renal Flashcards
5 functions of the kidney
- creating hormones to tell the bone marrow to create their blood cells - erythropeitin
- controls ph
- metabolises vitamin d
- blood volume /fliud management
- waste/toxin/drug extretion
how do we measure how well the kidney is doing?
creatinine -
- can only really be made in the body by muscles
- waste priduct of muscle metabolism
purely excreted by kidneys
- longstanding measure of kidney function
- small increases in creatinine = large changes in eGFR
causes of stepwise decline in GFR
medication
insterstitial cystitis
AKI gfr picture
rapid decline and then level off
newly identified CKD gfr
stable low gfr
what can suggest poor working kidneys
proteinuria/abluminuria
how do you measure proteinuria
problems with it
how to do it more accurately
urine dipstick
problems - just a snapshot, influenced by dilution, have to write it down
accuracy - albumin/creatinine ration
- albumin + creatinine is secreted into urine at constant rate therefore should always be the same ratio
how does kidney failure cause iron-deficiency anaemia
liverproduces hepcidin which is cleared by the kidney.
this doesnt happen as much so you get a build up …
what gfr would make you want to start dialysis
6-8
how does kidney failure cause iron-deficiency anaemia
liver produces toxin hepcidin which is cleared by the kidney.
this doesnt happen as much so you get a build up which inhibits iron absorption by the duodenum
AKI definition
sudden decline in GFR baseline/increase in creatinine with or without oliguria (<0.5ml/kg/hr) / anuria (< 50ml/day)
what is diagnosis of AKI based on
creatinine and urine output
causes of AKI
prerenal - hypovolaemia
- volume depletion - diarrhoea, blod loss, dehydration
- low cardiac output - MI, HF
- sepsis
- drugs - ACE i, NSAIDs
- renal artery stenosis
renal - internal structures
- vascular = vasculitis, malignant hypertension
- tubular = acute tubular necrosis, rhabdomyolysis, myeloma, **radiocontrast (common), drugs (antibiotics)
- glomerular eg glomerulonephritis
- interstitial eg interstitial nephririts
post-renal - obstruction with outflow tract of urine
- stones
- tumours
- strictures
- enlarged prostate
- blood clots
risk factors of AKI
- elderly
- CKD
- chronic conditions eg DM, HF (on eg ACEi, ARB, diuretics), liver disease
- neurological/cognitive impairment (low fluid intake)
- cancer - myeloma (light chains directly affect kidneys)
- previous AKI
- post-op
- medications
- radiocontrast
- sodium retaining states - CHF, cirrhosis, nephrotic syndrome
medications and how they affect the kidney causing AKI
direct effect
- NSAIDs - interstitial nephritis
- antibiotics - toxic effect to tubular cells (penicillin, rimapicin, gold, gentamycin), ATN - aminoglycosides, amphotericin, ciclosporin
accumulation during renal dysfunction
- metformin (can cause hyperglycaemia)
effects on renal/fluid/electrolyte physiology
- ACEi - cause AKI, increase potassium,
- diuretics - overdiuresis (prerenal)
drugs causing GI loss (laxatives - prerenal)
post-renal - causing retention
- anticholinergics
- alc
presentation of AKI
- depends on underlying cause
- incidental finding of raised creatinine
clinically =
- high urea from decreased excretion = nausea, vomiting, decreased consciousness
- hyponatraemia from excess of water relative to sodium = peripheral + pulm oedema, ascites, pleural effusion
- hyperkalaemia from decreased excretion + metabolic acidosis = muscle weakness + ECG changes
- met acidosis from decreased h+ ion secretion = kussmaul breathing
effect an AKI has on body
Impaired clearance and regulation of metabolic homeostasis, impaired acid-base, electrolyte and volume regulation
why is creatinine used as marker of GFR
creatinine
- waste product of normal muscle breakdown
- marker of GFR - used as its only excreted renally, freely filtered at glom, not reabsorbed, generally remains constant
- looking for changes in creatinine if problem
when is eGFR not valid
when creatinine is changing
what affects creatinine levels
muscle mass
ethnicity
gender
age
stages of AKI
KDIGO guidelines for adults
looks at serum creatinine and urine output - both dont need to be present for diagnosis
stage 1 - creatinine increase 1.5x in 7 days OR creatinine >/= 26.5 umol/L in 48 hrs. UO = <0.5ml/kg/hr for 6 hours
stage 2 - creatinine increase 2x in 7 days
UO = <0.5ml/kg/hr for 12 hours
stage 3 - creatinine 3x baseline in 7 days
cr >354
RRT started
UO = <0.3ml/kg/hr for 24 hours or anuria for 12 hours
false positives of AKI alerts from algorithm
causes
recent pregnancy
drugs - trimethoprim (they increase creatinine)
contamination
false negative of AKI alerts from algorithm causes
previous AKI within last year
what is AKI on CKD
when you have sudden decline in renal function with known CKD
normal size of kidneys
11-14cm
GFR normal
120 ml/min/1.73m
20% of CO
eGFR what is it
Predict creatinine generation age, gender, race, sex (n.b. Extreme muscle mass e.g. cachexia/body builder = misleading
creatinine
what is it
Chemical waste product from muscle metabolism
Secreted as well as filtered!
Therefore Cr clearance is > GFR
Therefore inhibitors of secretion will make Cr rise and function look worse e.g. trimethoprim
volume control
Aldosterone (adrenal) -> decreased excretion
Angiotensin II -> decreased excretion
ANP - released by heart in response to high pressure -> increases excretion
N.b. diuretics are not nephrotoxic but hypovolaemia is!
pressure control
RAAS - renin-angiotensin- aldosterone system
responds to low BP
angiotensinogen released from liver -> travels to kidney which spots low bp at juxtaglomerular apparatus in afferent arteriole and releases renin -> converts the angiotensinogen to angiotensin I
-> this gets converted to angiotensin II by ACE on surface of pulm and renal epithelium
angiotensin II =
1. increase sympth activity
2. tubular Na Cl reabsorption, and k excretion, h2o retention
3. adrenal gland cortex to secrete aldosterone -> 2.
4. arteriolar vasoconstriction, increase in blood pressure
5. pituitary gland post lobe -> ADH secretion -> collecting duct: H20 absorption
ACEi indications dose SE CI
indications
HTN, heart failure, post MI
dose
1.25/2.5mg PO ON
SE
- electrolytes - hyperkalaemia (by decrease aldosterone), reduce GFR
- post hypo
- dry cough - bradykinin
- fatigue
CI
Hypersensitivity. Pregnancy. Monitor closely if hepatic/renal impairment
ARB mech indication dose SE CI
angiotensin 2 receptor blockers
mech
Modulation of RAAS, similar to ACEI but no dry cough
indication
HTN, heart failure, diabetic nephropathy
dose
Losartan - usually 50mg PO OD, elderly =- 25mg PO OD
SE
Renal impairment
Postural hypotension
Hyperkalaemia
CI
Avoid in pregnancy, beware use with other RAAS drugs esp. Aliskiren (direct renin inhibitor) and other drugs causing hyperkalaemia
sodium reabsorption
70% proximal tubule
25% loop of henle
5% DCT
2% collecting duct
potassium control
hypo/per kal meds
Potassium freely filtered at proximal tubule and loop of henle
Distal secretion determines renal excretion (Na, aldosterone driven)
Hypokalaemia meds:
- Loop diuretics, thiazide diuretics
Hyperkalaemia meds:
- Spironolactone, amiloride, ACEI, ARB
erythropoietin function
stimulates RBC production
Renal cortex acts as an O2 sensor; blood flow and oxygen requirement matched. (GFR)
Therefore at low GFR anaemia may occur (GFR < 30)
what does 1-alpha hydroxylation of vitamin D cause kidney to do
inhibited by
@ proximal tubule calcitriol increases Ca and PO4 absorption from gut and suppresses PTH
*This process is inhibited by FGF-23 which is increased in CKD
whats in the renal medulla
loop of henle + collecting tubule
these are the pyramids
active transport
Move up concentration or electrochemical gradient. Energy dependent
passive transport
Move down concentration or electrochemical gradient.
PCT
% absorption
what absorbed?
70%
most essential stuff absorbed here
Nutrients - Glucose (why diabetics pee a loy) - Amino acids Ions - Na (As NA2HCO3 or NaCl), K, Cl Small plasma proteins Some urea and uric acid
sodium/pot ATPase channel
how many in/out
3 out sodium
2 in pot
maintains sodium conc gradient
requires energy
loop of henle
what is absorbed at thin descending limn
and thick ascending limb - key transporter, diuretic that works here + its effect
disorder that works on ascending thick limb
thin descending limb
water
thick ascending limb
- concentrates or dilutes fluid by countercurrent multiplication
- 25% sodium
- key transporter = NKCC2 (Na, k, Cl cotransporter - energy dependent)
- diuretic = furose
- effect = hypotens, hyponat, kal (dig tox), hypochlor, mag (indirect), calc (indirect), alkalosis (loss of hydrogen ions - indirect), inhibit uric acid excretion -> lead to gout
barters syndrome - same effect as loop diuretic , early childhood, low serum mag, urine calc high, conc capacity severely impaired, AR, met alk
DCT + CD
sodium
transporters
hormones
sodium
5% @ early DCT, 3% @ late DCT and CD determining how much sodium is excreted
transporters
Sodium/potassium ATPase drives reabsorption of calcium and chloride
hormones
Sodium reabsorption is regulated by hormones which stimulate or inhibit sodium resorption as required
Aldosterone and ADH
DCT function channel hormones diuretic syndrome
function
- Reabsorbs Na through coupled secretion of H+ or K+ ions into tubular fluid via aldosterone
- Acidifies urine (acid-base balance) through secretion of hydrogen or ammonium (LATE)
- Electrolyte homeostasis - Ca reabsorption via vitamin D dependent process
- Part of juxtaglomerular apparatus (renin for haemodynamic regulation, macula densa senses intra-cellular Cl)
channel
Passive Na/Cl co-transporter prevents reapsorption of sodium and water
hormones
1. PTH - Ca reabsorbed and phosphate excreted
2. *Aldosterone - More Na absorbed (ENaC), more K excreted
(ROMK) - mainly at CD
3. ANP - causes DCT to excrete Na
diuretic
thiazide
- Hypotension, hyponatraemia, hypokalaemia (increased delivery of
sodium to distal tubule where it may be exchanged for potassium)
- Over time may activate RAAS (normally prescribed with ACEI) -> hypokalaemia = cardiac arrhythmias
May increase plasma concentration of glucose
Gitelmans syndrome - same effect as thiazide
- late childhood
- serum mag always decreased, urine calc normal/low, conc cap may be impaired
- AR
- met alk
CD fucntion cell types channels hormones mechanism drugs acting here syndrome
function Concentration of urine and acid/base balance
cell types Principal cells (respond to aldosterone and vasopressin affecting sodium/potassium) + alpha intercalated cells \+ beta intercalated cells (secrete H+)
channels
ENaC
ROMK
both @ principle cells
hormones
aldosterone and ADH/vasopressin
mech
Aldosterone (steroid/binds nucleus) increases expression of
ENaC in apical membrane and N+/K+ antiporters
Vasopressin binds V2 channels inserts aquaporin 2 channel
to apical membrane allowing free movement of water
Alpha intercalated cells (damage can result in distal renal tubular
acidosis - classical) - secrete acid to urine
Beta intercalated cells - secrete bicarbonate to urine
drugs
1. aldosterone antagonists - spironolactone, competitive binding of aldosterone receptor, causes hypotension, hyponat, hyperkal, gynaecomastia
- potassium sparing diuretic - amiloride (may use with furose to counteract pot loss - co-amilofruse)
- @DCT inhibs absorb sodium and water @ ENaC
- hypotension, hyponat, hyperkal
liddles syndrome
= opposite effect to pot sparing diuretics, acts at ENaC, causes HTN, hypokalaemia, AD, met alk
how to calc, phos and mag move in kidney
calc similar to sodium
phosphate - glucose
mag - ascending limb of loop of henle
renal tubular acidosis what is it what it causes assoc syndrome types RFs pres ix mgmt comps
what is it
Numerous disorders in which excretion of acid or reabsorption of bicarbonate is absorbed disproportionately to GFR
results in
Hyperchloraemic metabolic acidosis + hypobicarbonataemia + decreased arterial pH + normal anion gap
May be hypokalaemic or hyperkalaemic depending on defect
fanconi syndrome
Generalised dysfunction of renal proximal tubule -> urinary loss of bicarb, glucose, aa, phosphate, peptides, organic acids. Leads to salt wasting and volume depletion
types 1 = CLASSIC DISTAL inability to excrete H+ in distal tubules min urine pH >5.5 low serum pot, plasma bicarb <10 comp = stones/nephrocalcinosis
2= INHERITED ISOLATED PROXIMAL inability to reabsorb bicarbonate min urine PH <5.5 serum pot low-normal plasma bicarb <12-20 comp = osteomalacia
3 = MIXED
extremely rare
caused by carbonic anhydrase II deficiency
results in hypokalaemia
4 = HYPERKALAEMIC DISTAL hyperkalaemia inhibits production of ammonia and decreases urine buffering capacity min urine ph <5.5 serum pot high plasma bicarb >17
FANCONI’S SYNDROME
myeloma proteins and various drugs cause proximal tubule injury and proximal RTA, or AD inherited
bicarb <18
RFs childhood urinary tract obstruction DM stones adrenal insufficency
pres
growth retardation/FTT
muscle weakness - fanconi
hypoglycaemia after fructose
rickets - Fanconi + T2 proximal have persistent phosphate loss
distal RTA with deafness - inherited AR - H+ATPase
kussmaul breathing if severe
ix ABG low serum bicarb high serum chloride variable pot low ph serum anion gap normal 12-18 serum aldosterone
MGMT
classic distal T1 = sodium or pot alkali (1mmol/kg) eg shohl’s solution +/- pot supplements
proximal T2 and fanconi - same as above + thiazide diuretic
(volume contraction will increase proximal absorption but will cause loss of potassium)
hyperkalaemia + mineralcorticoid deficiency - fludrocortisone + dietary restriction of pot
If resistant to mineralocorticoid give loop diuretic + potassium restriction + increased salt diet
comp
- Volume depletion - loss of sodium etc at proximal tubule dysfunction
- Nephrocalcinosis - classic distal, increased loads of filtered calcium because of release of calc phos and calc carb in bone buffering of acidosis
- Osteoporosis - bone buffering of acidosis leads to demineralisation
- Growth retardation - acidosis associated with muscle catabolism
- Renal rickets - Fanconi, can’t reabsorb phosphate
what is the anion gap
the negative electrolytes that cant be measured - protein, phosphate, citrate, sulfate
so difference between HCO3- + Cl- and Na+ levels = anion gap
causes of end stage renal failure
Glomerulonephritis
Pyelonephritis
Diabetes
PKD
pyelonephritis def aetiology who + ?complicated RF patho pres ix mgmt comp
def Infection/inflammatory disease of renal parenchyma, calyces and pelvis that may be acute, recurrent or chronic
causes
Enteric bacteria (e.g. Escherichia coli, UPEC uropathogenic with P pili) ascending from lower urinary tract or spread hematogenously to kidney
Gram -ve: E. coli (60%), proteus (15%), klebsiella (15%)
@Diabetes = klebsiella or candida
@HIV, malignancy, transplant = candida
who
women <35
complicated pyelonephritis = men, preg women, structural abnormalities, immunosuppression, obstruction, catheterisation
RF
Age - Infants and older
Anatomical abnormality - VUR, PKD, horseshoe, double ureter
Foreign body - Stone, catheter
Impaired renal function
Immunocompromised -
DM, sickle cell, transplant, malignancy, radio/chemo, alcohol, HIV, steroids
Instrumentation - Cystoscopy
Male sex
Obstruction - BPH, stone, foreign body, bladder neck obstruction, posterior ureteral valve, neurogenic bladder
Pregnant
patho
- Uncomplicated - bacterial ascent
- Men - prostatitis and BPH cause urethral blockage -> bacteriuria -> pyelonephritis
- Obstruction (calculi, tumour, BPH, neurogenic bladder) -> treatment failure and eventual abscess formation (re-infection)
pres TRIAD !!!! 1. loin pain 2. fever - or not if on steroids/antiinflam 3. renal tenderness/costovertebral angel \+ n/v, rigors
ix
Urine dip: blood, protein, nitrites, leukocyte esterase
Urinalysis (microscopy): WBC ≥ 10/HPF, RBC ≥ 5/HPF
Gram stain: G -ve rods (e.coli, klebsiella, proteus)
Urine culture: ≥ 100’000 CFU/ml
FBC: leukocytosis
ESR/CRP raised
Blood culture (systemic infection SEPSIS)
IMAGING - renal USS: gross abnormal, hydronephrosis, stones abscess
contrast CT: altered perfusion, structural abnormality
DMSA - renal scarring
mgmt mild/mod - ciprofloxacin or cefixime severe or comp or preg: admit IV ceftriaxone OR cipro OR gent (not preg) IV fluids, para catheter if needed
comp renal failure abscess formation parenchymal renal scarring reucrrent UTI
renal cell carcinoma % of renal cancers def types pres RF class stage spread via ix ddx mgmt comp
85%
def Renal malignancy arising from renal parenchyma/cortex
types
80% clear cell/adeno renal carcinoma (renal cortical parenchyma) -> due to cholesterol and glycogen
15% papillary tumor (types 1 and 2)
pres
asymp + dx incidentally
triad = haematuria, flank pain, abdo mass
b symps
left sided varicocele by invasion of left renal vein
lower limb oedema
RF
Smoking, obesity, HTN, age, renal transplant and dialysis (15%), cystic dis
+ve family history x4 risk:
- Von Hippel Lindau (AD): 30% develop RCC -> born with germline loss of one VHL tumour suppressor gene (Ch3) then lose the other (2nd hit hypothesis) -> tend to be bilateral and multifocal
class small renal mass <4cm = more likely to be benign
stage
T1 - confined to kidney and ≤ 7cm (a ≤ 4cm, b ≤ 7cm)
T2 - confined to kidney and > 7cm
T3 - to major veins or adrenals (e.g. vena cava)
T4 - beyond gerota fascia
LNs - para-aortic and hilar
spread
Direct - renal vein
Lymphatic - paraaortic then mediastinal
Haem - bone, liver, lung (cannonball mets + colono)
ix
BP - increased from renin secretion
Percutaneous renal biopsy
*FBC - polycythaemia (EPO)
LDH - raised is poor prognosis (x 1.5)
Corrected calcium - >2.5 mmol/l poor prognosis
LFT - raised AST/ALT = metastatic disease (cholestasis in absence of liver mets = stauffers syndrome)
*Cr - elevated with reduced clearance
Urinalysis - haematuria and/or proteinuria
*Abdominal/pelvis USS - cyst, mass, mets
*CT abdo/pelvis - lymphadenopathy, mass, bone mets inc contralateral kidney
MRI - for local invasion etc
CXR - cannonball metastasis, bone scan, MRI brain/spine
ddx benign cyst - bosniak classification on imaging simple = benign complex = cancer ureteric/bladder cancer
mgmt
NOTE - Contain high levels of multiple drug resistance protein P-glycoprotein therefore chemoresistant
S1/2 - small mass - surgical resection, local ablation, T1 = partial T2= lap nephrectomy
S3 = radical nephrectomy
S4 = targeted molecular therapy: tyrosine kinase inhibitor = 1st line eg SUNITINIB +/- local radiation + bisphos for bone mets
comp Paraneoplastic syndrome (30% of patients) - anaemia Hypercalcaemia (PNS) Erythrocytosis (PNS) SIADH (PNS)
childhood renal cancer
Wilm’s tumour -> nephroblastoma
Childhood tumour of primitive renal tubules and mesenchymal cells
Abdominal mass and haematuria
AKI ix
U+E+Cr:
- *Elevated creatinine, *high serum potassium (or on *VBG), *metabolic acidosis
Urine dip, MC + S
- Infection -> leukocytes/nitrates
- Glomerular disease -> blood/protein
FBC
- Anaemia (CKD/blood loss), leukocytosis (infx), thrombocytopenia (HUS, TTP)
Imaging *priority if anuric
- Renal USS -> obstruction, cysts, mass
*ECG
For *hyperkalaemia - increased PR, widened QRS, peaked T, sine wave
Ratio serum urea:creatinine + other tests of cause
- 20:1 -> pre-renal cause
AKI management
stop nephrotoxic drugs - MED REVIEW
ABCDE Catherise for accurate urine output urgent ABG for k+ and ECG Urgent USS KUB for obstruction urine dip for GN/infx if uraemic, severe metabolic acidosis, severe hyperkalaemia -> dialysis
CKD def causes stage pres ix mgmt comp
def Proteinuria or haematuria (evidence of kidney damage) and/or reduction in GFR to <60ml/min/1.73m2 for more than 3 months
causes most common = DM, HTN (+AI disorder, smoking, obesity) PKD glomerular nephrotic/nephritic sydromes obstructive uropathy
stage
Stage 1: kidney damage with normal or increased GFR (> 90)
Stage 2: kidney damage with mild decrease GFR (60-89)
CKD below
*Stage 3a: kidney damage with mod decrease GFR (45-59)
*Stage 3b: kidney damage with mod decrease GFR (30-44)
*Stage 4: kidney damage with severe decrease GFR (15-29)
*Stage 5: kidney failure (ESRD) with GFR < 15
-> Expected oliguric
This requires RRT: haemodialysis, peritoneal dialysis, transplantation
pres mainly asymp HTN diabetic >50 fatigue - lack of EPO oedema - salt/water retention nausea - toxic waste/uraemia arthralgia - AI disease large prostate pruritis - uraemia anorexia - uraemia infection related glomerular disease
ix
Serum creatinine elevated
Urinalysis: haematuria or proteinuria
Urine microalbumin: microalbuminuria
Renal USS: small kidney, obstruction/hydronephrosis, large kidney (infiltration myeloma, amyloidosis)
eGFR < 60
Blood sugar
FBC - anaemia, normochromic normocytic
Osteodystrophy: hypocalcaemia, hyperphosphataemia and hyperparathyroidism, high alkaline phosphatase
Antibodies: autoantibodies, antibodies to streptococcal antigens of hep B/C antibodies
mgmt
primary prev - DM - HbA1c <7%, HTN BP <140/90, smoking cessation, BMI <27
secondary - + salt/protein restriction
identify and treat cause
treat anaemia - EPO alpha +/- ferrous sulfate
renal bone disease - first line = reduce dietary phosphate. then calcium carbonate +/- calcitriol
met acid? sodium bicarb
oedema - furose
educate
stage 5 or uraemic - RRT
proteinuria - ACEi
comp high risk CVD chief cause of death = HF anaemia renal osteodystrophy protein malnutrition met acidosis hyperkalaemia pulm oedema
patho of CKD
- Insult leads to renal injury (DM, HTN, glomerular) - loss of nephrons
- Increase in intra-glomerular pressure with glomerular hypertrophy (adaptation to nephron loss) to maintain constant GFR
- Increased glomerular permeability to macro-molecules (TGF-beta, protein, fatty acids) leads to mesangial matrix toxicity
- Mesangial cell expansion, inflammation, fibrosis and glomerular scarring
- Renal injury leads to increased angiotensin 2 production -> TGF-beta is upregulated -> collagen synthesis and glomerular scarring
- Structural alterations and accompanying changes lead to progressive scarring and loss of kidney function
- All result in tubulointerstitial fibrosis
uraemia at GFR <15
symps
aka the uraemic syndrome
symp Uraemic tinge (grey/yellow) Nausea/vomiting Itch *Uraemic encephalopathy *Pericarditis *Bleeding metallic taste delirium/seizures pericardical friction rub
mgmt
RRT
RRT
when
indications
life expectancy
when
severe AKI
ESRD - stage 5 CKD
indications
- Uraemia (pericarditis, gastritis, encephalopathy)
- Pulmonary oedema (fluid retention) unresponsive med Rx
- Severe hyperkalaemia (>6.5) unresponsive to med Rx
- Severe hypo/hypernatramia
- Severe metabolic acidosis (<7.0) unresponsive to bicarb
- Severe renal failure (urea > 30)
life expectancy
Each year on dialysis increases risk of death by 6%
Main cause of death is cardiovascular
Will give 4-8 years
haemodialysis how? access regimen comp good for who?
how
Blood passed over semi-permeable membrane against dialysis fluid (opposite direction)
Blood meets less concentrated solution and small solutes may diffuse along concentration gradient
Blood drawn from AV fistula, heparin constantly infused
Access requires AV fistula (connect artery to vein to bypass capillaries), CVC (VC via IJV), or synthetic graft
regimen
Hospital 3x per week (4 hours), home 5x per week (2-3 hours)
40% of RRT
comp
Access: *infection, thrombosis, aneurysm, endocarditis, stenosis
*Hypotension (common), cardiac arrhythmia, air emboli
Nausea, vomiting, headache, cramps
*Anaphylaxis to sterilising agent
*Disequilibration syndrome: restless, tremor, fits, coma
good for
live alone
frail
elderly or unsuitable for PD eg surg
peritoneal dialysis how access regimen CI comp good for who
how
Dialysate infused into peritoneal cavity, uses blood in peritoneal capillaries
Waste collected below (gravity)
Ultrafiltration controlled by altering osmolality to draw water out of blood (e.g. glucose)
access
Catheter to peritoneum under LA or GA
regimen
May be continuous ambulatory peritoneal dialysis (CAPD) = 4 exchanges of 20 mins, or may be overnight with one or two in day
10% of RRT
CI
Intra-abdominal adhesions, stoma, obesity, intestinal disease
comp
Infection: peritonitis
Catheter problems: infection, blockage, leak
Constipation, fluid retention, hyperglycaemia + wt gain
Hernia
good for
young people
independant
lack of access to health service
renal transplant advantage types place match induction + maintenance meds CI risk prog
advantage
Survival, QoL, economic, enable pregnancy, reversal of anaemia and renal bone disease
types Cadaveric (90%), living donor (10%)
place
Iliac fossa
match 1. ABO group and crossmatch 2. HLA (tissue) match 3. Antibody screening 30% of living donors are antibody incompatible = paired/pooled programme
induction/main
At time of transplant with basiliximab + IV methylprednisolone
Long term immunosuppression: prednisolone, calcineurin inhibitors (tacrolimus/ciclosporin), anti-metabolites (azathioprine, mycophenolate mofetil)
CI
Cancer, active infection, uncontrolled IHD, AIDS with opportunistic infx
risk
Immediate operative: local infx, pain, DVT
Infections due to immunosuppression (viral HSV for 4 weeks then CMV, bact, fungal)
Urinary tract obstruction
Drug toxicity: bone marrow suppression
*Cancer (skin, lymphoma)
*CV disease (main cause of death), hypertension, dyslipidaemia
Rejection:
- Hyperacute (mins), rare due to crossmatch
- Accelerated (days), T cell mediated crisis -> fever, swollen kidney, increased Cr -> IV steroids
- Acute cellular (weeks), 25% in <3 weeks -> fluid retention, rising BP, rising Cr, high dose IV steroids
- Chronic (>6m), gradual rise in Cr and proteinuria, resistant HTN -> graft biopsy shows vascular changes, fibrosis and atrophy (non-responsive to immunosuppression)
Disease recurrence
glomerulonephritis def causes pres ix mgmt
def Glomerular injury by a group of diseases characterised by changes in the glomerular capillaries and glomerular basement membrane. Changes are most likely immune mediated
causes
Leukocyte infiltration, antibody deposition, complement activation
Commonly idiopathic
Infection - GABH streptococcus (pyogenes), resp/GI infection, hep B/C
Systemic inflammatory conditions - SLE, RA, Goodpasture’s, Wegener’s, HSP, HUS, scleroderma
Drugs - Penicillamine, gold, NSAIDs, ciclosporin, mitomycin
Metabolic - DM, HTN
Malignancy, hereditary, deposition - lung/colorectal, fabry’s/alport syndrome, amyloidosis
pres
RFs + haematuria + oedema + HTN + oliguria
Anorexia/nauseas -> vasculitic
Weight loss -> systemic
Fever -> infectious aetiology
Skin rash -> vasculitic
Arthralgia -> vasculitic
Abdo pain -> HSP and post-streptococcal glomerulonephritis
Haemoptysis -> in anti-glomerular basement membrane disease and Wegener’s
ix
FBC - anaemia -> systemic
U + E + Cr + LFT -> ?hepatitis, advanced disease, albumin
Urinalysis -> haematuria, proteinuria, RBC casts
GFR -> normal or reduced
Lipid profile + glucose
24 hour urine collection
ESR - vasculitis
Complement - low in immune complex
RF - RA
ANCA - anti GBM disease
Anti GBM antibody - anti-GBM disease or Goodpasture’s
Antistreptolysin O antibody/anti DNase - post strep
Anti DS DNA/ANA - SLE
Hep B/C/HIV serology
Electrophoresis - raised gamma globulin in lymphoma and amyloidosis
*Renal biopsy and light or electron + immunofluorescence microscopy
mgmt
mild - treat cause + supportive
E.g. antibiotics, antivirals, withdraw drug, *limit salt + fluid
+ ABX if post strep -> phenoxymethylpenicillin (or IM benpen 1 dose)
mod-severe - ORAL
Proteinuria reducing meds (ACEI/ARB), + ABX + furosemide + prednisolone (1 mg/kg/day) with immunosuppressant e.g. cyclophosphamide/az/mm (nephrotic)
rapidly progressing -IV
- anti-GBM - plasma exchange (remove aB) + IV methylprednisolone + IV cyclophos
- Immune complex - IV methylpred or oral pred ± ABX
- Lupus nephritis - IV methylprednisolone + cyclophosphamide
nephrotic or nephritic conditions
NEPHROTIC = NON-PROLIF
- Deposition disease (amyloidosis + light chain dep)
- Minimal change disease - abnormal podocytes, pred + support
- Focal and segmental GN - steroids ineffective, 50% RF
- Membranous nephropathy
- Membranoproliferative GN - thickened glomerular basement membrane, 1/3 chronic, 1/3 remission 1/3 progress to RF
Proteinuria (>3.5g/24 hours)
Hypoalbuminaemia (<30g/L)
Peripheral oedema
Hyperlipidaemia
NEPHRITIC = PROLIFERATIVE
IgA nephropathy (1ary) - most common, 24-48 hours post URTI/GI infection
Postinfectious GN (1ary) - weeks after URTI, strep pyogenes, supportive
Rapidly progressive GN
- Vasculitis - wegeners, microscopic polyangitis
- Anti-GBM GN (1ary) - good pastures
Oliguria/AKI (renal dysfunction)
HTN
Haematuria: active urinary sediment (red cells and casts)
glomerulonephritis patho
patho
1. immune mediated
- cellular immune response -> infiltration of glom by LC and MP and crescent formation in absence of antibody deposition (min change, focal glomerulosclerosis)
- humoral immune response -> immune deposit formation and complement activation in glom.
Antibodies deposited when react with intrinsic autoantigens (AGBM disease) or with extrinsic antigens trapped in glom (post-infective).
Injury due to activation and release of inflammatory mediators (complement, cytokines, growth factors) that lead to structural and functional characteristics of disease - non-immune - e.g. hyperglycaemia (diabetic nephropathy), high intraglomerular pressure (systemic HTN)
nephrotic syndrome
causes
ddx
comp
causes
PRIMARY
children = minimal change disease
younger adult = focal segmental glomerulosclerosis
adult = membranous nephropathy *antiphospholipase A2 antibody
diabetics - diabetic nephropathy
SECONDARY
(more freq in females): diabetes, amyloidosis, SLE, drugs (see above), infection
ddx
CCF (increased JVP, pulmonary oedema, oedema)
Liver disease (decreased albumin)
comp
Susceptibility to infection - increased urinary loss of IgG (streptococcal), or secondary to steroids
Hypercoagubility and thromboembolism - renal vein thrombosis (lupus or urinary loss of antithrombin, altered protein C and S)
Hypercholesterolaemia - increased hepatic lipoprotein synthesis and loss of lipid regulating proteins
Hypervolaemia - severe decrease in GFR resulting in oedema
AKI - more likely with acute GN
HTN - impaired GFR and increased reabsorption of salt and water
nephritic syndrome
what is it
causes
An acute kidney injury with rapid deterioration in function
CAUSES
Most common at adults - Buerger’s disease:
1. Macroscopic haematuria 24/48 hours post GI/URTI
2. IgA deposition in mesangial matrix
Membranoproliferative:
- Primary (immune mediated) or secondary (SLE)
- Thickening of glomerular basement membrane and mesangium
Post infection
1. Weeks after URTI -> strep pyogenes -> resolves
Rapidly progressive glomerulonephritis = CRESCENTIC - fibrin, epithelial and inflammatory cell matrix compress the glomerulus
- Goodpasture’s syndrome - AI, antiGBM
- Vasculitic: Wegener’s - cANCA, Microscopic polyangiitis - pANCA
polycystic kidney disease def forms characteristics causes patho pres ix mgmt comp
def inherited cystic disease of the kidneys
forms
2 forms, ADPKD (most common) and ARPKD
characteristics
Renal cysts, extrarenal cysts, intracranial aneurysms, aortic root dilation and aneurysms, mitral valve prolapse, abdominal wall hernias
causes
2 genes for ADPKD
- PKD1 @85% (Ch 16) encodes polycystin 1
- PKD2 @15% (Ch 4) encodes polycystin 2
patho Cysts (from tubular portion of nephron and CD) -> compression of normal renal architecture and intrarenal vasculature, increased renal size, interstitial fibrosis and tubular atrophy
pres fhx of PKD/ESRD or stroke flank/abdo discomfort lumbar pain haematuria HTN DUFS - infection, UTI palp kidneys headaches - intracranial aneurysm hepatomeg - liver cystic locations - liver (most common extra-renal manifestation), panc, seminal vesicles, brain
ix
Renal USS -> Ravine’s criteria (PPV = 100%)
<30 years - 2 total
30-60 - 2 in each
60 - 4 or more cysts in each
No fam Hx = 10 in each
Genetic testing - PKD1 or PKD2 mutation
CT abdo pelvis:
<30 = 2 or more unilateral or bilateral cysts, 30-60 = 2 cysts in each kidney, 60+ = 4 cysts in each kidney
No family history requires more than 10 cysts in each kidney
Relevant further testing:
- Urinalysis (protein, bacteria), ECG - LVH + echo - aortic root dilation, MR angiography - screen for aneurysm
mgmt symptomatic mgmt IC haem - neurosurg + nimodipine HTN - ACEi or ARB <130/80 UTI - cipro *Target fluid secretion - Calcium mimetics - CFTR inhibitors - Metformin *Target cell proliferation - Somatostatin
comp
HTN, increased CV morbidity, CKD, ruptured intracranial aneurysm -> SAH, ESRD
ARPKD
gene
pres
prog
Chromosome 6: fibrocystin -> renal collecting ducts and bile ducts
Patients often present in the neonatal period with enlarged echogenic kidneys, renal cysts congenital hepatic fibrosis.
This has a high mortality and many require ventilation
If survive infancy, probability of surviving till 15 is low (50-80%)
