TEST OF RENAL FUNCTIONS - PowerPoint Presentation

Slide1

TEST OF RENAL FUNCTIONS :

GLOMERULAR FUNCTIONS

:

About

200 L of plasma

ultrafiltrate

usually enter the tubular lamina daily ,glomerular function measured as GFR ( glomerular

filtrarion

rate ) which is mean the volume of fluid filtered from the renal glomerular capillaries into

Bowmans

capsule per unit time . it depend on :

1- the

net pressure across glomerular membrane .

2- physical

nature of the membrane .

3- the

surface area of the membrane .

Measurement of the GFR :

many substances concentration had been measured in blood to estimate the GFR but with a poor

guidness

like blood urea , then serum

creatinine

which is better than blood urea but still with a misleading results.

The most accurate

measurement

of the GFR is undertaking by measurement of clearance of

cr-labelled

EDTA or inulin .

Slide2

The GFR is determined

by measuring the concentration of specific substance in plasma and urine of this substances which must

fulfill

the following criteria :

1- It should be readily filtered from the plasma at the glomerulus into

glomerular

filtrate.

2- It should be neither

reabsorped

nor secreted.

There is misleading results when we measured urea clearance due to slightly

reabsorped

while

creatinine

clearance secreted in (PCT).

3- Its

concentration in plasma should remain constant through out the period of urine collection.

4- The

measurement of its concentration in plasma and urine should be analytically convenient and reliable.

Slide3

If a substance meet the four criteria listed , the amount of its excretion in the urine in unit time equal the amount clearance from the plasma so the clearance by the kidney of the substance (S) is given by the formula :

 

GFR = Us / Ps X V

Us

→ concentration of S in urine in the same unit ex:

(mg/dl)

or ( gm/ L ) .

Ps

→ concentration of sub. In

plasma ex : ( mg/dl )

V

→ rate of formation of urine ( ml/min.)

So the unit for the GFR is ( ml/min.)

Normal

range of GFR =

( 90-120 ) ml/min.

Slide4

Urea clearance :

-The

volume of plasma or blood that would be completely cleared of urea

by

one minutes excretion of urine.

Urea

clearance is not much used now for the GFR due to reabsorption in (PCT

)

T

he

proportion

reabsorped

varies

inversely with urine flow rate.

Slide5

Creatinine clearance :

The

creatinine

clearance test compares the level of

creatinine

in urine with the

creatinie

level in the

blood. (

creatinine

is a breakdown of product of

creatine

, which is an important part of

muscle).

The test helps provide information about kidney function

.

This

test requires both a blood and urine sample , you will collect urine for 24 hrs , and then have blood taken .it is more reliable than urea clearance and it closely correlate with inulin clearance a part from this

percent

of

creatinine

which is secreted

in (

PCT ) i.e. this will give over estimation ,

N.R

of

creatinine

clearance

( more

than

100

ml/min

.)

in a healthy adult.

Slide6

In children should be estimated according to the surface area Creatinine

clearnance

ml/min

.

=

creatinine

(urine)

µ

mol

/L

×

1000

Creatinine

(plasma) µ

mol

/L

1440

 

There is equation has been shown to be a reliable and consistent way of assess GFR from serum

creatinine

only :

Creatinine

clearance ( Cockcroft and

Gault

) =

 

(

140-age) X lean body wt.(Kg) X (1.22 male or 1.04 female)

serum

creatinine

(

µ

mol

/L

)

Slide7

The creatinine clearance may be impaired in a wide range of disorder affecting the renal tract these include the following :

1- Any

disease in which there is impaired renal perfusion ex. Hypotension, congestive heart failure , dehydration , shock and renal artery stenosis

.

2- Most

type of renal disease in which there is a loss of functioning nephron ex, chronic

pylonephritis

, acute renal failure .

3- Disease

in which there is increase pressure on tubular side (bladder outlet obstruction) ex, urinary tract obstruction by BPH.

Slide8

3- Inulin clearance :

This is reference procedure by which value of the GFR has been established and against which other methods of measuring GFR are

compared. Inulin

meet the criteria mention above , but it is not suitable for routine diagnostic use since it is an exogenous material and should be infused

.

Other clearance tests :

Several radioactively labeled substances have been used to estimate GFR including

chrom

Cr-

labelled

EDTA and Co-vit.B12 . they have not found general used since :

1- exogenous

material.

2-There

may be difficulty in maintaining a constant concentration in plasma during urine collection period.

3- Some

of substances become bound to plasma protein and are then not completely filtered at the glomerulus.

4- Test

involve exposure of patient to ionizing radiation.

Slide9

The plasma

creatinine

concentration may not exceed the upper limit of

the

reference range until the GFR, and therefore the

creatinine

clearance, has been reduced by approximately 60 % .

Thus

the measurement of

creatinine

clearance should be a more sensitive but less accurate indicator of early glomerular dysfunction than of plasma

creatinine

concentration

.

Clearance values will be low whether the reduced GFR is due to renal circulatory insufficiency, intrinsic renal damage or ‘post-renal’ causes, and it cannot distinguish among them,

creatinine

clearance has been said to be useful in deciding the dose of a

renally

excreted drug .

Slide10

RENAL TUBULAR FUNCTION

From 200 L of plasma filtered daily, only

about

2

L of urine are formed. The composition of urine differs markedly from that of plasma, and therefore of the filtrate. The tubular cells use ATP active transport, sometimes selectively, against physicochemical gradients. Transport of charged ions tends to produce an electrochemical gradient that inhibits further transport. This is minimized by two processes

.

Slide11

Isosmotic transport

:

This occurs mainly in the proximal tubules , active transport of one ion leads to passive movement of an ion of the opposite charge in the same direction, along the electrochemical gradient. The movement of sodium (Na+) depends on the availability of diffusible negatively charged ions, such as chloride (

Cl

–). The process is ‘isosmotic’ because the active transport of solute causes equivalent movement of water reabsorption in the same direction.

Isosmotic

transport also occurs to a lesser extent in the distal part of the nephron.

Slide12

Ion exchange :

This

occurs mainly in the more distal parts of the

nephrons

Ions of the same charge, usually

cations

,

are exchanged and neither electrochemical nor osmotic gradients are created. Therefore, during

cation

exchange there is insignificant net movement of anions or water. For example, Na+ may be reabsorbed in exchange for potassium (K

+)

or hydrogen (H+) ions

.

Other substances, such as phosphate and

urate

, are secreted into, as well as reabsorbed from, the tubular lumen. The tubular cells do not deal actively with waste products such as urea and

creatinine

to any significant degree. Most filtered urea is passed in urine (which accounts for most of the urine’s osmolality).

Slide13

Plasma measurement in the assessment of the glomerular functions:

Plasma urea and

creatinine

which are naturally substances found in the body and excreted as waste products in equal balance so urea and

creatinine

are widely used to provide an indicator of failure of glomerular function.

1-

Plasma

urea concentration.

2-

Plasma

creatinine

concentration

.

Urea

is derived in the liver from amino acids and therefore from protein, whether originating from the diet or from tissues. The normal kidney can excrete large amounts of urea. If the rate of production exceeds the rate of clearance, plasma concentrations rise.

Slide14

The rate of production is accelerated by : ●

a high-protein diet,

●

absorption of amino acids and peptides from digested blood after

haemorrhage

into the

gastrointestinal lumen or soft tissues,

●

increased catabolism due to starvation, tissue damage, sepsis or

steroid

treatment. In catabolic states, glomerular function is often impaired due to

circulatory

factors and this contributes more to the

uraemia

than does increased

production.

Slide15

The plasma urea concentration may be lower than 1.0

mmol

/L

,

the causes of

this decrement

include the following :

●

Those due to increased GFR or

haemodilution

(common):

–

pregnancy (the commonest cause in young women), – overenthusiastic intravenous infusion (the commonest cause in hospital patients), – ‘inappropriate’ ADH secretion (syndrome of inappropriate ADH secretion, SIADH).

●

Those due to decreased synthesis:

– use of amino acids for protein anabolism during growth, especially in children, – low protein intake, – very severe liver disease (low amino acid deamination), – inborn errors of the urea cycle are rare

Slide16

Creatinine

is largely derived from endogenous sources by muscle

creatine

breakdown. Plasma

creatinine

usually correlates with muscle mass, with 95 % of

creatine

occurring in skeletal muscle , sustained high-protein diets and catabolic states probably affect the plasma concentration of

creatinine

less than that of urea.

Creatinine

concentration is used to assess renal function; however, its assay may be less precise than that of urea, and can be prone to analytical interference by substances such as bilirubin, ketone bodies and certain drugs .

Slide17

If the plasma concentration of either urea or

creatinine

is significantly raised, and especially if it is rising, impaired glomerular function is likely

.

With

a reduced GFR, plasma urea concentrations tend to rise faster than those

of

creatinine

and tend to be disproportionately higher with respect to the upper reference limit. The rate at which urea is reabsorbed from the collecting ducts is dependent on the amount filtered by the glomerulus and by the rate of luminal

fluid flow .

Slide18

Reduced glomerular filtration

rate with normal tubular function :

The total amounts of urea and

creatinine

excreted are affected by the GFR. If the rate of filtration fails to balance that of production, plasma concentrations will rise. Phosphate and

urate

are released during cell breakdown , plasma concentrations rise because less than normal is filtered , most of the reduced amount reaching the proximal tubule can be reabsorbed, these contribute to high plasma concentrations.

Slide19

A large proportion of the reduced amount of filtered sodium is reabsorbed by isosmotic mechanisms; less than usual is then available for exchange with hydrogen and potassium ions distally. This has two main outcomes

:

1-

Reduced hydrogen ion secretion throughout the nephron: bicarbonate can

be

reclaimed only if hydrogen ions are secreted; plasma bicarbonate

concentrations

will fall,

2-

Reduced potassium secretion in the distal tubule, with potassium

retention

(potassium can still be reabsorbed proximally).

Slide20

If there is a low GFR accompanied by a low renal blood flow :

●

Systemic aldosterone secretion will be maximal

: in such cases, any sodium reaching the distal tubule will be almost completely reabsorbed in exchange for H+ and K+, and the urinary sodium concentration will be low.

●

ADH secretion will be increased

: ADH acting on the collecting ducts allows water to be reabsorbed in excess of solute, further reducing urinary volume and increasing urinary osmolality well above that of plasma and reducing plasma sodium concentration.

Slide21

In

summary, the findings in venous plasma and urine from the affected nephrons will be as follow

:

Plasma

● High urea (

uraemia

) and

creatinine

concentrations.

●

Low

bicarbonate concentration, with low pH (acidosis).

●

Hyperkalaemia

.

●

Hyperuricaemia

and

hyperphosphataemia

.

Urine

● Reduced volume (oliguria).

● Low (appropriate) sodium concentration – only if renal blood

flow

is low

,

stimulating aldosterone secretion.

Slide22

Acute Kidney injury :

This was previously known as acute renal failure. In adults,

oliguria

is defined as a

urine output of less than 400

mL

/day, or less than 15

mL

/h;

it usually indicates a low GFR and a rapid decline in renal function over hours to weeks, with retention of

creatinine

and nitrogenous waste products.

Oliguria

may be caused by the factors discussed below :

Acute

oliguria

with reduced GFR (pre-renal) :

This is caused by factors that reduce the hydrostatic pressure gradient between the renal capillaries and the tubular lumen. It is known as renal circulatory insufficiency (‘pre-renal

uraemia

’) and may be due to :

●

intravascular depletion of whole blood (

haemorrhage

) or plasma volume (usually

due to gastrointestinal loss), or reduced intake,

●

reduced pressure as a result of the vascular dilatation caused by ‘shock’,

i.e

( myocardial infarction, cardiac failure and mismatched blood transfusion ).

The patient is usually

hypotensive

, If renal blood

flow

is restored within a few hours, the condition is reversible, but, the longer it persists, the greater the danger of intrinsic renal damage.

Slide23

Acute

oliguria

due to intrinsic renal damage

This may be due to:

●

prolonged renal circulatory insufficiency,

●

acute

glomerulonephritis

, usually in children – the history of a sore throat and the

finding of red cells in the urine usually make the diagnosis obvious,

●

septicaemia

,

●

ingestion of a variety of poisons or drugs,

●

myoglobulinuria

.

●

Bence

Jones

proteinuria

.

Acute

oliguria

due to renal outflow obstruction (

postrenal

):

Oliguria

or

anuria

(absence of urine) may occur in post-renal failure.

The cause is usually, may be due to the following :

●

Intrarenal

obstruction, with blockage of the tubular

lumina

by

haemoglobin

,

myoglobin

and, very rarely,

urate

or calcium..

●

Extrarenal

obstruction, due to calculi,

neoplasms

, for example prostate or cervix, urethral strictures or prostatic hypertrophy, any of which may cause sudden obstruction. The finding of a palpable bladder indicates urethral obstruction, and in males is most likely to be due to prostatic hypertrophy.

Slide24

Investigation of acute kidney injury :

●

A careful clinical history, especially of taking

nephrotoxic

drugs, it is essential to

exclude reversible causes of pre-renal failure, including

hypovolaemia

or

hypotension , and also post-renal urinary tract obstruction (renal tract imaging may

be useful, such as abdominal radiograph if calculi are suspected, and renal tract

ultrasound)

●

Monitor urine output, plasma urea and

creatinine

and electrolytes, as well as acid-

base status.

●

Hyperkalaemia

,

hypermagnesaemia

,

hyperphosphataemia

,

hyperuricaemia

and

metabolic acidosis may occur

.

●

Urine microscopy may show granular casts supportive of the diagnosis of acute

tubular necrosis.

Slide25

●

The fractional excretion of sodium (

FENa

%) is also useful if less than 1% is typical of

prerenal

failure .

●

Urine sodium less than 20

mmol

/L in spot urine sample suggest

prerenal

failure.

●

Blood may be necessary for CBP , coagulation screen and blood cultures, also exclude myeloma, and look for

Bence

Jones

proteinuria

,

autoantibody screen, including (ANCA),antinuclear antibody(ANA), complement

,

antiglomerular

basement membrane

AB ,

and

antidouble

-

stranded

deoxyribonucleic acid (DNA)

.

●

In obscure cases, renal biopsy may be necessary to establish a diagnosis.

●

Recently, urine

neutrophil

gelatinase

-associated

lipocalin

(NGAL) has been suggested as a marker of renal injury and predictor of AKI.

Slide26

Chronic kidney disease :

Chronic renal dysfunction [defined as being reduced

eGFR

(estimated GFR),

proteinuria

,

haematuria

and/or renal structural abnormalities of more than 90 days’ duration , some causes of chronic kidney disease are the following :

Diabetes mellitus

-

Nephrotoxic

drugs

-Hypertension

-

Glomerulonephritis

-Chronic

pyelonephritis

-Polycystic kidneys

-Urinary tract obstruction

-Severe urinary infections

-

Amyloid

and

paraproteins

-Progression from acute kidney injury

-Severe hypothyroidism (rare)

Slide27

Abnormal findings in chronic kidney disease :

Apart from

uraemia

,

hyperkalaemia

and metabolic acidosis, other abnormalities that may occur in CKD include the following :

●

increase plasma phosphate concentrations rise and decrease plasma total calcium concentrations . The increased hydrogen ion concentration increases the proportion of free ionized calcium, the plasma concentration of which does not fall in parallel with the fall in total calcium concentration. Impaired renal tubular function and the raised phosphate concentration inhibit the conversion of vitamin D to the active metabolite and this contributes to the fall in plasma calcium concentration. After several years of CKD, secondary hyperparathyroidism may cause decalcification of bone, with a rise in the plasma alkaline

phosphatase

activity. Some of these features of CKD can also evoke renal

osteodystrophy

, associated with painful bones.

Slide28

The increase in plasma PTH occurs early when the GFR falls below 60

mL

/min per 1.73 m2.

●

Plasma

urate

concentrations rise in parallel with plasma urea .

●

Hypermagnesaemia

can also occur .

●

Normochromic

,

normocytic

anaemia

due to erythropoietin deficiency is common and, because

haemopoiesis

is impaired, does not respond to iron therapy; this can be treated with recombinant erythropoietin.

●

One of the commonest causes of death in patients with CKD is cardiovascular disease, in part explained by hypertension and a

dyslipidaemia

of

hypertriglyceridaemia

and low high-density lipoprotein cholesterol. Some of these effects may be due to reduced lipoprotein lipase activity.

●

Abnormal endocrine function, such as

hyperprolactinaemia

, insulin resistance, low plasma testosterone and abnormal thyroid function, may also be seen in chronic renal dysfunction.

●

The presence of increasing

proteinuria

may be the best single predictor of disease progression.

Slide29

Renal tubular function tests :

Reduced tubular function, with normal

glomerular

function, impairs the adjustment of the composition and volume of the urine with minimal effect on the plasma urea or

creatinine

concentration. The investigations used to diagnose tubular disorders can be divided into those that predominantly identify proximal tubular dysfunction and those that predominantly identify distal tubular dysfunction.

Proximal tubular function tests :

Impaired solute

reabsorption

from the proximal tubules reduces

isosmotic

water

reabsorption

, A large volume of inappropriately dilute urine is produced. The tubules cannot secrete hydrogen ions and so cannot reabsorb bicarbonate normally and therefore the urine is inappropriately alkaline for the degree of acidosis in the blood. The

reabsorption

of potassium, phosphate, magnesium,

urate

, glucose and amino acids is impaired.

The following

findings

may be present

Slide30

Plasma

●

Normal urea and creatinine concentrations (normal

glomerular

function).

●

Low bicarbonate concentration with low pH (metabolic acidosis).

●

Hypokalaemia

,

hypophosphataemia

, hypomagnesaemia and

hypouricaemia

Urine

●

Increased volume (

polyuria

).

●

pH may be inappropriately high

.

●

Phosphaturia

,

glycosuria

,

uricosuria

.

●

Generalized amino

aciduria

.

Tubular

proteinuria

can be diagnosed by measuring

specific

low-molecular-weight proteins such as

retinolbinding

protein

or

α

1-microglobulin are increased in the urine because of reduced tubular

reabsorption

and increased renal tubular secretion. If there is detectable

glycosuria

,

phosphaturia

and nonselective amino

aciduria

, the condition is known as

Fanconi’s

syndrome

.,

Slide31

Distal tubular function tests

Impaired distal tubular function primarily affects urine acidification, with a failure to excrete hydrogen ions; the urinary pH rarely falls below 5.5. There is an impaired response to

aldosterone

involving

reabsorption

of sodium, and the urine contains an inappropriately high concentration of sodium

The associated findings may include the following :

Plasma

●

Low bicarbonate and high chloride concentration with low pH (

hyperchloraemic

acidosis),

hypokalaemia

.

Urine

●

Increased volume.

●

pH inappropriately high.

●

An inappropriately high sodium concentration, even if renal blood flow is low (inability to respond to

aldosterone

)

Slide32

Urinary sodium estimation

Urinary sodium estimation may be used to differentiate acute

oliguria

due to renal damage from that due to renal circulatory insufficiency.

Aldosterone

secretion will be maximal only if renal blood flow is reduced; in such circumstances, functioning tubules respond appropriately by selectively reabsorbing sodium by distal tubular exchange mechanisms. A urinary sodium concentration of less than about 20

mmol

/L is usually taken to indicate that tubular function is not significantly impaired.

Slide33

Renal tubular damage

Renal tubular acidosis :

RTA is one of the important causes of

hyperchloraemic

acidosis , due to tubular transport defect there are various forms of renal tubular acidosis, which can present as a

hyperchloraemic

metabolic acidosis.

The more common, sometimes called classic,

RTA

(type I) is due to a distal tubular defect . The urinary pH can

not fall below that of plasma

even in severe acidosis.

I

n

RTA

type II there is impairment of HCO3–

reabsorption

in the proximal tubule. Loss of HCO3– may cause systemic acidosis, but the ability to form acid urine when acidosis becomes severe is retained,

Type II

RTA

is also associated with amino

aciduria

,

phosphaturia

and

glycosuria

, as in

Fanconi’s

syndrome

RTA

type IV is associated with

hyporeninism

hypoaldosteronism

and with a

hyperkalaemic

hyperchloraemic

acidosis. Sometimes plasma

renin

and

aldosterone

measurement may be useful to

confirm

this.

Slide34

Investigation of renal tubular acidosis

●

Measure the urinary anion gap and pH in a fresh spot urine sample along with the plasma anion gap. In practice, the urinary anion gap is the difference between the sum of the urinary [Na+] and [K+] minus the urinary [

Cl

–].

●

A urinary anion gap of less than 100

mmol

/L implies low urinary [NH4+].

●

In such cases a urinary pH of more than 5.5 in the presence of a

hyperchloraemic

metabolic acidosis and

hypokalaemia

is suggestive of type I, or distal, renal tubular acidosis.

a urinary pH of less than 5.5 in the presence of

hyperchloraemic

metabolic acidosis and

hyperkalaemia

is suggestive of renal tubular acidosis type IV. Plasma

aldosterone

and

renin

concentrations may show

hyporeninism

hypoaldosteronism

in renal tubular acidosis type IV.

Slide35

●

A urinary anion gap of more than 100 mmol/L implies high urinary [NH4+] , urine anion gap positive in both ( type I and type IV ) RTA .

●

Measure fractional excretion of HCO3– (FE% HCO3–), which is normally less than 5 % , but in type II RTA which usually more than 15 %

●

If the fractional excretion of HCO3– is increased, this is suggestive of renal tubular acidosis type II, particularly if

glycosuria

,

hypophosphaturia

and

hypophosphataemia

are also present.

●

Sometimes a diagnosis of acidosis is difficult to establish and additional tests are indicated , such as

furosemide

screening test and ammonium chloride test

Slide36

PROTEINS IN URINE

The loss of most plasma proteins through the

glomeruli

is restricted by the

size of the pores in, and by a negative charge on, the basement membrane

that repel negatively charged protein molecules. Alteration of either of these factors by

glomerular

disease may allow albumin and larger proteins to enter the filtrate. Low-molecular-weight proteins are filtered even under normal conditions; most are absorbed and metabolized by tubular cells.

Normal subjects excrete up to 0.08 g of protein a day in the urine

, amounts undetectable by usual screening tests.

Proteinuria

of (more than 0.15 g/day) almost always indicates disease.

Significant

proteinuria

may be due to renal disease or, more rarely, may occur because large amounts of low-molecular-weight proteins are circulating and therefore being

filtered

. Blood and pus in the urine and also urinary infection give positive tests for protein .

Slide37

Renal

proteinuria

Glomerular

proteinuria

Glomerular

proteinuria

is due to increased

glomerular

permeability, as in

nephrotic

syndrome. Albumin is usually the predominant protein in the urine .

Microalbuminuria

Microalbuimiuria

is an abnormal daily

urinary

excreation

of albumin range from (30-300 mg /day)

sensitive immunological assays have shown the normal daily excretion of albumin to be less than 0.05 gm. Patients with diabetes mellitus who excrete more than this, but to have

microalbuminuria

and to be at greater risk of developing progressive renal disease than those whose albumin excretion is normal.

Microalbuminuria

can be assessed from the urinary albumin to

creatinine

ratio (ACR) in female more than 3.5 mg /

mmol

and more than 2.5 mg /

mmol

in male The incidence of this complication may be reduced by optimization of

glycaemic

control and also blood pressure using

angiotensin

-converting enzyme (ACE) inhibitors .

Slide38

Tubular

proteinuria

Tubular

proteinuria

may be due to renal tubular damage from any cause, especially

pyelonephritis

. If

glomerular

permeability is normal,

proteinuria

is usually less than 1 g/day and consists mainly of low-molecular-weight globulins and not albumin. Low-molecular-weight α-globulins and β-globulins are sensitive markers of renal tubular damage. Tubular

proteinuria

can be diagnosed by measuring certain low-molecular-weight proteins in urine, such as retinol-binding protein (RBP), or

α 1-microglobulin Tubular

proteinuria

is associated with

Fanconi’s

syndrome and with

glycosuria

, amino

aciduria

,

hyperphosphaturia

(resulting in

hypophosphataemia

) and renal tubular acidosis. This can be primary or secondary, for example to heavy metals and drugs such as

cisplatin

.

Slide39

Overflow

proteinuria

This occurs when proteins of low molecular weight are filtered normally by the

glomerulus

and reabsorbed at the proximal tubule but are produced in amounts greater than the

reabsorptive

capacity of the proximal tubule. Overflow

proteinuria

can be due to the production of BJP (multiple myeloma), to severe

haemolysis

with

haemoglobinuria

, or to severe muscle damage (

rhabdomyolysis

) with

myoglobinuria

. In the last two cases, the urine may be red or brown in

colour

.

Nephrotic

syndrome :

The

nephrotic

syndrome is caused by increased

glomerular

basement membrane permeability, resulting in protein loss, usually daily

urinary protein loss of more than 3 gm a day

(or a urine protein to

creatinine

ratio of > 300 mg/

mmol

), with consequent

hypoproteinaemia

,

hypoalbuminaemia

and peripheral

oedema

. All but the highest molecular weight plasma proteins can pass through the

glomerular

basement membrane. The main effects are on plasma proteins and are associated with

hyperlipidaemia

and

hyperfibrinoginaemia

.

Uraemia

occurs only in late stages of the disorder, when many

glomeruli

have ceased to function.

Slide40

Nephritic syndrome :

This comprises reduced

eGFR

,

oedema

, hypertension and

proteinuria

with significant

haematuria

. It is usually associated with systemic disease such as

postinfectious

glomerulonephritis

, e.g. post-streptococcal or immunoglobulin A (

IgA

) nephropathy, ANCA associated

vasculitis

,

antiglomerular

basement membrane disease (

Goodpasture’s

disease).

Slide41