Re: For Connie Sink

October 24, 2002

What is HSP. Torrey

October 24, 2002

Torrey,

Here is the best email in the archives on HSP. I will copy and paste it here

for you.

Is Henoch-Schonlein Purpura the Systemic Form of IgA Nephropathy?

F. Bryson Waldo MD.

(From the Dept of Pediatrics.The Children's Hospital. The University of

Alabama at Birmingham. American Journal of Kidney Deseases Vol.X1I,NO 5

(November), 1988: pp 373-377 373

(c. 1988 by the National Kidney Foundation, Inc.)

INDEX WORDS: IgA nephropathy, , Henech-Schonlein purpura, nephritis;

pathegenesis.

PAGE 1.

Despite different clinical features, 1GA nephropathy (1gAN) and

Henoch-Schonlein purpura (HSP) are indistinguishable by histopathology,

leading to the suggestion that HSP is a systemic form of IgAN. This review

compares and contrasts the clinical, pathologic and experimental

similarities and differences of these two disorders. Many patients with HSP

have minimal extrarenal disease, while up to 30% of patients with IgAN will

subsequently have systemic symptoms. Although patients with HSP are usually

much younger than those with IgAN, the age distributions often overlap. Both

may have recurrent macroscopic hematuria associated with pharyngitis, a

similar risk of developing renal insufficiency, and recurrent disease after

kidney transplantation. Although the pattern of IgAN subclasses and

complement component deposition are similar, monocytic and

T. lymphocytic infiltrates have been observed only in HSP. Dermal blood

vessels of many patients with IgAN have lgA immunofluorescence similar to

that in HSP, supporting a systemic process in IgAN. Although the

pathogenesis is not clearly understood for either disease, investigations of

potential disease mechanisms have revealed striking similarities. These

include an upregulated

invitro IgA immune response, circulating IgA-containing immune complexes and

autoantibodies, and decreased Fc recepter-mediated immune clearance.

Finally, immunogenetic studies suggest that patients with both conditions

inherit a predisposition for disease.

HENOCH-SCHONLEIN. purpura (HSP) was first described in 1874 as a distinctive

clinical syndrome

of an acute systemic vasculitis of the skin, joints, gut, and kidney. In

1968 Berger and Hinglais described IgA nephropathy (IgAN) characterized by

mesangial proliferation and immunofluarescent staining for IgA in patients

with mild nephritis manifested by hematuria, minimal proteinuria, and normal

renal function, but without systemic symptoms. Berger also noted mesangial

lgA immunofluorescence in renal biopsy specimens from patients with HSP. In

the subsequent years, despite their different clinical features, HSP and

lgAN have remained indistinguishable by standard renal pathology. Several

investigators have postulated that HSP is a systemic form of lgAN. This

report will not attempt to prove or disprove that thesis, but rather will

review the numerous clinical and laboratory similarities between the two

conditions. Some distinctive, and potentially important, differences that

may provide helpful clues in the quest to understand their pathogenesis will

also be discussed.

CLINICAL FEATURES. The typical systemic presentation of HSP is so unique

that the diagnosis is usually made on clinical criteria alone; renal biopsy

is reserved for patients with severe or persistent nephritis. In contrast,

the diagnosis of lgAN always requires a renal biopsy. Patients with HSP

usually do not have all the major organ systems clinically involved.

Depending on the criteria to define nephritis, renal involvement occurs in

20 to 100% of patients. Although the systemic disease and nephritis in HSP

usually occur together, the renal involvement may either precede the

systemic symptoms or, conversely, appear months after the systemic signs

have resolved. Similarly, although most patents with IGA do not have

systemic signs or symptoms at presentation, over 30% will develop abdominal

pain, atypical rash, or arthralgia during

followup.

Most patients with HSP present in childhood, while those with lgAN present

in adolescence or early adult life. However, the age ranges in the two

groups significantly overlap; patients as young as 2 yrs have been reported

with lgAN, and 70yr old adults have developed HSP. The reason for this age

distribution is unclear. The lgA mucosal system is poorly developed at birth

and undergoes continual antigen-driven and antigen-dependent development

throughout childhood. The response of the immature immune system to an

antigenic challenge may more frequently produce circulating immune complexes

that deposit in tissue. Alternatively, differences in antigen exposure,

handling of immune complexes, or other unknowns in children may favor

development of systemic disease.

A systemic infection commonly precedes the onset of HSP in children, while

in many patients with 1gAN, macroscopic hematuria is often noted first

concomitant with an infection, leading to diagnosis. Because of the

insidious nature of IgAN the date of the true onset of the disease may not

be discernible. Many patients may develop the initial immunologic renal

lesion of IgAN months or even years, before the disease is

clinically manifest. Therefore, some patients with IgAN may develop their

initial renal lesion following an infection, as do patients with HSP. During

follow-up,10% to 30% of patients with either condition cxperience recurrent

bouts of macroscopic hematuria associated with upper respiratory tract

infections.

The Iong term clinical course of both HSP and IgAN are quite variable and

thus difficult to

compare. Few series of unselected patients with HSP are available and

prognostic data are drawn from groups of patients with significant renal

involvement. Most patients with HSP with or without renal disease resolve

their initial systemic symptoms within 3 months of onset. Many have one or

more relapses of purpura and systemic symptoms, which may include nephritis,

in the first 12 months after presentation but most will ultimately remit.

Similarly, patients with lgAN presenting with macroscopic hematuria

frequently have recurrent episodes associated with upper respiratory tract

infections during the first 2 years after diagnosis. As with HSP these

episodes usually become less frequent or cease during extended observation.

Approximately one third of patients with lgAN will progress to end-stage

renal disease (ESRD).

In an unselected series of patients with HSP, only 5% progressed to ESRD.

However, in patients with HSP referred for renal disease and followed for

six to 21 years one third developed renal in-sufficiency. A few patients

with HSP presenting with a severe necrotizing, cresentic glomerulo-nephritis

progress to ESRD. Most patients with HSP show persistent glomerular deposits

of lgA containing immune complexes indistinguishable from those in patients

with lgAN.

The renal transplant experience in patients with lgAiN has been very

instructive. Thirty percent to 40% of patients develop recurrent IgA

deposits in their allografts, suggesting that lgAN is a systemic disease. In

contrast, recurrence of the extrarenal manifestions of HSP after renal

transplantation is rare. However, one third of patients with HSP with a

renal allograft had recurrent IgA deposits in the kidney, although none had

systemic symptoms or allograft dysfunction. In both HSP and lgAN, recurrent

disease rarely causes loss of the allograft.

The reasons for this are unclear. The use of immunosuppressive drugs during

the potential

initiation period of disease (ie, immediately posttransplant) is one

possibility; a " burn out " effect as described with systemic lupus

erythematosus (SLE) is another.

PATHOLOGY. As noted above, the similar pathology of IgAN and HSP initially

suggested that they represented a spectrum of a single disorder. By light

microscopy, both diseases have mesangial proliferation and sometimes focal

sclerosis or necrosis and crescent formation. Both exhibit electron-dense

deposits containing IgA in the mesangium. The lgA is accompanied by C3 and

IgG or IgM, or both, in 80% of patients. Complement components Clq and C4

are usually absent, but properdin, C5, and the membrane attack complex are

detected. Furthermore, deposits may also occasionally occur in

subendothelial and less commonly, sub epithelial locations. Patients with

deposits in the capillary loops more often have necrotic lesions and

crescent formation. Crescentic disease was initially described more

conunonly in patients with HSP, but larger series have shown this pathologic

finding in a comparable number of patients with lgAN.

Much debate has focused on the subclass of lgA deposited in either disease.

Initial data indicated that lgA2 predominated, while many subsequent

reports using several different monoclonal antibodies found predominantly

lgAI. Although some authors expressed concern about possible nonreactivity

of the monocional antibodies with tissue-bound immunoglobulin, no study

found a different predominant lgA subclass in lgAN cormpared with HSP.

The hypercellularity in HSP and lgAN has traditionally been attributed to

mesangial cells.

PAGE 2.

A recent study Of infiltration of leukocytes in several forms of

glomerulonephritis found significant numbers of monocytes and T cells in the

glomeruli of patients with HSP but not with lgAN. All renal biopsies Of the

patients with HSP were performed early in the disease course

(13 = 1.4 weeks), compared with those of patients with IgAN (158 = 18.5

weeks). This time difference may explain a temporal difference in

immunopathology or, alternatively, it may suggest a basic difference in the

mechanism of glomerular injury. Further studies will be needed to clarify

this issue.

In patients with HSP, immune complexes containing lgA and C3 are not only

deposited in the kidney but also in blood vessels of the gut, joints, and

skin. Immunofluorescence staining of purpuric and normal skin in patients

with HSP reveals perivascular deposits of lgA. Although most patients with

lgAN have no rash, many have perivascular deposits of lgA in clinically

normal skin. This dermatologic finding suggests that the absence of purpura

in patients with lgAN may represent a quantitative rather than qualitative

difference in inununopathology.

DEMOGRAPHICS. Worldwide, lgAN is the most common primary inflammatory

glomerular disease however, its prevalence and incidence are not evenly

distributed. It is very common in the Orient, Australia, and southern

Europe, but less common in northern Europe and the United States. Within the

United States, some regions have a particularly high prevalence. The actual

prevalence in a given area is difficult to determine because of the varied

indications for renal biopsy. In the southern United Stares, IGAN and HSP

are common in whites, although rare in blacks. In Nigeria, the African

origin of many blacks in the southern United States, neither IGAN nor HSP is

seen (personal communication. Professor O.O. Akinkugbe, lbadan, Nigeria.

1987). The data on the geographic and racial distribution of HSP are

limited. HSP is common in western Europe, the United States, and Japan areas

where lgAN is also seen. No population has yet been described in which only

HSP or lgAN is commonly seen.

PATHOGENESIS. First, the pathogenesis of neither HSP nor lgAN is understood.

However, several general lines of active investigation have produced a

variety of stimulating results. Whether these data point to

causal mechanisms or epiphenomena is unclear. Nevertheless, the similarities

between HSP and lgAN have been striking and will be briefly reviewed.

Immune Complex Deposition. It has been hypothesized that mesangial

deposition of circulating immune complexes containing 1gA occur in lgAN and

HSP. Circulating immune complexes that bind to anti-C3 antibody or

conglutinin (a C3bi ligand) and contain IgA are easily detected in both

conditions. These complexes may also contain IgG and lgM. Although no large

series from a single center has compared the characteristics of circulating

immune complexes in lgAN and HSP, no obvious or significant differences are

apparent from small studies. The relationship between disease activity and

circulating immune complex levels in either disease is unclear. Despite a

few reports in which the two correlated, most investigators agree that a

correlation exists at best in only selected patients.

The possible role of autoimmunity in both diseases has generated recent

interest. lgA rheumatoid factor (anti-lgG Fc) has been found in patients

with either disease. One report revealed cross- reactive antibodies eluted

from kidney sections of patients with HSP and lgAN.These antibodies did not

bind to sections of normal kidney but did bind to diseased renal tissue. lgA

antibody against the Fab portion of normal IgG has recently been reported in

patients with lgAN. Similar studies have not been done in patients with HSP.

Immune Response. An upregulated lgA immune response has also been

hypothesized to occur in both diseases. About one third to one half of

patients with either condition had increased serum lgA concentrations. The

in vitro production of lgA by cultured lymphocytes from patients with lgAN

and HSP has been investigated.Whole mononuclear cells or B cells from

patients with HSP spontaneously produced increased amounts of lgA in culture

without mitogen stimulation. Pokeweed miitogen stimulation of whole

mononuclear cells decreased lgA production, presumably by activating T

suppressor cells; a similar response was shown for patients with systemic

lupus erythematosus.

PAGE 3.

Some studies of IgAN found similarly increased IgA production by

unstimulated cells. However, other investigators have shown lgA

production by cells from patients with lgAN was increased only after

pokeweed mitocen stimulation. Thus, the IgA irmmune response in patients

with either HSP

or IgAN may be upregulated, although the responsible cellular mechanisns may

differ. Two of the studies that showed increased spontaneous production of

lgA by lymphocytes from patients with IgAN (similar to that in HSP) used

cells from children. Age-related variations in the IgA

immune response, as noted earlier, may be important in the apparent

differences bewetn HSP and IgAN.

Immune Clearance. Defective clearance of IgA-containing immune complexes

has been hypothesized for both conditions. Fe-mediated clearance is

abnormal. in patients with IgAN or active HSP, but not in those

with inactive HSP. The etiology and significance of the reduced clearance

is unclear. In primates, soluble immune complexes containing C3b, such as

those in the circulation of these patients, bind to erythrocyte complement

receptor (CRI) and are transported to the liver for clearance. No data on

the clearance of soluble immune complexes are currently available for either

HSP or lgAN. Data from baboons suggest that immune complexes containing only

IgA and no C3 are not cleared normally and deposit in the kidney and other

tissue. This delayed clearance may also be true in lgAN. If abnormal immune

complex clearance is indeed important in the pathogenesis of lgAN, it will

be important to determine if this abnormality is also present in HSP.

Genetics. Neither lgAN nor HSP is usually considered a genetic disorder.

However, increasing evidence suggests that individuals inherit a

predisposition to develop lgAN, and probably also HSP. Scattered case

reports describe families with more than one member with lgAN. Several

families include one member with lgAN and another with HSP. One remarkable

family had twins, one with HSP the other with lgAN. In addition to these

families, I am aware of two others with one brother with lgAN and the other

with HSP. Brothers from one family were HLA typed and found to be

HLA-identical(AI1,31; B51, w62; DR 1,4). The fourth component of complement

is encoded by two loci on chromosome 6 within the major histocompatability

complex. Null genes(genes producing a nonfunctional gene product) occur at

one of the two loci on both chromosomes (homozygous null)

in < 10% of normal individuals. The frequency of homozygous null C4 genes at

either locus is significantly increased in patients with IgAN or HSP.

Whether this genetic finding relates to gene linkages within the major

histocompatibility complex or to a functional difference in the

compliment system, is unclear. An increased frequency of an unusual

restriction fragment length poly-morphism allele of the immunoglobulin heavy

chain switch region chromosome 14 was recently described in patients with

IgAN but not HSP. The patients with HSP in this study were unselected. Might

this all be more common in the subgroup of patients with HSP with a chronic

course of renal involvement, similar to patients with IgAN?

October 24, 2002

Hi Connie,

I love your attitude! I am so glad that you feel like you are taking your

life back. We just cannot allow IgAN to rule our lives!

I am so glad though that he is willing to cut back on your meds. You take

more than I do although we are at about the same stage. I only take

Lisinopril and Zocor for Cholesterol.

Keep your chin up Connie:-)

October 24, 2002

Thanks to Janie, , and and if I missed anyone for your

uplifting support, thanks to you also. I appreciate all of the information

on stiffness, joint/muscle pain too. I didn't really mention these issues

before because I didn't want to appear to be a whiner.

But alas, I am like a dog...I won't just let things lie. I almost had a

show down with my Neph yesterday about the amount of Altace that I take. I

now take 50mg of Altace along with 240mg Diltiazem and 160mg Diovan each

month. It seems that he continues to increase my dosages even though I am

remaining stable and also added Zocor at my last appointment for

cholesterol. I was sure that I had had a great decrease in my function

since I had felt so bad. When my numbers remained the same, I was really

perplexed and I had suspicions that the way I felt was directly related to

the medications.

Sorry to the group for rambling on, but as I said, I'm like a dog...Now I

didn't say I looked like a dog... well anyway, I came into work early and

did some research on these medications. I'm embarrassed to say that I did

not do any research prior to today on this issue A lesson that won't

need repeated I can assure you.

The bottom line is this...after looking into Altace as an example I have 13

of the twenty side effects that were listed and about the same ratio for

Diltiazem and Diovan. I feel that I have been set free with this

information! I am going to get my energy and my life back...starting today!

So to end this long, long posting, my Neph agreed to decrease my Altace to

40mg, but I have news for him, this is NOT the final deal that I will make

in regards to the medications. For the most part I have always felt very

good for living, working and functioning with a kidney disease and lately I

have difficulty sleeping because of pain, getting out of bed because of

rigormortis like stiffness, walking up a flight of stairs exhausts me, I

have difficulty breathing and shortness of breath, I have developed some

kind of severe allergies, I have bouts of vomiting, my hands and feet are

always numb, and I am extremely weak and fatigued and this is only the

really severe side effects!

Again, I'm sorry that I'm rambling, but emotionally I feel like a different

person today! There is indeed a reason for my exhaustion and sluggish

feelings. I know that I'm not a doctor, but I am talking about my body, my

well-being and MY decision, I am woman hear me roar! Today I take my life

back... Connie, skipping and hopping in the USA

For Connie Sink

Hi Connie

Glad to hear your good news.

I am now at serum Cr 407 and have not been asked to do a 24 hr

urine collection for at least two years!, it seems to me that my

neph. does not require this info just the blood tests, and a small

sample for dipstick analysis at each visit.

As for your comment about leg pains, I have not been diagnosed with

HSP, but I suffer a lot with feelings of pain in my legs, especially

at night. The pain is hard to describe but feels almost like bruising

that seems to move up and down my legs.

The only thing that seems to help is to drink more fluids, " water "

not alchohol.

Hope this helps

regards

October 24, 2002

Hi Connie

Stopped skipping yet? Sorry couldn't resist. You are not a whiner

Connie, you just care what is happening with your body. I am a great

believer in having an element of control over one's health issues, and

like you I always discuss with my team anything they plan for me, and

suffice to say to date I am more than happy with what I have been

advised.

I hope that with careful discussion and planning Connie, you can indeed

whittle down your medications, and remain stable. Not that I am

defending your teams regime, but in some instances, they take a hard

line with IGAN, and it seems like a lot of meds to the patient, when in

reality they are just trying to get some impact to either slow it down,

or eliminate problematic symptoms. Keep talking to them Connie, and

keep up the research, I keep saying this, but information is key to a

patient, appreciated by some Nephs, not by others. I am lucky my Neph

encourages my research, although 9/10 he disses things I run by him, but

that 1/10 he does approve of, has helped me have input to my treatment.

Keep us posted ok.

Best wishes

For Connie Sink

Hi Connie

Glad to hear your good news.

I am now at serum Cr 407 and have not been asked to do a 24 hr

urine collection for at least two years!, it seems to me that my

neph. does not require this info just the blood tests, and a small

sample for dipstick analysis at each visit.

As for your comment about leg pains, I have not been diagnosed with

HSP, but I suffer a lot with feelings of pain in my legs, especially

at night. The pain is hard to describe but feels almost like bruising

that seems to move up and down my legs.

The only thing that seems to help is to drink more fluids, " water "

not alchohol.

Hope this helps

regards

October 24, 2002

Connie,

Sound more like a tiger to me, your neph has really got the

adreniline going. It is good you are taking an active interest in

what is going on around you. Body chemistry maintenance is what it's

all about especially the closer you get to ESRD. Your fair dinkum,

good on ya!

Derrick

Sydney, Australia

October 25, 2002

Hi Connie,

Glad to hear your news.

Re your question........I haven't been diagnosed with HSP either but do have

bone and muscle flares that are extremely painful, in my shoulders arms and

legs and hips, not necessarily all at the same time ..... the pain can feel

as describes but at its worst feels almost like nagging kidney pain in

your bones and skin.....everything hurts. Luckily as says these only

happen about 3/4 times a year. I did get a positive blood test after one of

them confirming systemic inflammation.

On a daily basis I have very low grade bone ache and a little stiffness and

also have tender places like my shoulders and arms and my ribs.

Sally.

For Connie Sink

Hi Connie

Glad to hear your good news.

I am now at serum Cr 407 and have not been asked to do a 24 hr

urine collection for at least two years!, it seems to me that my

neph. does not require this info just the blood tests, and a small

sample for dipstick analysis at each visit.

As for your comment about leg pains, I have not been diagnosed with

HSP, but I suffer a lot with feelings of pain in my legs, especially

at night. The pain is hard to describe but feels almost like bruising

that seems to move up and down my legs.

The only thing that seems to help is to drink more fluids, " water "

not alchohol.

Hope this helps

regards

October 30, 2002

Thanks, , and Aarrgghh is for you Derrick! Yep, a tiger is on the

loose! I know that this posting is a little late, but I've been so busy at

work. Thanks for all of your responses. I finally felt like I had just had

it with the continued increase in medications and Altace in particular. I

really think that the way I feel is due to side effects of medication(s).

I guess because I was really maintaining my numbers and had for the last 2

years that I really let him use me as a guinea pig, until I started having

so many side effects and I felt so bad that I knew that my body was telling

me something was seriously wrong. I even considered taking time off of

work, something that I've never done, just because I can barely get up in

the morning, let alone make it through the day. I'm not normally a worrier,

but I even wondered if I had bone cancer because of the pain and not being

able to sleep at night. Just to let everyone know, I will be careful, I will

monitor my condition and I will confer with my Neph on my decision (s), but

I will be taking less of my medications with or without his consent. If he

doesn't understand or work with me, I will be looking in the yellow

pages...Again, thanks for all of your support and letting me blow off steam.

Connie, USA

and yes, because I feel like I've taken back some control, I'm still

skipping and jumping in the USA... C--

For Connie Sink

Hi Connie

Glad to hear your good news.

I am now at serum Cr 407 and have not been asked to do a 24 hr

urine collection for at least two years!, it seems to me that my

neph. does not require this info just the blood tests, and a small

sample for dipstick analysis at each visit.

As for your comment about leg pains, I have not been diagnosed with

HSP, but I suffer a lot with feelings of pain in my legs, especially

at night. The pain is hard to describe but feels almost like bruising

that seems to move up and down my legs.

The only thing that seems to help is to drink more fluids, " water "

not alchohol.

Hope this helps

regards

October 31, 2002

Connie,

Sounds like your almost back to normal again! At least you

still have a bit of fight left in you which is good to know.

Derrick

Sydney Australia

> Thanks, , and Aarrgghh is for you Derrick! Yep, a tiger

is on the

> loose! I know that this posting is a little late, but I've been

so busy at

> work. Thanks for all of your responses. I finally felt like I had

just had

> it with the continued increase in medications and Altace in

particular. I

> really think that the way I feel is due to side effects of

medication(s).

> I guess because I was really maintaining my numbers and had for the

last 2

> years that I really let him use me as a guinea pig, until I started

having

> so many side effects and I felt so bad that I knew that my body was

telling

> me something was seriously wrong. I even considered taking time

off of

> work, something that I've never done, just because I can barely get

up in

> the morning, let alone make it through the day. I'm not normally a

worrier,

> but I even wondered if I had bone cancer because of the pain and

not being

> able to sleep at night. Just to let everyone know, I will be

careful, I will

> monitor my condition and I will confer with my Neph on my decision

(s), but

> I will be taking less of my medications with or without his

consent. If he

> doesn't understand or work with me, I will be looking in the yellow

> pages...Again, thanks for all of your support and letting me blow

off steam.

> Connie, USA

>

> and yes, because I feel like I've taken back some control,

I'm still

> skipping and jumping in the USA... C--

>

> For Connie Sink

>

> Hi Connie

> Glad to hear your good news.

> I am now at serum Cr 407 and have not been asked to do a 24 hr

> urine collection for at least two years!, it seems to me that my

> neph. does not require this info just the blood tests, and a small

> sample for dipstick analysis at each visit.

> As for your comment about leg pains, I have not been diagnosed with

> HSP, but I suffer a lot with feelings of pain in my legs, especially

> at night. The pain is hard to describe but feels almost like

bruising

> that seems to move up and down my legs.

> The only thing that seems to help is to drink more fluids, " water "

> not alchohol.

> Hope this helps

> regards

>

October 31, 2002

Hi Connie,

I understand exactly how you feel. This is NOT something I recommend for

anybody else, but a year or so I felt like I just needed a break from the

entire IgAN, and I took 6 months off completely. I didn't even go to my Neph

to be monitored. I know that is not good under any circumstances, and again

I do not recommend anyone do this.

That being said, I felt ready to tackle IgAN again after the break, and was

in a much better place emotionally. Taking control back is therapeutic, but

please don't try it without being monitored. I suffered the consequences in

higher serum creatinine after my break, and I could never get it back to

where it was before I ignored it for 6 months.

October 31, 2002

One thing I neglected to mention is that during my 6 months of ignoring my

IgAN and not being followed, I did NOT stop taking BP meds. It was just a

mental/emotional break. Important clarification.

October 31, 2002

Just for the record Connie, I don't think it's a good idea to mess around

with your blood pressure medications on your own. Even a few more points of

high blood pressure will definitely shorten your time to end-stage.

Secondly, we can't really fool our doctors. They can tell when patients are

being non-compliant, and, it's really not something you want on your file

(remember the Seinfeld episode where Elaine gets a bad mark on her file,

well, this is true to some extent, and it can come back to haunt you when it

comes to transplant evaluation time or when you get on dialysis). Third, if

it's bone pain you're talking about, I wouldn't be too quick to blame the BP

meds about that. That's a known consequence of advancing renal failure, and

it may be due to various factors than can be corrected, such as a phosphorus

intake that is too high, or an adjustment in the calcium-based phosphate

binder, or you may need to take calcitriol...

There are more numbers in the lab reports than just creatinine.

Me, I highly recommend working with the doctor if there are any problems.

Pierre

RE: For Connie Sink

>

> Thanks to Janie, , and and if I missed anyone for your

> uplifting support, thanks to you also. I appreciate all of the

> information

> on stiffness, joint/muscle pain too. I didn't really mention these

> issues

> before because I didn't want to appear to be a whiner.

>

> But alas, I am like a dog...I won't just let things lie. I almost had

> a

> show down with my Neph yesterday about the amount of Altace that I take.

> I

> now take 50mg of Altace along with 240mg Diltiazem and 160mg Diovan each

> month. It seems that he continues to increase my dosages even though I

> am

> remaining stable and also added Zocor at my last appointment for

> cholesterol. I was sure that I had had a great decrease in my function

> since I had felt so bad. When my numbers remained the same, I was really

> perplexed and I had suspicions that the way I felt was directly related

> to

> the medications.

>

> Sorry to the group for rambling on, but as I said, I'm like a dog...Now

> I

> didn't say I looked like a dog... well anyway, I came into work early

> and

> did some research on these medications. I'm embarrassed to say that I

> did

> not do any research prior to today on this issue A lesson that

> won't

> need repeated I can assure you.

>

> The bottom line is this...after looking into Altace as an example I have

> 13

> of the twenty side effects that were listed and about the same ratio for

> Diltiazem and Diovan. I feel that I have been set free with this

> information! I am going to get my energy and my life back...starting

> today!

>

> So to end this long, long posting, my Neph agreed to decrease my Altace

> to

> 40mg, but I have news for him, this is NOT the final deal that I will

> make

> in regards to the medications. For the most part I have always felt

> very

> good for living, working and functioning with a kidney disease and

> lately I

> have difficulty sleeping because of pain, getting out of bed because of

> rigormortis like stiffness, walking up a flight of stairs exhausts me, I

> have difficulty breathing and shortness of breath, I have developed some

> kind of severe allergies, I have bouts of vomiting, my hands and feet

> are

> always numb, and I am extremely weak and fatigued and this is only the

> really severe side effects!

>

> Again, I'm sorry that I'm rambling, but emotionally I feel like a

> different

> person today! There is indeed a reason for my exhaustion and sluggish

> feelings. I know that I'm not a doctor, but I am talking about my body,

> my

> well-being and MY decision, I am woman hear me roar! Today I take my

> life

> back... Connie, skipping and hopping in the USA

>

October 31, 2002

I would like to add a note just for informational purposes.....I got tired of

taking all the meds and didn't think I needed them....my bp had been really good

so...I quit taking by bp meds...guess what happened. My body kinda freaked and

my bp spiked and it hasn't been normal since. My neph didn't say much...he just

sighed heavily and explained that you shouldn't just quit a med like that...it

does have adverse effects....

ok...enough of the lecture...just sharing my experience.

Janie