Nephrology - Passmedicine Flashcards
1
Q
How do you calculate an anion gap?
A
(Na + K) - (bicarb + Cl)
2
Q
What is considered a normal anion gap?
A
8-14mmol/L
3
Q
What are the two types of metabolic acidosis?
A
Normal anion gap (aka. hyperchloraemia) metabolic acidosis
Raised anion gap metabolic acidosis
4
Q
List causes of a normal anion gap (aka. hyperchloraemia) metabolic acidosis
A
GI bicarbonate loss - diarrhoea, ureterosigmoidostomy, fistula Renal tubular acidosis Drugs, e.g. acetazolamide Ammonium chloride injection Addison's disease
5
Q
List causes of a raised anion gap metabolic acidosis
A
Lactate: shock, hypoxia Ketones: DKA, alcohol Urate: renal failure Acid poisoning: salicyclates, methanol 5-oxoproline: chronic paracetamol use
6
Q
What is the anion gap?
A
Measure of the difference between cations and anions
7
Q
If the serum is neutral in charge why does an anion gap exist?
A
We are only measuring 4 ions to calculate it (there are a lot of significant anions not included, e.g. phosphate, negatively charged plasma proteins e.g. albumin)
8
Q
What does a high anion gap mean?
A
The negatively charged ions and proteins (not accounted for) are taking up a larger proportion of the serums negative charge than usual
9
Q
What causes a high anion gap?
A
Increased organic acid in the blood, e.g. lactate anions
10
Q
Explain why there is an increased anion gap in lactic acidosis
A
Lactic acid breaks down into lactate and H+, H+ is buffered by bicarb so there is less bicarb and more of the negative proportion of the serum being made up by lactate so the anion gap is increased
11
Q
What essentially causes a normal anion gap?
A
Bicarbonate loss
Kidneys compensate by reabsorbing more Cl keeping serum electroneutral
12
Q
What is the most common cause of bicarbonate loss causing normal anion gap?
A
Diarrhoea
Then renal tubular acidosis
13
Q
Does vomiting cause a metabolic acidosis?
A
Usually no
You are losing H+ ions in gastric acid
14
Q
Define acute interstitial nephritis
A
Pattern of kidney inflammation localised to the kidney tubulo-interstitial space
15
Q
What tends to trigger acute interstitial nephritis?
A
Medications, esp. antibiotics
16
Q
What antibiotics commonly cause acute interstitial nephritis?
A
Penicillin Rifampicin NSAIDs Allopurinol Furosemide
17
Q
What are causes of acute interstitial nephritis other than medications?
A
Systemic conditions - SLE, sarcoidosis, Sjogrens
Infections: Hanta virus, staphylococcus
18
Q
What do you see on histology in acute interstitial nephritis?
A
Marked interstitial oedema and interstitial infiltrates in the connective tissue between renal tubules
19
Q
What are the clinical features of acute interstitial nephritis?
A
Fever, rash, arthalgia
Eosinophilia
Mild renal impairment
HTN
20
Q
What can you see on investigation in acute interstitial nephritis?
A
Sterile pyuria
White cell casts
Raised urea and Cr
21
Q
Who does tubulointerstitial nephritis with uveitis tend to affect?
A
Young females
22
Q
What are features of tubulointerstitial nephritis with uveitis?
A
Fever
Wt loss
Painful, red eye
Urinalysis shows leukocytes + protein
23
Q
How do you manage acute interstitial nephritis?
A
Usually managed by stopping the offending medication
24
Q
What is the most common cause of a nephrotic syndrome in children/young people?
A
Minimal change disease
25
What causes the majority of cases of minimal change disease? What are other causes?
Idiopathic mostly
Drugs: NSAIDs, rifampicin
Hogdkin's lymphoma, thymoma
Infectious mononucleosis
26
What is the pathophysiology of minimal change disease?
T-cell + cytokine mediated damage to the glomerular basement membrane --> polyanion loss
Resultant reaction of electrostatic charge --> increased glomerular permeability to albumin
27
What are the features of minimal change disease?
Nephrotic syndrome
Normotension usually
Highly selective proteinuria (only medium sized proteins (e.g. albumin and transferrin) leak
28
What investigation will confirm a diagnosis of minimal change disease?
Renal biopsy
29
What will you see on electron microscopy of the renal biopsy in minimal change disease?
Fusion of podocytes + effacement of foot processes
30
How is minimal change disease managed?
80% corticosteroid responsive
| If steroid resistant --> cyclophosphamide
31
What is the prognosis of minimal change disease?
1/3rd --> 1 episode
1/3rd --> infrequent relapses
1/3rd --> frequent relapses which stop before adulthood
32
What is a nephrotic syndrome?
Damage to glomeruli allows leakage of proteins into urine --> proteinuria
Albumin leaving blood --> hypoalbuminaemia --> low oncotic pressure --> oedema
Unknown process --> hyperlipidaemia (which can also leak into urine)
33
What are the 4 hallmarks of nephrotic syndrome?
Proteinuria
Hypoalbuminaemia
Oedema
Hyperlipidaemia/lipiduria
34
What are the 3 layers of the glomerulus?
Endothelial cells (which line capillaries), basement membrane, podocytes
35
What are podocytes named podocytes?
They have foot like processes
36
How are the podocytes charged?
Negatively - helps them repel plasma proteins (e.g. albumin) and therefore podocytes act as a charge barrier
37
What happens in minimal change disease that means that proteins can leak into bowen's capsule?
T-cells release cytokines which specifically damage the foot processes of podocytes making them flatten out (effacement) --> reduced charge barrier and albumin can slip into nephron
NB larger proteins, e.g. Ig aren't allowed through
38
What technique do you need to see foot effacement in minimal change disease?
Electron microscopy
39
What is acute tubular necrosis?
Ischaemic/nephrotoxic injury to the kidney which leads to cell death
40
What area is most prone to AKI and why?
Renal medulla (it is relatively hypoxic making it prone to renal tubular hypoxia)
41
What is the best indicator of renal function?
eGFR
42
What parameters are required to estimate eGFR?
Serum creatinine, age, race, gender, body size
43
What sort of things may cause an AKI?
Nephrotoxic stimuli, e.g. aminoglycosides, contrasts --> apoptosis
Myoglobulinuria (e.g. after compartment syndrome) + haemolysis --> necrosis
44
What patients are more likely to be affected by post-op renal failure?
Early pts, with PVD, high BMI, COPD, on vasopressors or nephrotoxic medications
45
Avoiding hypertension/hypotension will reduce the risk of renal tubular damage
Hypotension
46
What is a typical history of acute tubular necrosis?
Worsening renal function
| Muddy brown casts
47
What are the three types of AKI?
Prerenal - cause before kidneys
Intrarenal - cause within kidneys
Post-renal - cause after kidneys
48
When is rhabdomyolysis typically seen?
After a fall or prolonged epileptic seizure
| May be in those who have AKI on admission
49
What are features of rhabdomyolysis?
```
AKI with disproportionately raised creatinine
Elevated CK
Myoglobulinuria
Hypocalcaemia
Elevated phosphate
Hyperkalaemia
Metabolic acidosis
```
50
Why do you get hypocalcaemia in rhabdomyolysis?
Myoglobin binds calcium
51
Why do you get elevated phosphate in rhabdomyolysis?
As it is released from myocytes
52
Why do you get hyperkalaemia in rhabdomyolysis?
Secondary to renal failure
53
What can cause rhabdomyolysis?
```
Seizure
Collapse/coma
Ectasy
Crush injury
McArdle's syndrome
Drugs - statins, esp. if co-prescribed with clarithromycin
```
54
How is rhabdomyolysis managed?
```
IV fluids (normal saline) to maintain good urine output
Urinary alkalinization is sometimes used
```
55
What is used as a diagnostic criteria in rhabdomyolysis?
CK >5x normal
56
How is Alport's syndrome inherited?
X linked dominant
57
What genetic defect causes Alport's syndrome?
Defect in gene which codes for IV collagen --> abnormal glomerular basement membrane
58
When does Alport's syndrome tend to present?
Childhood
59
What are features of Alport's syndrome?
```
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus
Retinitis pigmentosa
```
60
What is lenticonus?
Protrusion of the lens into the anterior chamber
61
What do you see on renal biopsy in Alport's syndrome?
Splitting of the lamina dense on electron microscopy (basket weave appearance)
62
How is Alport's syndrome diagnosed?
Molecular genetic testing
| Renal biopsy
63
At what K level should you give calcium gluconate etc. to treat hyperkalaemia?
>6.5 OR ECG changes
64
What biochemical pattern is more characteristic of dehydration as opposed to AKI?
Raised urea and cr but urea is proportionately more raised
| Hypernatraemia
65
Is eGFR more inaccurate in high or low muscle mass?
Both - it is most inaccurate at extremes of muscle mass
66
What are causes of transient non-visible haematuria?
UTI
Menstruation
Vigorous exercise
Sexual intercourse
67
What are causes of persistent non-visible haematuria?
```
Cancer (renal, bladder, prostate)
Stones
BPH
Prostatitis
Urethritis
Renal causes - e.g. IgA nephropathy
```
68
What things may mimic haematuria but no blood is actually in the urine?
Foods - beetroot, rhubard
| Drugs - rifampicin, doxorubicin
69
What is the test of choice for haematuria?
Urine dipstick
70
Define persistent non-visible haematuria
Blood in 2/3 samples tested 2-3 weeks apart
71
Which patients with haematuria should be urgently referred (within 2 weeks)?
Age >=45 AND unexplained visible haematuria in absence of UTI or visible haematuria that persists/recurs after treatment of UTI
Age >= 60 AND unexplained non-visible haematuria and either dysuria or raised WCC on blood test
72
Which patients with haematuria merit a non-urgent referal?
Age >=60 with recurrent or persistent unexplained UTI
73
Do patients under 40 with haematuria, with normal renal function, who are normotensive and have no proteinuria need to be referred?
No - they can be managed in primary care
74
Which test is most useful in distinguishing between acute tubular necrosis and prerenal uraemia?
Urinary sodium
75
What age group is HUS typically seen in?
Young chlidren
76
What are the triad of features of HUS?
AKI
Microangiopathic haemolytic anaemia
Thrombocytopenia
77
What classically causes HUS?
Shiga toxin producing E. coli 0157 (90% cases)
78
What other things can cause HUS?
Pneumococcal infection
HIV
Rare: SLE, drugs, cancer
79
What investigations should be done in suspected HUS?
FBC
UE
Stool culture
Severe cases - plasma exchange may be req.
Eculizumab
80
How is HUS managed?
Supportively, e.g. fluids, transfusion, dialysis
NO ANTIBIOTICS
81
What are the commonest causes of polyuria?
Diuretics, caffeine, alcohol
DM
Lithium
Heart failure
82
What are some infrequent causes of polyuria?
Hypercalcaemia
| Hyperthyroidism
83
What are some rare causes of polyuria?
Chronic renal failure
Primary polydipsia
Hypokalaemia
84
What is a very rare cause of polydipsia?
Diabetes inspidius
85
What is Henoch-Schonlein prupura?
An IgA mediated small vessel vasculitis
86
What condition does HSP overlap with?
Berger's disease
87
When is HSP most commonly seen?
Following an infection in children
88
What are the features of HSP?
Palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
Ab pain
Polyarthritis
Features of IgA nephropathy may occur, e.g. haematuria, renal failure
89
How is HSP treated?
Analgesia
| Nephropathy usually treated supportively
90
What is the prognosis of HSP?
Usually self limiting
| 1/3rd relapse
91
What are the two disease loci for ADPKD?
PKD1 and PKD2 which code for polycystin 1 and 2
92
How many types of ADPKD are there?
2
93
What is the best screening for relatives of ADPKD?
Abdominal US
94
What is the ultrasound diagnostic criteria for ADPKD in those with +ve FH?
2 cysts (uni/bilateral) if <30
2 cysts in both kidneys if 30-59
4 cysts in both kidneys if >60
95
What drug may be used in ADPKD and what patients can use it?
Tolvaptan (vasopressin receptor 2 antagonist)
Only used in adults to slow the rate of cyst development if they have CKD 2/3 at the start of treatment, there is evidence of rapidly progressive disease
96
How much glucose should nil by mouth patients be given per day to avoid starvation ketosis?
50-100g/day of glucose
97
What is diabetes inspidus?
Deficiency of ADH (cranial DI) or insensitivity to antiduretic hormone (nephrogenic DI)
98
What are causes of cranial DI?
```
Idiopathic
Post head injury
Pituitary surgery
Craniopharyngiomas
Histocystosis X
Wolfram's syndrome
Haemochromatosis
```
99
What are the features of Wolfram's syndrome?
DIDMOAD - cranial DI, DM, optic atrophy, deafness
100
What are causes of nephrogenic DI?
Genetic - most common affects vasopressin receptor, less common results from mutation in AQP2 channel
Electrolytes: hypercalcaemia, hypokalaemia
Lithium, demeclocycline
Tubulo-interstitial disease (obstruction, sickle cell, pyelonephritis)
101
What are the clinical features of DI?
Polyuria, polydipsia
102
What investigation results would you expect in DI?
High plasma osmolality, low urine osmolality
| Urine osmolality >700mOsm/kg excludes DI
103
What test can you do for DI?
Water deprivation test
104
How is nephrogenic DI treated?
Thiazides, low salt/protein diet
105
How is central DI treated?
Desmopressin
106
What is erythropoietin?
A haemopoietic growth factor that stimulates production of erythrocytes
107
What stimulates the kidneys to make EPO?
Cellular hypoxia
108
List side effects of EPO
Accelerated HTN potentially leading to encephalopathy + seizures
Bone aches
Flu like symptoms
Skin rashes, urticaria
Pure red cell aplasia (due to Abs against EPO)
Raised PCV increases risk of thrombosis
Iron deficiency
109
Why might patients fail to respond to EPO?
```
Fe deficiency
Inadequate dose
Concurrent inflammation/infection
Hyperparathyroid bone disease
Aluminium toxicity
```
110
What is there an increased risk of in patients with nephrotic syndrome?
VTE (LMWH prophylaxis indicated)
111
When might a patient with CKD require dialysis?
Uraemia (e.g. encephalopathy/pericarditis)
112
What are features of ADPKD?
```
HTN
Recurrent UTIs
Abdominal pain
Renal stones
Haematuria
CKD
```
113
What are the extra-renal manifestations of ADPKD?
Liver cysts (hepatomegaly)
Berry aneurysm (SAH)
CV - mitral valve prolpase, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
Cysts in other organs, e.g. spleen and pancreas
114
How does spironolactone work?
Aldosterone antagonist that acts in the cortical collecting duct
115
What are indications for spironolactone?
```
Ascites
HTN
HF
Nephrotic syndrome
Conn's syndrome
```
116
What adverse effects are associated with spironolactone?
Hyperkalaemia
| Gynaecomastia
117
If a patient gets troublesome gynaecomastia with spironolactone what can it be substituted with?
Eplerenone
118
How is hyperkalaemia classified?
Mild: 5.5-5.9mmol/L
Moderate: 6-6.4mmol/L
Severe: >= 6.5mmol/L
119
At what K level should a patient undergo an urgent ECG?
6 or more
120
How do the timing of onset of PSGN and IgA nephropathy differ after URTI?
PSGN develops 1-2 weeks post URTI
IgA nephropathy develops 1-2 days after URTI
121
What is the normal range for the anion gap?
10-18mmol/L
122
How do you calculate an anion gap?
(Na + K) - (Cl + HCO3)
123
What are causes of a normal anion gap metabolic acidosis?
```
GI bicarb loss - diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs, e.g. acetazolamide
Ammonium chloride injection
Addison's disease
```
124
What are causes of a raised anion gap metabolic acidosis?
Lactate: shock, sepsis, hypoxia
Ketones: DKA, alcohol
Urate: renal failure
Acid poisoning: salicyclates, methanol
125
What are the two types of lactic acidosis?
A: sepsis, shock, hypoxia, burns
B: metformin
126
In intrinsic AKI what is the urinary sodium and urine osmolality like and why?
It is high because the kidneys are not able to concentrate urine or retain sodium ---> urine osmolality low, urine sodium high
127
What is the urinary sodium and urine osmolality like in pre-renal AKI?
Urine osmolality high, urine sodium low
Kidneys act to concentrate urine and retain sodium
128
On what chromosome is HLA coded for?
6
129
What are post-op renal transplant problems?
ATN of graft
Vascular thrombosis
Urine leakage
UTI
130
What kinds of graft rejection can you get post-kidney transplant?
```
Hyperacute rejection (minutes to hours)
Acute rejection (<6 months)
Chronic rejection (>6 months)
```
131
What is the pathophysiology of hyperacute rejection?
It is due to pre-existing antibodies against donor HLA type 1 antigens (this is v. rare due to HLA matching)
132
What is the pathophysiology of acute rejection?
Usually due to mismatched HLA
| Other causes incl. CMV infection
133
Can acute rejection be treated?
May be reversible with steroids + immunosupressants
134
What happens in chronic graft failure?
Both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney
May get recurrence of original disease
135
How does acute rejection often present?
With signs and symptoms of infection
136
How do you confirm the acute graft rejection?
Biopsy
137
What is commonly see in the urine of someone with acute tubular necrosis?
Brown granular casts
138
What is reflux nephropathy?
Chronic pyelonephritis secondary to vesico-uretic reflux
139
How long does scarring take to occur in reflux nephropathy?
Usually occurs in first 5 years
140
How can reflux nephropathy lead to HTN?
Renal scarring may produce increased amounts of renin
141
How is reflux nephropathy best diagnosed?
On micturating cystography
142
How should all diabetic patients be screened for diabetic nephropathy?
Annual urinary albumin:creatinine ratio (ACR) from an early morning specimen
143
Define microalbuminuria
ACR >2.5
144
How is diabetic nephropathy managed?
```
Dietary protein restriction
Tight glycaemic control
BP aim <130/80mmHg
ACEi and ARBs can be used
Control dyslipidaemia, e.g. statins
```
145
What are signs of a negative fluid balance?
```
Tachycardia
Hypotension
Oliguria
Sunken eyes
Reduced skin turgor
```
146
What are signs of an over-filled fluid balance?
Ascites
Crackles
Tachypnoea
Elevated JVP
147
Why does rhabdomyolysis cause AKI?
Myoglobin released from muscle tissue is toxic to the kidneys
148
What are complications of nephrotic syndrome?
Inc. infection risk due to urinary Ig loss
Inc. TE risk due to loss of antithrombin III and plasminogen in urine (most common site - renal vein thrombosis)
Hyperlipidaemia
Hypocalcaemia (vitamin D and binding protein lost in urine)
Acute renal failure
149
Is renal biopsy always indicated in minimal change disease?
No - only indicated if response to steroids is poor
150
What is cyclosporin?
A calcineurin inhibitor
151
What are SEs of mycophenolate mofetil?
GI SEs
| Bone marrow suppression
152
What monitoring do those on long-term immunosupression for organ transplants require?
CV - tacrolimus + ciclosporin can cause HTN and hyperglycaemia, tacrolimus can --> hyperlipidaemia
Renal failure - nephrotoxic effects of tacrolimus + ciclosporin
Malignancy - esp. SCC and BCC
153
What is the first indicator of diabetic nephropathy?
Microalbuminuria
154
What is the recommended fluid challenge (in those with no heart failure)?
500ml normal saline STAT
| Reassess and decide if patient req. another 500ml
155
What is the recommended fluid challenge in those with heart failure?
250ml normal saline
156
What diuretic is used in high doses to prevent the reformation of ascites in patients with chronic liver disease?
Spironolactone
157
When does Wilm's nephroblastoma tend to present?
Typically in children under the age of 5
158
What are features of Wilm's nephroblastoma?
Abdominal mass
Flank pain
Painless haematuria
Anorexia, fever
159
What is the best way to differentiate between acute and chronic renal failure on US?
CRF tend to have small bilateral kidneys
(EXPECTIONS -
- AKPKD
- Diabetic nephropathy
- Amyloidosis
- HIV associated nephropathy
160
What electrolyte abnormality is more suggestive of chronic renal failure as opposed to acute renal failure?
Hypocalcaemia (due to lack of vit D)
161
What is the most common extra-renal manifestation of ADPKD?
Liver cysts
162
How can you remember the eGFR variables?
```
CAGE
C - serum Creatinine
A - Age
G - Gender
E - Ethnicity
```
163
Who should you consider a diagnosis of fibromuscular dysplasia in?
Young female patients who develop AKI after starting an ACE inhibitor
164
What does fibromuscular dysplasia cause?
Proliferation of cells in the walls of arteries causing the vessel to bulge/narrow
165
What is the classical appearance of fibromuscular dysplasia on US?
String of bead appearance of the renal arteries
166
What are the features of fibromuscular dysplasia?
HTN
CKD or acute renal failure (e.g. secondary to ACEi initiation)
Flash pulmonary oedema
167
What is the classic triad of symptoms seen in renal cell carcinoma?
Haematuria
Loin pain
Abdominal mass
Other features - left varicele (due to occlusion of L testicular vein)
168
What is dialysis disequilibrium syndrome?
A rare complication of dialysis that usually affects those who have just started RRT
Caused by cerebral oedema, exact mechanism is unclear
169
How do you calculate maintenance fluids for children for a 24h period?
100ml for first 10kg
50ml for next 10kg
20ml for subsequent kgs
170
How do you calculate maintenance fluids for children per hour?
4ml for first 10kg
2ml for next 10kg
1ml for subsequent kgs
171
What is someone with CKD on haemodialysis most likely to die from?
IHD
172
What are features of renal artery stenosis (secondary to atherosclerosis)?
HTN
CKD
Flash pulmonary oedema
173
What renin level will you see in someone with renal artery stenosis?
High renin (reduced perfusion --> decreased stimulation of baroreceptors in wall of afferent arteriole so RAAS is activated -> increased aldosterone (K low, Na high)
174
What are the WHO classes of lupus nephritis?
```
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
```
175
How is lupus nephropathy managed?
Treat HTN
Corticosteroids
Immunosupressants, e.g. azathioprine/cyclophosphamide
176
What things can cause metabolic alkalosis?
Loss of hydrogen ions or gain of bicarbonate
Mainly due to GI problems or kidney problems
177
List causes of metabolic alkalosis
```
Vomiting/aspiration
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia
```
178
What may cause a respiratory acidosis?
COPD
Decompensation in other respiratory conditions,e .g. life-threatening asthma/pulmonary oedema
Sedatives: benzos, opiate OD
179
What can cause respiratory alkalosis?
```
Anxiety --> hyperventilation
PE
Salicyclate poisoning
CNS disorders - stroke, SAH, encephalitis
Altitude
Pregnancy
```
180
When do nice recommend referring to a nephrologist from primary care in CKD?
If eGFR falls below 30 or by >15 in a year
181
What is the maximum recommended rate of potassium infusion via a peripheral line?
10mmol/hour
182
What are clinical features of hypokalaemia?
Muscle weakness, hypotonia
Palpations
Ascending paralysis
183
Hypokalaemia prediposes to toxicity from which drug?
Digoxin
184
What are the ECG features of hypokalaemia?
U waves
Small/absent T waves
Prolonged PR interval
ST depression
185
What are causes of hypokalaemia?
Inc. K loss (e.g. thiazides, laxatives, glucocorticoids, antibiotics)
GI loss: diarrhoea, vomiting, ileostomy
Dialysis
Endocrine disorders: hyperaldosteronism, Cushing's
Transcellular shift (e.g. insulin/glucose therapy, salbutamol, theophylline, metabolic alkalosis)
Decreased K intake
Mg depletion (assoc with increased K loss)
186
Define mild-moderate hypokalaemia
2.5-3.4
187
Define severe hypokalaemia
<2.5
188
How is mild-moderate hypokalaemia treated?
Oral K (if asymptomatic + no ECG changes)
189
How is severe hypokalaemia managed?
IV replacement (dilute K to low concentrations as higher concs can be pheblitic)
E.g. - 3 bags 0.9% saline with 40mmol KCl
