Если мы знаем количество мочи , например, за сутки, и концентрацию креатинина в этой моче, значит, мы знаем, сколько креатинина попало в мочу из крови.

Это понятно. Вопрос то мой был, что означает довольно резкое изменение моего кк за один год. И я получил на него ответ, за что всех благодарю.

В чем смысл тогда показателя "клиренс креатинина", который математически зависит

6.01.2012 ((Креатинин 87 (реф 80-115), Клиренс Креатинина 153 (88-146))
15.04.2012 ((Креатинин 84 (реф 80-115), Клиренс Креатинина 177 (88-146))
8.04.2013 (Креатинин 81 (реф 80-115), Клиренс Креатинина 112 (88-146))

Т.е. кагбы скачки какие-то

А что там Шпалыч хотел, я так и не понял.

Биопсия:

Заключение: ИгА-нефропатия с картиной мезангиопролиферативного гн (M1 E0 S0 T0).

Световая микроскопия: В препарате 10 клуб-в, клубочки не увеличены в размерах, отмечается расширение мезангия и мезангиальная пролиферация до 6-8 клеток на зону мезангия. Минимальный очаговый фиброз интерстиция и атрофия канальцев.
Артерии и артериолы - без особенностей.

Иммунофлюоресценция:
ИгГ - нет
ИгА - мезангий и периферия ++
ИгМ - нет
C1q - нет
C3 - то же, что ИгА ++
Kappa - то же, что ИгА +
Lambda - то же, что ИгА ++
Фибриноген - нет

4) Хочу отметить, что у меня с детства были проблемы с горлом, в основном – хр. Тонзиллит. А года 2-3 меня мучил стафилокок, нос был в корках, трещинах, ну в общем кошмар. Стафилокок так понимаю живет со мной, но сейчас под контролем, благодаря режиму образа жизни. Ну и плюс, я таки сделал профилактически тонзилэктомию – удалил частично миндалины криохирургией в Августе 2011 г

стр.139

Patients with IgA Nephropathy Respond
Strongly Through Production of IgA with
Low Avidity Against Staphylococcus aureus

Abstract
Background: Post-methicillin-resistant Staphylococcus aureus infection glomerulonephritis
(post-MRSA infection GN) is seen after MRSA infection and is a similar disorder
to IgA nephropathy (IgAN). We have found that immune complexes composed of staphylococcal
cell membrane antigen and IgA are deposited in the glomerular mesangial areas in
patients with post-MRSA infection GN and in more than 60% of patients with IgAN. Aim:
To examine the characteristics of serum IgA obtained from patients with IgAN. Patients and
Methods: Experiment 1. Serum samples were obtained from patients with IgAN (n
16)
and post-MRSA infection GN (n
19), and from healthy donors (n
13). Serum IgA and
IgG titers against Staphylococcus aureus (S. aureus) were measured using an ELISA.
Experiment 2. Relative antibody avidities of serum IgA and IgG against S. aureus from
patients and healthy donors were determined in a dissociation assay using an ELISA.
Results: Experiment 1. IgA class titers of anti-S. aureus antibodies in patients with IgAN
and post-MRSA infection GN were significantly higher than in healthy controls, and IgG
class titers of anti-S. aureus antibodies in patients with post-MRSA infection GN were significantly
higher than those in IgAN patients and healthy donors. A significant correlation
between IgG and IgA titers was found across all cases, and this was particularly evident in
patients with IgAN. Experiment 2. No significant correlation was observed between avidity
and titer of IgA class antibodies. The avidity of anti-S. aureus IgG did not differ significantly
between IgAN patients, post-MRSA infection GN patients, and healthy donors, but the avidity
of anti-S. aureus IgA from patients with IgAN was significantly lower than that from the
other groups. There was a significant correlation between antibody titer and antibody avidity
for the IgG class in patients with post-MRSA GN, but no significant correlation was
observed for the IgA class. Conclusion: These results suggest that patients with IgAN have
a strong response through production of IgA with low avidity against S. aureus.

Introduction
Although a large number of studies have examined the relationship between
infectious diseases and glomerulonephritis (GN), definite antigens have yet to
be found [3, 4]. IgA nephropathy (IgAN) is considered to be an infectionrelated
GN because urinary findings worsen after upper respiratory tract infection.
In 1995, we reported that rapidly progressive GN developed among patients
infected by methicillin-resistant Staphylococcus aureus (MRSA) [5]. These
patients showed a rapid loss in renal function with massive proteinuria and
hematuria, and mesangial proliferative GN with IgA, IgG, and C3 deposition
was observed in biopsy specimens. We designated this GN as post-MRSA
infection GN.
Post-MRSA infection GN serves as an appropriate model of bacterial
infection-related IgA-type GN owing to glomerular IgA deposition, and follows
an explicit clinical course. Although it has been suggested that hypercytokinemia
and polyclonal immunoglobulin activation by superantigens derived
from S. aureus play an important role in the pathogenesis of post-MRSA infection
GN [5], we found a 35 kDa staphylococcal cell-membrane antigen in the
glomeruli of the patients with post-MRSA infection GN [1]. Moreover, we also
found this antigen in the glomeruli of 60% patients with IgAN [1, 2]. We
identified this staphylococcal cell-membrane antigen (GenBank and DDBJ:
accession number; BAB 41819.1) by library screening with monoclonal anti-S.
aureus antibody S1D6 [1]. Therefore, we speculated that this staphylococcal
cell-membrane antigen was a possible antigen for IgAN.
S. aureus is a common bacterium that is present in all humans. Hence, we
developed a hypothesis that patients with IgAN show a specific response
against S. aureus and aimed to characterize the serum IgA against S. aureus in
patients with IgAN to prove our hypothesis.

Patients and Methods
Sixteen patients with IgAN, 19 patients with post-MRSA GN, and 13 healthy donors
were included in the study. First, the serum IgA and IgG titers against S. aureus were measured
in IgA-type GN patients, using an ELISA. Crude staphylococcal cell-membrane antigens
were prepared for ELISA by adsorption of protein A with human IgG-coated Sepharose
4B, as reported previously [6], and fixed to ELISA plates. Titers of anti-S. aureus IgA or IgG
were measured using mouse anti-human IgA or IgG as the primary antibody and horseradish
peroxidase-conjugated rabbit anti-mouse IgG as the second antibody.
Next, we examined the avidity of IgA and IgG among the patients. The bound antibodies
can be dissociated by sodium thiocyanate, and we measured the concentration of sodium
thiocyanate that inhibited 50% of antibody binding, the so-called ID50 [7]. The resulting
data were subjected to linear regression analysis, and the ID50 is referred to as the relative
antibody avidity.

Results
IgG and IgA Titers
Statistical analysis proved that patients with post-MRSA infection GN had
higher titers than those with IgAN and healthy controls. The IgA titers were statistically
different between the three groups. The highest titers were seen in
patients with post-MRSA infection GN, and the titers for IgAN patients were
higher than in healthy controls.
The correlation coefficients between serum IgG and IgA titers were 0.427
for all patients and 0.425 for IgAN patients. These data suggested a moderate
correlation between the IgG and IgA titers for all patients and for IgAN
patients.
Avidity of IgA and IgG
There were no statistical differences in IgG avidity between the three
groups. However, IgAN patients showed significantly lower IgA avidity than
healthy controls, and also showed a tendency to lower IgA avidity compared to
patients with post-MRSA infection GN (fig. 1).
Patients with post-MRSA infection GN showed a strong positive correlation
between antibody avidity and IgG titer. A similar analysis was performed
for antibody avidity and IgA titer, but no significant correlation was found in
any of the three groups. Moreover, no significant correlation between IgA and
IgG antibody avidity was observed in any of the groups.

Discussion
Patients with post-MRSA infection GN produce more IgG than IgAN
patients and healthy controls. The IgA titers were highest in patients with post-
MRSA infection GN, followed by those with IgAN. These two groups had IgA
titers that were statistically higher than the IgA titers of healthy controls. A
moderate correlation between IgA and IgG titers was observed for all patients
and IgAN patients. The antibody avidity for IgG did not differ significantly
between the three groups. However, patients with IgAN showed significantly
lower IgA avidity than healthy controls. IgAN patients also showed a tendency
to lower IgA avidity than that in patients with post-MRSA GN. For IgG, a
strong correlation between antibody avidity and titer was observed in patients
with post-MRSA infection GN, whereas IgA did not show such a correlation.
Collectively, these results lead us to conclude that patients with IgAN respond
strongly through production of IgA with low avidity against S. aureus.
This conclusion leads to a new hypothesis, in which we propose that under
conditions of an excess of antigens and antibodies with low avidity, small
immune complexes are formed due to the low efficiency of antibody-antigen
precipitation [8, 9]. These complexes then tend to be deposited in the glomeruli.

Acknowledgments
This work was supported by research grants from the Japanese Ministry of Education,
Culture, Sports, Science, and Technology, and from the University of Tsukuba. We are thankful
to the organizing committee of the 11th International Symposium on IgA nephropathy
and Professor Yasuhiko Tomino for giving us the opportunity to attend the symposium and to
present our work.