Renal Flashcards
1
Q
At what vertebral level do the kidneys lie?
A
T12-L3
2
Q
What surrounds the kidney?
A
a fibrous capsule which is covered in perinephric fat and then by perinephric fascia
3
Q
What makes up the renal medulla?
A
Renal pyramids
4
Q
Where are glomeruli found?
A
in the renal cortex
5
Q
Where does the renal artery arise from
A
the aorta
6
Q
is the ureter intraperitoneal or retroperitoneal?
A
Retroperitoneal
7
Q
What vertebral levels innervate the bladder?
A
S2,3,4
8
Q
Which type of nephron is more abundant?
A
Cortical (short loop)
9
Q
What is erythropoietin and where is it found?
A
it is a hormone that causes stem cells in the bone marrow to be differentiated into RBC’s. It is made in the fibroblast like cells in the renal cortex
10
Q
What is the function of mesangial cells?
A
provide a scaffold to support capillary loops and have contractile and phagocytic properties
11
Q
How does blood enter the glomerular capillaries?
A
from an afferent arteriole and leaves by an efferent arteriole once filtration has occurred at the Bowmans Capsule
12
Q
Why is there vasoconstriction of the efferent arteriole?
A
It creates a high hydrostatic pressure in the glomerular capillary forcing water, ions and small molecules through the filtration barrier into Bowmans space
13
Q
What are the layers of the filtration barrier?
A
Endothelial cells (thin with pores and -ve charge), glomerular basement membrane (2 layers made of type IV collagen, -ve charge), epithelial cells of the bowmans capsule (has foot processes which join with others to give slit pores e.g. nephrin- pores are the key selective barrier in the filtration process and prevent the passage of larger molecules, also -ve charge)
14
Q
What are podocytes?
A
cells in the bowmans capsule that wrap around capillaries of the glomerulus. They form a filtration barrier with endothelial cells and the GBM.
15
Q
Where in the tubule does most of reabsorption occur?
A
Proximal tubule
16
Q
What is the function of the loop of Henle on a basic level?
A
concentrates urine
17
Q
What type of epithelium is Bowmans capsule?
A
thin squamous epithelial cells
18
Q
What type of epithelium is in the tubules?
A
columnar epithelial cells which are specialised for transport processes
19
Q
Which substances are reabsorbed in the proximal tubule?
A
Na2+, K+, Cl-, PO3, glucose, amino acids and water
20
Q
Does water move with substances?
A
Yes- this keeps the filtrate diluted. Where salt goes, water goes
21
Q
What is the juxtaglomerular apparatus?
A
it consists of the macula densa, extraglomerular mesangial cells and granular cells.
22
Q
What is the function of the juxtaglomerular apparatus?
A
Regulates BP and monitor GFR
23
Q
What do the efferent arterioles form in the juxtaglomerular nephron?
A
Vasa recta and peritubular capillaries
24
Q
What is the function of the vasa recta?
A
it is the sole blood supply to the medulla of the kidney
25
Which hormones act on the kidney?
ADH, Aldosterone, natriuretic peptides and PTH
26
What effect does ADH have on the kidneys?
It promotes water reabsorption in the collecting ducts - concentrates urine
27
What effect does Aldosterone have on the kidneys?
Sodium reabsorption in the collecting ducts and excretion of potassium
28
What effect does natriuretic peptides have on the kidneys?
They are produced by the cardiac cells and promote sodium excretion in the collecting ducts
29
What effect does PTH have on the kidney?
it promotes renal phosphate excretion, calcium reabsorption and vitamin D production
30
What hormones are produced by the kidney?
Renin, Vitamin D, erythropoietin and prostaglandins
31
What is the effect of Renin?
It is released by the juxtoglomerular apparatus and results in the formation of angiotensin II which acts directly on the proximal tubules and via aldosterone on the distal tubules to promote sodium retention and vasodilates
32
When is renin released?
When baroreceptors sense a drop in BP and when the macula densa senses a drop in salt
33
What is the metabolism of vitamin D?
It is metabolised int he kidney to the active form 1,25-dihydroxycholecalciferol
34
What is the function of vitamin D?
Promotes calcium and phosphate absorption from the gut
35
Where does erythropoeitin work on?
The stem cells in the bone marrow to differentiate them into RBC's
36
What makes up the glomerular basement membrane?
collagen type IV, heparin sulfate proteoglycans and lamina
37
What are foot-like processes?
They are projected from podocytes (specialised epithelial cells) and interdigitate to form filtration slits
38
What is the importance of the foot like processes and podocytes?
They stop large anions from being filtrated
39
What factors of the substances affect filtration across the bowmans capsule?
weight and charge. Smaller substances cross easily, large ones don't. Negatively charged ions are not filtered as freely as positively charged ions because the epithelium is negatively charged
40
What is the triad of symptoms of nephrotic syndrome?
Proteinuria, hypoalbuminaemia and oedema
41
What is fucked in minimal change disease?
Under a light microscope there is nothing to see but under electron microscope there is pathology of the podocytes. There is diffuse effacement of the foot processes of podocytes causing the widening of filtration slits
42
What are the 2 sections of the proximal convoluted tubule?
Para convolute (renal cortex) and pars recta (renal medulla)
43
What is the driving force for the reabsorption in the PCt?
Sodium, which is followed by chloride ions to keep electro-neurtality
44
What is transcellular transport?
Transporting solutes through a cell
45
What is paracellular transport?
Transporting solutes via the tight junctions between cells
46
What is the effect of the sodium-potassium pump?
Sodium out, potassium in
47
Where are SGLUT transporters found and what do they transport?
Found on the apical membrane of the PCT and transport sodium and glucose
48
How does glucose cross the basolateral membrane?
Facilitated diffusion
49
Which is the most common primary renal cancer?
Renal cell carcinoma
50
Where does RCC originate?
The PCT
51
What are the symptoms of renal cell carcinomas?
Mostly occurs in men and causes haematuria, flank pain, weight loss and fever
52
What is the cause of acute tubular necrosis?
It can be caused by ischaemia which usually occurs secondary to reduced renal blood flow (hypotension or sepsis)
53
Where are Na/K-ATPase channels found?
the basolateral membrane
54
What happens to SGLT channels when there is too much glucose?
When glucose exceeds the transport max, glucose spills into the urine and water follows.
55
Where is the primary site of sodium reabsorption in the loop of henle?
thick ascending limb
56
Which part of the loop of Henle is impermeable to water?
Thick ascending limb
57
How is sodium reabsorbed in the loop of Henle?
It is reabsorbed via the NKCC2 transporter on the thick ascending loop
58
What is the action of the NKCC2 transporter?
Moves sodium, potassium and 2 chloride ions
59
What is the action of the ROMK transporter?
Moves potassium back into the tubule to prevent toxins from building up
60
Is sodium reabsorbed in the thin ascending limb?
Yes- it moves paracellularly due to the difference in osmolarity between the tubule and interstitium
61
What is the effect on water of sodium reabsorption in the thin ascending limb?
It is reabsorbed from the descending limb- counter current multiplication
62
Is sodium reabsorbed in the thin ascending limb?
No
63
What is Bartter Syndrome?
It is a group of autosomal recessive conditions caused by genetic mutations in the genes that code for NKCC2 which causes Na to get reabsorbed in the distal tubule leading K to be excreted into the tubule leading to hypokalaemia and hypovolaemia
64
Which group of drugs work on the NKCC2 transporter?
Loop diuretics (furosemide) to increase excretion of NaCl in the urine
65
What is the role of the early distal convoluted tubule?
Reabsorption of Na, Cl and Ca
66
What is the channel on the early DCT?
Sodium-potassium pump. Na out and K in. And the NCC symporter- Na and Cl in from the urine
67
What are the cells of the late distal convuluted tubule?
Principal cells: involved in sodium and potassium exchange and intercalated cells: control hydrogen and bicarbonate ions
68
How does hydrogen move into the lumen?
By the K/H-ATPase antiporter. It then binds to ammonia or phosphate so that it cannot cross again and is excreted in the urine
69
How does ADH increase sodium reabsorption?
It acts on the kidney to increase the number of aquaporin 2 channels in the apical membrane of the tubular cells of the collecting duct.
70
Which water channels are on the basolateral membrane?
Aquaporins 3 and 4
71
What are the features of the descending loop of henle?
it is permeable to water but not to salt
72
What are the features of the ascending loop of henle?
it is impermeable to water but permeable to salt. NaCl is pumped out the thick ascending limb actively to dilute the filtrate since it gets really salty in the LOH.
73
Where is bicarbonate reabsorbed?
in the PCT then the remaining in the DCT
74
Where is urea reabsorbed?
It is reabsorbed in the collecting duct and can be recycled at the loop of henle for water reabsorption.
75
What does a lack of ADH do to the collecting duct?
This happens when a patient is overhydrated. This will make the collecting ducts impermeable to water so that it has to pass into the urine
76
What makes up the renal corpuscle?
Glomerulus and Bowmans capsule
77
What is Oncotic pressure?
Pressure exerted by plasma proteins on the walls of the compartment in which they are contained
78
What pressure is the major driving force for filtration?
Hydrostatic pressure of the glomerulus (forces fluid out of the capillary)
79
What are the forces involved in filtration at the bowmans capsule?
From capillary to bowmans capsule:
Glomerular capillary blood pressure 55mmHg
Bowmans capsule oncotic pressure 0mmHg
From bowmans capsule acting on the capillary:
Bowmans capsule hydrostatic fluid pressure 15mmHg
Capillary oncotic pressure 15mmHg
Think: Glomerular Blood (55+0) and Bowmans Capsule (15+30)
80
What is the net filtration pressure?
(55+0) - (15+30) = 10mmHg
81
What is the GFR?
The total amount of filtrate formed by all the renal corpuscles in both kidneys per minute
82
What are the factors that influence GFR?
Net filtration pressure, surface area available for filtration and permeability of the glomeruli
83
What happens if the afferent arteriole is constricted?
Then this causes the hydrostatic pressure of the glomeruli to decrease due to a reduction of blood available for filtration and therefore GFR will decrease
84
Why can water move passively in the descending loop of henle?
Because the medulla is so salty
85
How does countercurrent multiplication work?
Water is passively pumped out of the descending loop because it is a salty environment which dilutes the interstitial fluid but then in the ascending loop NaCl is pumped out. There is a gradient in place of a difference of 200mosmol/L
86
What is the function of the Na+/H+ exchanger (NHE3)?
To move sodium out and hydrogen in
87
How is secretion of H+ by the sodium/hydrogen exchanger balanced?
by the exit of bicarbonate
88
What is the net effect of NKCC2 and ROMK channels in the thick ascending loop?
NKCC2: 1 sodium, 2 chloride and 1 potassium leave
ROMK: 1 potassium in
Net: 1 sodium and 2 chloride leave
89
What channel reabsorbs sodium in the distal convoluted tubule?
The NCC channel
90
What drug acts on the distal tubule to prevent sodium reabsorption?
Thiazide diuretics
91
What is the final stage of sodium chloride reabsorption?
In the collecting ducts, the principal cells have ENaC channels which lets sodium leave the cell. Chloride leaves the intercalated cells.
92
Which channel is most important for
a) the absorption of potassium
B) the secretion of potassium
A) Na/K ATPase
| B) ROMK
93
What factors increase K+ secretion?
Increased luminal flow which can be caused by volume expansion, acidosis and diuretics
94
What effect does Aldosterone have on K+ secretion?
high aldosterone: increase Na reabsorption and increase K secretion. Does this through ENaC channels
95
What is the clearance of glucose?
0
96
What is hypotonic?
More water outside than inside so increase in cell volume
97
What is hypertonic?
More water in the cell than outside so water moves out causing the cell to shrink
98
What is a normal GFR?
90-120mL/min/1.73 squared
99
What effect does an increase in glomerular capillary BP have on GFR?
Increased net filtration and increase GFR
100
How may the glomerular capillary BP fall?
From vasoconstriction of the afferent arteriole
101
What is autoregulation?
prevents short term changes in the systemic arterial pressure affecting GFR
102
What is the function of the macula densa?
sence NaCl content of tubular fluid and cause the afferent arteriole to constrict
103
What is inulin clearance?
It is a marker of GFr since it is freely filtered at the glomerulus, neither absorbed nor secreted, not metabolised by the kidney, not toxic and easily measured in urine and blood
104
What is used as a marker for GFR?
Creatinine- it is approximate and easier to measure than inulin
105
Where is glucose reabsorbed in the tubule?
PCT
106
What is the tonicity of the filtrate in the loop of henle?
It is isoosmotic in the descending loop and hypoosmotic in the descending loop
107
Where is the highest osmolarity? the Renal cortex or medulla?
Medulla
108
What is the point in countercurrent multiplication?
to concentrate the medullary interstital fluid to enable the kidney to produce urine of different volumes and concentration according to the amounts of circulating ADH
109
Why is the vasa recta a countercurrent exchanger?
Because as it dips down into the medulla water is lost and as it rises water is gained
110
What is diabetes insipidus?
It is due to too little ADH or insufficient response to ADH
111
What is the treatment of diabetes insipidus?
ADH replacement
112
What are the effects of Angiotensin II?
1. stimulates the adrenal cortex to release aldosterone to increase sodium reabsorption
2. arteriolar vasoconstriction
3. thirst
4. Vasopressin (ADH)- increase water reabsorption
113
What stimulates release of Renin?
Low salt, low ECF and a drop in BP
114
Where is Renin released from?
It is released from granular cells near the macula densa
115
When might RAAS be inappropriate in a falling BP?
Congestive heart failure
116
What is the treatment for congestive heart failure?
Loop diuretic
117
What is the mechanism of ACE inhibitors?
stop fluid and salt retention and arteriolar vasoconstriction- they lower BP
118
What is the effect of ANP?
It is released in response to the heart stretching and causes increased excretion of sodium, vasodilation (increase in GFR), decrease in BP from a decrease in CO and TPR
119
What are the mechanisms of micturation?
Micturation reflex and voluntary control
120
What is the micturation reflex?
It causes involuntary emptying of the bladder by simultaneous bladder contraction and opening of both the internal and external urethral sphincters
121
What does the Davenport diagram show?
Resp Acidosis metabolic acidosis
Metabolic acidosis resp acidosis
122
What are causes of respiratory alkalosis?
low inspired PCO2 at altitude, hyperventilation, hysterical overbreathing
123
What are causes of metabolic acidosis?
Starvation ketoacidosis, alcoholic ketoacidosis, DKA, paracetamol, increased urea, lactic acidosis, ethanol
124
What are causes of metabolic alkalosis?
Vomiting, aldosterone production, ingestion of alkali
125
What is stage 1 CKD?
GFR of >/= 90 with renal damage
126
What is stage 2 CKD?
GFR of 89-60 with kidney damage
127
What is stage 3 CKD?
GFR of 59-30
128
What is stage 4 CKD?
GFR of 15-29
129
What is stage 5 CKD?
GFR <15
130
At what stage of CKD would you consider prepping for dialysis?
Stage 4, Have to have dialysis by stage 5
131
What are the factors that may affect the creatinine level?
Age, sex, muscle mass, diet and race
132
What is eGFR?
Estimated GFR based on the patients serum creatinine, age, sex and race
133
What is proteinuria?
When there is more than 150mg/day in the urine which signifies significant glomerular damage
134
What is microalbuminuria?
Moderate increase in the level of urine albumin. it occurs when the kidney leaks small amounts of albumin into the urine. it is still low enough to be undetected by urine dipstick
135
What is ACR?
Albumin creatinine ration
136
What is ACR used for?
detecting small amounts of protein in the urine
137
What is PCR?
Protein creatinine ratio
138
What is PCR used for?
It should be used rather than ACR in pregnancy and where non-albumin proteinuria is suspected
139
What does an ACR of more than 30mg/mmol mean?
Proteinuria or nephrotic syndrome
140
What is a normal ACR?
Around 3mg/mmol
141
What causes a pre-renal AKI?
Reduced renal perfusion which can be caused by blood loss and hypovolaemia
142
What causes a post-renal AKI?
Ureteric/urethral obstruction by stones or malignancy
143
What causes a renal AKI?
intrinsic kidney tissue damage which can be due to GN or nephrotoxins
144
What effect does AKI's have on urea?
Urea is raised in kidney damage so the urine:serum urea ratio is much worse in renal AKI than pre-renal
145
What is an AKI?
An abrupt (<48 hours) reduction in kidney function defined as:
An absolute increase in serum creatinine by >25.4 micromols/L
OR an increase in creatinine by >50%
OR a reduction in urine output
Can only be applied following adequate fluid resuscitation and exclusion/ obstruction
146
What is a stage 1 AKI?
Increase >26 micromol/L or >50% increase in serum Cr (1.5-1.9x).
Urine: <0.5ml/Kg/hr for >6 consecutive hours
147
What is a stage 2 AKI?
Increase >/= 2-2.9x reference serum Cr
| Urine: <0.5ml/kg/hr for >15 hours
148
What is a stage 3 AKI?
Increase in more than 3x reference serum Cr or increase to more than or equal to 354 micromol/L or need for RRT
Urine: <0.3ml/Kg/hr for >24 hours
149
What is the normal creatinine level?
Women: 45-90
Men: 60-110
150
What is the normal urine output?
1.5ml/kg/hr
151
What are the causes of a pre-renal AKI?
Hypovolaemia (haemorrhage, volume depletion), hypotension (cardiogenic shock, anaphylaxis, sepsis) and renal hypoperfusion (NSAIDs, ACEi, ARBs, hepatorenal syndrome)
152
What can untreated pre-renal AKI lead to?
Acute tubular necrosis
153
What is acute tubular necrosis?
death of tubular epithelial cells that form the renal tubules. It is the most common cause of AKI. Often caused by sepsis and severe dehydration. Can also be caused by rhabdomyolysis and drug toxicity
154
What is the treatment for pre-renal AKI?
Assess for hydration and give fluid challenge- crystalloid 0.9% NaCl and reassess
155
What are the causes of renal AKI?
Blood vessels: Vasculitis, renovascular disease
Glomerular: GN
interstital injury: drugs, infection (TB), systemic (sarcoid)
Tubular injury: Ischaemia, drugs (gentamicin), contrast, rhabdomyolysis
156
What are the signs of a renal AKI?
anorexia, weight loss, fatigue, lethargy, N&V, itch, fluid overload (oedema, SOB), Oligiuria, uraemia
157
What is the treatment for Renal AKI's?
good perfusion, fluid resuscitation, dopamine/epinephrine/vasopressin. May require uregnat dialysis
158
What are the complications of an AKI?
Hyperkalaemia, fluid overload, severe acidosis, uraemic pericardial effusion, severe uraemia
159
What is a post-renal AKI?
AKI due to obstruction of urine flow leading to back pressure (hydronephrosis) and then loss of concentrating ability
160
What are the causes of a post renal AKI?
Stones, cancers, strictures, extrinsic pressures
161
What is the treatment of a post renal AKI?
Relieve obstruction, ureteric stenting, catheter
162
What are the ECG changes associated with hyperkalaemia?
Peaked T waves, flattened P wave, QRS prolonged, sine wave
163
What is the treatment for hyperkalaemia?
Calcium gluconate, insulin, dextrose, nebulised salbutamol, calcium resonium
164
What management protects the myocardium in hyperkalameia?
Calcium gluconate
165
What management moves potassium back into the cells?
Insulin, salbutamol
166
What drug prevents K+ absorption from the digestive tract?
Calcium resonium
167
What are urgent indications for haemodialysis?
Hyperkalaemia (>7), severe acidosis, fluid overload, urea >40, pericardial effusion
168
How do you treat pulmonary oedema?
```
sit up and give high flow oxygen
venous vasodilator e.g. diamorphine
furosemide
haemodialysis
Consider CPAP
```
169
What are the sick day rules?
if there is V&D or fevers, sweats or shakes for more than 24 hours then stop taking the tablets until the patients feel well enough.
170
Which medications should be stopped in the sick day rules?
NSAIDs, ACEi, ARBs, Diuretics, diabetic medication
171
What may low platelets in AKI may indicate?
haemolytic uraemic syndrome
172
What is bence jones protein? and What is the test for this?
Protein electrophoresis and it is indicative of myeloma
173
Does the risk of CKD increase with age?
Yes
174
What is needed to make a diagnosis of CKD?
2 samples 90 days apart
175
How bad is the prognosis based on eGFR and ACR?
The lower the eGFR and the higher the ACR the worse the prognosis
176
How is the stage of AKI done?
using creatinine and urine output
177
How long do you monitor patients for CKD after they have had an AKI?
2-3 years after
178
What accounts for an accelerated progression of CKD?
Decrease in serum Cr of 25% per year or 15ml/min/1.73 squared
179
When should someone be referred for a CKD?
```
CFR <30
ACR >70
ACR >30 with haematuria
decrease in GFR by 25% yearly
decrease in GFR by 15ml/min/1.73squared yearly
poorly controlled hypertension after use of 4 hypertensives
known genetic causes of CKD
suspected renal artery stenosis
```
180
What is the BP aims in those with CKD?
SBP below 140 and DBP below 90
181
What is given as a prophylaxis of CVD in those with CKD?
Atorvastatin
182
What are the causes of CKD?
Diabetes, hypertension, GN, renal artery stensosis, vasculitis, acute interstitial nephritis, ADPKD, calculi, prostatic, bladder malignancy, ureteric stricture
183
What are signs of advanced urea?
lemon yellow, uraemic frost (crystallised urea deposits), twitching, encephalopathic flap, confusion, pericardial rub, kassmaul breathing
184
What are the complications of CKD?
haemorrhage, haematuria, proteinuria, impaired salt balance, hypertension, acid base disturbance, electrolyte disturbance, end stage renal disease
185
What effect does kidney dysfunction have on mineral bone disease?
there is insufficient mineral homeostasis. Beginning in CKD3 the kidneys cannot excrete phosphate leading to hyperphosphataemia, increased PTH, decreased vit D. Vitamin D metabolism is impaired reducing calcium and increasing PTH
186
What is the treatment for CKD-MBD?
Alfacalcidol, phosphate binders, cinacalet
187
Which membrane do diuretics act on?
The apical membrane
188
How do diuretics enter the filtrate?
glomerular filtration, secretion by organic anion and cation transporters
189
Where do loop diuretics act?
e.g. furosemide actons on the NKCC2 transporter on the thick ascending limb to prevent reabsorption of Na, Cl and K (causes K loss due to ROMK)
190
What are the side effects of loop diuretics?
hypokalaemia, metabolic alkalosis and hypovolaemia
191
What are examples of thiazide diuretics?
Bendroflumethiazide
192
Where do thiazide diuretics work?
They work on the DCT to inhibit the NaCl transporter causing decrease salt and water reabsorption
193
What is an example of potassium sparing diuretics?
Spironolactone
194
Where do potassium sparing diuretics work?
They work on the late distal tubule and inhibit the action of aldosterone and block sodium channels decreasing potassium excretion and increasing sodium excretion
195
Where do osmotic diuretics (mannitol) work?
On the PCT to increase water excretion
196
Where do carbonic anhydrase inhibitors work (acetazolamide)?
Proximal tubule by increasing secretion of HCO3, Na, K, and H2O
197
What are the symptoms of nephrotic syndrome?
proteinuria, hypoalbuminuria, hypercholesterolaemia and oedema
198
What are the symptoms of nephritic syndrome?
proteinuria and haematuria
199
Does nephrotic or nephritic syndrome have a worse GFR?
Nephritic
200
What are the types of GN that cause nephrotic syndrome?
membranous, minimal change, focal segmental glomerulosclerosis, mesangiocapillary, SLE, amyloid, diabetes, hepatitis
201
What types of GN cause nephritic syndrome?
IgA nephropathy, mesangiocapillary, post strep, vasculitits, SLE, Anti-GBM, cyroglobulinaemia
202
What is the most common GN?
IgA nephropathy
203
What are the features of IgA nephropathy?
microscopic haematuria, increased IgA which forms immune complexes and deposits on mesangial cells of IgA and C3
204
What blood pressure medication is okay to take with IgA nephropathy?
ACEi
205
What is Henoch Schonlein purpura?
systemic variant of IgA nephropathy causing a small vessel vasculitis. Features are purpuric rash on extensor surfaces, polyarthritis, abdominal pain and nephritis
206
How do you confirm the diagnosis of HSP?
IgA and C3 on immunofluoresence
207
What are the classifications of SLE GN?
Class I: minimal mesangial lupus nephritis
Class II: mesangial lupus nephritis
Class III: focal proliferative lupus nephritis (<50%)
Class IV: diffuse proliferative lupus nephritis (>50%)
Class V: membranous lupus nephritis
208
What is Goodpastures syndrome?
When there is anti-GBM antibobies to the type IV collagen of the basement membrane
209
How does goodpastures syndrome present?
Haematuria and nephritic syndrome
210
What is the treatment of goodpastures syndrome?
plasma exchange, steroids and cytotoxics
211
What is post streptococcal GN?
a diffuse proliferative GN that occurs 1-12 weeks after a sore throat or skin infection. A streptococcal antigen is deposited on the glomerulus causing a host reaction and immune complex formation.
212
What can be seen on immunofluoresence of streptococcal GN?
IgG and C3
213
What is rapidly progressive GN?
proliferative GN characterised by acute deterioration of kidney function associate with cresent formation around the glomerulus. Most aggressive forms of GN
214
What are the 3 categories of rapidly progressive GN?
Immune complex disease: post-infectious, SLE, IgA/HSP
Pauci-immune disease- Vasculitis related
Anti-GBM disease
215
What is the presentation of rapidly progressive GN?
AKI with systemic features such as fever, myalgia, weight loss, haemoptysis, pulmonary haemorrhage
216
What is the treatment of rapidly progressive GN?
Aggressive immunosuppression with high dose steroids IV and cyclophosphamide +/- plasma exchange
217
What is the main cause of proteinuria?
injury to the podocyte
218
What is the most common cause of GN in children?
Minimal change
219
What is the treatment of Minimal change GN?
a trial of steroids or can resolve spontaneously
220
Do you biopsy patients with GN?
Yes in adults but not in children
221
Generally, what is the treatment of nephrotic syndrome?
Reduce oedema with loop diuretics, reduce proteinuria with ACEi, reduce risk of complications with statins and treat the underlying disease
222
What are the features of minimal change disease?
Normal biopsy, electron microscopy shows effacement of the podocyte foot processess. they have nephrotic syndrome and frothy urine.
223
What causes membranous nephropathy?
Usually idiopathic but can be due to malignancy, hep B, drugs (gold, penicillin, NSAIDs) and autoimmunity
224
What does biopsy in membranous nephropathy look like?
diffusely thickened GBM with IgG and C3 subepithelial deposits
225
What antibodies are found in those with idiopathic membranous nephropathy?
anti-PLA2
226
What is mesangiocapillary GN?
Can be immune complex mediated or complement mediated.
Immune complex:driven by circulating immune complexes which deposit in the kidney and activate complement via the classical pathway
Complement: less common and involves persistent activation of the alternative complement pathway e.g. C3 nephritic factor
227
What can be seen on biopsy in mesangiocapillary GN?
mesangial and endocapillary proliferation, a thickened capillary basement membrane, double contouring of the capillary walls
228
What is FSGS?
Segments of glomeruli develop sclerosis. presents with nephrotic syndrome. 50% progress to renal failure
229
What is seen on immunofluoresence of FSGS?
IgM and C3
230
What is the treatment of FSGS?
Corticosteroids or cyclophosphamide or ciclosporin if resistant
231
What is tubulointerstitial nephritis?
inflammation of the renal interstitium
232
What causes acute interstitial nephritis?
immune reaction to drugs, infections or autoimmune disorders e.g. NSAIDs, antibiotics, diuretics, allopurinol, omeprazole, phenytoin, staph/strep, SLE, sarcoid
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What is the treatment of interstital nephritis?
stop the drug, conservative treatment and if not improved in a week then consider starting prednisolone
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What things are nephrotoxic?
Gentamicin, NSAIDs and contrast
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What is Rhabdomyolysis?
results from skeletal muscle breakdown with release of its contents into the circulation including myoglobin, potassium, urate and CK
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How does rhabdomyolysis cause AKI's?
Myoglobin is filtered by the glomeruli and precipitates obstructing renal tubules
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What are the features of rhabdomyolysis?
muscle pain, swelling, tenderness and red-brown urine
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What confirms the diagnosis of rhabdomyolysis?
CK >1000, tea coloured urine, urinalysis +ve for blood
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What is the treatment of rhabdomyolysis?
Urgent treatment for hyperkalaemia, IV fluid rehydration is a priority to prevent AKI and sodium bicarbonate to alkalinse the urine
