Nephrology Flashcards

1
Q

how is the anion gap calculated?

A

(Sodium and potassium - positive cations) - (chlorine and bicarbonate - negative anions)

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2
Q

what is the anion gap?

A

the blood serum should have a neutral charge. the number of cations (positive) should equal the number of anions (negative). the reason we have an anion gap is because we don’t calculate all the anions present in the blood stream. we only look at chlorine and bicarbonate.

there are other anions e.g. sulphate, phosphate and organic acids. when there is a big anion gap - these anions are making up a bigger proportion of the anion molecules e.g. raised lactic acid (lactate anion)

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3
Q

how does lactic acidosis widen the anion gap?

A

lactic acid dissociates to form a lactate anion and hydrogen ion. the hydrogen is buffered by the bicarbonate, lowering its numbers.
less bicarbonate and more lactate anions leads to a bigger anion gap

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4
Q

what are causes for a raised anion gap?

A

lactic acid
ketoacids
urate - renal failure
acid poisoning - methanol (formic acid) and salicylate

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5
Q

what happens in a normal anion gap acidosis?

A

the bicarbonate falls and kidney compensates for the decrease in anions by increasing the production of chlorine anions.
therefore, can also be known as a hyperchloraemic acidosis

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6
Q

what are causes of normal anion metabolic acidosis?

A

loss of bicarbonate in the GI tract = e.g. diarrhoea
renal tubular acidosis (RTA) e.g. decreased bicarb re-absorption in DCT
addissons disease

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7
Q

what causes metabolic alkalosis?

A

caused by a loss of hydrogen ions or gain of bicarb
mainly due to problems in the kidneys or GI tract
- diuretics
- vomiting/aspiration
- cushings syndrome
- primary hyperaldosteronism
- hypokalaemia

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8
Q

what is diabetes insipidus?

A

characterised by raised plasma osmolarity and low urinary osmolarity
due to a deficiency of ADH (cranial DI) or decreased sensitivity to ADH (nephrogenic DI)

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9
Q

what are causes of cranial DI?

A

idiopathic
head injury
pituitary surgery
craniopharyngomas

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10
Q

what are causes of nephrogenic DI?

A

genetic - mutations affection vasopressin receptor / aquaporin channel
electrolytes- hypercalcaemia, hypokalaemia
tubulo-interstital disease (pyelonephritis, sickle-cell, obstruction)

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11
Q

what are features of diabetes insipidus?

A

polyurea
polydipsia
high plasma osmolarity
low urine osmolarity (<700 )

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12
Q

what is rhabdomyolosis?

A

break down of muscle fibres and the release of their content into the blood stream - can cause serious complications such as renal failure
due to direct or indirect muscle injury

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13
Q

what is myoglobinuria?

A

the presence of myoglobin in the urine

usually associated with rhabdomyolosis or muscle destruction

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14
Q

what can cause renal tubular apoptosis?

A

aminoglycosides and radio contrast medium

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15
Q

what can cause renal tubular necrosis? ATN

A

myoglobinuria and haemolysis

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16
Q

how is an AKI defined?

A

an AKI is a syndrome of reduced renal function, measured by creatinine or urine output. There are a number of different aetiologies
clinically defined as:

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17
Q

how is AKi clinically defined?

A

1) creatinine rise >26 in 48 hours
2) Creatinine rise in adults by 50% + in 7 days
3) eGFR fall in children by 25% + in 7 days
3) urine output < 0.5ml/kg/h for >6 consecutive hours

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18
Q

what are the clinical parameters for the severity staging of AKIs?

A

Stage 1 = Creatining rise 1.5x baseline or Urine output <0.5 for > 6 hours
Stage 2 = Creatinine rise 2-2.9 x baseline or Urine output <0.5 for >12 hours
Stage 3 = creatinine rise >3 x baseline or urine output <0.3 for >24 hours

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19
Q

how are causes for AKI classified?

A

Pre-renal 85%
Renal 10%
Post renal 5%

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20
Q

what are pre-renal causes for an AKI?

A

anything causing decreased renal perfusion

  • sepsis, shock
  • haemorrhage, burns, pancreatitis, D and V
  • cardiogenic shock, severe HF, MI (decreased cardiac output)
  • drugs - vasodilation
  • hypotension
  • ACE-I, ARBs, hepatorenal syndrome, NSAIDs ( renal vasoconstriction)
  • dehydration
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21
Q

what are renal causes for AKI?

A

anything damaging the actual kidney
glomerular = glomerularnephritis, acute tubular necrosis
interstitial = drug reaction, infection, infiltration
vessels = vasculitis, DIC (disseminated intravascular coagulation), TTP (Thrombotic thrombocytopenic purpura), HUS (haemolytic ureamic syndrome)

drugs - NSAIDs, ARBs, ACEi, gentamycin, radio contrast,
rhabdomyelosis

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22
Q

what are post-renal causes of AKI?

A

anything obstructing the output

  • within renal tract: stone, renal tract malignancy, clot, stricture
  • extrinsic pressure: retroperitoneal fibrosis, pelvic malignancy, prostatic hypertrophy
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23
Q

what are the most common causes of AKI?

A
  1. sepsis
  2. major surgery
  3. cardiogenic shock
  4. other hypovolaemias
  5. drugs
  6. hepatorenal syndrome
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24
Q

how does a patient with an AKI present?

A

dizzy, nausea, vomiting, fluid overload (orthopnea, pulmonary oedema etc), hypotension, tachycardia,

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25
how is an AKI managed?
need to treat underlying cause almost all AKI patients will need to have the following addressed: (regardless of aetiology): fluid balance (overload or dehydration), acidosis and hyperkalaemia.
26
how is fluid resuscitation in hypovolaemic AKI patients carried out?
500mL crystalloid bolus given over 15 mins and then reassessed. continue giving boluses of 250-500mL and then reassessing. stop when euvolaemic if 2L given and no change - seek advice Buffered solutions e.g. Hartmanns/ Ringers contain Potassium - be cautious if patient hyperkalaemic non-buffered solutions e.g. 0.9% saline = contains chlorine. be wary of hyperchloraemic acidosis Blood components should be used in haemorrhage (colloid)
27
how is fluid overload managed in AKI patients?
- oxygen if patient has pulmonary oedema - fluid restriction - venous vasodilator e.g. diamorphine (with antiemetic) - diuretics can be used in symptomatic overload. not useful if the cause is oliguria a patient with persistent fluid overload and oliguria/anuria needs urgent referral to critical care
28
what are causes of fluid overload?
sepsis - increased capillary permeability aggressive fluid resuscitation oliguria Heart failure
29
how is hyperkalaemia treated in AKI?
1) calcium gluconate/calcium chloride (calcium chloride best given via central line) - stabilises heart cell membrane potentials 2) IV insulin - encourages cell take up of K+ 3) salbutamol (nebuliser) - also shifts K+ into cells, at high doses
30
when is renal replacement therapy indicated?
- persistent fluid overload despite medication - persistent hyperkalaemia - severe/prolonged acidosis - uraemic symptoms e.g. encephalopathy, pericarditis
31
what does the SALFORD pneumonic for AKI checklist stand for?
``` Sepsis? ACEi/ARBs/NSAIDs? - suspend! Labs - repeat creatinine levels Fluid resuscitation Obstruction - US for non- resolving AKI Renal replacement therapy? Dip the urine ```
32
how does the RAAS counteract hypovolaemia?
it attempts to increase circulating volume by 1) increasing reabsorption of Sodium and water 2) causing vasoconstriction of efferent arteriols to maintain GFR (ACEi, ARBs and NSAIDs prevent this protective mechanism)
33
what is Acute Tubular Necrosis?
a condition involving the death of tubular epithelial cells that make up the renal tubules. ATN presents with AKI and is one of the most common causes of AKI
34
what are common causes of ATN?
sepsis and nephrotoxic drugs
35
what are the 3 phases of ATN?
1) oligoruic phase - patient produces <500ml urine /day - at risk of fluid overload and electrolyte imbalance - creatinine levels shoot up 2) maintenance phase - creatinine levels stabilise/ rise slowly - normal urine quantities produced - fluid and electrolyte balance maintained 3) polyuric recovery phase - large amounts off dilute urine produced - patients can become hypovolaemic and unwell, hypokalaemic (electrolyte loss) - DCT and collecting ducts recover last so water not reabsorbed by aquaporins - creatinine levels drop
36
what is sepsis?
overwhelming and damaging systemic inflammatory response to infection. can cause organ dysfunction recognised by worsening vital signs
37
what is the pathophysiology of sepsis?
pathogen gains access to patient - risk increased with surgery, foreign bodies e.g. catheter and poor immunity widespread inflammation leads to the systemic release of inflammatory molecules. NO causes vasodilation, other molecules activate endothelins - causing increase capillary permeability. fluid leaks out into tissue - causing oedema and hypovolaemia. increased coagulapathy causes formation of microthrombi the above compounds organ hypo-perfusion and dysfunction. lactic acidosis and multi organ failure results
38
what are the SIRS criteria for sepsis?
``` need 2 or more of the below criteria tachycardia >90bpm RR> 22 acutely altered mental state temp >38.3 or <36 leukocytosis or leukopenia hyperglycaemia >7.7 ```
39
what is the SOFA score for sepsis?
``` Sequential Organ Failure Assessment if a patient with infection scores 2 or more, suspect sepsis Resp; PaO2 liver: bilirubin Coagulation: platelets renal; urine output CV; catecholamine doses CNS; GCS score ```
40
what is the risk stratification approach to sepsis and how are moderate and high risk patients classified?
identifying infective patients who are high risk for sepsis looking at 1) history 2) respiratory, >20 in moderate, >25 in severe 3) blood pressure, high in moderate, low in severe 4) circulation and hydration - raised HR, prolonged anuria 5) skin - cyansis, non-blanching skin rash
41
what investigations should be performed in suspected sepsis?
``` examination and culture of potential sites of infection blood culture FBC, LFTs, U and E, renal profile ABGs - hypoxia and Lactate? coagulation screening CRP, procalcitonin - raised in inflammation/sepsis glucose ECGs, CXR, CT - source of infection? ```
42
what is the sepsis six?
``` must be completed within the first hour mnemonic -O2 FLUID 1. Oxygen therapy - high flow 2. Fluid challenge - bolus 3. Lactate levels checked 4. Urine output - hourly measurement 5. Infection, blood culture 6. Drugs - ASAP antibiotics - broad spec at max dose ```
43
what electrolyte imbalance can omeprazole and furosemide cause?
hyponatraemia
44
what is chronic kidney disease?
impaired renal function or structure for >3 months with implication for health or markers of kidney damage and GFR <60 (on 2 separate occasions) for over 3 months
45
what are the 5 stages of CKD?
1) >90 2) 60-89 3a) 45-59 3b) 30-44 4) 15-29 5) <15
46
at what GFR do symptoms of renal failure become apparent?
usually <30 GFR
47
what are causes of CKD?
1) hypertension and diabetes are responsible for majority of cases 2) glomerulonephritis - mainly IgA nephropathy 3) renovascular disease 5) pyelonephritis / reflux nephropathy others = following AKI, ATN, adult polycystic kidney disease, interstitial nephritis, obstructive uropathy, lupus
48
what are symptoms of CKD??
often vague - requiring lab evidence begins with fatigue, nausea, possible oedema then as renal function worsens = uraemic symptoms such as pruritis, bone pains, restless legs, vomiting, fatigue, weakness, yellowish tinge to skin signs of fluid overload signs of hyperkalaemia - seizures, encephalopathy, coma, arrhythmias
49
what investigations should be performed in suspected CKD?
- Renal profile; GFR and creatinine levels - Urine dipstick and analysis - haematuria, proteinuria, Pyuria? - renal ultrasound - diabetes revision/screen - glucose levels etc
50
how is proteinuria defined?
ACR - albumin: Creatinine ratio > 30 mg/mmol Albumin >200mg/L PCR: urine protein: creatinine ration > 45mg /mmol ACR is more conclusive than PCR
51
how is STAGE 1-4 CKD treated?
- aim to slow down renal damage and prevent RRT 1) ACEi or ARBs = decreases the pressure in the kidneys (ramipiril or losarton) 2) Statins 3) additional hyptertensive medication - beta blockers, thiazide diuretics 2nd line = non -dilhydropyridine CCB e.g. diltiazam or verpamil
52
how is STAGE 5 CKD treated?
1st line = dialysis | 2nd line = kidney transplant
53
what is the pathophysiological mechanisms behind diabetic nephropathy?
1) Raised glomerular pressure - due to HTN and RAAS activation by hyperglycaemia 2) barotrauma of mesangial cells 3) nephron ischaemia (microvascular damage, efferent arteriole vasoconstriction)
54
what are side effects of ACEi/ ARBs?
``` dry cough hyperkalaemia hypotension angio oedema AKIs - must be stopped in this case ( they prevent body's protective mechanism against pre-renal AKI) ```
55
how do ACEi and ARBs work in CKD?
they prevent salt retention and vasoconstriction this reduced bllood volume and pressure in the kidneys relaxes the efferent arteriole - prevents the viscous cycle HTN causing hypoperfusion of kidney, which then activates the RAAS, raising BP
56
can you take ACEi/ARBs in pregnancy?
NO
57
what are the metabolic complications of CKD?
1) anaemia - decreased erythropoietin produced 2) Acidosis - failure to excrete various anions 3) CKD mineral bone disease - bone pain and muscle cramps
58
how is metabolic acidosis treated in CKD?
oral sodium bicarbonate
59
How is anaemia treated in CKD?
EPO stimulating agents e.g. epoetin-alfa darbepoetin-alfa
60
how does CKD lead to mineral bone disease?
hypocalcaemia is caused by kidneys inability to activate Vit D, and inability to excrete adequate phosphate. Hypocalcaemia leads to secondary hyperparathyroidism - excess PTH causes excess phosphate
61
how is mineral bone disease in CKD treated?
alfacalcidol - vitamin D supplement / calcitriol | phosphate binding medication
62
when should a CKD patient be referred to a renal specialist?
Stage 5 - immediate referral Stage 4 - urgent referral, or routine if stable Stage 3 - routine referral if any of the following: uncontrolled BP, PCR>45, GFR fall by 15% after ACEi, unexplained anaemia, abnormal K, Ca, Phosphate, microscopic haematuria, systemic illness e.g. SLE Stage 1 and 2 - referral not required proteinuria w/ oedema and decreased serum albumin (nephrotic syndrome) hyperkalaemia malignant hypertension
63
which diabetic medication is contraindicated if eGFR < 30 ?
metformin
64
what is the target BP in all stages of CKD?
130/80
65
what are the features of hemodialysis?
- AV fistula created (better flow, less complications for needle insertion) - dialysis carried out 3 times a week for 4 hours - diet and fluid is restricted - difficult to go abroad, unless dialysis clinics arranged - lots of time travelling to/from hospital, spent in hospital
66
what are features of peritoneal dialysis ?
- tenckhoff catheter is fitted - usual requirement = 4-6 exchanges per day with 4-6 hours of dwell time per exchange - absolute CIs : IBD, ischaemic bowel, abdo abscess, pregnancy 3rd trimester, diverticulitis - carried out at home, less bulky, portable equipment - there are 2 forms: CAPD (continuous ambulatory PD) or APD (assisted PD). - CAPD doesn't require a machine - the patient fills the stomach with dialysate, leaving it to dwell whilst carrying out normal daily activities and then drains it with gravity - APD uses a machine that automatically does exchanges whilst you sleep. the dwells are shorter. in the morning you fill with dialysate and leave it to dwell all day. - risk of peritonitis, malnutrition
67
what is the average waiting time for a kidney transplant in manchester?
3 years
68
what is the annual cost of dialysis per patient?
£30800
69
how is the new kidney plumbed into the patient?
the renal artery is anatomised onto the iliac artery the renal vein onto the iliac vein and the ureter onto the bladder the old kidney is left where it was
70
what immunosuppressant drugs can be used for kidney transplant patients?
calcineurin inhibitors: cyclosporine or tacrolimus antiproliferative agents: mycophenolate mofitil, mycophenolate sodium or azathioprine prednisolone mTOR inhibitor: sirolimus
71
what are the complications of a kidney transplant?
1) Rejection 2) Infection- most commonly UTI then Chest. Diverticulitis = ~100% mortality in transplant patients 3) Malignancy 4) CV disease 5) Immunosuppressant drug interacts. 6)
72
how is transplant rejection diagnosed?
via US guided transplant biopsy biopsy shows lymphocyte infiltration of tubularinterstitium and tubules. Can be treated with steroids if lymphocytes have infiltrated vasculature - under endothelium - this is very serious.
73
risk of which malignancy is increased most in transplant patients?
squamous cell carcinoma of the skin
74
which immunosuppressant drug has numerous interactions?
tacrolimus
75
give examples of phosphate binders used in CKD?
lanthanum, sevelamer, calcium carbonate/acetate
76
what is tertiary hyperparathyroidism?
after a long period of secondary hyperparathyroidism, the regulation of PTH hormone can become autonomous and dysregulated. excessive PTH can be secreted leading to hypercalcaemia treated with cinacalcet
77
what are side effects of erythropoietin treatment?
accelerated hypertension (leading to encephalopathy or seizures) increased risk of thrombosis (b/c increased PCV) iron deficiency bone aches flu-like symptoms skin rashes red cell aplasia (due to autoimmune antibodies)
78
how much protein and albumin is excreted daily in the urine?
<150 mg protein <30 mg albumin 30-300 mg albumin = moderately increased albuminurea
79
what is glomerulonephritis?
- A group of diseases which cause injury to the glomeruli - present with proteinuria and/or haematuria - covering a spectrum from nephrotic syndrome to nephritis - can cause CKD - diagnosed on biopsy
80
what is nephrotic syndrome? (triad)
1) Proteinuria (hyperalbuminuria) >3.5g/24hr, PCR>300, ACR>250 2) Hypoalbuminaemia 3) Oedema ALSO hyperlipidaemia (serum proteins suppress lipid production usually) lipiduria
81
what is the pathophysiology of Nephrotic syndrome?
damage to the filtration barrier of the glomeruli leads to proteins entering the urine. (>3.5g/24hr) decreased protein in the serum leads to decreased oncotic and osmotic pressures. Fluid leaves the blood causing Oedema. (?)lack of proteins/albumin in blood causes a rise in lipids. this results in hyperlipidaemia and lipiduria
82
which diseases fall under the umbrella of nephrotic glomerulonephritis?
Minimal Change disease Focal Segmental Glomerulosclerosis Membranous nephropathy mebranoproliferative GN
83
which diseases fall under the umbrella of nephritic GN?
IgA nephropathy Post-streptococcal GN Anti GBM disease (Good Pastures)
84
What causes Minimal change disease?
``` most cases are idiopathic 10-20% have cause - drugs: NSAIDs, rifampicin - Hodgkin's lymphoma, thymoma - infectious mononucleosis ```
85
what are features of minimal change disease?
- nephrotic syndrome - normotensive - highly selective proteinuria (only intermediate sized proteins leek through) - change only visible on electron microscopy - shows effacement of podocytes. - responsible for 75% cases of GN in children - and 25% cases in adults
86
what is the pathophysiology of minimal change disease?
t cell and cytokine mediated damage of the glomerular basement membrane leads to polyanion loss and podocyte foot damage the loss of the electrostatic charge barrier leads to increased permeability of the glomerular filter and thus passage of albumin into the urine
87
how is minimal change disease treated?
steroids this works in 90% cases cyclophosphamide is second line
88
what is Focal Segmental Glomerulosclerosis?
scarring of segments in glomeruli. not all glomeruli are affected - only a small section. characterised by sclerosis and hyalonosis - where scarring occurs, the filtration barrier is damaged and proteins escape into the urine - most common GN in adults - can cause chronic renal failure
89
what are causes of FSGS?
in primary FSGS - idopathic in secondary FSGS - clear underlying cause. secondary is associated with Sickle cell, HIV, heroin abuse, lithium, kidney hyperpurfusion, raised pressure in glomeruli
90
how is FSGS treated?
steroids ACEi/ARBS and BP control 2nd line = calcinuerin inhibitors e.g. tacrolimus , cyclosporine
91
what is membranous nephropathy?
- the glomerular basement membrane becomes inflammed. this leads to increased permeability and proteins escaping into the urine. nephrotic syndrome
92
what is the pathophysiology of membranous nephropathy ?
inflammation of the basement membrane leads to nephrotic syndrome the damage is caused by immune complexes. these immune complexes are either 1) auto-antibodies which target the GBM. these include M type phospholiase A2 antibodies and neutral endopeptidase or 2) complexes which are formed outside of the kidney and then carried to the GBM. these include complexes with the antigen: cationic bovine serum albumin, from beef and cows milk. these immune complexes are known as subepithelial deposits - sandwiched between the GBM and podocytes. they activate the complement system - leading to damage of podocytes and mesangial cells and recruits further inflammatory mediators which cause damage to the GBM. in response to the subepithelial deposits, GBM matrix is laid down - creating a spiky thickened GBM
93
which antibodies are found in membranous nephropathy?
M type phospholipase A2 antibody Neutral endopeptidase complexes with cationic bovine serum albumin
94
what are the causes for membranous nephropathy?
``` primary = idiopathic secondary = autoantibodies are generated in response to malignancy, infections (Hep c,b, strep, malaria), autoimmune conditions (lupus, arthritis), and drugs (gold, penincilinamine) ```
95
how is membranous nephropathy treated?
``` secondary = treat underlying cause primary = steroids, BP control and ACEi/ARBs ```
96
what is the pathophysiology of membranoproliferative GN (MPGN)??
a mixture of: (1) immune complex deposition in btwn the endothelial layer and basement membrane. (subendothelial deposits) (2) inappropriate complement activation - (perhaps by IgG binding C3 activase which stabilises it and causes it to continually activate C3 - this antibody is known as nephritic Factor (C3NeF)) The inflammation leads to mesangial cell proliferation and growth into the BM Type 1 MPGN = mixture of (1) and (2) Type 2 MPGN = only complement deposits - no immune complexes. this is also known as Dense Deposit Disease Type 3 MPGN = mixture of (1) and (2). deposits are also found in subepithelial space as well as subendothelial space
97
how does MPGN present?
- present as nephrotic and maybe nephritic syndrome
98
what are characteristics of nephritic syndrome?
INFLAMMATION haematuria oliguria azotemia (nitrogen containing compounds in urine)
99
how is MPGN treated?
steroids | ACE/ARB/BP control
100
what is IgA nephropathy?
abnormal, galactose deficient IgA antibodies are not recognised by the body. they accumulate in high numbers. IgG anti-glycan antibodies are formed against them and complexes are formed which are then carried to the kidney. immune complexes are deposited in the mesangium
101
what is the most common cause of renal AKI?
Acute tubular necrosis
102
how do you differentiate between pre-renal AKI and ATN (renal AKI)?
in prerenal AKI, the kidneys hold onto sodium to preserve volume. In ATN: raised sodium in the urine, wont respond to fluid challenge
103
what fluid challenge should be given to a patient without known HF?
500mls 0.9% saline
104
what fluid challenge should be given to a patient with known HF?
250mls 0.9% saline
105
what are the requirements for maintenance fluids?
25-30 ml/kg/24hours saline 1mmol/kg/day sodium, potassium and chloride 50-100g glucose/day
106
what are the complications of nephrotic syndrome??
1) hypocalcaemia (vit d not activated) 2) infection - immunoglobulin lost in urine 3) coagulopathy - antithrombin 3 and plasminogen lost in urine (can cause renal vein thrombosis) 4) acute renal failure 5) hyperlipidaemia
107
how is lupus nephritis picked up?
regular urine testing of all lupus patients, even if asymptomatic proteinuria will be present
108
what is the commonest cause of GN worldwide?
IgA nephropathy
109
what is the histology of IgA nephropathy?
mesangial hypercellularity and positive immunofluoresence for IgA and C3
110
how does IgA nephropathy typically present?
young male recurrent episodes of macroscopic haematuria associated with infection, usually URTI renal failure
111
how do you differentiate between IgA Nephropathy and Post-strep GN?
``` POST STREP: - GN is seen 1-2 weeks after URTI - proteinuria also seen - IGA NEPH - seen 1-2 days after URTI - macroscopic haematuria proteinuria very rarely seen ```
112
what is Henoch Schonlein purpura ??
small vessel vasculitis and system variant of IgA nephropathy IgA complexes are deposited in joints/skin/gut/kidney
113
how does henoch schonlein purpura present?
purpuric rash on extensor surfaces polyarthritis abdo pain GI bleeding renal biopsy identical to IgA nephropathy IgA nephropathy - renal failure, haematuria
114
How is IgA nephropathy treated?
steroids
115
What are features of post-strep GN?
- occurs ~2 weeks after an infection | - strep antigen deposits in the glomerulus leading to immune complex formation and inflammation
116
how is maintenance fluid prescribed for children?
100ml/kg for the first 10 kg 50ml/kg for the next 10kg and 20ml/kg for the remainder of the kgs
117
how does post-strep GN present?
haematuria oedema raised BP oliguria
118
how is post-strep GN treated?
supportive antibiotcis
119
what are the features of Anti - GBM disease (Good Pastures)?
- autoimmune antibodies against type 4 collagen - found in glomerular and alveolar BM - diagnosed by presence of Anti-GBM antibodies in circulation/kidney
120
how does Good-Pastures disease present?
renal disease (oliguria, haematuria, AKI, RF) and lung disease (pulmonary haemorrhage, SOB, haemoptysis)
121
what is rapidly progressive GN (Crescentric GN) ?
a type of nephritic syndrome inflammation in the glomerulus leads to proliferation of cells producing a crescent like shape in the bowmans space. this change leads to renal failure in weeks to months
122
what causes rapidly progressing GN?
idiopathic 1) type 1 - Anti-GBM antibodies (Goodpastures) 2) Type 2 - immune complex mediated e.g. Post-strep GN, lupus, IgA nephropathy and henoch schonlein 3) type 3 - Pauci- immune (no immune complexes/abs in kidney) - ANCA in blood (Anti Neutrophil Cytoplasmic Antibodies)
123
what are the autosomal dominant cystic kidney diseases?
1) AD polycystic kidney disease 2) Von Hippel Landau 3) tuburous sclerosis 4) medularry cystic disease
124
what are the features of AD PKD?
- commonst genetic renal disease - make up 10% of the end stage renal failure ppln - 50% reach ESKF by 60s - 1 in 800 births - patient also presents with extra renal cysts e.g. hepatic cysts (most common), berry aneurysm, pancreas, spleen and mitral valve prolapse)
125
how does a patient with ADPKD present?
``` flank/abdo pain renal colic gross haematuria renal stones cystitis headaches recurrent UTIs history of dysuria, suprapubic pain and urgency HTN often Hernias chronic kidney disease early satiety = kidneys occupy large amount of space in abdo ```
126
what imaging should be performed if ADPKD is suspected?
1) ultrasonography | 2) contrast enhanced CT or MRI
127
what are the US diagnostic criteria for ADPKD?
for patients with 50% risk: - < 30 yrs = 2 cysts unilaterally or bilaterally - 30-60 yrs = 2 cysts in each kidney - > 60 yrs = 4 cysts in each kidney
128
what is a common finding in ADPKD patients?
renal stones are found in 20% cases | low urine citrate and pH predisposes to this
129
how is ADPKD treated?
1) treat HTN -lifestyle mods and medication 2) UTIs - antibiotics 3) infected renal cyst = antibiotics, drainage and 2nd line = nephrectomy 4) analgesia for renal pain 5) nephrolithiasis (renal stones) =potassium citrate 6) symptomaic polycysts - drainage, resection and then nephroctomy
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what antibiotic do we use in renal cyst infection?
ciprofloxacin
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which new medication may slow cyst progression in PKD?
Tolvaptan (Jinarc) - a vasopressin receptor 2 antagonist - patient needs regular blood tests to monitor liver and kidney - and annual imaging of kidney
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what are examples of large vessel vasculitis?
``` Giant Cell (elderly, headaches, raised ESR) Takayasu arteritis (pulseless disease, aorta and main branches) ```
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what are examples of medium vessel vasculitis??
kawasaki disease | polyarterius nodosum - assoc. with Hep C and B
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what are examples of small vessel vasculitis?
ANCA associated | others... SLE
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what does ANCA stand for?
Anti Neutrophil Cytoplasmic Antibodies
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what are the 3 clinical entities of ANCA assoc. vasculitis?
1) microscopic polyangitis 2) granulomatosis polyangitis 3) eosinophilic granulomatosis polyangitis
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what are the 2 types of ANCA?
pANCA = perinuclear staining. specific for myeloperioxidase staining. seen mostly in Pauci immune GN cANCA = diffuse cytoplasmic staining. specific for proteinase 3 enzmye both enzymes are present in neutrophil granules
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what is the pathogenesis of ANCA assoc. vasculitis??
1) neutrophil is primed - expression of auto antibodies 2) binding of ANCA and activation of neutrophil 3) tissue damage
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how does ANCA assoc. vasculitis present?
renal - Pauci immune GN / RPGN | lungs - haemoptysis, granuloma/alveolar haemorrhage, cough, dyspnoea
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how is ANCA + vasculitis treated?
1) induction of remission = steroids and cyclophosphamide | 2) maintenance of remission = azathioprine and steroids
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what are features of von hippel landau disease?
- a mutation in the tumour suppressor gene (VHL protein) - autosomal dominant - 1 in 36000 - presents in 20's-30's with an array of benign tumours and cysts in the CNS, abdomen, pancreas, retina
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what are the kidney mainfestations of VHL syndrome?
- cortical renal cysts (70%) - renal cell carcinoma (20-40%) - renal cell adenoma, renal haemaginoma
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how is VHL syndrome monitored?
annual US | 3 yearly CT scan
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what are causes of transient non-visible haematuria?
sexual intercourse vigorous exercise UTI menstruation
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what are causes of persistent non-visible haematuria?
``` cancer (bladder, prostate, renal) stones BPH Renal causes (GN nephritis, IgA nephropathy,) prostasis urethritis (chlamydia) ```
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when do you make an urgent referal for haematuria?
> 45 years with haematuria without UTI or after successful treatment of UTI > 65 years with haematuria without UTI AND dysuria or raised WBC
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when do you make a non-urgent referral for haematuria?
unexplained persistent/recurrent UTIs in > 60 YO
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which GN presents with nephrotic syndrome?
minimal change GN FSGN membranous GN
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which GN presents with nephritic syndrome?
IgA nephropathy | Rapidly progressing GN
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which GN present with mixed nephritic/nephrotic picture?
Post - strep GN | membranoproliferative GN
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what are extra-renal features of ADPKD?
hepatic cysts - manifest as hepatomegaly ovarian cysts intracranial aneurysms diverticulosis
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what is the prognosis of Henoch schonlein purpura?
usually excellent, self-limiting disease | 1/3 will relapse
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how may contrast media nephrotoxicity defined?
25% rise in creatinine within 3 days of IV contrast media administration
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how is the risk of contrast media administration reduced in CKD patients?
administration of 0.9% saline solution at a rate of 1mL/kg/h for 12 hours pre-and post-procedure N acetyl cysteine (oral) has been shown to help but poor evidence base
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what are risk factors for contrast media nephrotoxicity?
``` known renal impairment dehydration cardiac failure >70 YO nephrotoxic drugs ```
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how would a patient with a ruptured berry aneurysm present?
subarachnoid haemorrhage -sudden severe headache -meningitic features= neck stiffness and vomiting CT findings = hyper attentuation around circle of willis
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what is the characteristic triad of haemolytic uraemic syndrome?
1) haemolytic anaemia 2) thrombocytopenia - low platelet count 3) acute kidney failure (Uraemia)
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what are causes of haemolytic uraemic syndrome?
``` post dysentry e.g. E Coli tumours pregnancy cyclosporin, the pill HIV SLE ```
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how does minimal change disease present?
young child periorbital swelling frothy urine
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what is the prognosis of minimal change disease?
1/3 have 1 episode 1/3 have infrequent relapses 1/3 have frequent relapses which stop before adulthood
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what is the first step after receiving a patients blood results which show hyperkalaemia?
urgent ECG | if ECG changes consistent with hyperkalaemia are seen - stabilise myocardium with calcium gluconate infusion
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how is severity of hyperkalaemia classified??
mild 5.5-5.9 moderate 6 - 6.4 severe >6.5mmol/l
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what are features of rhabdomyolosis?
- renal failure with disproportionately raised creatinine - CK rise - myoglobinuria - hypocalcaemia (myoglobin binds calcium) - elevated phosphate - released from myocytes
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eosinophilic casts are found on microscopic inspection of urine. what is this a sign of?
acute interstitial nephritis | usually caused by a drug reaction e.g. penicillin
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which bacteria is associated with post-strep GN?
streptococcus pyogenes
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what are the different causes of anaemia in CKD?
reduced erythropoietin reduced erythropoiesis in bone marrow due to toxic ureamic affect reduced iron absorption nausea and vomiting due to uraemia reduced red cell survival (especially in haemodialysis)
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what are signs/symptoms of anaemia?
pallor tachycardia fatigue aortic flow murmur
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what are acceptable changes in CK and GFR after starting on an ACEi in patients with CKD?
a rise in creatinine of 30% | and fall in GFR of 25%
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what antihypertensive medication should be used if GFR falls below 45 (or 30)?
furosemide
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what is the most commonly used formula for calculating eGFR?
MDRD | modification of diet in renal disease
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what variables does the MDRD formula take into account?
``` CAGE creatinine age gender ethnicity ```
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which factors may affect the eGFR?
pregnancy muscle mass eating red meat 12 hours prior to tests
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what are causes for diffuse proliferative GN?
post-strep | SLE
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why are diuretics nephrotoxic?
they prevent water being reabsorbed into the capillaries. this means the capillaries have a lower volume as they move to the end of the nephrons. this can cause hypoxia and then acute tubular necrosis
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muddy brown casts found in urine microscopy are suggestive of?
acute tubular necrosis
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what is an example regime for immunosuppression following a transplant?
initial: ciclosporin/tacrolimus with monoclonal antibody maintenance: ciclosporin/tacrolimus with MMF or sirolimus add steroids after 1 rejection episode
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what is Alports syndrome?
a rare X linked dominant genetic disease | caused by a mutation in gene coding for collagen 4 resulting in abnormal glomerular basement membrane
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what are features of Alports syndrome?
- presents in childhood - progressive renal failure - microscopic haematuria - bilateral sensorineural loss - retinitis pigmentosa - lenticonus - protrusion of the lens into the anterior chamber
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what is seen on electron microscopy of a renal biopsy from a patient wit Alport syndrome?
splitting of the lamina densa
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what is gold standard for bladder cancer diagnosis?
cystoscopy
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what are complications of peritonal dialysis ?
peritonitis | sclerosing peritonitis
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which bacteria is most commonly responsible for peritonitis in peritoneal dialysis?
staphylococcus epidermidis | staph aureus is another common one
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how is diabetes insipidus treated?
cranial DI = treated with vasopressin analogue e.g. desmopressin nephrogenic DI = treated with thiazide diuretic. prevents the plasma serum osmolarity for getting too high e..g chlorothiazide
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what changes predispose to thrombosis in CKD?
loss of antithrombin 3, proteins C and S | and subsequent raise in fibrinogen
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what are potential complications of an arteriovenous fistula?
infection thrombosis stenosis steal syndrome
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when should calcium glucanate be administered for hyperkalaemia?
if potassium >6.5 or ECG changes
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what are symptoms of hypokalaemia?
weakness, leg cramps, ascending paralysis, arrhythmias causing palpitations
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what are ECG changes seen in hypokalaemia?
u waves absent/flat T waves prolonged PR interval ST depression
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how is hypokalaemia treated?
depends on severity mild to moderate: 2.5 - 3.4 treated with oral potassium severe < 2.5 : cardiac monitoring and saline with potassium infusion. not exceeding 20mml/hr
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what are the 2 types of ADPKD?
type 1 - 85% cases. mutation in polycistin 1 on chromosome 16 type 2 - 15% cases, mutation in polycistin 2 on chromosome 4
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what is Wilm's nephroblastoma?
one of the most common childhood malignancy | typically presents in under 5s (mean age 3)
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what are features of Wilm's nephroblastoma?
``` abdominal mass painless haematuria flank pain other = fever, anorexia unilateral in 95% cases 20% metastasised ```
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how does acute graft rejection present?
<6 months post transplant | signs and symptoms of infection
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what is the most common viral infection in organ transplant recipients?
cytomegalovirus | treated with ganciclovir
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what are causes for hypokalaemia associated with hypertension?
cushings syndrome conns syndrome (primary hyperaldosteronism) liddle's syndrome
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what are causes of hypokalaemia without HTN?
GI loss diureti renal tubular acidosis
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can a CKD diagnosis be made on eGFR alone?
no, need supporting evidence from urinalysis or renal ultrasound
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how does a urine dip differentiate between causes of AKI?
- presences of proteins basically rules out any pre or post renal causes - absence of nitrates rules out infection - high white blood count will point towards an inflammatory process
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what is the most likely cause of death for CKD patient on haemodialysis?
ischaemic heart disease | CV events acount for over 50% of mortality
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what can spironolcatone be switched for?
eplerenone (another aldosterone antagonist)
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what are features of renal cell carcinoma?
-classic triad = loin pain, abdo mass, haematuria -pyrexia - left varicocele (due to occlusion of left testicular vein) -endocrine effects -may secrete erythropoietin, PTH, renin, ACTH -
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what are the investigations for goodpastures?
renal biopsy - linear IgG deposits along linear BM | increased transfer factor b/c of haemorrhage
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how is pyelonephritis treated?
24-48 hours of IV gentamicine or temocillin
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what abnormalities may predispose a patient to UTIs?
urinary tract tumours urinary stones incomplete bladder emptying vesicoureteral reflux
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what is defined as recurrent UTIs?
>3 episodes /year
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how do urological stones present?
``` pain haematuria infection 3rd-5th decade of life male > female ```
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what are causes of urological stones?
metabolic (50%) - renal tubular acidosis, hyperparathyroidism, crohns disease, cystinuria, sarcoidosis - infection - immobilisation - urological
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what are urological stones composed of?
75% calcium oxalate 10% struvate 10% urate
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how are urological stones managed?
increase fluid intake treat infection surgery for large stones >8mm
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what is the most common kidney malignancy?
renal cell carcinoma (80%) | next is TCC
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what are benign renal tumours?
angiomyolipomas | oncocytoma
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what is papillary necrosis?
necrosis and shedding of medullary papillae | the papillae may cause obstruction and pyonephrosis
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what are RFs for papillary necrosis?
analgesia, sickle cell, infection, DM
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how is papillary necrosis treated?
emergency drainage | and antibiotics