Medicine: AKI and CKD Flashcards
What’s AKI?
Definition/criteria (3)
- Serum creatinine rises by ≥ 26µmol/L within 48 hours
- Serum creatinine rises ≥ 1.5 from baseline (50% greater rise in serum creatinine over past 7 days)
- Urine output < 0.5ml/kg/hr for >6 hours
diagnostic criteria (1) for AKI in children
>= 25% fall in eGFR in children / young adults in 7 days
Risk factors for AKI
- Emergency surgery, ie, risk of sepsis or hypovolaemia
- Intraperitoneal surgery
- CKD, ie if eGFR < 60
- Diabetes
- Heart failure
- Age >65 years
- Liver disease
- Use of nephrotoxic drugs
When AKI needs a referral to a nephrologist?
Refer to a nephrologist if any of the following apply:
- Renal tranplant
- ITU patient with unknown cause of AKI
- Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
- AKI with no known cause
- Inadequate response to treatment
- Complications of AKI
- Stage 3 AKI (see guideline for details)
- CKD stage 4 or 5
- Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
Stages (3) of AKI
Examples of nephrotoxic drugs
- NSAIDs
- ACE-i/ARB
- diuretics
- aminoglycosides
- chemotherapy
- ciclosporin
- tacrolimus
- contrast
Prerenal causes of AKI
- pathophysiology
Prerenal
- ischaemia, or lack of blood flowing to the kidneys
- Impaired renal perfusion → reduced glomerular capillary filtration pressure
Examples of conditions/problems leading to prerenal causes of AKI
Examples:
- hypovolaemia secondary to diarrhoea/vomiting
- renal artery stenosis
- cardiac failure
- hepatorenal syndrome
- large or medium vessel vasculitis
What are compensatory mechanisms to maintain GFR and examples of how those mechanisms could be damaged (2)
Compensatory mechanisms to maintain GFR:
- Afferent arteriolar dilation - Impaired by NSAIDs
- Efferent arteriolar vasoconstriction - Impaired by ACE-I / ARBs
Examples of Intrinsic causes of AKI
- glomerulonephritis
- acute tubular necrosis (ATN)
- acute interstitial nephritis (AIN), respectively
- rhabdomyolysis
- tumour lysis syndrome
Pathophysiology of intrinsic AKI
- intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves
- may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis
Pathophysiology of Postrenal AKI
Postrenal = problems after the kidneys
- obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function
Examples of causes of postrenal AKI (3)
- kidney stone in ureter or bladder
- benign prostatic hyperplasia
- external compression of the ureter
What’s the most common cause of AKI?
Acute Tubular Necrosis
- necrosis of renal tubular epithelial cells severely affects the functioning of the kidney
- in the early stages ATN is reversible if the cause if removed
Causes of Acute Tubular Necrosis
-
ischaemia
- shock
- sepsis
-
nephrotoxins
- aminoglycosides
- myoglobin secondary to rhabdomyolysis
- radiocontrast agents
- lead
Signs and symptoms (2) of Acute Tubular Necrosis
- features of AKI: raised urea, creatinine, potassium
- muddy brown casts in the urine
(3) Histopathological features of Acute Tubular Necrosis
Histopathological features
- tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
- dilatation of the tubules
- necrotic cells obstruct the tubule lumen
(3) phases of Acute Tubular Necrosis
- oliguric phase
- polyuric phase
- recovery phase
Pathophysiology of Acute Tubular Necrosis
Reduced renal blood flow → hypoxia → endothelial/epithelial injury
Prognosis in Acute Tubular Necrosis
- 50% left with degree of renal impairment
- Up to 10% will require RRT
Symptoms of AKI
Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:
- reduced urine output
- pulmonary and peripheral oedema
- arrhythmias (secondary to changes in potassium and acid-base balance)
- features of uraemia (for example, pericarditis or encephalopathy)
Investigations in AKI
- Urinalysis ± ACR → blood, protein, casts, nitrites etc
- Bloods
- FBC →infection, anaemia, platelets (e.g. HUS/TTP/DIC)
- U&Es
- Bone profile → high phosphate, low / high calcium)
- LFTs → hepatorenal, albumin
- clotting →DIC
- Lactate
- CK
- CRP
- Blood gas
- ECG
- Microbiology: urine, blood, Hep B / C /HIV
- CXR
- Renal ultrasound
•Immunology: ANCA, ANA, Anti-GBM, Complement, cryoglobulins
•Myeloma screen:
Immunoglobulins, Bence Jones Protein,
Electrophoresis, Serum free light chains,
Skeletal survey (pepper pot skull, lytic lesions)
•Renal biopsy
What does myeloma screen consist of?
Myeloma screen:
Immunoglobulins, Bence Jones Protein,
Electrophoresis, Serum free light chains,
Skeletal survey (pepper pot skull, lytic lesions)
Management of AKI
- Identify and treat cause and complications of AKI
- Stop nephrotoxics
- Assess volume status
- Hypovolaemic → fluid bolus
- Euvolaemia → maintenance fluids
- Hypervolaemic → diuretics / RRT
- Consider urinary catheter - input / output monitoring
- Daily weights
- Nephrology/critical care referral
- AKI3
- indication for acute dialysis (see below)
- unclear aetiology
- vasculitis / GN
•Urology referral if post-renal
Indications for nephrology/critical care referral in a patient with AKI
- AKI3
- indication for acute dialysis
- unclear aetiology
- vasculitis / GN
(4) Indications for acute dialysis
- Refractory hyperkalemia
- Refractory pulmonary oedema
- (Progressive/severe metabolic acidosis (pH <7.2, HCO3- <10)
- (Symptomatic uraemia (e.g. pericarditis, encephalopathy)
Abnormalities seen on ECG at different levels of hyperkalaemia (3 levels)
> 5.5 mEq/L → repolarization abnormalities:
•Peaked T waves
> 6.5 mEq/L → progressive paralysis of the atria:
- P wave flattening
- PR prolongation
> 7.0 mEq/L → conduction abnormalities / cardiac arrest:
- Wide QRS
- AV / conduction blocks
- sine wave
- Asystole/ VF/ PEA
Management of hyperkalaemia
- *Stabilisation of the cardiac membrane**
- intravenous calcium gluconate
+ does NOT lower serum potassium levels
Short-term shift in potassium from extracellular to intracellular fluid compartment
- combined insulin/dextrose infusion
- nebulised salbutamol
- *Removal of potassium from the body**
-
calcium resonium (orally or enema)
- enemas are more effective than oral as potassium is secreted by the rectum
- loop diuretics
-
dialysis
- haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia
Management of Pulmonary Oedema
- Stop IV fluids
- Upright position + 100% oxygen
- Strict hourly input/output
- Fluid / salt restriction
- IV furosemide
- IV nitrates
- Consider CPAP
- If anuric → dialysis
Features of Pulmonary Oedema on an X-ray
Features of pulmonary oedema on a chest x-ray may include:
- interstitial oedema
- bat’s wing appearance
- upper lobe diversion (increased blood flow to the superior parts of the lung)
- Kerley B lines
- pleural effusion
- cardiomegaly may be seen if there is cardiogenic cause
Function of the kidney (physiology)
- Execretory function:
- Metabolites, drugs, toxins
- Homeostatic function:
- maintaining of acid-based balance
- maintenance of electrolyte
- maintenance of water balance
- Endocrine( hormonal secretory function)
- Renin by juxtaglomerular
- Erythropoietin hormone
- Endocrine(hormonal) metabolic function
- Vitamin D3-1,25OH vitamin D
Equation used to estimate kidney function in adult and its disadvantages
- Serum creatinine is correlated with muscle mass → in people with extremes of muscle mass is subject to inaccuracy
(In those with increased muscle mass, GFR will be under estimated and in those with reduced muscle mass GFR will be over estimated)
- This equation is accurate in patients with chronic kidney disease (CKD), but it significantly underestimates GFR in healthy persons (probably due to the exclusion of healthy persons from the study used to develop this equation). Do not over-interpret slightly low values.
- Stages 1 or 2 CKD should not be diagnosed on GFR alone - unless there are urinalysis, structural abnormalities or genetic factors to indicate renal disease
- These calculations assume that the creatinine levels are relatively stable (over a few days) and not rapidly changing
- The MDRD equation is not valid for children - use the Counahan-Barrat method
Name equation used to estimate kidney function in children
Counahan-Barrat method
CKD stages
Causes of CKD
- Diabetes
- Glomerulonephritis
- Hypertension / renovascular
- Pyelonephritis / reflux
- Polycystic / familial
- Unknown
How can CKD present?
Chronic renal failure presents in three ways:
- Routine blood tests (e.g. annual DM / hypertension check up)
- Anaemia
- Acute on chronic renal failure
- Emergencies requiring urgent management for life threatening complications of renal failure (e.g. uraemia / hyperkalaemia)
Complications of CKD
- Fluid overload
- Hypertension
- Hyperkalemia
- Acidosis
- Anaemia
- Uraemic syndrome
- Mineral bone disease
- Increase cardiovascular risk (majority of CKD patients die from cardiovascular disease before experiencing end stage kidney disease !!!)
Management of CKD
- Life style advice:
- Encourage exercise
- Offer smoking cessation
- Healthy diet ( low K, low PO4 diet )
- Meticulous BP control
- Management of lipids
- Glycemic control
Manage complications e.g. mineral bone disease
Management of renal related bone disease (mineral bone disease)
- reduced dietary intake of phosphate is the first-line management
- phosphate binders
- vitamin D: alfacalcidol, calcitriol
- parathyroidectomy may be needed in some cases
Acidosis and CKD?
- at what level to treat
- why to treat
- how to treat
Level: Treat when venous HCO3 is <21mmol/l
Why: Correction of acidosis might:
- slow progression of eGFR decline and development of “renal bone disease
- Reduce risk of Hyperkalaemia
Treatment:
Give sodium bicarbonate 0.5-1.5 g TDS aim for high normal serum bicarbonate
*Refractory acidosis is an indication for dialysis
Renal anaemia
- diagnosis
- treatment
- treatment target Hb
Diagnosis:
- prevalence and severity increase as eGFR falls
- diagnosis of exclusion
Treatment:
- EPO supplementation
- Target Hb range 10-12
Hypertension targets in CKD
- BP target < 140/90 mmHg for non-diabetic, non proteinuric CKD patient
- BP target < 130/80 if proteinuria (diabetic or not)
* ACE-I/ARB especially IF ACR>70 mg/mmol
How mineral bone disease in CKD can manifest?
- Abnormalities of calcium, phosphate, PTH or vitamin D metabolism
- Abnormalities of bone turnover, mineralization, volume, linear growth or strength
- Vascular or soft tissue calcification
Types of Renal Replacement Therapies
oHemodialysis / Haemodiafiltration (In Center / Home)
o Peritoneal dialysis (In Center / mostly Home)
o Transplantation (living- / vs. deceased- donor (brain / cardiac death)
o Conservative management
How does haemodialysis work?
- Removal of certain elements from the blood while it being circulate and exposed to dialysate across a semi-permeable membrane
- The concentration difference across the membrane allow molecules to diffuse down a gradient which allows waste product to be removed
- Can be done at home or in hospital
- Patients need vascular access
Difference between haemodialysis vs haemofiltration
Principles of peritoneal dialysis
