Evidence based facts on ESKD
It was known the life expectancy for dialysis patients was about 15 years. It well noted that in spite of improvement in dialysis field, that become 5 years.
Here will review the patients data who there still on dialysis or have kidney transplant with treatment interval more than 15 years
We analyze retrospective data in our hemodialysis center who spent more than 15 years on dialysis taking several variable and hopefully to applied it to rest of patients that may increase their life expectancy
Factore affect life expectancy
Age of starting dialysis
Sex
Causes of ESKD
Pre renal causes
Diabetic nephropathy
Blood pressure on starting dialysis
Blood transfusion
Hospitalization days and time
Blood access history
Skipping dialysis sessions
Metabolic bone disease
Itching
Commitment of medication
Urgent dialysis sessions
Education
Average intradialytic weight gain
total no of patents: 13
m :9
f :4
age starting dialysis
oldest :48
youngest :12
average "30
cause
GN :9
Alport :2
Polycystic :1
neurogenic bladder :1
pre renal cause :0
diabetic 0
High Blood pressure on starting dialysis :13
blood transfusion : 0 -1
hospitalization : 0-1
PTH
<150 :5
150- 1000 :3
>1000 :5
itching
0
skipping dialysis sessions
0
urgent dialysis
1
medication commitment
2
education
elementary school 9
college 2
university 2
duration of dialysis treatment
max :25
min :15.3
average :20
Age of starting dialysis
It well known that average of our ages is about sixty to seventy, for that the patents who start dialysis after fifty, will expire before 15 years of dialysis, main while patient how start dialysis at forty or less there be a chance to have treatment more than fifty or even twenty.
Sex
It noted the male patients was double the female, this may related to hormonal factors
Causes of ESKD
The primary cause in this group of patients was glomerulonephritis, or genetic Allport syndrome
Pre renal causes
There was no prerenal causes among our populations, that mean that on starting they was not suffer from heart disorders as heart failure, myocardiopathy nor ventricular hyper atrophy
Diabetic nephropathy
No one have diabetes either Type I or Type II, which mean the diabetic disease effect the system in way that increase mortality
High Blood pressure on starting dialysis
All the patients have hypertension on starting dialysis, this may reflect primary hypertension due to antigens
Not secondary hypertension due to heart failure or atherosclerosis
Blood transfusion
Null of the them need blood transfusion as a management of anemia which is proven to primary cause of mortality and
morbidity in dialysis patients
Hospitalization days
Almost all the patient does not require admissions
Blood access history
All patients experience all types of access as perm catheter, internal jugular, arteriovenous fistula and arteriovenous graft.
Skipping dialysis sessions
Null of them skip any session
Metabolic bone disease
The PTH was in these patients very low and very high,
3 patients were in accepted value
Itching
Null of them suffer from itching regardless the phosphorus level
Commitment of medication
They are commit to take the prescribed drugs
Urgent dialysis sessions
Do not have any urgent dialysis except one patient mostly doing 4 time per week
Education
Majority of them have only elementary education
Average intradialytic weight gain
Weight gain not more than 4 kg in average 3 kg
It is noted these patients that they have adaptation and understanding to their disease, which reflect minimum stress.
It is evidence that there is significant increase in the synthesis of inflammation oxidative stress mediators as appear in early stages of CKD advances along with worsening of renal failure
inflammation in CKD pathophysiology
Despite being a “silent epidemic” disease, CKD is now recognized as one of the major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Mounting evidence suggests implication of inflammation in CKD pathophysiology, thereby shifting the perception of inflammation as no longer a new risk factor but rather a traditional one linked to morbidity and mortality in these patients. The pathophysiology of inflammation may not be the same in CKD patients; nevertheless, a persistent, low-grade inflammation has been established as a hallmark feature of CKD.
Among various factors that contribute to the setting of an inflammatory milieu in the context of CKD, the inflammasome has recently become the focus of extensive research, gaining recognition for its key role in the pathogenesis of CKD and its complications.
s such, the inflammasome represents an attractive potential therapeutic target in renal diseases.
Another underestimated source of smouldering inflammation related to CKD was assigned to gut microbiota dysbiosis, a condition intensively studied, since it was postulated that may represent the starting point of many diseases, including malignancy.
Modulating the microbiota balance has become a subject of intense research; therefore, different dietary patterns have been proposed, along with administration of pre-, pro-, and synbiotics, with quite remarkable results.
In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up.
Advances in proteomics, in searching for the ideal biomarker, have become increasingly popular over the last decades, offering novel insights in deciphering the CKD mechanisms, thus moving the boundaries forward.
The identification of novel biomarkers using high-throughput technologies will provide the molecular signature of the disease, with impact on early diagnosis, monitoring, and prognosis.
Understanding the role of inflammation in the setting of CKD will foster the development of therapeutic strategies in order to treat and even prevent the underlying inflammation, thus improving CKD outcomes.
