J de Zoysa: Renal Failure Flashcards
Vascular supply of the kidneys and describe/draw the nephron.
Blood supply: aorta
Venous supply: drains to IVC
Ureters to the bladder
The five key roles of the kidneys
- Elimination of waste products
- control of fluid balance: either conc or dilute urine
- regulate acid-base balance
- Produce hormones
- Regulation of electrolytes (minerals eg; salt, K+ and calcium)
The major role of the kidneys is to
Describe this.
- Major role; to remove waste products
- GFR: rate at which the blood is cleared of the waste products
- GFR > 120 ml/min usually
- if reduced = renal impairment
acute vs chronic kidney injury
AKI:
- Hours to days
- Potentially reversible
- ‘Acute renal failure’ had an inconsistent diagnosis and refeered to different set points.
CKD
- weeks/ months/years
- Progressive, irreversible
Rates of AKI, and what does it consist of?
- AKI is a syndrome with multiple aetiologies
- The incidence in the community is unclear
- Primary cause of admission in 5% of cases and affects 20% of acute admissions
- It is associated with ~50% of preventable hospital deaths
What are the KDIGO guidelines for staging?
Why is this important
- We measure serum creatinine and urine output?
- SC: 1.5-1.9 x baseline UO: <0.5ml/kg/hr for 6-12hr
- SC: 2 - 2.9x baseline UO: <0.5 ml/kg/hr for >12hr
- SC: 3x baseline UO: <0.3 ml/kg/hr for >24hr or anuria for >12 hours
- non elective mortality 3.3%
- AKI stage 1 mortality 16%
- AKI stage 2 mortality 16-33%
- AKI stage 3 mortality 33%
Types of AKI
- Pre-renal
- Renal
- Post-renal
What are the risk factors of AKI
- Chronic KD
- Age >75 (this can be variable)
- Diabetes
- Emergency surgery (sepsis and hypovolaemic)
- Intraabdominal surgery
- Congestive HF
- Liver failure
- Nephrotoxic medications (NSAIDs, dabigatrin, gentamicin, ACE inhibitors)
- past history of AKI
- Acute illness
- hypotension
- sepsis
- hypovolaemia
- High EWS
General approaches (1 and 2) to high-risk patients with/or suspected to have AKI
Approach 1: deal with symptoms
- Identify patient at high risk
- assess and optimise volume status
- Stop all nephrotoxic agents
- Review medications; dose adjust (or stop)
- Monitor creatinine and UO
Approach 2: target primary source
- Non-invasive diagnostic workup
- CT, xray, lab tests
- invasive diagnostic workup
- renal biopsy
- Daily weights
- Diet
- Targetted therapy
Chronic Kidney disease
“an abnormality of kidney structure or function, present for >3months, with implications for health”
- Slowly declining renal function over time*
- Based off cause, GFR and albuminuria
How to calculate the GFR
-
Clearance of artificially injected substances
- Inulin clearance: Sugar which is filtered by the glomerulus and neither reabsorbed nor secreted into the tubule
- GOLD STANDARD: inject inulin in blood and measure the clearance in urine
- Isotope clearance: inject radioactive substance (Cr-EDTA or I-IOT) and measure the clearance over time, very accurate measurement
- Inulin clearance: Sugar which is filtered by the glomerulus and neither reabsorbed nor secreted into the tubule
-
Creatinine clearance
- It’s produced by creatinine metabolism and freely filtered at the glomerulus and can be used to estimate the GFR
- Cr Clearance= (urine Ct x urine volume) / (plasma Cr x time period)
Potential issues with Creatinine clearance measures?
- As it’s also secreted in small amounts by the tubules, therefore Cr Cl tends to overestimate the GFR
- Serum Cr also reflects body size and muscle mass
- Presence of mod-severe CKI can confound CrCl
- As GF declines, extrarenal excretion of creatinine increases and there is decreased muscle mass → overestimation of GFR at end stage renal failure
Estimated GFR
most typically derived formula, using a single blood test of serum creatinine are used. (there’s over 80 formulas)
- CKD- EPI formula the most common: using age etc
STaging of GFR related to differing GFR levels
- ** we also measure albuminuria as a marker of renal disease
- A1 <30mg/mmol
- A2 30-300 mg/mmol
- A3 >300mg/mmol
- REMEMBER that renal function naturally declines with age so link their age to their levels accordingly
CKI Can be a marker of issues, such as heart disease etc.
How common is it?
What are the sociodemographic risk factors?
- Over 10% of the population is at risk of CKD
Sociodemographic Risk Factors
- age (M>F)
- sex (maori and pacific islanders > pakeha)
- ethnicity
- low income
- obesity
Causes of CKD?
- Diabetic nephropathy 45%
- Glomerulonephritis 25%
- Hypertensive nephrosclerosis 10%
- Polycystic kidney disease 5%
IgA nephropathy the most common cause
*
What happens if we don’t control CKD?
It will progress to end stage kidney disease (ESKD)
Irrespective of the primary disease, secondary factors develop and lead to deterioration
Secondary factors that cause CKD→ ESKD
- Systemic Hypertension
- intra-glomerular hypertension
- glomerular hypertrophy
- calcium and phosphate
- dyslipidaemia
- proteinuria
- Tubulo-interstitial fibrosis
- toxicity of iron/ammonia/middle molecules
By lowering hypertension (and controlling diabetes), you can manage CKI. How do you manage the hypertension
- Target 140/80 mmHg or better
- Weight loss
- salt restriction
- exercise
- moderation of alcohol
- stop smoking
So lifestyle, naturesis (diuretics), renin (angiotensin) and the SNA
Many patients will also need drugs to control their BP
they will need multiple complementary drugs specifically combined to target these for systems
- **ACE inhibitors, angiotensin II receptor blockers, spirolactone: block the RAAS
- alpha blockers, B-blockers, calcium channel blockers: block the SNS
Proteinuria is an important prognostic factor and can improve outcome. Reduction of this improves outcome, how is this done/
- Weight loss
- ACE-I and AIIRB
- Aldosterone antagonists
- statins
- moderate protein restriction: to avoid fibrosis from the toxic protein process
- BP <125/70
Dyslipidaemia
Common in CKD and no proof of benefit in terms of preserving kidney function
- Potential benefits in moderate kidney disease zetamide and a statin
Calcium and Phosphate content of the kidneys is increased in CRF and ESRF
What is this used for
Used as an indication of renal function and Ca/P increased with progressive renal impairment.
Improvement in the Ca/P product is associated with a reduction in the rate of decline.
- Stage 3 CKD (30-60 GFR) hyperphosphatemia
- Stage 4 CKD: Hyperphosphatemic and get secondary HPT, start to see a fall in serum creatinine (when GfR falls below 30ml/min)
- Depostion of Ca/P in tissue can be found here and it is thoguht by normalising this we can improve the outcome.
- Done by diet (limiting phosphate), medication (phosphate binders) etc
- Aim for a Ca x P <4.5mmol/litre2
As kidneys regulate the volume state, CKD patients are more prone to ?
Both dehydration and volume overload
- Advise the patient to avoid volume depletion
What hormones does the kidney produce?
- Erythropoietin: in response to hypoxia by liver and kidney, produce RBC, why kidney disease patients suffer from anemia
- 1,25 OH vitamin D
- BMP-7
- Renin, angiotensin, bradykinin
- control BP and electrolytes which can lead to dysfunction of electrolytes
How does the kidney do Acid-base regulation?
- Kidneys are long-term regulatory mechanisms of pH maintenance
-
Typically with CKD a metabolic acidosis develops due to a lack of excretion of non-organic acids
- dietary changes can alter
- addition of oral sodium bicarbonate may be required
Uraemia
Symptomatics ESKD
- THe manifestations of organ dysfunction seen in CKD 4 and 5
- the uraemic syndrome resembles a systemic intoxication
- Unfortunately, no singles compound has been found to produce the clinical picture of uraemia
Symptoms: faitgue/lethargy, headache, seizures, encephalopathy, peripheral neuropathy
Haematological, cardiovascular, respiratory and GI ymptoms of anaemia
Haematological
- anaemia
- bleeding tendency
- platelet dysfunction
- infection
CVS
- pericarditis
- hypertension
- HF
- IHD
- Cardiomyopathy
- CVA
Resp:
- pleuritis
- ischaemic lung
GI tract
- anorexia, nausea
- vomiting
Treatment of Uraemia
- Treat primary disease
- treat secondary factors
- avoid nephrotoxins
- Correct abnormalities
- Ca/P PTH
- other electrolytes
- Acid-base balance
- volume
- Renal replacement therapy
ESKD treatment option
- conservative
- Dialysis
- peritoneal
- haemodialysis
- Renal transplant
- cadaveric
- living
- cadaveric
