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RBF > J de Zoysa: Renal Failure > Flashcards

J de Zoysa: Renal Failure Flashcards

1
Q

Vascular supply of the kidneys and describe/draw the nephron.

A

Blood supply: aorta
Venous supply: drains to IVC
Ureters to the bladder

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2
Q

The five key roles of the kidneys

A
  1. Elimination of waste products
  2. control of fluid balance: either conc or dilute urine
  3. regulate acid-base balance
  4. Produce hormones
  5. Regulation of electrolytes (minerals eg; salt, K+ and calcium)
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3
Q

The major role of the kidneys is to

Describe this.

A
  • 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
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4
Q

acute vs chronic kidney injury

A

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
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5
Q

Rates of AKI, and what does it consist of?

A
  • 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
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6
Q

What are the KDIGO guidelines for staging?

Why is this important

A
  • We measure serum creatinine and urine output?
  1. SC: 1.5-1.9 x baseline UO: <0.5ml/kg/hr for 6-12hr
  2. SC: 2 - 2.9x baseline UO: <0.5 ml/kg/hr for >12hr
  3. 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%
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7
Q

Types of AKI

A
  • Pre-renal
  • Renal
  • Post-renal
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8
Q

What are the risk factors of AKI

A
  • 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
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9
Q

General approaches (1 and 2) to high-risk patients with/or suspected to have AKI

A

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
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10
Q

Chronic Kidney disease

A

“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
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11
Q

How to calculate the GFR

A
  1. 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
  2. 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)
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12
Q

Potential issues with Creatinine clearance measures?

A
  • 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
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13
Q

Estimated GFR

A

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
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14
Q

STaging of GFR related to differing GFR levels

A
  • ** 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
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15
Q

CKI Can be a marker of issues, such as heart disease etc.

How common is it?

What are the sociodemographic risk factors?

A
  • 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
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16
Q

Causes of CKD?

A
  • Diabetic nephropathy 45%
  • Glomerulonephritis 25%
  • Hypertensive nephrosclerosis 10%
  • Polycystic kidney disease 5%

IgA nephropathy the most common cause

*

17
Q

What happens if we don’t control CKD?

A

It will progress to end stage kidney disease (ESKD)

Irrespective of the primary disease, secondary factors develop and lead to deterioration

18
Q

Secondary factors that cause CKD→ ESKD

A
  • Systemic Hypertension
  • intra-glomerular hypertension
  • glomerular hypertrophy
  • calcium and phosphate
  • dyslipidaemia
  • proteinuria
  • Tubulo-interstitial fibrosis
  • toxicity of iron/ammonia/middle molecules
19
Q

By lowering hypertension (and controlling diabetes), you can manage CKI. How do you manage the hypertension

A
  • 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

20
Q

Many patients will also need drugs to control their BP

A

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
21
Q

Proteinuria is an important prognostic factor and can improve outcome. Reduction of this improves outcome, how is this done/

A
  • Weight loss
  • ACE-I and AIIRB
  • Aldosterone antagonists
  • statins
  • moderate protein restriction: to avoid fibrosis from the toxic protein process
  • BP <125/70
22
Q

Dyslipidaemia

A

Common in CKD and no proof of benefit in terms of preserving kidney function

  • Potential benefits in moderate kidney disease zetamide and a statin
23
Q

Calcium and Phosphate content of the kidneys is increased in CRF and ESRF

What is this used for

A

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
24
Q

As kidneys regulate the volume state, CKD patients are more prone to ?

A

Both dehydration and volume overload

  • Advise the patient to avoid volume depletion
25
Q

What hormones does the kidney produce?

A
  • 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
26
Q

How does the kidney do Acid-base regulation?

A
  • 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
27
Q

Uraemia

A

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

28
Q

Haematological, cardiovascular, respiratory and GI ymptoms of uraemia

A

Haematological

  • anaemia
  • bleeding tendency
  • platelet dysfunction
  • infection

CVS

  • pericarditis
  • hypertension
  • HF
  • IHD
  • Cardiomyopathy
  • CVA

Resp:

  • pleuritis
  • ischaemic lung

GI tract

  • anorexia, nausea
  • vomiting
29
Q

Treatment of Uraemia

A
  1. Treat primary disease
  2. treat secondary factors
  3. avoid nephrotoxins
  4. Correct abnormalities
    • Ca/P PTH
    • other electrolytes
    • Acid-base balance
    • volume
  5. Renal replacement therapy
30
Q

ESKD treatment option

A
  • conservative
  • Dialysis
    • peritoneal
    • haemodialysis
  • Renal transplant
    • cadaveric
      • living

RBF (29 decks)

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