Renal disease Flashcards

1
Q

What are the types of lower tract UTI

A

Cystitis and Prostatitis

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2
Q

When should ramipril be started in patients with CKD

A

Patients with chronic kidney disease should be started on an ACE inhibitor if they have an ACR > 30 mg/mmol

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3
Q

What is fibromuscular dysplasia

A

Fibromuscular dysplasia describes the proliferation of cells in the walls of the arteries causing the vessels to bulge or narrow. This most commonly affects women. These patients are susceptible to AKI after the initiation of an ACE inhibitor. The classic description is ‘string of beads’ appearance.

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4
Q

Who should be referred for a urinary tract cancer

A

Visible haematuria in over 45s that either is not associated with a UTI or that persists after successful treatment of UTI should be referred urgently under the 2-week wait pathway. This is because visible haematuria can be a sign of bladder or renal cancer.

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5
Q

Compare and contrast pre-renal azotemia and acute tubuler necrosis.

A

Pre-renal uraemia (‘azotemia’) Acute tubular necrosis
Urine sodium < 20 mmol/L > 40 mmol/L
Urine osmolality > 500 mOsm/kg < 350 mOsm/kg
Fractional sodium excretion* < 1% > 1%
Response to fluid challenge Good Poor
Serum urea:creatinine ratio Raised Normal
Fractional urea excretion** < 35% >35%
Urine:plasma osmolality > 1.5 < 1.1
Urine:plasma urea > 10:1 < 8:1
Specific gravity > 1020 < 1010
Urine Normal/ ‘bland’ sediment Brown granular casts

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6
Q

What is a normal anion gap

A

A normal anion gap is 8-14 mmol/L

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7
Q

What is diagnostic of ADPKD

A

in patients with a positive family history, diagnosis is made by the visualisation of two cysts, unilateral or bilateral, if aged <30 years. If between 30-59 years of age, two cysts in both kidneys are the diagnostic criteria. If 60 or over, the diagnostic criteria are four cysts in both kidneys.

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8
Q

What symptoms might be seen with acute interstitial nephritis

A

Sterile pyuria and white cell casts in the setting of rash and fever should raise the suspicion of acute interstitial nephritis, which is commonly due to antibiotic therapy

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9
Q

At what level should an ACE inhibitor be discontinued in patients with ckd.

A

NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs).

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10
Q

How is HUS treated?

A

In most cases of haemolytic-uraemic syndrome, the mainstay of treatment is supportive, with fluids, blood transfusions and dialysis as required.

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11
Q

What is membranous nephropathy?

A

Membranous glomerulonephritis histology:
basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2

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12
Q

WHAT ARE THE CAUSES OF NORMAL ANION GAP ACIDOSIS?

A

Hyperchloraemia
Renal tubular acidosis
Addison’s disease
Diarrhoea

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13
Q

How is diabetic nephropathy investigated?

A

Screening
all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

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14
Q

Who should be referred for nephrology?

A

Refer to a nephrologist if:
g4 or g5 CKD
If ACR is above >70 and no diabetes
If ACR is >30 and haematuria
If eGFR decreases by 25% or remains at 15
not controlled by 4 antihypertensives
genetic or rare syndrome

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15
Q

Who should be prescribed ACE inhibitors with CKD?

A

Patients with ACR >3 with diabetes
>30 with hypertension
and any CKD more than 70

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16
Q

What are the complications of CKD?

A

Bone abnormalities
Anaemia
Restless legs
Oedema
CKD
Acidosis

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17
Q

What should be prescribed in CKD to manage the ‘BAROCA’ complication?

A

darbepoetin alfa injections i

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18
Q

How long for an AV fistula to form?

A

The time taken for an arteriovenous fistula to develop is 6 to 8 weeks

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19
Q

What is FSGS?

A

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

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

Focal segmental glomerulosclerosis is noted for having a high recurrence rate in renal transplants.

Investigations
renal biopsy
focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

Management
steroids +/- immunosuppressants

Prognosis
untreated FSGS has a < 10% chance of spontaneous remission

20
Q

What are the features of a nephritic syndrome?

A

haematuria, proteinuria/oedema, hypertension and oliguria

21
Q

How do you treat nephrogenic diabetes insipidus?

A

Chlorthiazide

22
Q

What should be monitored frequently with HSP?

A

Patients with active Henoch-Schonlein purpura: blood pressure and urinanalysis should be monitored to detect progressive renal involvement

23
Q

What does annual screening for diabetes nephropathy involve?

A

All diabetic patients require annual screening for albumin:creatinine ratio (ACR) in early morning specimens

24
Q

What medications are recommended in people with CKD?

A

NICE guidelines recommend prescribing an angiotensin converting enzyme (ACE) inhibitor to all patients with chronic kidney disease (CKD) who have a urinary ACR or 70mg/mmol or more. Lipid-lowering therapy with a statin is also recommended for all patients with CKD for the primary or secondary prevention of cardiovascular disease.

25
Q

What is a feature of acute tubular necrosis?

A

Acute tubular necrosis - urine sodium > 40 mmol/L

26
Q

What is interstitial nephritis?

A

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

Pathophysiology
histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

Features
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

27
Q

Why does nephrotic syndrome cause of hypercoagulable state?

A

antithrombin III via the kidneys

28
Q

How is Goodpasture’s managed?

A

Management
plasma exchange (plasmapheresis)
steroids
cyclophosphamide

29
Q

What are the causes of FSGS?

A

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

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

Focal segmental glomerulosclerosis is noted for having a high recurrence rate in renal transplants.

Investigations
renal biopsy
focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

Management
steroids +/- immunosuppressants

Prognosis
untreated FSGS has a < 10% chance of spontaneous remission

30
Q

What are the features of membranous nephropathy?

A

Membranous glomerulonephritis is the commonest type of glomerulonephritis in adults and is the third most common cause of end-stage renal failure (ESRF). It usually presents with nephrotic syndrome or proteinuria.

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

Causes
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

Management
all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB):
these have been shown to reduce proteinuria and improve prognosis
immunosuppression
as many patients spontaneously improve only patient with severe or progressive disease require immunosuppression
corticosteroids alone have not been shown to be effective. A combination of corticosteroid + another agent such as cyclophosphamide is often used
consider anticoagulation for high-risk patients

Prognosis - rule of thirds
one-third: spontaneous remission
one-third: remain proteinuric
one-third: develop ESRF

Good prognostic features include female sex, young age at presentation and asymptomatic proteinuria of a modest degree at the time of presentation.

31
Q

What is needed to make a diagnosis of rhabdomyolysis?

A

The creatinine kinase should be 5 times the baseline

32
Q

How should incomplete bladder emptying be managed with neurogenic bladder?

A

Self catheteritisation

33
Q

What can be used apart from resonium to remove potassium

A

Calcium polystyrene sulphonate

34
Q

What is HIVAN?

A

HIV associated nephropathy
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

35
Q

What are some causes of membranous nephropathy?

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

36
Q

What are the criteria for eGFR?

A

eGFR variables - CAGE - Creatinine, Age, Gender, Ethnicity

36
Q

What is the effect of too much sodium replacement?

A

Use of 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes = risk of hyperchloraemic metabolic acidosis

37
Q

What are some causes of FSGS?

A

Heroin
HIV
Lithium
Lymphoma

38
Q

What are the causes of membranous nepropathy?

A

Malignancy
Infection
Sarcoidosis
SLE
Hep B/C
Idiopathic
Gold / Penicillamine
Srojens

39
Q

What is pathogmonic of membranous nephropathy?

A

> 25% of adult nephrotic syndrome
Silver stain
subepithelial spikes
PLAR2

40
Q

How is membranous nephropathy treated?

A

ACE inhibition
Ponticelli method of immunosuppression

41
Q

How is FSGS?

A

ACE inhibition
Calcineurin inhibitor,
Corticosteroids

42
Q

What are the complications of nephrotic syndrome?

A

Hyperlipidemia
Infection
Thrombocytopenia

43
Q

What are the examples of glomerulonephritis?

A

IgA nephropathy
HSP
Post-streptococcal glomerulonephritis
Anti- GBM
Rapidly progressive GN

44
Q

What is Fabry disorder?

A

A lipid storage disorder X linked alpha galactosidase

45
Q

What is acute graft failure?

A

<6 months
Acute graft failure happens within months, is usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
Use steroids

46
Q

What is dialysis disequilibrium syndrome?

A

Dialysis disequilibrium syndrome is a rare complication and usually affects those who have recently started renal replacement therapy. It is caused by cerebral oedema, but the exact mechanism is unclear. Therefore this is a diagnosis of exclusion.