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pp2 quiz 2
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- 1TESTS OF RENAL FUNCTION: GLOMERULAR FILTRATION RATE• Total surface area available for filtration is about 6 m
2
• 10% of plasma delivered to kidneys enters the tubules
• Glomerular Filtration Rate (GFR) = the amount of
filtrate produced by the kidneys/minute
120-125 mL/min
around 180 L /day ( compare that with the amount of
urine excreted : 1 to 2 L/day) - 2GLOMERULAR FILTRATION RATEAny changes in blood pressure/blood flow, the integrity of the
filtration membrane, or capsule pressure will have an impact on
GFR, e.g.:
increase in arterial blood pressure ( ________________ in
GFR)
dehydration (______________________ in GFR)
obstructions to urine flow (_____________________in GFR)
glomerular loss (_______________________ in GFR) - 3CLEARANCE• GFR is calculated looking at clearance of a substance that
easily passes from the blood across the filter into the tubules and
is excreted in the urine. It is calculated as follows:
[substance]urine x urine volume secreted/min
[substance]plasma
• According to this equation:
if filtration is not optimal=>more of the substance stays in
the plasma and less gets excreted=>what happens to the
measured clearance? - 4FOR EXAMPLE: CREATININE CLEARANCECreatinine is waste product from energy metabolism in the
muscle.
rate of production determined by total muscle mass
readily filtered through the glomerulus
not reabsorbed and
normally an insignificant amount is secreted by the tubules.
• The subject provides:
one blood sample
24 h urine
Exercise
24h urine sample: 1500 mL
plasma creatinine: 0.1 mmol/L
urine creatinine: 10 mmol/L - 5CREATININE CLEARANCEHOWEVER:
• 24 h urine collection is very prone to error
• So estimations using urinary clearance have been found to
under estimate actual clearance
• Equations using only serum creatinine level are available,
avoiding the inconvenience of 24 h urine clearance and also
allowing serial estimations over a period of interventions
As glomerular function falls what you expect to happen to
the levels of creatinine in the blood? - 6DISORDERS OF THE GLOMERULUSThere are three categories of glomerular disorders
immunological (e.g. glomerulonephritis)
non-immunological (e.g. diabetic glomerulosclerosis)
inherited (such as certain types of nephrotic syndrome) - 7GLOMERULONEPHRITISThis is a group of conditions with an inflammatory basis. There will be:
: an increase in the number of the different cell types
damage to the endothelium
dramatic changes in the permeability of the filtration membrane which
allows the passage of red blood cells
a decrease in glomerular filtration GFR ( measured by decrease in
clearance) (and so :an _____________ in the blood levels of nitrogencontaining
wastes such as urea and creatinine
)
o These last two points don’t actually contradict each other: while
damage to the endothelium may make this leakier: the
accumulation of cells and proteins of inflammatory response in the
capsular space can reduce blood flow through the capillaries
o There are also structural changes to the basement membrane which
also impact upon GFR - 8GLOMERULONEPHRITIS: Underlying causesExamples include:
induced by the complexes of infectious agents and antibodies
becoming trapped in the glomerulus
induced by binding of antibodies to glomerular or basement
membrane components
In either case the accumulation of antibodies at the glomerulus
triggers an inflammatory response at that site - 9GLOMERULONEPHRITIS: Clinical SignsThe person may present with (cross out the incorrect answer):
High/low blood pressure
Increased /decreased urine output
Upon analysis of urine and blood:
haematuria and the presence of red blood cell casts
proteins may also be detected in the urine
azotaemia: elevated blood urea or elevated levels of other
nitrogen-containing compounds - 10ACUTE NEPHRITIC SYNDROME• A syndrome is a particular pattern of symptoms and signs in
a presenting patient. It is not the disease itself. Several
diseases may be under the “umbrella” of a syndrome
• With the different occurrences of glomerulonephritis acute
nephritic syndrome is a set of signs and symptoms that are
result of blockage, and damage to the walls, of the glomerular
capillaries.
• This clinical presentation will be:
sudden onset of haematuria
oliguria
oedema
hypertension - 11NEPHROTIC SYNDROMEA syndrome where the principle sign is a increased
glomerular permeability to protein. Diagnosis is based
upon:
substantial proteinuria, that is > 3.5 g/day
• This is accompanied with
a hypoalbuminaemia and generalised oedema
lipiduria
hyperlipidaemia which in this case is an elevated
triglycerides and LDL-cholesterol possibly due to elevated
lipoprotein production by the liver - 12NEPHROTIC SYNDROME: MechanismsIn nephrotic syndrome there have
been substantial modifications to the
architecture of the filtration
membrane leading to defects in
filtration
• Primary (inherited) defects e.g.
minimal change disease where the
foot-shaped processes of the
podocytes (the visceral cells of the
Bowman’s capsule) are absent
• Secondary defects e.g. associated
with an autoimmune disease like
systemic lupus erythromatosus; or
associated with diabetes mellitus - 13REVISION: MESANGIAL CELLSA network of fibres and cells
surrounds the glomerulus and holds
the structure together: the
mesangium
There are several types of
mesangial cells
One type are phagocytic cells
which engulf material that can
pass through the fenestrations
but not through the filtration slits
Others are contractile and so
reduce the surface area of
glomerulus available for
filtration - 14DIABETIC GLOMERULOSCLEROSIS• The prevalence of nephropathy amongst people with diabetes
mellitus is high.
• The glomerulus is most common site for such changes
increased basement membrane collagen production
(“sclerosis”)
expansion of the area occupied by the mesangial cells
• In the early stages modifications to the filtration membrane results
in and increased GFR and an increased permeability to protein.
• As the mesangial cells proliferate there is a reduction in the
surface area of the glomerulus available for filtration
• As the disease progresses there is a loss of nephrons
Q: So as the disease progresses over time: what will happen
to GFR? - 15DIABETIC GLOMERULOSCLEROSIS: Microalbuminuria• In the early stage of this disease: microalbuminuria.
24-hour urine albumin excretion of 30 to 300
mg.
•The presence of microalbuminuria is indicator of
a poor prognosis with regard to not only
nephropathy but also cardiovascular disease. - 16KEY POINTSDiseases of the glomerulus modify its filtration functions
vital materials (like protein, blood and lipids) may be lost
wastes may be retained
• The manifestations of glomerular disease reflect these defects
in filtering function as measured by urine output, clearance and
blood levels of nitrogenous wastes and the presence of vital
materials in the urine
• Glomerulonephritis involves changes to glomerular function
wrought by inflammatory damage
• Nephrotic syndrome is a specific set of signs and symptoms
which are manifestations of an dramatic increase in
permeability to proteins
• A serious complication of diabetes are the changes in
glomerular (and tubular) function and these may become
progressively worse - 17CHRONIC KIDNEY DISEASEThis is the result of irreversible renal damage that may progress
over several years
There is a progressive decline in renal function
That is a progressive drop in GFR + other signs of failures
in renal function
• However, humans are endowed with 2.5 million nephrons
Also with nephron loss, surviving nephrons manifest an
increase in activity - 18CHRONIC KIDNEY DISEASEIt means that renal function can be progressively declining in
someone without any symptoms
• While symptoms and signs can become manifest when GFR <
50% ; renal function can drop as low as 10% of normal and
remain undiagnosed
At a 90% loss it is currently not possible to prevent the
disease worsening - 19Risk factors for CKDHypertension (15% of new cases in Australia)
• Diabetes (34% of new cases in Australia)
• Smoking
• BMI >=30
• Family history of chronic kidney disease
• Being over 50 years of age
The cluster of risks factors (as well as others) means that
indigenous Australians are a high risk group for CKD - 20CLINICAL MANIFESTATIONS OF CKDDisturbances in fluid, electrolyte and acid-base balance
• loss of sodium balance can lead to sodium (and water) retention
or loss (“wasting”) depending upon principal site of damage.
Thus: glomerular = retention whereas tubular = wasting
• possibly also
Elevated blood potassium level
Depleted blood bicarbonate level - 21Clinical manifestations of CKDBone and Mineral Disorders
• phosphate excretion is impaired in CKD leading to a
hyperphosphataemia.
The increasing amount of phosphate reduces the availability
of calcium in the blood.
• vitamin D activation is impaired
• The sum effects of impaired phosphate excretion and
depleted vitamin D activation result in a persistent
hypocalcaemia
• This in turn leads to a persistent elevated secretion of PTH into
the blood stream.
Which will target, amongst other sites: the bones - 22CLINICAL MANIFESTATION OF CKDPTH stimulates bone
resorption
• Thus people with CKD
are at risk of renal
osteodystrophy or renal
rickets - 23Clinical manifestations of ckdHaematological Disorders
• The rate of production of rbc is
regulated by erythropoietin
(EPO): produced by cells of the
juxtaglomerular apparatus of the
kidneys.
In CKD, EPO production is
usually insufficient.
• This is made worse with an
elevated
Blood
Urea
Nitrogen as
urea suppresses rbc production.
• Also people on dialysis often
become iron-deficient - 24Clinical manifestations of ckdSkin disorders
• dry skin and mouth
• disorders due to the deposition of
phosphate, and later, urea crystals
e.g. pruritis (itching) - 25CLINICAL MANIFESTATIONS OF CKDCardiovascular disease
• Hypertension (decreased GFR) , pericarditis
Gastrointestinal problems
• nausea, vomiting, anorexia
Neurological problems
• peripheral neuropathy: often the patient has “restless leg
syndrome” where, when their legs are still, they experience
unpleasant sensations in their legs
• uraemic encephalopathy: often first seen as a loss of alertness,
memory loss commonly follows. In the later stages there can be
delirium and coma
Uraemia is the term given for azotaemia with symptoms - 26CLINICAL MANIFESTATIONS OF CKDToxicological problems
• With depleted renal function there will be impaired drug
excretion
• Loss of albumin means loss of a protein that makes a major
contribution to reducing the concentration of free, and thus
active, drug in the blood stream
• Impaired drug metabolism occurs both due to defects in the
kidneys and also an inhibitory effect associated with azotaemia
• Thus choice of drugs as well as dosage regimes need to be
reviewed when the person has CKD - 27KEY POINTSChronic Kidney Disease represents a progressive loss of renal
function which may go undetected until the nephron loss is
substantial
• This means that it is critical for those at risk to be monitored so
that any problems can be picked up early
• Glomerular filtration rate, as a measure of nephron loss, is
used to stage CKD
• Amongst the complications of CKD are: hyperphosphataemia,
hypocalcaemia and an associated loss of bone density;
anaemia; skin diseases; GIT, CVS and neurological problems
as well as greater sensitivity to the side effects of drug
treatment
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