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Finals > Renal > Flashcards

Renal Flashcards

1
Q

When can an official diagnosis of an AKI be made ?

A
  • Rise in serum creatinine of 26 micromol/litre or greater within 48 hours
  • 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  • Fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
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2
Q

What are the pre renal causes of an AKI ?

A
  • Hypovolaemia secondary to D&V
  • HF
  • Renal artery stenosis
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3
Q

What are the intrinsic causes of AKI ?

A
  • Glomerulonephritis
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis (AIN)
  • Rhabdomyolysis
  • Tumour lysis syndrome
  • HUS
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4
Q

What are the postrenal causes of AKI?

A
  • Kidney stone in ureter or bladder
  • BPH
  • External compression of the ureter
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5
Q

what are the signs of an AKI?

A
  • Reduced urine output
  • Pulmonary and peripheral oedema
  • Rise in K+ = arrhythmias
  • Rise in urea / creatinine
  • Features of uraemia (pericarditis / encephalopathy)
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6
Q

RF for an AKI

A
  • CKD
  • Other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
  • History of AKI
  • Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACEI/ARBs within the past week
  • Use of iodinated contrast agents within the past week
  • AGge >=65 years
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7
Q

What is acute tubular necrosis and what can it be caused by ?

A
  • Most common cause of AKI
  • Necrosis of renal tubular epithelial cells
  • Caused by : ischaemia due to hypoperfusion or nephrotoxins
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8
Q

What will be seen on urinalysis in acute tubular necrosis ?

A

Muddy brown casts

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9
Q

What can cause acute interstitial nephritis ?

A
  • Drugs : acute interstitial nephritis accounts for 25% of drug-induced AKI
  • Systemic disease : SLE, sarcoidosis and Sjogrens
  • Infection : Hanta virus, staphylococci
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10
Q

What drugs can cause acute interstitial nephritis

A
  • Penicillin
  • Rifampicin
  • NSAIDs
  • Allopurinol
  • Furosemide
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11
Q

what will be seen on urinalysis in acute interstitial nephritis

A
  • Sterile pyuria
  • White cell casts
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12
Q

4 features of acute interstitial nephritis

A
  • Fever, rash, arthralgia
  • Eosinophilia
  • Mild renal impairment
  • HTN
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13
Q

what medications should be stopped in an AKI

A
  • NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
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14
Q

what is involved in the management of AKI

A
  • Careful fluid balance
  • Stop any nephrotoxic medications
  • Correction of hyperkalaemia if present
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15
Q

Give 5 causes of CKD

A
  • Diabetes
  • HTN
  • Polycystic kidney disease
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
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16
Q

what investigations are used to assess CKD

A
  • eGFR
  • Proteinuria quantified with urine albumin:creatinine ratio
  • Haematuria
  • Renal USS
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17
Q

How does nephrotic syndrome present ?

A
  • Oedema
  • Possible frothy urine due to the high protein content
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18
Q

How is CKD classified based on eGFR ?

A
  • 1 : Greater than 90 ml/min, with some sign of kidney damage on other tests
  • 2 : 60-90 ml/min with some sign of kidney damage
  • 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
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19
Q

How is CKD classified based on albumin:creatinine ration ?

A
  • A1 : <3mg/mmol
  • A2 : 3-30 mg/mol
  • A3 : >30mg/mol
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20
Q

what are the group of features seen in nephritic syndrome

A

-> Haematuria (blood in the urine), which can be microscopic (not visible) or macroscopic (visible)
-> Oliguria (significantly reduced urine output)
-> Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome)
-> Fluid retention

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21
Q

what is nephritis ?

A

Inflammation in the kidney

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22
Q

Primary causes of nephrotic syndrome

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis (FSGS),
  • Membranous nephropathy.
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23
Q

Most common type of inherited kidney disease

A
  • AD
  • PKD1 gene on chromosome 16 (85% of cases)
  • PKD2 gene on chromosome 4 (15% of cases)
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24
Q

What is nephrotic syndrome ?

A
  • The basement membrane of the glomerulus becomes highly permeable resulting in significant proteinuria
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25
Q

what are the group of features seen in nephrotic syndrome ?

A
  • Proteinuria (more than 3g per 24 hours)
  • Low serum albumin (less than 25g per litre)
  • Peripheral oedema
  • Hypercholesterolaemia
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26
Q

what is the eGFR based on ?

A
  • Serum creatinine
  • Age
  • Gender
  • Ethnicity
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27
Q

4 extra-renal manifestations of ADPKD

A
  • Cerebral aneurysms
  • Hepatic, splenic, pancreatic, ovarian and prostatic cysts
  • Mitral regurgitation
  • Colonic diverticula
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28
Q

6 complications of ADPKD

A
  • Chronic loin/flank pain
  • Hypertension
  • Gross haematuria can occur with cyst rupture (usually resolves within a few days)
  • Recurrent urinary tract infections
  • Renal stones
  • End-stage renal failure occurs at a mean age of 50 years
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29
Q

Presentation of ARKPD

A
  • Picked up on antenatal scans with oligohydramnios
  • Leads to pulmonary hypoplasia and resp failure shortly after birth
  • Dysmorphic features (underdeveloped ear cartilage, low set eats, flat nasal bridge)
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30
Q

Chromosome involved in ARPKD

A

mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6

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31
Q

what can be given to slow the development of cysts and progression of renal failure in ADPKD

A

Tolvaptan (vasopressin receptor antagonist)

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32
Q

Causes of hyperkalaemia

A

D : Drugs (ACEI, ARB, NSAID, aldosterone antagonist)
R : Renal failure
E : Endocrine (Addison’s)
A : Artefact
D : DKA / DI

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33
Q

what 5 conditions can cause hyperkalaemia

A

Acute kidney injury
Chronic kidney disease (stage 4 or 5)
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome

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34
Q

what ECG changes are seen in hyperkalaemia

A

Tall peaked T-waves
Flattening or absence of P waves
Prolonged PR interval
Broad QRS complexes

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35
Q

when do people require urgent treatment for hyperkalaemia

A

ECG changes
Serum potassium above 6.5 mmol/L

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36
Q

what is the treatment for hyperkalaemia

A
  • Insulin and dextrose infusion and IV calcium gluconate
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37
Q

what is rhabdomyolysis and 5 possible causes

A

-> Skeletal muscle breakdown

  1. Prolonged immobility
  2. Extreme rigorous exercise
  3. Crush injuries
  4. Seizures
  5. Statins
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38
Q

What chemicals are released from muscle in rhabdomyolysis and why is this dangerous

A

Myoglobin = AKI
Potassium = arrythmias / arrest
Phosphate
Creatine kinase

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39
Q

7 signs and symptoms of rhabdomyolysis

A

Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)

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40
Q

Diagnostic blood test for rhabdomyolysis

A

-> Creatinine kinase (CK) : remains elevated for 1-3 days

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41
Q

what will a urine dipstick show in rhabdomyolysis

A
  • Positive for blood due to presence of myoglobin (red-brown colour to urine)
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42
Q

Mainstay of treatment for rhabdomyolysis

A
  • IV fluids to correct hypovolaemia and filter breakdown products
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43
Q

what is HUS and the usual trigger ?

A
  • Thrombosis in small blood vessels
  • Triggered y shiga toxins for E.coli O157 or Shigella
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44
Q

Who does HUS usually affect and what increases the risk of it ?

A
  • Children following an episode of gastroenteritis
  • Abx and anti-motility medication (e.g. loiperamide)
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45
Q

what triad is seen in HUS ?

A
  • AKI
  • Thromboytopenia (formation of blood clots)
  • Microangiopathic haemolytic anaemia
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46
Q

what is the presentation of HUS ?

A
  • Diarrhoea from gastroenteritis, turns blood in 3 days
  • After a week, Sx of HUS develop :

Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

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47
Q

How is HUS managed

A

-> Medical emergency = admit and treat :

Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

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48
Q

Correction of hypokalaemia due to diarrhoea

A

IV sodium chloride with IV potassium chloride at 10mmol/hour

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49
Q

Secondary causes of nephrotic syndrome

A
  • DM
  • SLE
  • Amyloidosis
  • Infections (HIV, hepatitis B and C), - Drugs (NSAIDs, gold therapy).
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50
Q

Common presentation of amyloidosis

A
  • 50-65 yr old
  • Worsening SOB and weakness
  • Loss of renal function & proteinuria
  • Massive hepatosplenomegaly
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51
Q

Results in keeping with a diagnosis of acute tubular necrosis

A
  • Raised urinary sodium
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52
Q

What urea to creatinine ratio would suggest a pre renal cause of an AKI

A

Urea rise&raquo_space;» Creatinine rise

  • Urea : creatinine ratio of >100
  • In pre renal causes, blood flow to kidney is reduce and so kidneys reabsorb more water and solutes including urea
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53
Q

New onset chest pain on a background of CKD with raised urea

A

Pericarditis caused by uraemia

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54
Q

Treatment of encephalopathy (confusion) or pericarditis caused by uraemia

A

Haemodialysis

55
Q
  • Presents with allergic type reaction after commencing new medication
  • Fever, joint pains
  • Pruritic macular rash
  • AKI

Diagnosis and what will be seen on urinalysis

A

Acute interstitial nephritis
White cell casts

56
Q

How do u calculate an anion gap

A

(Sodium + potassium) - (bicarbonate + chloride)

57
Q

How is the anion gap used to classify metabolic acidosis

A
  1. Raised anion gap = DKA
  2. Normal = seen in pts with diarrhoea due to GI bicarb loss
58
Q

Management of anaemia due to CKD

A

Oral iron (if not on ESAs or haemodialysis)

59
Q

IF target Hb Levels in a pt with anaemia caused by CKD are not reached within 3 mnths of oral iron what should they be switched too ?

A

IV iron

60
Q

If a patient on ESAs or haemodialysis develop anaemia due to CKD what do they generally require

A

IV iron

61
Q

Screening test for adult ADPKD

A

Abdominal USS

62
Q

USS diagnostic criteria for ADPKD (In pts with a +ve family history)

A
  • Two cysts, unilateral or bilateral, if aged < 30 years
  • Two cysts in both kidneys if aged 30-59 years
  • Four cysts in both kidneys if aged > 60 years
63
Q

What are pts with ADPKD at risk of ?

A

Subarachnoid haemorrhage due to ruptured berry aneurysms

64
Q

what cardiac condition is ADPKD associated with

A

Mitral valve prolapse

65
Q

Most common cause of post operative oliguria

A

Hypovolaemia

66
Q

Management of poster operative oliguria if stab le and not clinically fluid overload

A

Fluid challenge = 500ml fluid bolus

67
Q

What can be seen on microscopic examination of urine in acute interstitial nephritis ?

A

Eosinophilic casts

68
Q

Investigation of AKI of unknown origin

A

Renal USS

69
Q

What is the exception to the rule of stopping NSAIDs in AKI

A

Aspirin at cardio-protective doses

70
Q

Stage 1 AKI

A
  • Increase in creatinine to 1.5-1.9 times baseline, or
  • Increase in creatinine by ≥26.5 µmol/L, or
  • Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
71
Q

Stage 2 AKI

A
  • Increase in creatinine to 2.0 to 2.9 times baseline, or
  • Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
72
Q

Stage 3 AKI

A
  • Increase in creatinine to ≥ 3.0 times baseline, or
  • Increase in creatinine to ≥353.6 µmol/L or
  • Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
  • The initiation of kidney replacement therapy, or,
  • In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
73
Q

What is the primary action of ADH

A
  • Acts on the kidney to increase the reabsorption of water
74
Q

Cranial DI

A

Decreased secretion of ADH from the pituitary

75
Q

Causes of cranial DI

A
  • Idiopathic
  • Post head injury
  • Pituitary surgery
  • Craniopharyngiomas
  • Infiltrative : histiocytosis X, sarcoidosis
  • DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
  • Haemochromatosis
76
Q

Nephrogenic DI

A

Insensitivity of the kidney to ADH

77
Q

Causes of nephrogenic DI

A
  • Genetic:
  • Electrolytes : hypercalcaemia, hypokalaemia
  • Lithium
  • Demeclocycline
  • Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
78
Q

Features of DI

A

Nocturia
Polyuria
Polydipsia

79
Q

Gold standard investigation for DI

A

Water deprivation test

80
Q

Investigation findings in DI

A

high plasma osmolality
low urine osmolality

81
Q

Management of nephrogenic DI

A

thiazides
low salt/protein diet

82
Q

Management of cranial DI

A

Desmopressin - vasopression V2 agonist

83
Q

Management of ascites in pts with chronic liver disease

A
  • Aldosterone antagonist = spironolactone
84
Q

Type of tubulointerstitial nephritis seen in young females

A

Tubulointerstitial nephritis with uveitis

Fever, weight loss, painful red eyes
Leukocytes and protein on urinalysis

85
Q

why does urinary sodium decrease in pre renal causes of AKI

A
  • The kidneys reabsorb more sodium in order to preserve volume
86
Q

U&E result suggest kidney disease is chronic and not acute

A

Hypocalcaemia

87
Q

First line management of pts with proteinuria that have CKD and coexistent HTN if the ACR >30mg/mmol

A

ACEI

88
Q

If max dose ACEI is not efficient in managing proteinuia in pts with CKD + ACR >30 what can be added

A

SGLT-2 inhibitor

89
Q

Direct complication of nephrotic syndrome

A

Increased VTE risk -> prophylactic LMWH required

90
Q

Cause of ABG showing metabolic acidosis (low HCO3, normal CO2) with a NORMAL anion gap and possible hypokalaemia

A

Diarrhoea

91
Q

what does vomiting show on an ABG

A
  • Metabolic alkalosis = loss of gastric secretions which are acidotic
  • Hypochloraemia, hypokalaemia
92
Q

Most common cause of nephrotic syndrome in adults and often associated with malignancy

A

Membranous nephropathy

93
Q

Renal biopsy in membranous nephropahty

A
  • Thickened basement membrane
  • Subepithelial electron dense deposist
94
Q

Management of membranous nephropathy

A
  • ACEI to reduce proteinuria
95
Q

Cause of metabolic acidosis with raised chloride

A

Large volume fluid resuscitation with 0.9% sodium chloride

96
Q

what would suggest the cause of AKI is intrinsic ?

A
  • Urea : creatinine ration of <100
  • No response to fluid challenge
97
Q

Common cause of nephrotic syndrome in pts with HIV

A

Focal segmental glomerulosclerosis

98
Q

Common presenting history causing tubular cell necrosis

A
  • Fall with prolonged lie
  • Rhabdomyolysis = myoglobinuria
  • Causes acute tubular cell necrosis
99
Q

what are pts who have had an organ transplant and are on long term immunosuppression at increased risk of ?

A
  • Skin cancer -> esp squamous cell carcinoma
100
Q

Signs of an under-filled fluid balance

A
  • Tachycardia
  • Hypotension
  • Oliguria
  • Sunken eyes and reduced skin turgor
101
Q

Pt presents >24hrs after paracetamol overdose + jaundice, hepatic tenderness or elevated ALT

A

Start acetylcysteine

102
Q

Pt presents 8-24 hrs after paracetamol overdose of more than 150mg/kg

A

Start acetycysteine

103
Q

When should acetylcysteine be given for paracetamol overdose

A
  • Plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
  • Staggered overdose or doubt over time of ingestion
104
Q

Presentation of renal adenocarcinoma

A
  • HTN and haematuria
  • Associated polycythamie a
  • Left renal mass
105
Q

Presentation of transitional cell carcinoma

A
  • Ureteric colic
  • Heematuria
  • Dilatation of renal pelvis but outline is irregular
106
Q

Presentation of nephroblastoma

A
  • 4 y/o
  • Haematuria
  • Renal mass

It is also known as Wilms tumours

107
Q

small vessel vasculitis causing pullmonary haemorrhage and glomerulonephritis

A

Granulomatosis with polyangitis = Anti-glomerular basement membrane disease (Goodpastures)

108
Q

Presentation of anti-glomerular basement membrane disease

A
  • Haemoptysis and SOB
  • Proteinuria and haematuria
109
Q

Antibodies seen in granulomatosis with polyangitis

A

ANCA
Anti-glomerular basement membrane

110
Q

Most common cause of glomerulonephritis world wide

A

IgA nephropathy

111
Q

Features of IgA nephropathy

A
  • Preceeding URTI
  • 3 days later -> frank haematuria, no or little protein.
112
Q

what is seen histologically in IgA nephropathy

A
  • Mesangial hypercellularity
  • Positibe immunofluoresecene for IgA and C3
113
Q

Treatment of IgA nephropathy if persistnent proteinuria

A

ACEI

114
Q

Presentation of Wilms’ nephroblastoma

A
  • Child <5
  • Painless haematuria
  • Abdominal mass
115
Q

Most common cause of peritonitis associated with peritoneal dialysis

A

Staphylococcus epidermis

116
Q

4 common causes of polyuria

A
  1. Lithium
  2. HF
  3. DM
  4. Diuretics, caffeine and alcohol
117
Q

what is seen on the bloods in post streptococcal glomerulonephritis

A
  • Low C3
  • Raised anti-streptolysin O titre confirms a recent strep infection
118
Q

How to reduce the risk of contrast induced nephropathy

A

IV 0.9% sodium chloride pre and post procedure

119
Q

Presentation of alport’s syndrome in a child

A

Microscopic haematuria
Progressive renal failure
Bilateral sensorineural hearing loss

120
Q

5 causes of metabolic acidosis with a normal anion gap (Hyperchloraemic metabolic acidosis)

A
  • GI bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
  • Renal tubular acidosis
  • Drugs: e.g. acetazolamide
  • Ammonium chloride injection
  • Addison’s disease
121
Q

4 causes of metabolic acidosis with a raised anion gap

A
  • Lactate: shock, hypoxia
  • Ketones: diabetic ketoacidosis, alcohol
  • Urate: renal failure
  • Acid poisoning: salicylates, methanol
122
Q

8 causes of metabolic alkalosis

A

Caused by either loss of H+ or gain of bicarbonate

  • Vomiting
  • Diuretics
  • Hypokalaemia
  • Primary hyperaldosteronism
  • Cushing’s syndrome
  • Bartter’s syndrome
  • Congenital adrenal hyperplasia
  • Liquorice, carbenoxolone
123
Q

3 causes of respiratory acidosis

A
  • COPD
  • Decompensatation of resp conditions : Asthma, pulmonary oedema
  • Sedative drugs : Opiate overdose, benzos
124
Q

6 causes of respiratory alkalosis

A
  • PE
  • Anxiety : Hyperventilation
  • CNS disorders : stroke, SAH, encephalitis
  • Altitude
  • Pregnancy
  • Salicylate poisoning
125
Q

how should diabetics be screened for diabetic nephropathy

A

annually using albumin:creatinine ratio (ACR)

126
Q

When should an ACEI be started for diabetic nephropathy

A

If urinary ACR is 3mg/mmol or more

126
Q

Management of diabetic nephropathy

A
  • Dietary protein restriction
  • Tight glycaemic control
  • BP control: aim for < 130/80 mmHg
  • ACEI
  • Control dyslipidaemia e.g. Statins
127
Q

4 presenting features of henoch-schonlein purpura

A
  • Palpable purpuric rash over buttock and extensor surface
  • Abdo pain
  • Polyarthritis
  • IgA nephropathy : haematuria, renal falure
128
Q

what should parents be educated on monitoring in HSP

A

BP and urinalysis for progressive renal involvmenet

129
Q

5 complications of nephrotic syndrome

A
  • Increased risk of VTE
  • Hyperlipidaemia
  • CKD
  • Increased risk of infection
  • Hypocalcaemia
130
Q

Presentation of post-streptococcal glomerulonephritis

A

Strep pyogenes infection 7-14 days prior

  • Visible haematuria
  • Headache, malaise
  • HTN
  • Oliguria
131
Q

5 causes of rhabdomyolysis

A
  • Seizure
  • Collapse/coma (e.g. elderly patient collapses at home, found 8 hours later)
  • Ecstasy
  • Crush injury
  • Drugs: statins (especially if co-prescribed with clarithromycin)
132
Q

Risk in creatining kinase required for diagnosis of rhabdomyolysis

A

5 times upper limit of normal

133
Q
A

Finals (92 decks)

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