels?

A

post-streptococcal glomerulonephritis
subacute bacterial endocarditis
systemic lupus erythematosus
mesangiocapillary glomerulonephritis

80
Q

What is the most likely outcome following the diagnosis of minimal change nephropathy in a 10-year-old male?

A

Full recovery but 2/3 have relapses - 1/3 frquent and 1/3 infrequent

81
Q

CKD proteinuria ix?

A

Spot ACR sample

the NICE guidelines state ‘regard a confirmed ACR of 3 mg/mmol or more as clinically important proteinuria’

‘if the initial ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested.’

82
Q

NICE recommendations for referral to a nephrologist for proteinuria when?

A

a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated

a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection

consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease

83
Q

Subendothelial and mesangial immune deposits resulting in a ‘tram-track’ appearance

renal biopsy findings - dx?

A

T1 membranoproliferative glomerulonephritis

84
Q

focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy

Seen in what dx?

A

HIV nephropathy

84
Q

Thickened basement membrane with subepithelial electron-dense deposits creating a ‘spike and dome’ appearance

dx?

A

membranous glomerulonephritis

85
Q

Common causes of chronic kidney disease?

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease

86
Q

Most likely cause of death in CKD with haemodialysis?

A

most likely cause of death is IHD

87
Q

Diffuse proliferative glomerulonephritis - presentation?

A

classical post-streptococcal glomerulonephritis in child

presents as nephritic syndrome / acute kidney injury

most common form of renal disease in SLE

88
Q

Membranoproliferative glomerulonephritis (mesangiocapillary)

types?

A

type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy

89
Q

Benign prostatic hyperplasia - ethnicity?

A

Black > white > asian

90
Q

GnRH agonists - what should be given alongside when used in mx of prostate ca?

A

Lead to lower LH levels long term by causing overstimulation -> -ve feedback

initially causes rise in testosterone which can lead to tumour flare

Hence need anti-androgen therapy in meanwhile eg cyproterone acetate

91
Q

Stages of diabetic nephropathy?

A

5 stages - this is for T1DM, T2DM is same but can progress to later stages quicker

1 - hyperfiltration (rise in GFR) ?reversible
2 - silent / latent - most dont develop microalbuminuria for 10 y - can see persistent rise in GFR
3 - incipient nephropathy - microalbuminuria - dipstick -ve
4 - overt neprhropathy - persistne proteinuria >300 albumin and dipstick +ve, HTN in most
Histology: diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
5 - ESRD <10 GFR, RRT needed

92
Q

Which organ can be dysfunctioning in RCC?

A

paraneoplastic hepatic dysfunction syndrome
(Stauffer syndrom)e
- a paraneoplastic disorder associated with renal cell cancer
- typically presents as cholestasis/hepatosplenomegaly
- it is thought to be secondary to increased levels of IL-6

93
Q

What endocrine effects can RCC have?

A

may secrete erythropoietin (polycythaemia)
parathyroid hormone-related protein (hypercalcaemia), renin
ACTH

94
Q

Features and associations of retroperitoneal fibrosis?

A

Lower back/flank pain is the most common presenting feature. Fever and lower limb oedema is also seen in some patients.

Associations
- Riedel’s thyroiditis
- previous radiotherapy
- sarcoidosis
- inflammatory abdominal aortic aneurysm
- drugs: methysergide

95
Q

SLE kidney disease mx in pregnancy

A

Azathioprine

However if this doesnt work consider Ciclosporin but associated w premature delivery and LBW

96
Q

Which BPH med reduces PSA levels?

A

Finasteride

97
Q

What can increase PSA?

A

Prostate ca
benign prostatic hyperplasia (BPH)
prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 6 weeks after treatment)

ejaculation (ideally not in the previous 48 hours)
vigorous exercise (ideally not in the previous 48 hours)

urinary retention
instrumentation of the urinary tract

98
Q

Ix of renal artery stenosis?

A

MR angiography

99
Q

How to distinguish between ATN and acute interstitial nephritis?

A

Urine dip - ATN = proteinuria minimal haematuria

Nephritis = haematuria

100
Q

Mx of HUS?

A

Largely supportive - Fluids, blood transfusion and dialysis if required

No ABX

Plasma exchange in rare cases - more often if not associated w diarrhoea + severe HUS

Eculizumab C5 inh MAb - better than plasma exchange in adult atypical HUS

101
Q

The cyanide-nitroprusside test - when is it +ve

A

The cyanide-nitroprusside test +ve = Homocystinuria + cystinuria

Differentiation = renal stones in latter

102
Q

Causes of normal anion gap met acidosis?

A

GI bicarb loss - prolonged diarrhoea, ureterosigmoidoscopy, fistula

RTA

Drugs eg acetazolamide

Ammonium chloride injections

Addisons

103
Q

Light microscopy renal biopsy:
Mesangium: normal, with no hypercellularity. The capillary walls are thickened. Subepithelial deposits are seen. (‘spike and dome’ appearance)

Suggestive of ? mx?

A

Membranous glomerulonephritis

Mx = ACEi / ARB -> improves prognosis and reduces proteinuria

104
Q

RFs for renal stones?

A

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

105
Q

RFs for urate stones?

A

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

106
Q

drugs that promote calcium stones?

A

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

107
Q

Hepcidin in CKD?

A

CKD -> raised hepcidin due to reduced renall clearance

Hepcidin -> preventing iron absorption by blocking the action of ferroportin, a transmembrane protein that maintains iron homeostasis hence reduced iron absorption

108
Q

RFs for contrast nephropathy?prevention?

A

known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs

prevent with 1ml/kg/hr for 12hr pre + post procedure + hold metformin 48h before due to risk of lac acidosis

109
Q

Requirements for maintainence fluids per 24h?

A

Sodium - 1mmol/kg
Potassium - 1 mmol/kg
Water - 30ml/Kg
Glucose - 50-100g

110
Q

Prognosis in IgA nephropathy?

A

markers of good prognosis: frank haematuria

markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

25% develop ESRF

111
Q

Complications of plasma exchange?

A

hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system

metabolic alkalosis

removal of systemic medications

coagulation factor depletion

immunoglobulin depletion

112
Q

Histology in IgA nephropathy?

A

mesangial hypercellularity, positive immunofluorescence for IgA & C3

113
Q

urpuric rash on the extensor surfaces of his lower legs. He also has a history of abdominal pain and an urticarial rash

Urine dip ++ blood

dx? renal biopsy?

A

HSP aka IgA vasculitis -> mesangial hypercellularity due to the deposition of IgA immune complexes within the mesangium.

114
Q

PLEX indications?

A

Guillain-Barre syndrome
myasthenia gravis
Goodpasture’s syndrome
ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
TTP/HUS
cryoglobulinaemia
hyperviscosity syndrome e.g. secondary to myeloma

115
Q

When is AA and AL amyloidosis seen?

A

AL - more common - L = light chain seen with myeloma, MGUS + Waldenstroms

AA - A = acute phase reactant - seen in chronic infection / inflammation

116
Q

eGFR and CKD stage?

A

1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)

2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)

3a 45-59 ml/min, a moderate reduction in kidney function

3b 30-44 ml/min, a moderate reduction in kidney function

4 15-29 ml/min, a severe reduction in kidney function

5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

117
Q

(patients classically have a loss of subcutaneous tissue from their face),

Condition? renal issue?

A

Partial lipodystrophy

Renal - Membranoproliferative glomerulonephritis T2

118
Q

Alcohol bingeing effect on kidneys?

A

ADH suppression in the posterior pituitary gland subsequently leading to polyuria

+ raised urinary sodium and reduced urinary osmolality

119
Q
A

MRCP - Passmed (17 decks)

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