Renal Failure (Zoysa) Flashcards

1
Q

Describe the anatomy of the kidneys

A

Kidneys sit posteriorly, connecting to ureters, which go to the bladder.

  • There are nephrons in kidneys.
  • Renal arteries supply afferent arterioles ® glomerulus ® efferent arterioles
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2
Q

What are the key roles of Kidneys?

A
  • Elimination of waste products (major role)
  • Control of fluid balance
  • Regulate acid-base balance
  • Produce hormones

Elimination Of Waste Products: Glomerular Filtration Rate (GFR)

Glomerular filtration rate (GFR) is defined as rate at which blood is cleared of waste products

  • Normal GFR ³120mL/min
  • Reduced GFR indicates renal impairment

Control Of Fluid Balance (Concentrate Or Dilute Urine)

Kidneys regulate volume state of fluid, including water and electrolytes (sodium, potassium, calcium, phosphate).

CKD patients are more prone to both dehydration and volume overload.

Acid Base Regulation

Kidneys are the long term regulatory mechanism of maintaining pH

  • Typically, CKD patients develop metabolic acidosis due to lack of excretion of metabolic organic acids

Addition of oral sodium bicarbonate (NaHCO3) may be needed

Endocrine Organ

Kidneys produce hormones (endocrine organ):

  • Erythropoietin (RBC production stimulated by hypoxia)
    • Most patients with CKD starts to develop anemia
    • Corrected with recombinant EPO (injected form)
  • 1, 25-OH vitamin D
  • BMP-7
  • Renin, angiotensin, bradykinin etc.
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3
Q

What is GFR?

A

Glomerular filtration rate (GFR) is defined as rate at which blood is cleared of waste products

  • Normal GFR ³120mL/min
  • Reduced GFR indicates renal impairment
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4
Q

Classify the 2 types of renal failure

A

Renal failure may be divided into acute kidney injury or chronic kidney disease.

AKI

Acute kidney injury is characterised by sudden decline in kidney function. It can be hours to days, potentially reversible.

It is a wide clinical syndrome that may be due to many potential aetiologies (some may be due to several causes at the same time). It can either be:

  • Severe kidney failure (traditional clinical focus),

Mild impairment of kidney function, that is characterised by changes in either urine output or serum creatinine (may also associated with significant clinical consequence).

CKD

Chronic kidney disease is characterised by progressive loss of kidney function. It can be weeks/months/years; progressive, irreversible.

It is a major public health issue.

  • It is now 18th most common cause of death worldwide with a steady increase in disease burden of over 50% between 1990 and 2010 and a 50% increase in global years of life lost.

In New Zealand, it is estimated that over 10% population are affected by CKD, the number of patients needing life-sustaining renal replacement therapy (RRT), has steadily grown with annual increase of ~3.7% over last decade.

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5
Q

Describe the types of AKI ***

A

Acute kidney injury can be classified into (1) pre-renal; (2) renal; (3) post-renal. It provides a framework for different management.

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6
Q

How do you stage AKI **** Exam****

A

Either Serum creatinine or a certain level of urine output

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7
Q

What are the risk factors for AKI?

A

General Risks

  • Underlying chronic kidney disease
  • Age >75 years
  • Diabetes mellitus
  • Congestive heart failure (lack of renal perfusion)
  • Liver failure
  • Nephrotoxic medications (e.g. NSAIDs, ACEi)
  • Past history of acute kidney injury
  • Acute illness (e.g. hypotension, sepsis, hypovolemia)
  • High early warning scores (markers of physiology)
    • Temperature, pulse, BP, O2 saturation
    • Requires further assessment to eliminate illness if outside parameter
  • Surgery (e.g. emergency surgery (increases risk of sepsis, hypovolemia), intraperitoneal surgery)
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8
Q

What are the General approaches to AKI? ***

(Initial then further management)

A

General Approach I: Initial Management

  • Identify patient at high risk
  • Assess and optimize volume status
    • _​_JVP inspection
    • (third heart sound also suggests fluid overload)
  • Review medications (dose adjustment) and stop nephrotoxic agents
    • Revise meds that may be nephortoxic e.g. NSAIDs, gentamicin, anti-hypertesnive agents
    • Revise meds that are renally excreted e.g. hypoglycaemic agents
  • Monitor creatinine and urine output daily (and other renal function tests)

General Approach II: Further Management

  • Non-invasive diagnostic workup
    • (e.g. ultrasound/CT scan to identify whether AKI is pre-renal, renal or post-renal)
  • Invasive diagnostic workup
    • (e.g. renal biopsy)
  • Daily weight (marker of fluid balance)
  • Regulate diet
  • Targeted therapy (e.g. hypovlemia requires fluid therapy)
    • Give them fluid or restric their fluid intake- depending on if they’re hypo and hyper-volemic.
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9
Q

Define CKD

A

CKD is defined as a_bnormalities of kidney structure or function_ (slow declining renal function), present for >3 months, with i_mplications for health._

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10
Q

Stage CKD ***** Exam *****

A

CKD is classified based on cause of disease, GFR category, and albuminuria category (CGA). These are markers of renal disease and prognosis (G1-G5, A1-A3).

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11
Q

We tend to think of CKD based on…… ________**** Exam ****

A

We tend to think of CKD based on the cause, GFR, and the degree of albumin uria

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12
Q

Stage some ways you can measure the GFR

A

Measuring Glomerular Filtration Rate (GFR)

There are several ways to measure GFR via:

  • Clearance of artificially injected substances (inulin, isotope)
  • Creatinine clearance
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13
Q

Describe the Insulin CLerance test

A

Inulin is a sugar which is filtered by the glomerulus, and is neither reabsorbed nor secreted into the tubule

  • Injection of inulin into the blood and measure the clearance of inulin in the urine
  • This is not commonly done as it is quite invasive and time-consuming (more common in research settings)
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14
Q

Describe the Isotope Clearance Test

A

Injection of a radioactive substance and measure their levels in blood and its excretion over time.

  • Radioactive substance can be 51Cr-EDTA (ethylenediaminetetraacetic acid); 125I-IOT (iothalamate); 99mTc-DTPA (diethylenetriaminepentaacetic acid); 99mTc-MAG3 (mercaptoacetyltriglycine).
  • This is often done in people who wants to donate a kidney to see if they are fit to survive with only one kidney.
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15
Q

Describe the Creatinine Clearance Test

A

Creatinine is produced by creatine metabolism. It freely filtered at glomerulus thus can be used to estimate GFR.

  • CrCl (creatinine clearance rate) tends to overestimate GFR, since creatinine is also secreted in small amounts by tubules.
  • Serum creatinine also reflects body size and muscle mass (increase muscle mass, increase CrCl)
  • Moderate to severe CKD confounds CrCl interpretation
    • As GFR drops, there is increased extra-renal creatinine secretion (tubular secretion) and decreased muscle mass
    • This results in an overestimation of GFR in patients nearing end-stage renal disease
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16
Q

Describe how you might calculate the eGFR

A

Calculating Estimated Glomerular Filtration Rate (eGFR)

Using a single blood test of serum creatinine, estimated glomerular filtration rate (eGFR) is calculated from more typically derived formula (many other formulae exist).

  • It depends on age, sex and ethnicity.
  • Parameters for normal e_GFR decreases with age_ as renal function tend to deteriorate with age.
17
Q

Describe how you might predict the outcome of CKD (renal prognosis of CKD)

A

We use the Ga staging because it’s a marker of renal prognosis

In predicting risk for outcome of CKD, identify the following variables: (1) cause of CKD; (2) GFR category; (3) albuminuria category; (4) other risk factors and comorbid conditions.

For example, if GFR <15mL/min, patient has high risk of progressing to end stage renal failure, and higher risk with reduced GFR and albuminuria.

18
Q

What are the Sociodemographic Risk Factors of CKD?

A

Sociodemographic Risk Factors

  • Age
  • Sex (more common in men)
  • Ethnicity (more common in Maori/PI)
  • Low income (poverty)
  • Obesity
  • Smoking
19
Q

What are the causes of CKD?

A

Most common causes of CKD are

  • Diabetic nephropathy (45%)
  • Glomerulonephritis (25%) (most common form is IgA nephropathy)
  • Hypertensive nephrosclerosis (10%)
  • Polycystic kidney disease (5%)
20
Q

Describe the Progression of CKD

A

Lack of control of primary disease will lead to progression of CKD to end stage kidney disease (ESKD)

Irrespective of primary disease, secondary factors develop, which are likely to contribute to progression.

  • Systemic hypertension
  • Intra-glomerular hypertension
  • Glomerular hypertrophy
  • Calcium and phosphate
  • Dyslipidaemia
  • Proteinuria
  • Tubulo-interstitial fibrosis
  • Toxicity of iron/ammonia/middle molecules
21
Q

Name some areas you can form interventions to slow progression of CKD

A

Intervention into the primary renal disease, e.g. diabetes control

Intervention into secondary factors

1) Hypertension
2) Proteinuiria
3) Smoking
4) Dyslipidemia
5) Ca and P

22
Q

Describe how you might address: Hypertension

A

Progression of chronic renal failure (CRF) has been linked to hypertension.

_Lowering BP slows the speed of progression (i_ncreases renal survival), with target of 140/80mmHg or lower (better). This can be treated by:

  • Lifestyle changes include (1) weight loss; (2) salt restriction; (3) exercise; (4) moderation of alcohol; (4) quit smoking
  • Natriuresis by excreting salt (thiazide/loop diuretics)
  • RAAS cascade (ACE inhibitors or AIIA, aldosterone antagonists, e.g. spironolactone)
  • Inhibition of sympathetic nervous system (ABC) (a-blockers, b-blockers, calcium channel blockers)

We aim to use “complementary drugs” (combine different classes of drugs to achieve therapeutic BP)

23
Q

Describe how you might address: Proteinuria

A

Proteinuria is an important prognostic risk factor. In a wide range of glomerulonephritis, outcome is determined by degree of proteinuria

_Reducing urine albumi_n leads to improved outcome. Modification of proteinuria can be done by:

  • Weight loss
  • RAAS cascade (ACEi/AIIA, aldosterone antagonists)
  • Statins (lowers cholesterol)
  • Moderate protein restrictions
  • Drop BP <125/70mmHg

There is risk of nephrotoxicity (thus risk of AKI) with these drugs, but balance between risks and benefits.

24
Q

Describe Uraemia

A

Uraemia is the manifestation of organ dysfunction typically seen in CKD stage 4 and 5 (kidney toxins not being removed).

  • Uraemic syndrome resembles a systemic intoxication.
  • No single compound has been found to produce clinical picture of ureamia.

Putative uraemic toxins are listed on the right.

25
Q

Describe how you might address Ca2+ P + abnormality?

A

Slowing Progression: Calcium (Ca) and Phosphate (P)

Ca2+ and PO42- abnormality common in CKD. Ca2+ and PO42- content of the kidney is increased in experimental CRF and ESRF.

  • Increased Ca2+ and PO42- is associated with progressive renal impairment and decline in renal function
  • Improvement in Ca2+ PO42- product (<4.5) is associated with reduction in rate of renal function decline

Management includes:

  • Limiting phosphate in diet
  • Phosphate binders (calcium carbonate, aluminium hydroxide, severlemar, lanthrunum)
26
Q

Define and Describe the manifestations of Uraemia

A

Uraemia is the manifestation of organ dysfunction typically seen in CKD stage 4 and 5 (kidney toxins not being removed).

  • Uraemic syndrome resembles a systemic intoxication.
  • No single compound has been found to produce clinical picture of ureamia.

Putative uraemic toxins are listed on the right.

27
Q

How would you manage Uraemia?

A
  • Treat primary disease, and treat secondary factors
    • Correct abnormalities (haemologlobin, calcium phosphate PTH, other electrolytes, acid base balance, volume)
    • Renal replacement therapy
  • Avoid nephrotoxins
28
Q

What are the treatment options for End Stage Kidney Disease?

A

ESKD Treatment Options

  • Conservative (due to scarcity of resource)
  • Dialysis (peritoneal, hemodialysis)
  • _Renal transplan_t (cadaveric, living)