Renal medicine Flashcards
1
Q
where in the nephron does Type 2 renal tubule acidosis affect and what are the biochemical signs?
A
PCT - glycosuria, aminoaciduria, acidosis
2
Q
where in the nephron do loop diuretics act on?
A
ascending loop
3
Q
where in the nephron do thiazide diuretics act on
A
distal tubule
4
Q
where in the nephron do drugs like spironolactone act on?
A
collecting ducts
5
Q
how and why does trimethoprim affect creatinine results
A
it raises serum creatinine without affecting GFR because it inhibits the secretion of creatinine in the tubules.
6
Q
how do NSAIDs and ACEi affect renal perfusion
A
NSAIDs vasoconstrict afferent arterioles while ACEi dilate efferent arterioles.
7
Q
what happens if someone takes both an NSAID and an ACEi?
A
reduce blood going in and increased blood leaving, would severely starve the nephron of blood causing kidney failure or exacerbating one.
8
Q
how do drugs like metformin and sulphonylurea affect the kidney?
A
they are not nephrotoxic, but they are both renally excreted. metformin has an increased risk of lactic acidosis and sulphonylurea has a risk of hypoglcyaemia, in renal impairment, these risks are elevated.
9
Q
describe the anatomy of the kidney
A
fibrous capsule surrounding cortex whith the medulla in the centre. renal artery goes in and supplies afferetn arterioles and leaves via the efferent arterioles to continue to surround the nephrons and transport blood back out through the renal vein.
filtrate goes through nephron, into CD, into renal papilla, minor calyx and into major calyx finally into renal pelvis and to the ureter
10
Q
describe the anatomy of the glomerulus
A
nest of capillaries surrounding by fenestrated epithelium and podocytes to ensure large and charged particles don’t get throught. PCT -> loop of henle -> DCT -> CD
11
Q
what happens at the PCT
A
most solutes reabsorbed
60-80% water 60-70% sodium 80-90% calcium 90% potassium 90% bicarb 90% glucose 100% amino acids
secretion of creatinine and uric acid
12
Q
what happens in the loop of henle
A
one-way membranes cause the solute to concentrate as the interstitium is higher in concentration than the loop
13
Q
what happens in the DCT
A
5% sodium reabsorbed, potassium reabsorbed
14
Q
what happens in the collecting duct
A
action of ADH inserting aquaporins
secretion of acid
absorption of remaining sodium
15
Q
describe the endocrine function of the kidney
A
EPO
vitamin D
16
Q
how does kidney failure affect bone metabolism
A
cannot activate vit D, so gut doesn’t absorb calcium, kidney doesn’t absorb calcium, result in hypocalcemia and 2ndary hyperparathyroidism
17
Q
most common cause of ckd
A
diabetes
18
Q
what to ask about in renal history
A
diabetes, cdvs (incl. hypertension), urinary changes, pain, systemic symptoms, signs of infection
19
Q
what can be assessed in observation of someone with suspected kidney impairment
A
fluid status - dehydration or fluid overload?
(pulmonary)edema? or dry/mottled skin?
20
Q
what does a raised JVP tell you ?
A
fluid overload
21
Q
what does urinalysis tell you
A
assessment of filtration ability, by seeing things that aren’t supposed to be in the urine like lecocytes, glucose, portein, blood, ketones, ph, specific gravity, nitrites
22
Q
what is creatinine and how is it affected
A
byproduct of muscle respiration. affected by age and muscle mass. but also in renal impairment due to decreased ability to filter it caused by reduced GFR
23
Q
what is urea and how can it be interpreted in renal impairment
A
metabolite of ammonia metabolism. raised in illness, but not specific to renal causes.
24
Q
how are electrolyte levels changed in renal impairment - potassium sodium calcium pH?
A
hyperkalaemia, hyponatraemia, hypocalcaemia, and acidaemia usually.
25
what other investigations can be done in renal impairment
immunology, cultures, microscopy, imaging, biopsy.
26
what is postobstructive diuresis?
complication that happens after relieve of post-renal obstruction where kidney starts to loose more fluid and sodium than it should causing hypovolaemia
27
what 5 things are required for a functioning kidney
```
adequate perfusion
intact glomerular vasculature
patent tubules
functioning tubular cells
patent outflow
```
28
causes of pre-renal AKI
hypovolaemia
low cardiac output
distributive hypovolaemia
vasoconstrictive drugs
29
risk factors of AKI
preexisting CKD
older age
diabetes, atherosclerosis, liver disease, hypertension. heart failure
30
what can trigger AKI in a vulnerable patient?
hypovolaemia, antihypertensives, nsaids, imaging contrast
31
most common intrinsic cause of AKI?
acute tubular necrosis
32
what is ATN ?
vascoconstriction and ischaemia of intrarenal micro vessels causing cell injury and necrosis/apoptosis
33
what can cause ATN?
renal ischaemia, toxins like aminoglycosides, platinum, lithium
34
what can trigger ATN
sepsis, infection, cholestatic jaundice, hypotension, rhabdomyolysis
35
what are the biochemical signs of ATN
```
hyperkalaemia
hyperphosphataemia
hypocalcaemia
hyponatraemia
uraemia
```
36
other signs of ATN
```
fluid overload
purritis
anorexia, nausea, vomiting
reduced GCS
haemorrhagic events - GI bleeding, epistaxis
```
37
what other causes of intrinsic AKI are there
tubular interstitial disease
tubular obstruction by casts
glomerulonephritis
microvascular injury
38
what can cause post renal AKIs?
BPH or prostate cancer causing obstruction
kidney stones
retroperitoneal masses
constipation
39
complications of AKI?
hyperkalaemia causing cardiac instability
salt and water accumulation causing fluid overload
uraemia and toxin accumulation
metabolic acidosis
40
what are features of uraemia and toxin accumulation?
nausea vomiting anorexia
pericarditis, pleurisy, ECG changes
fitting, coma
bleeding risk
41
why is there bleeding risk in uraemia?
because of toxicity to platelets
42
what are features of metabolic acidosis
haemodynamic instability
circulatory collapse
reduces GCS
arrhythmias
43
what investigations to do for AKI?
```
urinalysis, ECG
bloods - FBC, LFTs, U&Es, creatinine, CRP, ESR, calcium
cultures, blood film, microscopy
antibody testing
imaging, biopsy
```
44
when should urine microscopy be done?
if urinalysis shows protein and blood
45
what might be seen on urine microscopy in haematuria and proteinuria?
red cell casts, or myoglobin casts in rhabdomyolysis
46
how to tell the difference between an AKI and a CKD?
previous bloods, trend of creatinine
USS kidneys to see if atrophied
duration of symptoms
if discrete cause can be identified
47
what is the criteria for stage 1 AKI?
1.5-2x increase in creatinine in 7 days, or increase of 26 mmol/L within 48 hours.
or less than 0.5ml/kg/hr in 6 hours urine outpue
48
what is the criteria for stage 2 AKI?
2-3x increase in creatinine in 7 days
or less than 0.5ml/kg/hr in 12 hours urine outpue
49
what is the criteria for stage 3 AKI?
>3x increase in creatinine over 7 days OR higher than 354 mmol/L
or urine output less than 0.3ml/kg/hr for 24 hours or anuria for 12 hours
50
what drugs should be modified or stopped in AKI?
NSAIDs, ACEi/ARBs, opioid analgesics, some antibiotics, metformin, insulin, benzos, diuretics,
51
What is the definition of CKD
Abnormal urinary sediments (haematuria and/or proteinuria)
Fall in gfr
Anatomical abnormality in kidney
For longer than 3 months
52
What anatomical changes account for the physiological changes in CKD?
Glomerular filtration damage which causes sedimentation abnormality
Reduced number of functional nephrons and reduced function of remaining nephrons - account for fall in GFR
53
What are the most some causes of CKD
Diabetes
Hypertension
Intrinsic glomerular or tubular disease
Urinary tract obstruction
54
How does CKD present usually?
Early CKD is usually asymptomatic, features would usually only include hypertension, some microalbuminuria. Usually found incidentally or in screening.
55
What are some features of late CKD (when is late CKD defined as?)
<30 GFR
Reduced concentration, poor sleep, fatigue, nausea and vomiting, anorexia
Bruising, itching, skin pigmentation
Fluid retention (Edema)
Bone pain
56
What are features of severe CKD
Uraemic encephalopathy
| Pericarditis - chest pain
57
What are some complications of late stage CKD
```
Anaemia
Cardiovascular risk
GI complications
Bone disease
Neurological abnormalities
Endocrine dysfunction
```
58
What is renal osteodystrophy?
A host of bone dysfunction caused by CKD, due to calcium and phosphate levels leading to PTH changes and vitamin D abnormalities.
Results in brittle bones
59
How is CKD diagnosed
Urinary sample for ACR measurement and eGFR calculation
For more than 3 months.
60
How is hypertension and ckd related
One may cause the other. Always screen for the other if presenting if one.
61
What can be done to diagnose CKD, if someone with hypertension develops CKD?
Biopsy
62
What are the downsides of using creatinine to estimate GFR?
Varys according to patient factors, non-linear relationship with GFR, some secretion in tubules.
63
What is required to stage CKD as G4A2
EGFR or 15-29
| ACR if 3-30
64
What is a better biochemical marker than creatinine to estimate GFR?
Cystatin C
65
What is the clinical course of CKD like
Most symptoms come at stage 3 CKD. Most will die of cardiovascular compliations, few will progress to stage 5 CKD.
66
What factors in CKD are most useful in managing to increase life span
Blood pressure - ACEi
Proteinuria - ACEi
Glycaemic control - SGLT2 inhibitor
67
Explain why cardiovascular risk increases in CKD
Increased risk of MI, strokes, heart failure due to calcification of vessels causing increased BP and increased afterload.
68
What are some associated risk factors of cardiovascular risk in CKD
Calcium and phosphate levels
Hyperparathyroidism
Uraemia
Inflammation
69
Describe pathophysiology of diabetic nephropathy
Increased blood glucose leads to
Haemodynamic changes, overactive RAAS, and hypoxia and inflammation of kidneys
This progresses to albuminuria and intrinsic kidney damage in the form of glomerulosclerosis and tubulointerstitial fibrosis
These lead to loss of filtration function
70
How long does diabetic nephropathy usually take to progress to end stage kidney disease?
25 years
71
How does GFR change in the early stages of Diabetic nephropathy?
Increased GFR due to GBM thickening and mesangial expansion
72
How should diabetics be screened for diabetic nephropathy>
Annual screening includes urinary testing for ACR and serum testing for eGFR
73
What test results is required for CKD to be diagnosed?
EGFR <60 and/or ACR more than 3mg/mmol for mnore than 3 months
74
what are the indications for starting dialysis in AKI?
```
Acidosis
Electrolytes (esp potassium)
Ingestions (poisoning e.g. ethylene glycol)
Ooverload (pulmn edema)
Uraemic encephalopathy/pericarditis
```
75
how does haemodialysis work?
moving blood through semipermeable membrane to remove toxins and let water back in through osmosis.
76
complications of haemodialysis?
rapid shift in electrolyte balance results in nausea, vomiting, cramps, cardiac arrythmias, headaches.
77
how does peritoneal dialysis work?
dialysate is pumped into peritoneal cavity, using peritoneum as membrane for dialysis
78
disadvantages of peritoneal dialysis?
weight gain, hyperglycaemia, peritonitis
79
possible iatrogenic complications of haemodialysis?
infection
thrombosis
bleeding
bleeding
80
what must be considered in a patient before renal transplant
no contraindicated comorbidities, no malignancy, no chronic infections.
where the kidney is coming from
matching of donor - HLA and blood type
81
what are the complications of organ transplant
organ dysfunction, rejection, GvHD, immunosuppresion leading to infection, malignancy
82
what are the 5 characteristics of nephrotic syndrome?
```
>3.5g/day proteinuria
hypertension
edema due to salt and water retention
lipiduria
hyperlipidaemia
```
83
what are 2 classifications of nephritic syndromes
acute or rapidly progressing
84
features of acute nephritis
```
haematuria
<3.5g/day proteinuria
edema
AKI
hypertension
```
85
difference between acute nephritis and rapidly progressing nephritis
rapidly progresing nephritis has features of focal necrosis, +/- crescents and rapid renal failure over weeks
86
what syndrome would mainly podocyte damage cause?
nephrotic
87
what structures are mainly damage in nephritic syndrome
endothelial and mesangial cells
88
what happens if there is damage in podocytes, endothelial cells and mesangial cells
mixed nephrotic/nephritic syndrome
89
hypertension is a feature of nephrotic syndrome, T or F?
F
90
what immunological features are present in FSGS
C3 and IgM
91
how do amyloid deposits stain?
they stain pink with green bifringence under polarised light with congo red
92
what are 4 features of nephrotic syndrome?
heavy proteinuria (>3.5g/day)
edema
hypoalbuminaemia
hyperlipidaemia
93
what causes hypoalbuminaemia in nephrotic syndrome?
increased catabolism of albumin resorbed in the tubules
94
what causes hyperlipidaemia in nephrotic syndrome?
increased lipoprotein production in hypoalbumin state
95
what causes edema in nephrotic syndrome?
increased sodium and water retention
96
what causes proteinuria in nephrotic syndrome?
damage to glomerular filtration barrier
97
describe the causes of physiological proteinuria
PU without HU
PU <1g/day
asymptomatic
normal renal function
can be caused by postural PU or post infection PU
98
what are 3 non systemic causes of nephrotic syndrome
minimal change disease
membranous glomerulopathy
focal segmental glomerulosclerosis
99
what are some features of minimal change disease
facial edema, proteinuria. no immune complexes found.
100
minimal change disease often leads to CKD, T or F
F
101
what can trigger minimal change disease
atopy
drugs (NSAIDs, antibiotics, etc)
infections
102
C3 and IgM are a common feature of minimal change disease, T or F
F, usually no immune complexes found
103
describe FSGS
sclerosis of some glomeruli, not all, and some sections of each tuft.
104
what are the types of FSGS
primary and secondary
105
describe the clinical course of primary FSGS
progressive destruction of glomeruli, tubules and interstitium.
106
what immunological features are present in FSGS
C3 and IgM
107
what are some clinical signs of FSGS
massive PU
| HU, H/T and renal impairment
108
what can cause secondary FSGS
drugs
infection
genetics
109
who usually gets membranous glomerulopathy
mostly male
110
clinical features of membranous glomerulopathy
asymptomatic PU, nephrotic SD, +/- microscopic HU, H/T or renal impairment
111
what is the prognosis for membranous glomerulopathy
1/3 get better
1/3 get partial recovery
1/3 progress to CKD
112
what are some good prognostic factors in membranous glomerulopathy
female
younger
asymptomatic at presentation
113
what immune features are present in membranous glomerulopathy
IgG4 and C3
114
how does amyloid deposits stain?
they stain pink, and exhibit green birefringence under polarised light in red congo stain.
115
macroglossia, racoon eyes, and shoulder pad sign; these are pathognomonic for what disease?
amyloidosis
116
what immunologic criteria are associated with SLE?
```
ANA
anti dsDNA antibodies
anti smooth muscle antibodies
anti-phospholipid antibodies
low complement C3, C4
positive direct coomb's test
```
117
what disease exhibits effacement of foot processes
minimal change disease
118
what forms the the 'crescent' seen in rapidly progressing glomerulonephritis?
macrophages and epithelial cells in bowman's space.
119
what investigation is done to identify ANCA proteins
immunofluorescence
120
how does ANCA vasculitis cause damage?
the ANCA antibodies bind to neutrophils, activating them to bind to endothelium, causing degranulation of neutrophils, promoting inflammation and causing damage.
121
what are 5 complications of nephrotic syndrome and how to manage them
```
hyperlipidaemia - statins
thromboembolism - anticoagulation
infections - vaccinations
protein malnutrition
AKI - CKD
```
122
difference between nephrotic and nephritic syndrome
nephrotic - insidious onset, edematous, no hypertension, no raised jvp, high PU, minimal HU and red cell casts, low serum albumin
nephritic - acute/rapidly progressing, edematous, hypertnsive, raised jvp, minimal PU, HU with red cell casts, +/- low serum albumin
123
most common cause of nephrotic syndrome?
diabetes
124
what investigations to do in proteinuria?
urinaysis, then quantification with 24 hour collection OR urine albumin/creatinine ratio (ACR)
125
what is the ACR diagnostic of microproteinuria? and frank proteinuria
>2,5 in men, >3 in women,
>30 in both for frank PU
126
what are the features of nephritic syndrome
```
hypertension
edema
haematuria
non-nephrotic proteinuira
redufction in eGFR
```
127
list some causes of nephritic syndrome
```
post streptococcal nephritis
IgA nephropathy
anti-GBM GN
alport's syndrome
ANCA +ve vasculitis
```
128
what are some mixed nephritic nephrotic causes
SLE
HSP
mesangiocapillary glomerulonephritis
129
what are some causes of haematuria
non-glomerular - stones, cancer, infection, sickle cell, pckd, BPH, exercise induced, renal vein thrombosis, trauma,
glomerular- glomerulonephritis, IgA nephropathy, alport's sd
130
what are some painful causes of visible haematuria
```
trauma
stones
renal vein trhombosis
infection
pckd
```
131
what are some painless causes of frank haematuria
bladder cancer
exercise induced
post streptococcal glomerulonephritis
132
what can cause a false +ve haematuria dipstick
myoglobinuria after rhabdo
semen
drugs
menses
133
what are features of glomerular disease
symmetrical kidney involvement
dysfunctional filtration
injury to filtration structure
134
what comprises the filtration structure of the nephron
endothelial cells
basement membrane
podocytes
mesangial cells
135
damage to what structures cause nephrotic syndrome, nephritic syndrome and mixed?
damage to podocytes cause nephrotic syndrome
damage to endothelium and mesangial cells cause nephritic syndrome
damage to both cause mixed
136
2 classifications of nephritic syndrome
acute and rapidly progressing
137
how to differentiate acute and rapidly progressing nephritis
acute has - HU, edema, AKI, hypertension, proteinuria (<3.5g/day)
RPGN - includes necrotic features and +/- crescentic features, renal failure occurs over weeks
138
how to investigate proteinuria or haematuria?
```
ask about UTI symptoms
urinalysis
urine microscopy
blood tests - U&Es, ACR, eGFR
biopsy
imaging
```
139
for someone with newly diagnosed renal anaemia, what should be prescribed?
iron supplement, then EPO
140
how to treat mineral bone disease in diabetic nephropathy?
check PTH
low phosphate diet, phosphate binders
vitamin D
141
in an intrinsic AKI where are 3 possible sites of damage?
tubular
glomerulonephritis
interstitial
142
what happens in acute tubular necrosis?
acute ischaemia to tubules cause necrosis and sloughing off of epithelial cells, creating casts. these casts obstruct the tubules causing back pressure, resulting in reduced GFR.
143
what are the effects of acute tubular necrosis?
reduced GFR causes more toxins to be left in the blood, resulting in azotemia, metabolic acidosis and an increased BUN
144
what can cause acute tubular necrosis?
from a prerenal AKI or toxins
145
what kind of toxins cause ATN?
```
aminoglycosides antibiotics
lead
myoglobin in rhabdo
ethylene glycol
radiocontrast
uric acid (TL sd)
```
146
what kind of AKI would tumour lysis syndrome cause?
ATN
147
what kind of casts would be seen on microscopy in ATN?
epithelial casts
148
pathophysiology of acute glomerulonephritis?
inflammation in glomerulus characterised by AgAb complexes with complement activation. this causes damage to podocytes, resulting in PU and HU. increased membrane permeability then also causes reduced GFR because of reduced pressure, thus causing azotemia, oliguria, edema and hypertension
149
why does GFR go down in acute glomerulonephritis?
damage to podocytes cause increased permeability, reduced Glomrular filtration pressure, reducing GFR.
150
what characterises acute interstitial necrosis?
eosinophils and neutrophil infiltration of interstitium
151
clinical features of acute interstitial necrosis?
eosinophiluria, oliguria, rash, fever
152
what can acute interstitial necrosis lad to?
renal papillary necrosis, causing haematuria and flank pain
153
what is the BUN:Creatinine ratio, FENa, and urine osmolality in acute interstitial necrosis?
BUN:creatinine ratio goes below 15:1 because tubules cannot resorb stuff
FENa increases to >2%
urine osmolalitiy increases because of impaired resorption
154
what is the BUN:Creatinine ratio, FENa, and urine osmolality in prerenal AKI?
BUN:creatinine ratio >20:1 (RAAS activation, more Na reabsorption, urea follows)
FENa <1%
urine osmolality will be low
155
what is the normal BUN:creatinine ratio?
5-20:1
156
what happens in postrenal AKI?
blockage or compression causes pressure to build up in tubules, this reduces pressure gradient, causing reduced GFR, causing azotemia, oliguria.
increased pressure in tubules will then increased reabsorption of whatever was filtered out, causing increased BUN:crt ratio, reduced FENa, reduced Urine Na+ concentration.
157
what happens in prolonged postrenal AKI
tubules get damaged, reduced ability to reabsorption things, causing FENa to rise, BUN:Crt to fall
