r e n a l Flashcards
what are the pre renal causes of AKI
Shock - dehydration, hypovolaemia
RAS
Hepatorenal syn.
what are the renal causes of AKI
Glomerulonephritis
Acute Tubular Necrosis
Interstitial disease
what are the post renal causes of AKI
- Diseases of renal papillae, pelvis, ureters, bladder or urethra.
SNIPPIN
Stone Neoplasm Inflammation: stricture Prostatic hypertrophy Posterior urethral valves Infection: TB, schisto Neuro: post-op, neuropathy
what are the presentations relating to AKI
Uraemia / Azotaemia Acidosis Hyperkalaemia Fluid overload Oedema, inc. pulmonary ↑BP(or↓) S3 gallop ↑ JVP
how would you assess for AKI clinically
1. Acute or chronic? Can’t tell for sure: Rx as acute Chronic features Hx of comorbidity: DM, HTN Long duration of symptoms Previously abnormal bloods (GP records) 2. Volume depleted? Postural hypotension ↓ JVP ↑ pulse Poor skin turgor, dry mucus membranes 3. GU tract obstruction? Suprapubic discomfort Palpable bladder Enlarged prostate Catheter Complete anuria (rare in ARF) 4. Rare cause? Assoc. ̄c proteinuria ± haematuria Vasculitis: rash, arthralgia, nosebleed
what are the investigations required in AKI
Bloods: FBC, U+E, LFT, glucose, clotting, Ca, ESR
ABG: hypoxia (oedema), acidosis, ↑K+
GN screen: if cause unclear. f blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) too look for vasculitis, anti-GBM, ANA,
C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma
Urine: dip, MCS, chemistry (U+E, PCR, osmolality, BJP)
ECG: hyperkalaemia
CXR: pulmonary oedema
Renal US: Renal size, hydronephrosis
describe how AKI is classified
RIFLE = 3 grades of AKI and 2 outcomes
Classification determined by worst criteria
table
in pre renal failure what is happens to osmolality and sodium
in pre-renal failure, urine is concentrated and Na is reabsorbed = increase osmolality, Na less than 20mM
what is the general management for AKI
Identify and Rx pre-renal or post-renal causes
Urgent US
Rx exacerbating factors: e.g. sepsis
Give PPIs
Stop nephrotoxins: NSAIDs, ACEi, gent, vanc
Stop metformin if Cr > 150mM
What are the features to be monitored in AKI
Catheterise and monitor UO
Consider CVP
Fluid balance Wt.
what are the ECG changes seen in hyperkalamia
ECG Features (in order) Peaked T waves Flattened P waves ↑ PR interval Widened QRS Sine-wave pattern → VF
how do you treat hyperkalaemia
10ml 10% calcium gluconate
100ml 20% glucose + 10u insulin (Actrapid) Salbutamol 5mg nebulizer
Calcium resonium 15g PO or 30g PR
Haemofiltration (usually needed if anuric)
how do you treat pulmonary oedema
Sit up and give high-flow O2
Morphine 2.5mg IV (± metoclopramide 10mg IV)
Frusemide 120-250mg IV over 1h
GTN spray ± ISMN IVI (unless SBP <100)
If no response consider:
CPAP
Haemofiltration / haemodialysis ± venesection
what are the indications for acute dialysis (in AKI)
- Persistent hyperkalaemia (>7mM)
- Refractory pulmonary oedema
- Symptomatic uraemia: encephalopathy, pericarditis 4. Severe metabolic acidosis (pH <7.2)
reabsorbed → ↑osmolality, Na <20mM - Poisoning (e.g. aspirin)
what are the life threatening complications in AKI
Hyperkalaemia
Pulmonary oedema
how do you manage acute renal failure
refer to notes
- A-E
- life threatening complications
- shock or dehydration
- monitor
- look for evidence of post renal causes
- hx and lx
- manage sepsis
- further management
what are the features of chronic renal disease?
Kidney damage ≥3mo indicated by ↓ function
Symptoms usually only occur by stage 4 (GFR<30)
ESRF is stage 5 or need for RRT
how is CKD classified
based on eGFR
stage 1 = Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
stage 2 = 60-90ml/min if kidney tests are normal, no CKD
stage 3a = 45-59ml/min
stage 3b = 30-44ml/min
stage 4 = 15- 29ml/min
stage 5 = less than 15 ml/ min = dialysis or kidney transplant needed
what are the common causes of CKD
Common
DM
HTN = Chronic raised BP causing nephrosclerosis.
Other RAS GN Polycystic disease Drugs: e.g. analgesic nephropathy Pyelonephritis: usually 2O to VUR SLE Myeloma and amyloidosis
describe the inheritance pattern for adult polycystic disease and chr affected by type 1 and 2
2 Types (both are autosomal dominant)
Type 1 (85%; PKD1 mutation on Chromosome 16)
Type 2 (15%; PKD2 mutation on Chromosome 4)
what are sx seen in APKD
size of the kidney, infection of the cysts (flank pain, haematuria, and fever) or can be asymptomatic
what are the factors affecting anaemia in chronic kidney disease
Decreased production of erythropoietin from the kidney
Absolute iron deficiency (poor absorption and malnutrition)
Functional iron deficiency (inflammation, infection) Blood loss
Shortened Red Blood Cell survival
Bone marrow suppression from uraemia Medication induced
Deficiency of Vit B12 and folate
in CKD, mineral bone disease leads
CKD leads to
Increased Fibroblast Growth Factor-23 Increased Alkaline Phosphatase and PTH Increase Phosphate
Decreased Serum Calcium
decreased 1,25 - vitamin D
describe tertiary hypothyroidism in CKD
Occurs when PTH release continues despite raised serum Calcium levels (independently)
• As a result of parathyroid gland nodular hyperplasia
• Consequence of advanced CKD
how is anaemia of CKD managed
Measure haematinics – Vitamin B12, Folate, Ferritin, Iron, Transferrin Saturation, CHr
If deficient in any of above – replace this first
• IV Iron may be better tolerated than PO Discuss with renal team regarding starting ESA
aim for Hb 100-120
describe management of ADPKD
Control BP
As per CKD management
Tolvaptan (Vasopression receptor-2 antagonist) is
available for some patients to slow progression of
CKD.
Genetic counselling and testing
how id ADKPD DX
Family history is KEY
USS
describe the pathophysiology and investigations for HTN nephropathy and treatment
Chronic raised BP causing nephrosclerosis.
Investigations to identify if primary or secondary HTN (based on clinical findings and index of suspicion):
24 hour Urinary metanephrines (Phaeochromocytoma)
Aldosterone: Renin ratio (Primary aldosteronism)
Cortisol & Dexamethasone suppression test
(Cushing’s syndrome)
TSH (hyperthyroidism)
MRA (Renal artery stenosis)
Treatment
Anti-hypertensives (see ABCD guidelines)
in CKD what are questions to ask
past UTI HTN, DM FH DH sx
what are the investigations in CKD
BLOOD = ↓Hb, U+E, ESR, glucose, ↓Ca/↑PO4, ↑ALP, ↑PTH
Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep
Film: burr cells
Urine: dip, MCS, PCR, BJP
Imaging
CXR: cardiomegaly, pleural/pericardial effusion, oedema
AXR: calcification from stones
Renal US
Usually small (<9cm)
May be large: polycystic, amyloid
Bone X-rays: renal osteodystrophy (pseudofractures)
CT KUB: e.g. cortical scarring from pyelonephritis
renal biopsy if cause unclear and size normal
what are the complications of CKD
CRF HEALS
Cardiovascular disease Renal osteodystrophy Fluid (oedema) HTN, Hypothyroidism secondary and tertiary Electrolyte disturbances: K, H Anaemia Leg restlessness Sensory neuropathy
describe the features our renal osteodystrophy
osteoporosis: ↓ bone density
Osteomalacia: ↓ mineralisation of osteoid (matrix)
describe the mechanism of renal osteodystrophy
↓ 1α-hydroxylase → ↓ vit D activation → ↓ Ca → ↑ PTH
Phosphate retention → ↓ Ca and ↑ PTH (directly)
↑ PTH → activation of osteoclasts ± osteoblasts
Also acidosis → bone resorption
describe the management of CKD
MDT focused
general = rx reversible causes
stop nephrotoxic drugs
lifestyle = exercise, healthy weight, stop smoking, Na, fluid and PO4 restriction
CV risk = statins, low dose aspirin, manage DM
HTN = target 140/90 and 130/80 if DM. in DM kidney disease give ACEi/ARB
ACEi/ ARB = reduce proteinuria
Oedema = furesomide
Bone disease = phosphate binders = sevelamar. vit D analogues - alfacalcidiol. Ca supplements
Anaemia = exclude IDA and ACD. EPO to raise Hb to 11g/dl (higher thrombosis risk)
Restless legs = clonazepam
Refer for fistula o Venous mapping Refer for PD tube insertion Work-up for transplant o Further tests o Refer to Transplant work-up clinic
describe RRT options
H.D
P.D
kidney transplant
diabetic nephropathy is the biggest cause of…
ESKD
describe the pathology of diabetic nephropathy
Hyperglycaemia → renal hyperperfusion → hypertrophy and ↑ renal size
Hypertrophy and metabolic defects inc. ROS production → glomerulosclerosis and nephron loss
Nephron loss → RAS activation → HTN
clinically, what are the progression of diabetic nephropathy
Microalbuminuria (30-300mg/d or albumin:creatinine >3)
Strong independent RF for CV disease
Progresses to proteinuria (albuminuria >300mg/d)
Diabetic retinopathy usually co-exists and HTN is
common
describe screening for diabetic nephropathy
T2DMs should be screened for micrroalbuminuria 6 monthly
how is diabetic nephropahty managed
Good glycaemic control delays onset and progression BP target 130/80
Start ACEi/ARB even if normotensive
Stop smoking
Combined kidney pancreas Tx possible in selected pts
renal transplant is the treatment of choice in …
ESRF
what factors needs to be checked/ or assessed before renal transplant
Virology status: CMV, HCV, HBV, HIV, VZV, EBV
CVD
TB
ABO and HLA haplotype
what are the contraindications to renal transplant
Active infection
Cancer
Severe HD or other co-morbidity
what are the types of renal graft?
cadaveric: brainstem death ̄c CV support
Non-heart beating donor: no active circulation
Live-related = Optimal surgical timing + HLA-matched + Improved graft survival
Live unrelated
what immunosuppression is required in renal transplant
pre and post op
pre = campath/alemtuzumab post = pred short term and tacrolimus/ciclosporin long term
what is the prognosis for cadaveric renal allografts
15 years
what are the complications of renal transplant
Post-op Bleeding Graft thrombosis Infection Urinary leaks Hyperacute rejection (minutes) ABO incompatibility Thrombosis and SIRS
Acute Rejection (<6mo)
↑ing Cr (± fever and graft pain)
Cell-mediated response
Responsive to immunosuppression
Chronic Rejection (>6mo)
Interstitial fibrosis + tubular atrophy
Gradual ↑ in Cr and proteinuria
Not responsive to immunosuppression
Ciclosporin / tacrolimus nephrotoxicity
Acute: reversible afferent arteriole constriction → ↓GFR
Chronic: tubular atrophy and fibrosis
↓ Immune Function
↑ risk of infection: opportunists, fungi, warts
↑ risk of malignancy: BCC, SCC, lymphoma (EBV)
Cardiovascular Disease
Hypertension and atherosclerosis
what are differentials for raising Cr in Tx pt
Rejection
Obstruction
ATN
Drug toxicity
what are the causes of hyperkalaemia
CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)
Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/ Heparin/ LMWH/Cyclosporin or calcineurin inhibitors/High dose Trimethoprim/ Digoxin toxicity/B- blockers)
Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use
Rarer – Hyperkalaemic periodic paralysis, Gordon’s syndrome
Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis
what does each drug used in hyperkalaemia do?
Treatment of hyperkalaemia involves:
1. Stabilizing the myocardium to prevent arrhythmias
10mls of 10% Calcium Gluconate over 5-10 minutes
- shifting potassium into intracellular space
IV fast acting insulin (actrapid)
10 units and IV glucose/dextrose 50% 50mls
Sodium Bicarbonate
500mls of 1.4% Sodium Bicarbonate
Only effective at driving Potassium intracellullarly
if the patient is acidotic
Salbutamol
5-10mg via nebulizer - Eliminating Potassium From the Body: Calcium Resonium
15-45g orally or rectally, mixed with sorbitol or lactulose
Frusemide
20-80mg depending on hydration status
Dialysis
If resistant to medical treatment
what are sx of hypokalaemia
Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias, worsened glucose control in diabetics, hypertension
what are the causes of hypokalaemia
Pseudohypokalaemia – acute leukaemia
Extra-renal losses - Inadequate PO intake, Gut
losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)
Redistribution – Delirium tremens, beta agonists, insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)
Refeeding syndrome, alkalosis, vigorous exercise, glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)
Primary hyperaldosteronism (conn’s syndrome) Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),
Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.
what are the ECG changes seen in hypokalaemia
ECG Changes
Small T waves
U wave (after T)
Increased PR interval
what are the rx of AKI
Diabetes CKD IHD/CCF/CVD Any major medical co-morbidity Elderly >75 Sepsis Medications – ACEi, ARBs, NSAIDs, Antibiotics
how is hypokalaemia treated
Replace magnesium
Oral K replacement
IV K replacement (Usually in 0.9% NaCl - avoid in
dextrose as induces further hypokalaemia)
