Is this getting too academic for some out there?  Please let me know and if
so, I will go back to trying to bleat rather that roar :0  heh heh  no
offense, a dig at myself actually.

and from links in that page, a specific reference to Hepatitis C
(goodpasture's syndrome)

cryoglobulemia is loosely described by me as the gunk of left-over viruii
that have a tendency to accumulate.  maybe.

(I think increased bile production may be of help for the liver itself and
thereby the gallbladder and the kidneys)  -  cj
Preamble then link to Goodpasture's syndrome:

Autoimmune diseases are usually:

 a.. Systemic lupus erythematosus, rheumatoid arthritis, Sjögren syndrome
 b.. Vasculitis - Polyarteritis nodosa, Henoch-Schönlein purpura.
Differential Diagnosis The differential diagnosis includes looking for the
underlying cause of the cryoglobulinaemia:

Antiphospholipid Syndrome
Chronic Lymphocytic Leukemia
Cirrhosis
Glomerulonephritis

Goodpasture Syndrome
Haemolytic Uraemic Syndrome
Hepatitis A, B or C  <<<<<<<<<< ####

Non-Hodgkin lymphoma
Multiple Myeloma
Polyarteritis Nodosa

Sarcoidosis
Systemic Lupus Erythematosus
Waldenstrom's macroglobulinaemia.

Investigations

 a.. Check for serum cryoglobulins. The blood must be kept warm and then
serum incubated at 4°C. Type I tends to precipitate within the first 24
hours but type III may take a week. Correct handling is essential for
reliable diagnosis2.
 b.. FBC: leucocytosis may occur with infection or leukaemia. There may be
anaemia.
 c.. Urinalysis may show evidence of renal disease.
 d.. U&E: in case of renal disease
 e.. LFTs: may show hepatitis. If so get serology for hepatitis.
 f.. Rheumatoid Factor: RF is positive in type II and III.
 g.. Antinuclear antibody: if SLE suspected.
 h.. ESR will be elevated with rouleaux formation.
 i.. Complement levels may be reduced, especially C4.
 j.. Electrophoresis of serum and urine if there is suspicion of an
underlying gammopathy.
 k.. Further tests will be required if other diseases are suspected.
 l..
 m.. ............ specifically to Hep C .........
Goodpasture's syndrome
An autoimmune disease which is characterised by

 a.. deposition of antibodies to the glomerular basement membrane along
with compliment
 b.. a progressive glomerulonephritis and often renal failure.
 c.. Cross reaction with the basement membrane in the lungs causing
pulmonary haemorrhage.
Epidemiology
Incidence It is uncommon. It affects mostly young, white men aged 15 to 35
with a further peak after 55 when it is more common in women1 and tends to
affect just the kidneys. The male preponderance is between 2 and 9 to 1. It
affects both sexes equally in children. Classification can be difficult in
that sometime either the lungs or the kidneys are affected but not both.
However, the presence of autoantibodies to the glomerular basement membrane
is the diagnostic feature.

In the USA it represents 1 to 2% of all cases of rapidly progressive
glomerulonephritis. In England the incidence is about 1 in 2 million.
Wegener granulomatosis is about 10 times as common.

Risk Factors Insults to the lungs are probably required to produce both the
renal and pulmonary disease.

Genetic predisposition2,3 with possession of HLA-DRw2.
Exposure to organic solvents or hydrocarbons4   <<<<<<  carbon tet for
instance?
Smoking
Infection (eg, influenza)
Cocaine inhalation
Exposure to metal dusts
Goodpasture's syndrome can occur after renal transplantation in Alport's
syndrome5.
Presentation
Symptoms Between 60 and 80% have both renal and pulmonary disease. The
kidneys alone are affected in 20 to 40% and in about 10% only the lungs are
affected.

 a.. Chills and fever present in about 25% of patients.
 b.. There is nausea and vomiting in 40%.
 c.. Weight loss occurs in about 15%.
 d.. Chest pain is present in approximately 40% of patients.
 e.. Anaemia may result from persistent intrapulmonary bleeding.
 f.. Massive pulmonary haemorrhage can cause respiratory failure.
 g.. There is a rapidly progressive glomerulonephritis that may lead to
acute renal failure and volume overload
 h.. Arthralgia.
Sometimes the pulmonary haemorrhage may precede the renal disease by weeks
or months.
Signs

 a.. Tachypnoea
 b.. Inspiratory crackles over lung bases.
 c.. Cyanosis
 d.. Hepatosplenomegaly (sometimes)
 e.. Hypertension in 20%
 f.. Skin rash
Dyspnoea can be severe. Death is often due to respiratory failure. There may
be gross haematuria and pallor from anaemia.
Differential Diagnosis Pulmonary haemorrhage with renal failure can also
occur in collagen vascular diseases like SLE and RA, idiopathic rapidly
progressive glomerulonephritis, microscopic polyarteritis, Wegener's
granulomatosis, and essential mixed cryoglobulinemia. All these diseases
have specific laboratory features. In Goodpasture's syndrome the essential
feature is antibody to the glomerular basement membrane.

Investigations

FBC. Iron-deficiency anaemia from intrapulmonary bleeding. Leukocytosis.

U&E and creatinine: Watch for renal failure.

ESR is raised in vasculitis but not in this disorder.

Urinalysis is typical of acute glomerulonephritis, with low-grade
albuminuria, gross or microscopic haematuria, and red blood cell casts.
Anti-GBM antibodies are diagnostic: Assays for antibodies are valuable for
confirming the diagnosis and monitoring therapy. Radioimmunoassays or
enzyme-linked immunosorbent assays (ELISAs) for anti-GBM antibodies are
highly sensitive (>95%) and specific (>97%) but are performed only in a few
laboratories. Although the peak of serum anti-GBM antibody titre does not
correlate with the severity of disease, changes in titre over time may be a
guide to the efficacy of treatment.

Antineutrophilic cytoplasmic antibodies (ANCA). At sometime during the
illness, one third of patients with Goodpasture syndrome have circulating
ANCA in addition to anti-GBM antibody.

Imaging: CXR. Patchy consolidation, usually bilateral, symmetrical,
perihilar, and bibasilar. The apices and costophrenic angles are usually
spared. 18% may have normal CXR. Recurrent pulmonary haemorrhage causes new
opacities.

Other Tests: Pulmonary function tests are not helpful. Spirometry may show
some restriction.

Procedures: Percutaneous kidney biopsy is the preferred invasive procedure
to substantiate the diagnosis. Not indicated if anti-GBM antibodies are
present. Lung biopsy: Either transbronchial or open lung biopsy may be
performed in cases where renal biopsy cannot be performed.

Management
Non-Drug

 a.. Intubation, assisted ventilation, and haemodialysis are often required
in the acute phase.
 b.. Repeated plasmapheresis6 removes anti-glomerular basement membrane
antibodies from the circulation.
 c.. End-stage renal disease can be managed by long-term haemodialysis or
renal transplantation.
Drugs High-dose corticosteroids (methylprednisolone 7 to 15 mg/kg/day IV in
divided doses) with cyclophosphamide or azathioprine are of benefit.
Duration of immunosuppressive therapy varies considerably and may be
necessary for longer than 12 to 18 months in some patients. Early use of
these measures in combination may preserve renal function.

Surgical Cessation of pulmonary haemorrhage has been described after
bilateral nephrectomy.
Renal transplantation has been used and although there are IgG deposits in
the graft it does not appear to damage the kidney. Most centres still like
to wait 6 to 12 months before transplantation.

Complications

 a.. Pulmonary haemorrhage with respiratory failure is the commonest cause
of death.
 b.. Renal failure in 90%.
 c.. The circulating antibodies clear within 8 weeks, but an early relapse
within 2 months may occur when circulating antibodies are still present.
This typically presents as alveolar haemorrhage.
 d.. The risk factors for relapse include infection, volume overload, and
cigarette smoking.
 e.. Pneumocystis carinii pneumonia has an annual incidence of 1% but is a
potentially deadly complication of immunosuppressive therapy in patients
with Goodpasture syndrome. Prophylaxis with co-trimoxazole may be useful.
Prognosis In the past, the disease was almost invariably fatal, and
sometimes rapidly so. Now the mortality rate is about 10%,
Most progress to end stage renal failure within months. Early, energetic
treatment may delay or prevent this. It can last from a couple of weeks to 2
years.

Prevention No known prevention but avoid glue sniffing and siphoning petrol.

References Used

 1.. Savage CO, Pusey CD, Bowman C, et al; Antiglomerular basement membrane
antibody mediated disease in the British Isles 1980-4.;Br Med J (Clin Res
Ed) 1986 Feb 1;292(6516):301-4.[abstract]
 2.. D'Apice AJ, Kincaid-Smith P, Becker GH, et al; Goodpasture's syndrome
in identical twins.;Ann Intern Med 1978 Jan;88(1):61-2.
 3.. Gossain VV, Gerstein AR, Janes AW; Goodpasture's syndrome: a familial
occurrence.;Am Rev Respir Dis 1972 Apr;105(4):621-4.
 4.. Bombassei GJ, Kaplan AA; The association between hydrocarbon exposure
and anti-glomerular basement membrane antibody-mediated disease
(Goodpasture's syndrome).;Am J Ind Med 1992;21(2):141-53.[abstract]
 5.. Hudson BG, Tryggvason K, Sundaramoorthy M, et al; Alport's syndrome,
Goodpasture's syndrome, and type IV collagen.;N Engl J Med 2003 Jun
19;348(25):2543-56.
 6.. Lockwood CM, Rees AJ, Pearson TA, et al; Immunosuppression and
plasma-exchange in the treatment of Goodpasture's syndrome.;Lancet 1976 Apr
3;1(7962):711-5.[abstract]
Internet and further reading

 a.. Sharma.S, Verrelli.M on eMedicine
 b.. Valentini.R.P. on eMedicine
Acknowledgements EMIS is grateful to Dr P Hewish for authoring this article.
The final copy has passed peer review of the independent Mentor GP authoring
team. ©EMIS 2004.

Hi group.  There are two not-so-academic articles on this page about
hcv-realted cryoglobulins written for a general audience.  They are from
the Janis7hepc.com website.  Ping Eileen (if you are reading) can you tell
us if your routine blood tests for kidney function were usually normal
until you lost a kidney to glomerulonephritis caused by cryoglobulins?  I
mean was your attack sudden or were there detectable  abnormalities that
led up to it, before your kidney failed?  Did your neuropathy develop long
before the kidney failure?  I have several  cryoglobulin-related symptoms.
My peripheral joint pain is worsening and cold makes it worse :-(  I did
test negative for cryoglobulins at the end of tx.  I might ask to be
tested again soon, but I don't think our local labs are equipped to run
the test, which is a problem.  

Below is an excert from one of the articles that briefly explains what
cryoglobs are.  

Solstice soon!  Yay!  I hate these short days.  Grumble.
kj

"When the body senses an invasion by foreign organisms, such as HCV,
chemical responses are triggered. Among those responses are various kinds
of immunoglobulin  proteins that help kill the foreigners or regulate the
immune response. For some reason -- biologists are not sure why -- these
immunoglobulins can "glob" together and lodge on the walls of medium and
small blood vessels.  The immunoglobulins that are involved are called
cryoglobulins because they turn into a gel at cool temperatures. Since
cold temperature readily affects the small and middle-sized vessels in the
body's extremities, the cryoglobulins are most likely to form in them. It
appears that this glob-and-lodge action causes the inflammation of blood
vessels. Cryoglobulinemia is the condition of having cryoglobulins in the
blood. "

http://www.janis7hepc.com/related_conditions2.htm#cryoglobulinemia