Re: Question about IGA- and another question...

[Guest guest]

Hi Chuck,

I was not diagnosed with IgAn until I was about 28, after having 2 kids.

In college I always had strep throat, every single winter. There is no one else

in my family with kidney disease, so like you I strongly suspect the strep to

have started it.

However , I also have thin basement membrane. How could that be when I didn't

inherit it (no one in my family has it), I don't know. My kid's neph says that

thin basement membrane is just a sign of kidney disease, not a disease onto

itself. He said that " benign familial hematuria " does not cause nephrotic range

proteinuria, like I've had.

Any ideas? Who's right and who's wrong here, my neph or my kids' neph? (Mine

says thin GBM is a disease)...

-beth

[Guest guest]

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

Phil, I'm no expert either. I have read different articles and on different

web sites different things. One I read, if I understood everything right

was that you can have different triggers.... streppe, upper respiratory

infections, etc. I don't know if that helps much. But hopefully it does.

Tara

Re: Question about IGA- and another question...

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

Phil, I'm no expert either. I have read different articles and on different

web sites different things. One I read, if I understood everything right

was that you can have different triggers.... streppe, upper respiratory

infections, etc. I don't know if that helps much. But hopefully it does.

Tara

Re: Question about IGA- and another question...

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

Phil, I'm no expert either. I have read different articles and on different

web sites different things. One I read, if I understood everything right

was that you can have different triggers.... streppe, upper respiratory

infections, etc. I don't know if that helps much. But hopefully it does.

Tara

Re: Question about IGA- and another question...

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

Phil, this is the best I can do...

There is something called post-strep glomerulonephritis. In this case, the

strep infection is definitely the cause of the nephritis, but this kind of

nephritis usually is not permanent. It does NOT turn into IgAN. Some people

may already have a mild, undetected IgAN which does become diagnosed by

coincidence after a strep infection.

What happens with IgAN is not really understood by even the best

nephrologists and the most expert researchers in the field, but with the

knowledge we have about it at present, it seems like the problem is not with

having IgA immune complexes circulating in our blood (which everyone in the

world has), but rather a problem with their structure. To put it simply,

they end up binding with something in the kidneys where they shouldn't. The

defect appears at this time to be with the IgA immune complexes themselves,

rather than a defect in the kidneys themselves. Many experts think that IgAN

is simply the same thing as HSP (Henoch-Schönlein purpura), but with only

the one symptom in the kidneys. Nobody knows what causes HSP either. All we

know is that HSP appears to be triggered by bacterial or viral infections,

medicines, insect bites, vaccinations or exposure to chemicals or cold

weather. Is is the same with just IgAN without the other HSP symptoms? This

is unknown.

Now, is there a precipitating event that causes triggers the IgA complexes

to become defective? Is it something that people who eventually develop IgAN

had all along since they were born, something they were genetically

pre-disposed to get whenever the right trgger came along? Or is there

something we are doing or being exposed to in life that causes this defect

to occur? Nobody can answer that. We, ie. medical science, simply do not

know.

When people say they got an upper respiratory infection of some kind and had

visible blood in their urine, and then were diagnosed with IgAN, it could be

that the upper respiratory infection only caused the little flare-up of

hematuria (blood in urine), because the IgAN was already there, too mild to

be detected.

Others may do so, but I can guarantee that I would never, ever suggest IgAN

starts with a single event. What I think happens is that for most people, a

single event just happens to cause the existing underlying condition to

generate hematuria, which gets the attention of the person or parent, and

then the doctor for what would have otherwise not have been noticed until

there was more renal failure. But of course, I have no proof of that. It's

only what I think.

I think this because other people with IgAN never get the visible blood in

the urine. Like me, they just happen to have a routine medical examination

and they are found to have microscopic blood in the urine. Further

investigation eventually leads to diagnosis of IgAN.

Some people are probably more prone than others to have the underlying IgAN

flare up into a more significant inflammation, which causes the hematuria

(usually harmless on its own), and/or proteinuria. Everyone with IgAN has

proteinuria, but for the majority, it just stays at a mild to moderate

level. For others, it flares up into a heavier proteinuria which must be

treated. Why? We don't know. There are a lot of things that aren't known

about all glomerular kidney diseases.

Pierre

P.S. It's not easy to operate a support group for a disease with no cure and

with so many unknowns. There is almost nothing that anyone can say for sure

about IgAN. We only have observational studies, clinical trials, clinical

experience as well as personal and anecdotal experience to go by. Nothing is

merely black or white.

Re: Question about IGA- and another question...

>

>

>

> I don't understand something about IGA. In many emails, you guys talk

> about how it started as if one single event caused IGA. But yet my

> understanding is that IGA is not caused by something but more related

> to how your body produces the IGA antibody. Is my understanding foggy?

>

> Phil

>

> BTW: The members in this group are the sweetest, most loving group and

> supportive group than any group that I was a member.

>

[Guest guest]

Phil, this is the best I can do...

There is something called post-strep glomerulonephritis. In this case, the

strep infection is definitely the cause of the nephritis, but this kind of

nephritis usually is not permanent. It does NOT turn into IgAN. Some people

may already have a mild, undetected IgAN which does become diagnosed by

coincidence after a strep infection.

What happens with IgAN is not really understood by even the best

nephrologists and the most expert researchers in the field, but with the

knowledge we have about it at present, it seems like the problem is not with

having IgA immune complexes circulating in our blood (which everyone in the

world has), but rather a problem with their structure. To put it simply,

they end up binding with something in the kidneys where they shouldn't. The

defect appears at this time to be with the IgA immune complexes themselves,

rather than a defect in the kidneys themselves. Many experts think that IgAN

is simply the same thing as HSP (Henoch-Schönlein purpura), but with only

the one symptom in the kidneys. Nobody knows what causes HSP either. All we

know is that HSP appears to be triggered by bacterial or viral infections,

medicines, insect bites, vaccinations or exposure to chemicals or cold

weather. Is is the same with just IgAN without the other HSP symptoms? This

is unknown.

Now, is there a precipitating event that causes triggers the IgA complexes

to become defective? Is it something that people who eventually develop IgAN

had all along since they were born, something they were genetically

pre-disposed to get whenever the right trgger came along? Or is there

something we are doing or being exposed to in life that causes this defect

to occur? Nobody can answer that. We, ie. medical science, simply do not

know.

When people say they got an upper respiratory infection of some kind and had

visible blood in their urine, and then were diagnosed with IgAN, it could be

that the upper respiratory infection only caused the little flare-up of

hematuria (blood in urine), because the IgAN was already there, too mild to

be detected.

Others may do so, but I can guarantee that I would never, ever suggest IgAN

starts with a single event. What I think happens is that for most people, a

single event just happens to cause the existing underlying condition to

generate hematuria, which gets the attention of the person or parent, and

then the doctor for what would have otherwise not have been noticed until

there was more renal failure. But of course, I have no proof of that. It's

only what I think.

I think this because other people with IgAN never get the visible blood in

the urine. Like me, they just happen to have a routine medical examination

and they are found to have microscopic blood in the urine. Further

investigation eventually leads to diagnosis of IgAN.

Some people are probably more prone than others to have the underlying IgAN

flare up into a more significant inflammation, which causes the hematuria

(usually harmless on its own), and/or proteinuria. Everyone with IgAN has

proteinuria, but for the majority, it just stays at a mild to moderate

level. For others, it flares up into a heavier proteinuria which must be

treated. Why? We don't know. There are a lot of things that aren't known

about all glomerular kidney diseases.

Pierre

P.S. It's not easy to operate a support group for a disease with no cure and

with so many unknowns. There is almost nothing that anyone can say for sure

about IgAN. We only have observational studies, clinical trials, clinical

experience as well as personal and anecdotal experience to go by. Nothing is

merely black or white.

Re: Question about IGA- and another question...

>

>

>

> I don't understand something about IGA. In many emails, you guys talk

> about how it started as if one single event caused IGA. But yet my

> understanding is that IGA is not caused by something but more related

> to how your body produces the IGA antibody. Is my understanding foggy?

>

> Phil

>

> BTW: The members in this group are the sweetest, most loving group and

> supportive group than any group that I was a member.

>

[Guest guest]

Phil, this is the best I can do...

There is something called post-strep glomerulonephritis. In this case, the

strep infection is definitely the cause of the nephritis, but this kind of

nephritis usually is not permanent. It does NOT turn into IgAN. Some people

may already have a mild, undetected IgAN which does become diagnosed by

coincidence after a strep infection.

What happens with IgAN is not really understood by even the best

nephrologists and the most expert researchers in the field, but with the

knowledge we have about it at present, it seems like the problem is not with

having IgA immune complexes circulating in our blood (which everyone in the

world has), but rather a problem with their structure. To put it simply,

they end up binding with something in the kidneys where they shouldn't. The

defect appears at this time to be with the IgA immune complexes themselves,

rather than a defect in the kidneys themselves. Many experts think that IgAN

is simply the same thing as HSP (Henoch-Schönlein purpura), but with only

the one symptom in the kidneys. Nobody knows what causes HSP either. All we

know is that HSP appears to be triggered by bacterial or viral infections,

medicines, insect bites, vaccinations or exposure to chemicals or cold

weather. Is is the same with just IgAN without the other HSP symptoms? This

is unknown.

Now, is there a precipitating event that causes triggers the IgA complexes

to become defective? Is it something that people who eventually develop IgAN

had all along since they were born, something they were genetically

pre-disposed to get whenever the right trgger came along? Or is there

something we are doing or being exposed to in life that causes this defect

to occur? Nobody can answer that. We, ie. medical science, simply do not

know.

When people say they got an upper respiratory infection of some kind and had

visible blood in their urine, and then were diagnosed with IgAN, it could be

that the upper respiratory infection only caused the little flare-up of

hematuria (blood in urine), because the IgAN was already there, too mild to

be detected.

Others may do so, but I can guarantee that I would never, ever suggest IgAN

starts with a single event. What I think happens is that for most people, a

single event just happens to cause the existing underlying condition to

generate hematuria, which gets the attention of the person or parent, and

then the doctor for what would have otherwise not have been noticed until

there was more renal failure. But of course, I have no proof of that. It's

only what I think.

I think this because other people with IgAN never get the visible blood in

the urine. Like me, they just happen to have a routine medical examination

and they are found to have microscopic blood in the urine. Further

investigation eventually leads to diagnosis of IgAN.

Some people are probably more prone than others to have the underlying IgAN

flare up into a more significant inflammation, which causes the hematuria

(usually harmless on its own), and/or proteinuria. Everyone with IgAN has

proteinuria, but for the majority, it just stays at a mild to moderate

level. For others, it flares up into a heavier proteinuria which must be

treated. Why? We don't know. There are a lot of things that aren't known

about all glomerular kidney diseases.

Pierre

P.S. It's not easy to operate a support group for a disease with no cure and

with so many unknowns. There is almost nothing that anyone can say for sure

about IgAN. We only have observational studies, clinical trials, clinical

experience as well as personal and anecdotal experience to go by. Nothing is

merely black or white.

Re: Question about IGA- and another question...

>

>

>

> I don't understand something about IGA. In many emails, you guys talk

> about how it started as if one single event caused IGA. But yet my

> understanding is that IGA is not caused by something but more related

> to how your body produces the IGA antibody. Is my understanding foggy?

>

> Phil

>

> BTW: The members in this group are the sweetest, most loving group and

> supportive group than any group that I was a member.

>

[Guest guest]

What a great email Pierre! Thanks for posting such an in-depth explanation

of IgAN.

In a message dated 2/9/2005 10:06:19 A.M. Pacific Standard Time,

pgl-groups@... writes:

Phil, this is the best I can do...

There is something called post-strep glomerulonephritis. In this case, the

strep infection is definitely the cause of the nephritis, but this kind of

nephritis usually is not permanent. It does NOT turn into IgAN. Some people

may already have a mild, undetected IgAN which does become diagnosed by

coincidence after a strep infection.

What happens with IgAN is not really understood by even the best

nephrologists and the most expert researchers in the field, but with the

knowledge we have about it at present, it seems like the problem is not with

having IgA immune complexes circulating in our blood (which everyone in the

world has), but rather a problem with their structure. To put it simply,

they end up binding with something in the kidneys where they shouldn't. The

defect appears at this time to be with the IgA immune complexes themselves,

rather than a defect in the kidneys themselves. Many experts think that IgAN

is simply the same thing as HSP (Henoch-Schönlein purpura), but with only

the one symptom in the kidneys. Nobody knows what causes HSP either. All we

know is that HSP appears to be triggered by bacterial or viral infections,

medicines, insect bites, vaccinations or exposure to chemicals or cold

weather. Is is the same with just IgAN without the other HSP symptoms? This

is unknown.

Now, is there a precipitating event that causes triggers the IgA complexes

to become defective? Is it something that people who eventually develop IgAN

had all along since they were born, something they were genetically

pre-disposed to get whenever the right trgger came along? Or is there

something we are doing or being exposed to in life that causes this defect

to occur? Nobody can answer that. We, ie. medical science, simply do not

know.

When people say they got an upper respiratory infection of some kind and had

visible blood in their urine, and then were diagnosed with IgAN, it could be

that the upper respiratory infection only caused the little flare-up of

hematuria (blood in urine), because the IgAN was already there, too mild to

be detected.

Others may do so, but I can guarantee that I would never, ever suggest IgAN

starts with a single event. What I think happens is that for most people, a

single event just happens to cause the existing underlying condition to

generate hematuria, which gets the attention of the person or parent, and

then the doctor for what would have otherwise not have been noticed until

there was more renal failure. But of course, I have no proof of that. It's

only what I think.

I think this because other people with IgAN never get the visible blood in

the urine. Like me, they just happen to have a routine medical examination

and they are found to have microscopic blood in the urine. Further

investigation eventually leads to diagnosis of IgAN.

Some people are probably more prone than others to have the underlying IgAN

flare up into a more significant inflammation, which causes the hematuria

(usually harmless on its own), and/or proteinuria. Everyone with IgAN has

proteinuria, but for the majority, it just stays at a mild to moderate

level. For others, it flares up into a heavier proteinuria which must be

treated. Why? We don't know. There are a lot of things that aren't known

about all glomerular kidney diseases.

Pierre

P.S. It's not easy to operate a support group for a disease with no cure and

with so many unknowns. There is almost nothing that anyone can say for sure

about IgAN. We only have observational studies, clinical trials, clinical

experience as well as personal and anecdotal experience to go by. Nothing is

merely black or white.

[Guest guest]

Phil,

One thing that might be causing confusion is that viral illness while not

necessarily a trigger for the IgAN itself, certain can trigger a flare up of the

IgAN and cause the IgAN symptoms to become visible.

In a message dated 2/9/2005 9:30:17 A.M. Pacific Standard Time,

tnewman@... writes:

Phil, I'm no expert either. I have read different articles and on different

web sites different things. One I read, if I understood everything right

was that you can have different triggers.... streppe, upper respiratory

infections, etc. I don't know if that helps much. But hopefully it does.

Tara

[Guest guest]

Hi Phil,

The " single event theory " is a little misleading. Everything that I know points

to a genetic pre-disposition. Given that IgAN (and other immunologically

mediated glomerular diseases) are loosely associated with other autoimmune

disorders), it appears that they may share a common genetic basis.

That being said, there are a number of instances in which IgAN (and other

similar diseases) are specifically related to a single event - such as an

infection with strep, HIV or hep C. It's my hunch that the immune response to

such infections directly or indirectly activates the gene (or genes) that cause

IgAN.

I think many people feel a need to know where their disease came from - which is

natural. However, you have to be very careful when postulating causal

relationships.

Cy

phil_m_palmer wrote:

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

Hi Phil,

The " single event theory " is a little misleading. Everything that I know points

to a genetic pre-disposition. Given that IgAN (and other immunologically

mediated glomerular diseases) are loosely associated with other autoimmune

disorders), it appears that they may share a common genetic basis.

That being said, there are a number of instances in which IgAN (and other

similar diseases) are specifically related to a single event - such as an

infection with strep, HIV or hep C. It's my hunch that the immune response to

such infections directly or indirectly activates the gene (or genes) that cause

IgAN.

I think many people feel a need to know where their disease came from - which is

natural. However, you have to be very careful when postulating causal

relationships.

Cy

phil_m_palmer wrote:

I don't understand something about IGA. In many emails, you guys talk

about how it started as if one single event caused IGA. But yet my

understanding is that IGA is not caused by something but more related

to how your body produces the IGA antibody. Is my understanding foggy?

Phil

BTW: The members in this group are the sweetest, most loving group and

supportive group than any group that I was a member.

> Hi Chuck,

>

> I was not diagnosed with IgAn until I was about 28, after having 2 kids.

> In college I always had strep throat, every single winter. There is

no one else in my family with kidney disease, so like you I strongly

suspect the strep to have started it.

>

> However , I also have thin basement membrane. How could that be

when I didn't inherit it (no one in my family has it), I don't know.

My kid's neph says that thin basement membrane is just a sign of

kidney disease, not a disease onto itself. He said that " benign

familial hematuria " does not cause nephrotic range proteinuria, like

I've had.

> Any ideas? Who's right and who's wrong here, my neph or my kids'

neph? (Mine says thin GBM is a disease)...

>

> -beth

>

>

>

>

>

[Guest guest]

Can you explain the rapid onset aggessive form this way too? I'm

still trying to understand how the aggessive form of IgAN works...I

understand the genetic predisposition to it but if a single event

doesn't trigger the rapid form, where does it come from?

Amy G.

> Phil, this is the best I can do...

>

> There is something called post-strep glomerulonephritis. In this

case, the

> strep infection is definitely the cause of the nephritis, but this

kind of

> nephritis usually is not permanent. It does NOT turn into IgAN.

Some people

> may already have a mild, undetected IgAN which does become

diagnosed by

> coincidence after a strep infection.

>

> What happens with IgAN is not really understood by even the best

> nephrologists and the most expert researchers in the field, but

with the

> knowledge we have about it at present, it seems like the problem

is not with

> having IgA immune complexes circulating in our blood (which

everyone in the

> world has), but rather a problem with their structure. To put it

simply,

> they end up binding with something in the kidneys where they

shouldn't. The

> defect appears at this time to be with the IgA immune complexes

themselves,

> rather than a defect in the kidneys themselves. Many experts think

that IgAN

> is simply the same thing as HSP (Henoch-Schönlein purpura), but

with only

> the one symptom in the kidneys. Nobody knows what causes HSP

either. All we

> know is that HSP appears to be triggered by bacterial or viral

infections,

> medicines, insect bites, vaccinations or exposure to chemicals or

cold

> weather. Is is the same with just IgAN without the other HSP

symptoms? This

> is unknown.

>

> Now, is there a precipitating event that causes triggers the IgA

complexes

> to become defective? Is it something that people who eventually

develop IgAN

> had all along since they were born, something they were genetically

> pre-disposed to get whenever the right trgger came along? Or is

there

> something we are doing or being exposed to in life that causes

this defect

> to occur? Nobody can answer that. We, ie. medical science, simply

do not

> know.

>

> When people say they got an upper respiratory infection of some

kind and had

> visible blood in their urine, and then were diagnosed with IgAN,

it could be

> that the upper respiratory infection only caused the little flare-

up of

> hematuria (blood in urine), because the IgAN was already there,

too mild to

> be detected.

>

> Others may do so, but I can guarantee that I would never, ever

suggest IgAN

> starts with a single event. What I think happens is that for most

people, a

> single event just happens to cause the existing underlying

condition to

> generate hematuria, which gets the attention of the person or

parent, and

> then the doctor for what would have otherwise not have been

noticed until

> there was more renal failure. But of course, I have no proof of

that. It's

> only what I think.

>

> I think this because other people with IgAN never get the visible

blood in

> the urine. Like me, they just happen to have a routine medical

examination

> and they are found to have microscopic blood in the urine. Further

> investigation eventually leads to diagnosis of IgAN.

>

> Some people are probably more prone than others to have the

underlying IgAN

> flare up into a more significant inflammation, which causes the

hematuria

> (usually harmless on its own), and/or proteinuria. Everyone with

IgAN has

> proteinuria, but for the majority, it just stays at a mild to

moderate

> level. For others, it flares up into a heavier proteinuria which

must be

> treated. Why? We don't know. There are a lot of things that aren't

known

> about all glomerular kidney diseases.

>

> Pierre

> P.S. It's not easy to operate a support group for a disease with

no cure and

> with so many unknowns. There is almost nothing that anyone can say

for sure

> about IgAN. We only have observational studies, clinical trials,

clinical

> experience as well as personal and anecdotal experience to go by.

Nothing is

> merely black or white.

>

>

> Re: Question about IGA- and another question...

>

>

> >

> >

> >

> > I don't understand something about IGA. In many emails, you guys

talk

> > about how it started as if one single event caused IGA. But yet

my

> > understanding is that IGA is not caused by something but more

related

> > to how your body produces the IGA antibody. Is my understanding

foggy?

> >

> > Phil

> >

> > BTW: The members in this group are the sweetest, most loving

group and

> > supportive group than any group that I was a member.

> >

[Guest guest]

Amy,

You go to the E.R. and they tell you your son is in kidney failure.

Then the biopsy confirms IGAN. That's the simple explanation. Kidney

failure in children stunts their growth and they have to take hormones.

is 6'5 " barefoot. So it couldn't have been that long. He grew

10 " in 3 years. We grow em big round here. <S>

Deb/tn

deborah@...

Our 18 year old son is in End Stage Renal Disease on Hemo

Dialysis since Dec 24, 2003

Transplant scheduled for Feb 15, 2005

Please sign his guest book

http://www.caringbridge.org/tn/dbowman

Amy Griswold wrote:

>Can you explain the rapid onset aggessive form this way too? I'm

>still trying to understand how the aggessive form of IgAN works...I

>understand the genetic predisposition to it but if a single event

>doesn't trigger the rapid form, where does it come from?

>

>Amy G.

>

>

>

[Guest guest]

I think my theory fits the rapidly aggressive form as well.

First of all, there's the question of proper diagnosis. What seems like

rapidly progressive gn might not be. A person could conceivably have a

certain degree of acute renal failure on top of the existing IgAN. There

could be various mechanisms for this, including some medications that might

precipitate acute renal failure (ACE inhibitors can actually cause this,

even though they are the drug of choice for chronic kidney disease at

present). In this case, the acute phase could resolve and then the person is

back to a more typical, more slowly progressive kidney disease.

There could be misdiagnosis, since, as we know, the more advanced renal

failure is when it's discovered, the harder it is to diagnose accuretely

which kidney disease caused it. Also, what might initially seem like rapidly

progressive gn might simply be a late diagnosis of kidney disease that has

already progressed to advanced chronic renal insufficiency. It happens.

If the diagnosis of rapidly progressive kidney disease (IgAN or whatever) is

correct, then, I think that a plausible explanation is that the kidney

disease already existed, and some unknown event, like a bad flu or

something, suddenly made it worse, in a person who might be more prone to

getting a lot of inflammation in the kidneys once they get it.

It's important to note again that I'm just thinking out loud here,

suggesting various possibilities. My reasoning for predisposition is simply

that the incredibly vast majority of people who are exposed to the same

things do NOT develop IgAN or any other kidney disease. So, there must be

some other factor at work, and it's probably either genetic predisposition,

existing low-level kidney disease that was previously undetectable, or, it's

a combination of events.

As I've posted before, I used to be convinced that a series of multiple

vaccinations I had to take within a short time while in the navy in my early

20's could have triggered it. I still think that's a possibility, but I

think I must have already had the disease at a very low level. In that

scenario, it would simply have taken a few years to develop to the point

where a then civilian doctor checked my urine and found blood in it. But,

it's just pure speculation. I don't know, and nobody else knows. The 1000's

of other guys and gals who had the same vaccinations that same year didn't

all develop kidney disease, I'm sure. In the navy in the 1970's, I was

exposed to a lot of things that the average person might not be: smoke and

chemicals during firefighting training, tear gas, radioactive material, lots

of gas and diesel fumes, lots of paint (including lead paint), insects in

tropical parts of the world, pesticides, herbicides used on land training

bases, cold and heat extremes, going days without sleep, etc. Now, the blood

in my urine was only found after I had left the navy about 4-5 years later,

but, maybe the seeds had already been planted.

But whatever, I have no way to prove anything, no way of knowing, and even

if I did, it wouldn't restore my kidney function. So, while I was very

active in trying to find reasons like most of you in my early years with

this IgAN, I eventually just let it go since that past is not something I

can control, and there's no way at this point to relate the disease to my

military service, ie. no medical pension. At some point, you just have to go

on, and I've organized my life to be able to do so by getting a social

security type disability pension (which ensured low but also stable income

for my family, getting subsidized housing so we wouldn't have to move onto

the street, etc.

Pierre

Re: Question about IGA- and another question...

Can you explain the rapid onset aggessive form this way too? I'm

still trying to understand how the aggessive form of IgAN works...I

understand the genetic predisposition to it but if a single event

doesn't trigger the rapid form, where does it come from?

Amy G.

> Phil, this is the best I can do...

>

> There is something called post-strep glomerulonephritis. In this

case, the

> strep infection is definitely the cause of the nephritis, but this

kind of

> nephritis usually is not permanent. It does NOT turn into IgAN.

Some people

> may already have a mild, undetected IgAN which does become

diagnosed by

> coincidence after a strep infection.

>

> What happens with IgAN is not really understood by even the best

> nephrologists and the most expert researchers in the field, but

with the

> knowledge we have about it at present, it seems like the problem

is not with

> having IgA immune complexes circulating in our blood (which

everyone in the

> world has), but rather a problem with their structure. To put it

simply,

> they end up binding with something in the kidneys where they

shouldn't. The

> defect appears at this time to be with the IgA immune complexes

themselves,

> rather than a defect in the kidneys themselves. Many experts think

that IgAN

> is simply the same thing as HSP (Henoch-Schönlein purpura), but

with only

> the one symptom in the kidneys. Nobody knows what causes HSP

either. All we

> know is that HSP appears to be triggered by bacterial or viral

infections,

> medicines, insect bites, vaccinations or exposure to chemicals or

cold

> weather. Is is the same with just IgAN without the other HSP

symptoms? This

> is unknown.

>

> Now, is there a precipitating event that causes triggers the IgA

complexes

> to become defective? Is it something that people who eventually

develop IgAN

> had all along since they were born, something they were genetically

> pre-disposed to get whenever the right trgger came along? Or is

there

> something we are doing or being exposed to in life that causes

this defect

> to occur? Nobody can answer that. We, ie. medical science, simply

do not

> know.

>

> When people say they got an upper respiratory infection of some

kind and had

> visible blood in their urine, and then were diagnosed with IgAN,

it could be

> that the upper respiratory infection only caused the little flare-

up of

> hematuria (blood in urine), because the IgAN was already there,

too mild to

> be detected.

>

> Others may do so, but I can guarantee that I would never, ever

suggest IgAN

> starts with a single event. What I think happens is that for most

people, a

> single event just happens to cause the existing underlying

condition to

> generate hematuria, which gets the attention of the person or

parent, and

> then the doctor for what would have otherwise not have been

noticed until

> there was more renal failure. But of course, I have no proof of

that. It's

> only what I think.

>

> I think this because other people with IgAN never get the visible

blood in

> the urine. Like me, they just happen to have a routine medical

examination

> and they are found to have microscopic blood in the urine. Further

> investigation eventually leads to diagnosis of IgAN.

>

> Some people are probably more prone than others to have the

underlying IgAN

> flare up into a more significant inflammation, which causes the

hematuria

> (usually harmless on its own), and/or proteinuria. Everyone with

IgAN has

> proteinuria, but for the majority, it just stays at a mild to

moderate

> level. For others, it flares up into a heavier proteinuria which

must be

> treated. Why? We don't know. There are a lot of things that aren't

known

> about all glomerular kidney diseases.

>

> Pierre

[Guest guest]

Pierre,

Is there a difference in prognosis if a person has both protein and blood in the

urine when diagnosed as opposed to just blood in the urine? Do people first

have blood and then get the protein in the urine? The neph told me that my son,

who is 12, already has about 10% scarring of the kidneys. He hasn't lost any

renal function though. The doctor thinks he must have had this for a long time

undetected, but a routine urine test in August 03 was normal. A routine urine

test in August 04 showed 300 units of protein and blood at 3+. Now is January

05 the protein is at 2000 units and blood at 4+. Can you tell me what you make

of this? You have a lot of knowledge that is much appreciated. Thank you.

Elaine

Re: Question about IGA- and another question...

I think my theory fits the rapidly aggressive form as well.

First of all, there's the question of proper diagnosis. What seems like

rapidly progressive gn might not be. A person could conceivably have a

certain degree of acute renal failure on top of the existing IgAN. There

could be various mechanisms for this, including some medications that might

precipitate acute renal failure (ACE inhibitors can actually cause this,

even though they are the drug of choice for chronic kidney disease at

present). In this case, the acute phase could resolve and then the person is

back to a more typical, more slowly progressive kidney disease.

There could be misdiagnosis, since, as we know, the more advanced renal

failure is when it's discovered, the harder it is to diagnose accuretely

which kidney disease caused it. Also, what might initially seem like rapidly

progressive gn might simply be a late diagnosis of kidney disease that has

already progressed to advanced chronic renal insufficiency. It happens.

If the diagnosis of rapidly progressive kidney disease (IgAN or whatever) is

correct, then, I think that a plausible explanation is that the kidney

disease already existed, and some unknown event, like a bad flu or

something, suddenly made it worse, in a person who might be more prone to

getting a lot of inflammation in the kidneys once they get it.

It's important to note again that I'm just thinking out loud here,

suggesting various possibilities. My reasoning for predisposition is simply

that the incredibly vast majority of people who are exposed to the same

things do NOT develop IgAN or any other kidney disease. So, there must be

some other factor at work, and it's probably either genetic predisposition,

existing low-level kidney disease that was previously undetectable, or, it's

a combination of events.

As I've posted before, I used to be convinced that a series of multiple

vaccinations I had to take within a short time while in the navy in my early

20's could have triggered it. I still think that's a possibility, but I

think I must have already had the disease at a very low level. In that

scenario, it would simply have taken a few years to develop to the point

where a then civilian doctor checked my urine and found blood in it. But,

it's just pure speculation. I don't know, and nobody else knows. The 1000's

of other guys and gals who had the same vaccinations that same year didn't

all develop kidney disease, I'm sure. In the navy in the 1970's, I was

exposed to a lot of things that the average person might not be: smoke and

chemicals during firefighting training, tear gas, radioactive material, lots

of gas and diesel fumes, lots of paint (including lead paint), insects in

tropical parts of the world, pesticides, herbicides used on land training

bases, cold and heat extremes, going days without sleep, etc. Now, the blood

in my urine was only found after I had left the navy about 4-5 years later,

but, maybe the seeds had already been planted.

But whatever, I have no way to prove anything, no way of knowing, and even

if I did, it wouldn't restore my kidney function. So, while I was very

active in trying to find reasons like most of you in my early years with

this IgAN, I eventually just let it go since that past is not something I

can control, and there's no way at this point to relate the disease to my

military service, ie. no medical pension. At some point, you just have to go

on, and I've organized my life to be able to do so by getting a social

security type disability pension (which ensured low but also stable income

for my family, getting subsidized housing so we wouldn't have to move onto

the street, etc.

Pierre

Re: Question about IGA- and another question...

Can you explain the rapid onset aggessive form this way too? I'm

still trying to understand how the aggessive form of IgAN works...I

understand the genetic predisposition to it but if a single event

doesn't trigger the rapid form, where does it come from?

Amy G.

> Phil, this is the best I can do...

>

> There is something called post-strep glomerulonephritis. In this

case, the

> strep infection is definitely the cause of the nephritis, but this

kind of

> nephritis usually is not permanent. It does NOT turn into IgAN.

Some people

> may already have a mild, undetected IgAN which does become

diagnosed by

> coincidence after a strep infection.

>

> What happens with IgAN is not really understood by even the best

> nephrologists and the most expert researchers in the field, but

with the

> knowledge we have about it at present, it seems like the problem

is not with

> having IgA immune complexes circulating in our blood (which

everyone in the

> world has), but rather a problem with their structure. To put it

simply,

> they end up binding with something in the kidneys where they

shouldn't. The

> defect appears at this time to be with the IgA immune complexes

themselves,

> rather than a defect in the kidneys themselves. Many experts think

that IgAN

> is simply the same thing as HSP (Henoch-Schönlein purpura), but

with only

> the one symptom in the kidneys. Nobody knows what causes HSP

either. All we

> know is that HSP appears to be triggered by bacterial or viral

infections,

> medicines, insect bites, vaccinations or exposure to chemicals or

cold

> weather. Is is the same with just IgAN without the other HSP

symptoms? This

> is unknown.

>

> Now, is there a precipitating event that causes triggers the IgA

complexes

> to become defective? Is it something that people who eventually

develop IgAN

> had all along since they were born, something they were genetically

> pre-disposed to get whenever the right trgger came along? Or is

there

> something we are doing or being exposed to in life that causes

this defect

> to occur? Nobody can answer that. We, ie. medical science, simply

do not

> know.

>

> When people say they got an upper respiratory infection of some

kind and had

> visible blood in their urine, and then were diagnosed with IgAN,

it could be

> that the upper respiratory infection only caused the little flare-

up of

> hematuria (blood in urine), because the IgAN was already there,

too mild to

> be detected.

>

> Others may do so, but I can guarantee that I would never, ever

suggest IgAN

> starts with a single event. What I think happens is that for most

people, a

> single event just happens to cause the existing underlying

condition to

> generate hematuria, which gets the attention of the person or

parent, and

> then the doctor for what would have otherwise not have been

noticed until

> there was more renal failure. But of course, I have no proof of

that. It's

> only what I think.

>

> I think this because other people with IgAN never get the visible

blood in

> the urine. Like me, they just happen to have a routine medical

examination

> and they are found to have microscopic blood in the urine. Further

> investigation eventually leads to diagnosis of IgAN.

>

> Some people are probably more prone than others to have the

underlying IgAN

> flare up into a more significant inflammation, which causes the

hematuria

> (usually harmless on its own), and/or proteinuria. Everyone with

IgAN has

> proteinuria, but for the majority, it just stays at a mild to

moderate

> level. For others, it flares up into a heavier proteinuria which

must be

> treated. Why? We don't know. There are a lot of things that aren't

known

> about all glomerular kidney diseases.

>

> Pierre

To edit your settings for the group, go to our Yahoo Group

home page:

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iga-nephropathy-unsubscribe

Visit our companion website at www.igan.ca. The site is entirely supported by

donations. If you would like to help, go to:

http://www.igan.ca/id62.htm

Thank you

[Guest guest]

Pierre,

Is there a difference in prognosis if a person has both protein and blood in the

urine when diagnosed as opposed to just blood in the urine? Do people first

have blood and then get the protein in the urine? The neph told me that my son,

who is 12, already has about 10% scarring of the kidneys. He hasn't lost any

renal function though. The doctor thinks he must have had this for a long time

undetected, but a routine urine test in August 03 was normal. A routine urine

test in August 04 showed 300 units of protein and blood at 3+. Now is January

05 the protein is at 2000 units and blood at 4+. Can you tell me what you make

of this? You have a lot of knowledge that is much appreciated. Thank you.

Elaine

Re: Question about IGA- and another question...

I think my theory fits the rapidly aggressive form as well.

First of all, there's the question of proper diagnosis. What seems like

rapidly progressive gn might not be. A person could conceivably have a

certain degree of acute renal failure on top of the existing IgAN. There

could be various mechanisms for this, including some medications that might

precipitate acute renal failure (ACE inhibitors can actually cause this,

even though they are the drug of choice for chronic kidney disease at

present). In this case, the acute phase could resolve and then the person is

back to a more typical, more slowly progressive kidney disease.

There could be misdiagnosis, since, as we know, the more advanced renal

failure is when it's discovered, the harder it is to diagnose accuretely

which kidney disease caused it. Also, what might initially seem like rapidly

progressive gn might simply be a late diagnosis of kidney disease that has

already progressed to advanced chronic renal insufficiency. It happens.

If the diagnosis of rapidly progressive kidney disease (IgAN or whatever) is

correct, then, I think that a plausible explanation is that the kidney

disease already existed, and some unknown event, like a bad flu or

something, suddenly made it worse, in a person who might be more prone to

getting a lot of inflammation in the kidneys once they get it.

It's important to note again that I'm just thinking out loud here,

suggesting various possibilities. My reasoning for predisposition is simply

that the incredibly vast majority of people who are exposed to the same

things do NOT develop IgAN or any other kidney disease. So, there must be

some other factor at work, and it's probably either genetic predisposition,

existing low-level kidney disease that was previously undetectable, or, it's

a combination of events.

As I've posted before, I used to be convinced that a series of multiple

vaccinations I had to take within a short time while in the navy in my early

20's could have triggered it. I still think that's a possibility, but I

think I must have already had the disease at a very low level. In that

scenario, it would simply have taken a few years to develop to the point

where a then civilian doctor checked my urine and found blood in it. But,

it's just pure speculation. I don't know, and nobody else knows. The 1000's

of other guys and gals who had the same vaccinations that same year didn't

all develop kidney disease, I'm sure. In the navy in the 1970's, I was

exposed to a lot of things that the average person might not be: smoke and

chemicals during firefighting training, tear gas, radioactive material, lots

of gas and diesel fumes, lots of paint (including lead paint), insects in

tropical parts of the world, pesticides, herbicides used on land training

bases, cold and heat extremes, going days without sleep, etc. Now, the blood

in my urine was only found after I had left the navy about 4-5 years later,

but, maybe the seeds had already been planted.

But whatever, I have no way to prove anything, no way of knowing, and even

if I did, it wouldn't restore my kidney function. So, while I was very

active in trying to find reasons like most of you in my early years with

this IgAN, I eventually just let it go since that past is not something I

can control, and there's no way at this point to relate the disease to my

military service, ie. no medical pension. At some point, you just have to go

on, and I've organized my life to be able to do so by getting a social

security type disability pension (which ensured low but also stable income

for my family, getting subsidized housing so we wouldn't have to move onto

the street, etc.

Pierre

Re: Question about IGA- and another question...

Can you explain the rapid onset aggessive form this way too? I'm

still trying to understand how the aggessive form of IgAN works...I

understand the genetic predisposition to it but if a single event

doesn't trigger the rapid form, where does it come from?

Amy G.

> Phil, this is the best I can do...

>

> There is something called post-strep glomerulonephritis. In this

case, the

> strep infection is definitely the cause of the nephritis, but this

kind of

> nephritis usually is not permanent. It does NOT turn into IgAN.

Some people

> may already have a mild, undetected IgAN which does become

diagnosed by

> coincidence after a strep infection.

>

> What happens with IgAN is not really understood by even the best

> nephrologists and the most expert researchers in the field, but

with the

> knowledge we have about it at present, it seems like the problem

is not with

> having IgA immune complexes circulating in our blood (which

everyone in the

> world has), but rather a problem with their structure. To put it

simply,

> they end up binding with something in the kidneys where they

shouldn't. The

> defect appears at this time to be with the IgA immune complexes

themselves,

> rather than a defect in the kidneys themselves. Many experts think

that IgAN

> is simply the same thing as HSP (Henoch-Schönlein purpura), but

with only

> the one symptom in the kidneys. Nobody knows what causes HSP

either. All we

> know is that HSP appears to be triggered by bacterial or viral

infections,

> medicines, insect bites, vaccinations or exposure to chemicals or

cold

> weather. Is is the same with just IgAN without the other HSP

symptoms? This

> is unknown.

>

> Now, is there a precipitating event that causes triggers the IgA

complexes

> to become defective? Is it something that people who eventually

develop IgAN

> had all along since they were born, something they were genetically

> pre-disposed to get whenever the right trgger came along? Or is

there

> something we are doing or being exposed to in life that causes

this defect

> to occur? Nobody can answer that. We, ie. medical science, simply

do not

> know.

>

> When people say they got an upper respiratory infection of some

kind and had

> visible blood in their urine, and then were diagnosed with IgAN,

it could be

> that the upper respiratory infection only caused the little flare-

up of

> hematuria (blood in urine), because the IgAN was already there,

too mild to

> be detected.

>

> Others may do so, but I can guarantee that I would never, ever

suggest IgAN

> starts with a single event. What I think happens is that for most

people, a

> single event just happens to cause the existing underlying

condition to

> generate hematuria, which gets the attention of the person or

parent, and

> then the doctor for what would have otherwise not have been

noticed until

> there was more renal failure. But of course, I have no proof of

that. It's

> only what I think.

>

> I think this because other people with IgAN never get the visible

blood in

> the urine. Like me, they just happen to have a routine medical

examination

> and they are found to have microscopic blood in the urine. Further

> investigation eventually leads to diagnosis of IgAN.

>

> Some people are probably more prone than others to have the

underlying IgAN

> flare up into a more significant inflammation, which causes the

hematuria

> (usually harmless on its own), and/or proteinuria. Everyone with

IgAN has

> proteinuria, but for the majority, it just stays at a mild to

moderate

> level. For others, it flares up into a heavier proteinuria which

must be

> treated. Why? We don't know. There are a lot of things that aren't

known

> about all glomerular kidney diseases.

>

> Pierre

To edit your settings for the group, go to our Yahoo Group

home page:

http://groups.yahoo.com/group/iga-nephropathy/

To unsubcribe via email,

iga-nephropathy-unsubscribe

Visit our companion website at www.igan.ca. The site is entirely supported by

donations. If you would like to help, go to:

http://www.igan.ca/id62.htm

Thank you

[Guest guest]

Elaine,

Good question. My son had a urine test today. No blood but 1+ protein.

Yesterdays' mid-day urine was normal.

What does this mean?

Phil

> > Phil, this is the best I can do...

> >

> > There is something called post-strep glomerulonephritis. In this

> case, the

> > strep infection is definitely the cause of the nephritis, but this

> kind of

> > nephritis usually is not permanent. It does NOT turn into IgAN.

> Some people

> > may already have a mild, undetected IgAN which does become

> diagnosed by

> > coincidence after a strep infection.

> >

> > What happens with IgAN is not really understood by even the best

> > nephrologists and the most expert researchers in the field, but

> with the

> > knowledge we have about it at present, it seems like the problem

> is not with

> > having IgA immune complexes circulating in our blood (which

> everyone in the

> > world has), but rather a problem with their structure. To put it

> simply,

> > they end up binding with something in the kidneys where they

> shouldn't. The

> > defect appears at this time to be with the IgA immune complexes

> themselves,

> > rather than a defect in the kidneys themselves. Many experts think

> that IgAN

> > is simply the same thing as HSP (Henoch-Schönlein purpura), but

> with only

> > the one symptom in the kidneys. Nobody knows what causes HSP

> either. All we

> > know is that HSP appears to be triggered by bacterial or viral

> infections,

> > medicines, insect bites, vaccinations or exposure to chemicals or

> cold

> > weather. Is is the same with just IgAN without the other HSP

> symptoms? This

> > is unknown.

> >

> > Now, is there a precipitating event that causes triggers the IgA

> complexes

> > to become defective? Is it something that people who eventually

> develop IgAN

> > had all along since they were born, something they were genetically

> > pre-disposed to get whenever the right trgger came along? Or is

> there

> > something we are doing or being exposed to in life that causes

> this defect

> > to occur? Nobody can answer that. We, ie. medical science, simply

> do not

> > know.

> >

> > When people say they got an upper respiratory infection of some

> kind and had

> > visible blood in their urine, and then were diagnosed with IgAN,

> it could be

> > that the upper respiratory infection only caused the little flare-

> up of

> > hematuria (blood in urine), because the IgAN was already there,

> too mild to

> > be detected.

> >

> > Others may do so, but I can guarantee that I would never, ever

> suggest IgAN

> > starts with a single event. What I think happens is that for most

> people, a

> > single event just happens to cause the existing underlying

> condition to

> > generate hematuria, which gets the attention of the person or

> parent, and

> > then the doctor for what would have otherwise not have been

> noticed until

> > there was more renal failure. But of course, I have no proof of

> that. It's

> > only what I think.

> >

> > I think this because other people with IgAN never get the visible

> blood in

> > the urine. Like me, they just happen to have a routine medical

> examination

> > and they are found to have microscopic blood in the urine. Further

> > investigation eventually leads to diagnosis of IgAN.

> >

> > Some people are probably more prone than others to have the

> underlying IgAN

> > flare up into a more significant inflammation, which causes the

> hematuria

> > (usually harmless on its own), and/or proteinuria. Everyone with

> IgAN has

> > proteinuria, but for the majority, it just stays at a mild to

> moderate

> > level. For others, it flares up into a heavier proteinuria which

> must be

> > treated. Why? We don't know. There are a lot of things that aren't

> known

> > about all glomerular kidney diseases.

> >

> > Pierre

>

>

>

>

>

> To edit your settings for the group, go to our Yahoo Group

> home page:

> http://groups.yahoo.com/group/iga-nephropathy/

>

> To unsubcribe via email,

> iga-nephropathy-unsubscribe

> Visit our companion website at www.igan.ca. The site is entirely

supported by donations. If you would like to help, go to:

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>

> Thank you

>

[Guest guest]

Elaine,

Good question. My son had a urine test today. No blood but 1+ protein.

Yesterdays' mid-day urine was normal.

What does this mean?

Phil

> > Phil, this is the best I can do...

> >

> > There is something called post-strep glomerulonephritis. In this

> case, the

> > strep infection is definitely the cause of the nephritis, but this

> kind of

> > nephritis usually is not permanent. It does NOT turn into IgAN.

> Some people

> > may already have a mild, undetected IgAN which does become

> diagnosed by

> > coincidence after a strep infection.

> >

> > What happens with IgAN is not really understood by even the best

> > nephrologists and the most expert researchers in the field, but

> with the

> > knowledge we have about it at present, it seems like the problem

> is not with

> > having IgA immune complexes circulating in our blood (which

> everyone in the

> > world has), but rather a problem with their structure. To put it

> simply,

> > they end up binding with something in the kidneys where they

> shouldn't. The

> > defect appears at this time to be with the IgA immune complexes

> themselves,

> > rather than a defect in the kidneys themselves. Many experts think

> that IgAN

> > is simply the same thing as HSP (Henoch-Schönlein purpura), but

> with only

> > the one symptom in the kidneys. Nobody knows what causes HSP

> either. All we

> > know is that HSP appears to be triggered by bacterial or viral

> infections,

> > medicines, insect bites, vaccinations or exposure to chemicals or

> cold

> > weather. Is is the same with just IgAN without the other HSP

> symptoms? This

> > is unknown.

> >

> > Now, is there a precipitating event that causes triggers the IgA

> complexes

> > to become defective? Is it something that people who eventually

> develop IgAN

> > had all along since they were born, something they were genetically

> > pre-disposed to get whenever the right trgger came along? Or is

> there

> > something we are doing or being exposed to in life that causes

> this defect

> > to occur? Nobody can answer that. We, ie. medical science, simply

> do not

> > know.

> >

> > When people say they got an upper respiratory infection of some

> kind and had

> > visible blood in their urine, and then were diagnosed with IgAN,

> it could be

> > that the upper respiratory infection only caused the little flare-

> up of

> > hematuria (blood in urine), because the IgAN was already there,

> too mild to

> > be detected.

> >

> > Others may do so, but I can guarantee that I would never, ever

> suggest IgAN

> > starts with a single event. What I think happens is that for most

> people, a

> > single event just happens to cause the existing underlying

> condition to

> > generate hematuria, which gets the attention of the person or

> parent, and

> > then the doctor for what would have otherwise not have been

> noticed until

> > there was more renal failure. But of course, I have no proof of

> that. It's

> > only what I think.

> >

> > I think this because other people with IgAN never get the visible

> blood in

> > the urine. Like me, they just happen to have a routine medical

> examination

> > and they are found to have microscopic blood in the urine. Further

> > investigation eventually leads to diagnosis of IgAN.

> >

> > Some people are probably more prone than others to have the

> underlying IgAN

> > flare up into a more significant inflammation, which causes the

> hematuria

> > (usually harmless on its own), and/or proteinuria. Everyone with

> IgAN has

> > proteinuria, but for the majority, it just stays at a mild to

> moderate

> > level. For others, it flares up into a heavier proteinuria which

> must be

> > treated. Why? We don't know. There are a lot of things that aren't

> known

> > about all glomerular kidney diseases.

> >

> > Pierre

>

>

>

>

>

> To edit your settings for the group, go to our Yahoo Group

> home page:

> http://groups.yahoo.com/group/iga-nephropathy/

>

> To unsubcribe via email,

> iga-nephropathy-unsubscribe

> Visit our companion website at www.igan.ca. The site is entirely

supported by donations. If you would like to help, go to:

> http://www.igan.ca/id62.htm

>

> Thank you

>

[Guest guest]

Pierre,

The Neph from Hopkins said that even with a benign case of Acute Glom.

(the non-IGA, kind caused by staph) Protein can be in the urine for 6

months before clearing.

Do you believe this one?

Phil

[Guest guest]

Hi Elaine

A person in the early stages of IgAN could have blood in the urine but not

yet protein. This is what happened to me, in fact. Well, let me qualify

that. There's always a little bit of protein in the urine, and also a little

bit of red blood cells. It's not considered clinically significant

proteinuria unless it's more than about 150 mg per day, so unless it's

higher, you would be told there's no proteinuria. It's possible at that time

that the inflammatory process in the glomeruli has simply not developed to

the point that a lot of protein leaks through into the urine. As the

glomerular wall becomes more leaky, it lets more protein through. Once the

more active inflammation is resolved or resolves itself, the proteinuria

will probably go back down, while he may or may not continue to have

microscopic blood in the urine for a long time.

Good luck.

Pierre

Re: Question about IGA- and another question...

Pierre,

Is there a difference in prognosis if a person has both protein and blood in

the urine when diagnosed as opposed to just blood in the urine? Do people

first have blood and then get the protein in the urine? The neph told me

that my son, who is 12, already has about 10% scarring of the kidneys. He

hasn't lost any renal function though. The doctor thinks he must have had

this for a long time undetected, but a routine urine test in August 03 was

normal. A routine urine test in August 04 showed 300 units of protein and

blood at 3+. Now is January 05 the protein is at 2000 units and blood at

4+. Can you tell me what you make of this? You have a lot of knowledge

that is much appreciated. Thank you.

Elaine

[Guest guest]

Hi Elaine

A person in the early stages of IgAN could have blood in the urine but not

yet protein. This is what happened to me, in fact. Well, let me qualify

that. There's always a little bit of protein in the urine, and also a little

bit of red blood cells. It's not considered clinically significant

proteinuria unless it's more than about 150 mg per day, so unless it's

higher, you would be told there's no proteinuria. It's possible at that time

that the inflammatory process in the glomeruli has simply not developed to

the point that a lot of protein leaks through into the urine. As the

glomerular wall becomes more leaky, it lets more protein through. Once the

more active inflammation is resolved or resolves itself, the proteinuria

will probably go back down, while he may or may not continue to have

microscopic blood in the urine for a long time.

Good luck.

Pierre

Re: Question about IGA- and another question...

Pierre,

Is there a difference in prognosis if a person has both protein and blood in

the urine when diagnosed as opposed to just blood in the urine? Do people

first have blood and then get the protein in the urine? The neph told me

that my son, who is 12, already has about 10% scarring of the kidneys. He

hasn't lost any renal function though. The doctor thinks he must have had

this for a long time undetected, but a routine urine test in August 03 was

normal. A routine urine test in August 04 showed 300 units of protein and

blood at 3+. Now is January 05 the protein is at 2000 units and blood at

4+. Can you tell me what you make of this? You have a lot of knowledge

that is much appreciated. Thank you.

Elaine

[Guest guest]

Deb I hear you! I had perfectly normal labs in November '02 and a

full physical that showed me healthy (but overweight) by July of '03

I was at 35% kidney function. In March '03 my entire family was

laid up with a nasty bout of food poisioning from a local

resturant....I just never felt like I recovered from it. Really

makes you wonder about a single event trigger for the rapid form.

Had I not had a snius infection in July I could have easily gone

into full failure without realizing what was happening. In

hindsight I can see the 'signs' cold extremeties, tired all the

time, seriously foamy urine, etc. But in the midst of it I had no

clue my b/p was so high or that my kidneys were failing so quickly.

Thankfully they caught mine with some function left and the

aggessive prednisone treatment I've been on for the past 16 months

along with quite a few antibiotic treatments for random weird

infections have done something to slow things down it seems...my

labs have stayed stable since starting pred anyhow. I really feel

that my constant state of infections had something to do with the

food poisioning bacteria, my white count was constantly elevated for

close to a year until the doctors put me on a full 8 weeks on

antibiotics. So far my white count has been normal and my other

labs stable.

I just finally saw the message about getting a transplant!

Congratulations and I will add my good energy to everyone elses, I

wish him an easy surgery and speedy recovery.

Amy G.

>

> >Can you explain the rapid onset aggessive form this way too? I'm

> >still trying to understand how the aggessive form of IgAN

works...I

> >understand the genetic predisposition to it but if a single event

> >doesn't trigger the rapid form, where does it come from?

> >

> >Amy G.

> >

> >

> >