This document discusses chronic kidney disease (CKD), including its history, importance, risk factors, progression, and relationship to cardiovascular disease. Some key points:
- CKD concepts were developed in 2002 to standardize criteria, classification, and terminology. Goals include early detection, slowing progression, and reducing cardiovascular risk.
- CKD prevalence is 12-15% for stages 1-5 and 6-8% for stages 3-5. Renal mortality is low but cardiovascular disease is a major cause of death.
- Risk factors include diabetes, hypertension, smoking, obesity, dyslipidemia, proteinuria, inflammation, and others. CKD itself is an independent risk factor for cardiovascular disease.
Hepatitis C virus infection is associated with many renal diseases.
Renal disease caused by
• Virus itself
• Drugs used for treatment of hepatitis c
• Associated condition with hepatitisadvanced liver cell failure.
A. The renal disease associated with hepatitis c due to advanced liver cell failure:
• Prerenal (Hypovolemia , shock and hepatorenal syndrome )
• ATN ( sepsis or shock)
B. Drugs used for treatment of hepatitis c:
• Interstitial nephritis secondary to Interferon
C. Hepatitis c itself
o Hepatitis c is RNA flavivirus( single strand)
o Has extrahepatic manifestation like arthritis, DM, cryglobulinemia and glomerulonephritis
o Renal diseases associated with hepatitis C
1. The most common types is MPGN with cryoglobulinemia
2. Others are
MPGN without cryoglobulinemia
Membranous nephropathy (MN)
Focal segmental glomerulosclerosis
IgA nephropathy
Fibrillary glomerulopathy
Immunotactoid glomerulopathy
Thrombotic microangiopathy
Amyloid
Vasculitis
Interstitial nephritis secondary to virus
HCV-associated PAN
Hepatitis C virus infection is associated with many renal diseases.
Renal disease caused by
• Virus itself
• Drugs used for treatment of hepatitis c
• Associated condition with hepatitisadvanced liver cell failure.
A. The renal disease associated with hepatitis c due to advanced liver cell failure:
• Prerenal (Hypovolemia , shock and hepatorenal syndrome )
• ATN ( sepsis or shock)
B. Drugs used for treatment of hepatitis c:
• Interstitial nephritis secondary to Interferon
C. Hepatitis c itself
o Hepatitis c is RNA flavivirus( single strand)
o Has extrahepatic manifestation like arthritis, DM, cryglobulinemia and glomerulonephritis
o Renal diseases associated with hepatitis C
1. The most common types is MPGN with cryoglobulinemia
2. Others are
MPGN without cryoglobulinemia
Membranous nephropathy (MN)
Focal segmental glomerulosclerosis
IgA nephropathy
Fibrillary glomerulopathy
Immunotactoid glomerulopathy
Thrombotic microangiopathy
Amyloid
Vasculitis
Interstitial nephritis secondary to virus
HCV-associated PAN
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Всемирный день почки 2016 в НИКИ им. академика Ю.Е. ВельтищеваKidneyOrgRu
9 марта 2016 г в конференц-зале Научно-Исследовательского Клинического Института имени академика Ю.Е. Вельтищева проведено праздничное мероприятие, посвященное Всемирному Дню Почки, который отмечается во всем мире с 2006 года по инициативе Международного Общества Нефрологов (http://www.worldkidneyday.org). Впервые в этом году Всемирный День Почки был посвящен детям с акцентом на ранней профилактике развития заболеваний почек.
Сотрудники отделения наследственных и приобретенных болезней почек представили для детей презентации об истории проведения праздника, распространенности заболеваний почек с рекомендациями здорового образа жизни для сохранения функций почек.
Было организовано праздничное веселое интерактивное представление для детей с участием Центра детского и юношеского творчества "Бибирево", театра-студии «Рампа», танцевально-акробатических студий «Овация» и «Альфа». Все дети получили праздничные подарки с символом Всемирного Дня Почки.
a precise presentation over CKD made for house officers/medical interns . It focuses over signs and symptoms and in-hospital management of resulting problems , material taken majorly from medscape, CMDT and oxford hand book
Diabetic nephropathy considered one of the most common complications of DM. This presentation answer the question are some diabetic patient immune to diabetic nephroapthy
Abstract: Uremia is a clinical manifestation of chronic kidney failure (CKD) and is defined as the elevation of urea levels in plasma associated to fluid, electrolytes and hormonal imbalances and metabolic abnormalities. Uremia even though arises from CKD, it can also occur with Acute Kidney injury (AKI). The terms uremia was first coined by Piorry which translates to urine in blood. Also, Uremia and uremic syndrome have been used interchangeably for a long time. Comparatively, Azotemia is also uremia but the only difference is that the urea elevation in azotemia is not high enough to have manifesting signs or symptoms. Thus, Uremia is pathological and symptomatic manifestations of severe azotemia.
Urea itself has direct and indirect toxic effects on our body; parathyroid hormone (PTH), beta2 microglobulin, polyamines, advanced glycosylation end products, and other middle molecules, are thought to contribute to the clinical syndrome. Patient’s symptoms range from mild bleeds to severe congestive heart failure. If left untreated complications include seizure, coma, cardiac arrest, and death. He most severe is cardiac arrest secondary to electrolyte abnormalities such as hyperkalemia, metabolic acidosis, or hypocalcemia. The patients, who are diabetic, tend to develop severe hypoglycemic reactions if the medications are not adjusted for creatinine clearance. Renal failure and renal osteodystrophy may cause early onset osteoporosis or formation of adynamic bone which predisposes the patient to fractures on mild trauma. Also medications the patient was previously on can lead to unwanted side effects due to impaired clearance e.g. Digoxin toxicity secondary to renal failure, increased sensitivity to narcotics.
Key Words: Uremia, Uremic syndrome, Chronic kidney failure, azotemia, beta 2 microglobulins, congestive heart failure, electrolyte abnormalities, hyperkalemia, hyocalcemia, metabolic acidosis, creatinine, osteodystrophy
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...
8-1. Progression of CKD to CRF. Vladimir Dlin (eng)
1. Progression of chronic kidney
diseases: mechanisms, risk factors,
treatment strategies
Dlin V.V., Konkova N.E.
Nephrology department of Research Institute of
Pediatrics & Children surgery, Moscow, Russia
2. History and conception of problem
•
The conception was developed at the beginning of XXI century by U.S.
National Kidney Foundation (National Kidney Foundation) and published
in 2002. It’s development was continued by experts from the European
Dialysis and Transplant Association (ERA-EDTA) and KDIGO (Kidney
Desease: Improving Global Outcomes)
• The purpose of the conception:
- early detection of kidney disease
- slowing down the progression of kidney disease
- reduction the risk of cardiovascular complications
- prevention of kidney lesions
- the use of common criteria and universal classification
- the use of common terminology
3. Importance of the problem
The high prevalence of CKD in the world:
1-5 stage of CKD - 12-15% of the population
3-5 stage of CKD - 6-8 % of the population
5. Importance of the problem
Renal mortality in patients with kidney disease is low.
Cardiovascular pathology as a major factor of patient’s death is
ignored.
6. Importance of the problem
Renal factors of cardiovascular risk:
albuminuria / proteinuria
systemic inflammation
oxidative stress
anemia
hyperhomocysteinemia
Smirnov A. et al., 2005
7. FREQUENCY OF CARDIOVASCULAR DISEASE IN
CHRONIC KIDNEY DISEASE
(per 100 patients / year)
kidney
diseases
infarction
disturbance
of cerebral
blood flow
peripheral
vasculopathy
atheroscler
osis
cardiovascul
ar death
CKD -
1,6
7,6
6,9
14,1
5,5
CKD+
3,9
16,6
19,9
35,7
17,7
CKD – chronic kidney disease
C.R.. Harper, 2008
8. FREQUENCY OF CARDIOVASCULAR DISEASE IN
PATIENTS IN RELATION TO GLOMERULAR
FILTRATION RATE
the estimated frequency
GFR – glomerular filtration rate
Matthew R., 2005
9. The structure of mortality (%) in patients with ESRD by age
(Russian Register of renal replacement therapy, 1998-2007)
CVD – cardiovascular disease
10. The main markers of kidney damage,
suggestive of the presence of CKD
marker
Albuminuria / proteinuria
notes
persistent increasing in urinary albumin
excretion greater than 10 mg/day (10 mg
albumin/g creatinine) –
see recommendation
hematuria, cylindruria, leykotsituriya (piura)
Persistent changes of the urinary
sediment
Changes of renal imaging studies anomalies of the kidney cysts,
hydronephrosis, resizing kidneys, etc.
Changes of of blood and urine
composition
Persistent decrease of GFR less
than 60 mL/min/1,73m2
Morphological changes of the
lifetime nephrobiopsy
changes in serum and urinary electrolyte
concentration, impaired HGA and others,
including the characteristic of the "tubular
dysfunction syndrome" (Fanconi's syndrome,
renal tubular acidosis, Bartter's syndrome and
Gitelman, nephrogenic diabetes insipidus,
etc.)
in the absence of other markers of kidney
damage
should be taken into account the signs of
“chronization” (sclerotic changes of kidneys,
changes of membranes, etc.)
11. Terminology
• CKD - the common notion reflecting the presence
of common risk factors of development and
progression of different nephropathy.
• The diagnosis of CKD is based on the presence of
markers of kidney damage and/or GFR < 60 ml/
min for at least 3 months.
12. Normal GFR in children and
adolescents
Age / Sex
The average GFR ± σ
(ml/min/1,73m2)
1 week
41 ± 15
2-8 weeks
66 ± 25
> 8 weeks
96 ± 22
2-12 years
133 ± 27
13-21 years(m)
140 ± 30
13-21 years(f)
126 ± 22
13. Estimation of GFR
• estimation of GFR in general clinical practice
(outpatient) will be based of calculation formulas
(eGFR), including gender, age, the patient and the
concentration of creatinine in serum
• clearance methods of GFR’s determination will be
used at the hospital
14. Methods of GFR’s estimation
• Simple ways to calculate GFR based on measurements of
serum parameters without hour urine collection:
1. Schwart’s formulas
2. Formulas of Cockroft DW., Gault MH.
3. MDRD (Modification of Diet in Renal Disease)
4. CKD-EPI method eGFR (the most suitable in the clinical
practice)
Levey AS. et al., 2000
15. eGFR in children on the basis of serum creatinine
and growth (according to Schwartz)
• GFR (ml/min/1,73m2)= [0,0484*х Height
(сm)]/Scr (mmol/l)
*k= 0,0616 for boys >13 years
16. CKD-EPI formula (modification of 2011 year)
race
gender
Serum
creatinine
mg/100 ml
formula
White and
other
female
≤ 0.7
144*(0.993) Age*Cr/0.7)-0.328
White and
other
female
> 0.7
144*(0.993)Age*Cr/0.7)-1.21
White and
other
male
≤ 0.9
141*(0.993) Age*Cr/0.9)-0.412
17. Stages of CKD in based on GFR
(National Kidney Foundation KD, 2002 in modification of Smirnov et al., 2008)
stages
Kidney function
GFR
ml/min/1,73 m2
С1
high and optimal
>90
С2
slightly decreased
60-89
С3а
moderately reduced
45-59
С3б
significantly reduced
30-44
С4
drastically reduced
15-29
С5
ESRD
<15
18. Albuminuria
• Albuminuria (normal < 10 mg/day) – integral sign of CKD
[A. Smirnov et al., 2010] and represents:
- increased permeability of cell membranes (size-selectivity, the chargeselectivity);
- transport changes in the proximal tubule;
- increased hemodynamic burden on the glomerules;
- presence of systemic and renal endothelial dysfunction;
- the degree of glomerular/interstitial sclerosis due to glomerular and
tubular transport protein disturbances and subsequent activation of
profibrotic cytokines
• Albuminuria – risk factor of total and cardiovascular mortality,
ESRD, acute kidney injury and progression of CKD
19. Stage of albuminuria/proteinuria
(Levey A.S. et al., 2010 )
urea albumine
(mg/creatinine, g)
Stage
Kidney function
А0
optimum
А1
increased
А2
high
А3
very high
<10
10-29
30-299
300-1999
А4
nephrotic
≥2000
20. The stage of CKD should be indicated in the
diagnosis after the nosologic form of renal disease
Examples of diagnosis:
• Kidney’s anomaly: a partial doubling of right renal pelvis. CKD
C1A0
• Hypertensive nephrosclerosis. CKD C3aA1
• Focal segmental glomerulosclerosis. Nephrotic syndrome.
CKD С3аА3
• IgA-nephropathy. Isolated urinary syndrome. CKD С1А3.
21. Classification and characteristic of main risk factors of
CKD
type
definition
description
increase susceptibility of
factors increasing
susceptibility to CKD kidney to damage
older age, family history of CKD, low renal
weight, low birth weight, racial and ethnic
differences
factors of initiation
of CKD
cause direct damage of
kidneys
diabetes, blood hypertension, autoimmune
diseases, systemic infections, urinary tract
infections, urinary stones, urinary tract
obstruction, drug toxicity, genetic diseases
factors of
progression of CKD
promote the progression
of renal damage and
accelerate the rate of
decline in renal function
high level of proteinuria, high blood
pressure, poor control of blood glucose
level in diabetic patients, dyslipidemia,
smoking
factors of ESRD
increase morbidity and
mortality in patients with
ESRD
inadequate dialysis (Kt/V); temporary
vascular access, low albumin level, high
levels of phosphorus and delayed treatment
22. Risk factors of CKD
nonmodifiable
modifiable
older age
diabetes
male sex
blood hypertension
low number of nephrons
(low birth weight)
autoimmune diseases
racial and ethnic peculiarities
chronic inflammation, systemic infections
hereditary factors (including family
history of CKD)
urinary stones, urinary tract infection
urinary tract obstruction
drug toxicity
high protein diet
dyslipidemia
smoking
obesity/metabolic syndrome
hyperhomocysteinemia
pregnancy
23. Factors of progression of CKD
nonmodifiable
modifiable
older age
persistent activity of the basic renal pathology
male sex
high levels:
- systemic blood pressure
- proteinuria
low number of nephrons
(low birth weight)
uncontroled diabetes
racial and ethnic peculiarities
obesity/metabolic syndrome
dyslipidemia
smoking
anemia
metabolic acidosis
pregnancy
disturbed calcium-phosphorus metabolism
(hyperparathyroidism)
high protein and sodium diet
24. CKD as independent risk factor for the development and
progression of cardiovascular disease
Groups of risk for cardiovascular disease:
• group of intermediate risk - CKD stages C1-C2 and
albuminuria A1;
• group of high risk - CKD stages C1-C2 and
albuminuria A2-A3 or CKD stage C3a, regardless of
the level of albuminuria/proteinuria;
• group of very high risk - CKD stages C3B - C5
regardless of the level of albuminuria/proteinuria
26. The incidence of arterial hypertension in patients with chronic
kidney disease
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow,
Russia)
%
100
90
80
70
60
BH by Korotkov method
BH by ABPM
50
40
30
20
10
0
SRNS
AS
Aspr
ADPKD
TMAP
(HUS)
RN
SRNS – steroid resistant nephrotic syndrome
AS – Alport syndrome
ТМАP (HUS) – thrombotic microangiopathy (hemolytic uremic syndrome)
AD PKD – autosomal-dominant polycystic kidney disease
RN – reflux nephropathy
27. PECULIARITIES OF RENAL ARTERIAL
HYPERTENSION
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
RN
RN
TM
AP
AD
(H
PK
U
S)
D
TMAP
(HUS)
ADPKD
AS
AS
SR
N
S
SRNS
0%
50%
nightly / daily BH
100%
daily BP
0%
50%
100%
diastolic / systolo-diastolic HP
systolic HP
SRNS – steroid resistant nephrotic syndrome
AS – Alport syndrome
ТМАP (HUS) – thrombotic microangiopathy (hemolytic uremic syndrome)
AD PKD – autosomal-dominant polycystic kidney disease
RN – reflux nephropathy
28. FREQUENCY OF COMPLICATIONS OF ARTERIAL HYPERTENSION
IN PATIENTS WITH PROGRESSIVE KIDNEY DISEASE
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
100
80
60
62,5
40
44,4
20
0
40,0
30,4
17,4
SRNS
angiopathy
33,3
28,6
23,1
4,5
11,8
AS
Aspr
ADPKD
TMAP (HUS)
RN
left ventricular hypertrophy
SRNS – steroid resistant nephrotic syndrome
AS – Alport syndrome
AD PKD – autosomal-dominant polycystic kidney disease
ТМАP (HUS) – thrombotic microangiopathy (hemolytic uremic syndrome)
RN – reflux nephropathy
29. The risk of cardiovascular complications in children with
steroidresistant nephrotic syndrome
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
data
Left ventricular
hypertrophy
retinal angiopathy
SRNS ≥ 4 years
2,8
2,7
the severity of blood
hypertension (explicit)
9,7
0,56
systolo-diastolic blood
hypertension
2,1
7,2
the lack of
antihypertensive therapy
2,3
9,2
RR>2,0 – high risk of cardiovascular disease
30. Primary prevention of CKD
is the elimination or minimization of the risk factors for
its development:
• clinical supervision of patient from high-risk group;
• the control of modifiable risk factors of development and
progression of CKD;
• control of GFR and albuminuria.
31. Secondary prevention of CKD
• slowing the progression of CKD (renoprotection)
• preventing the development of cardiovascular disease
(cardioprotection)
32. Correction of common risk factors for the development
and progression of renal and cardiovascular disease
•
•
•
•
•
•
metabolic and hemodynamic changes
glycemia
dyslipidemia
uricemia
blood hypertension
anemia
33. Common approaches of primary and
secondary prevention of CKD
stage
recommendations
The presence of risk factors for CKD
Regular screening for CKD, measures for reduction of
the risk of development CKD
С1 (normal renal function)
Diagnosis and treatment of the kidney disease,
correction of common risk factors of progression of
CKD. Identification of CVD, correction of therapy,
monitoring of risk factors of progression of CVD.
С2 (initial reduction of GFR)
previous measures + estimation of the rate of
progression CKD, correction therapy
С3 А и В (moderate reduction of GFR)
previous measures + detection, prevention and
treatment of systemic complications of renal
dysfunction (anemia, dizelektrolitemiya, acidosis,
hyperparathyroidism, hyperhomocysteinemia, etc)
С4 (marked reduction of GFR)
previous measures + preparations for renal replacement
therapy
С5 (ESRD)
renal replacement therapy + identification, prevention
and treatment of systemic complications of renal
dysfunction
35. Treatment of blood hypertension in patients with chronic
kidney disease
medicines with nephroprotective
effect
• inhibitors of angiotensinconverting enzyme
• blockers of ATII receptor type 1
• calcium channel blockers (nondihydropyridine)?
medicines without nephroprotective
effect
• beta-blockers
• diuretics
• calcium channel blockers
(dihydropyridine)
36. Indications for ACE inhibitors and
BRA in patients with CKD
• in patients with blood hypertension (for
achievation of target blood pressure levels)
• in patients with albuminuria / proteinuria A2-A3
(even in the absence of hypertension)
37. Antihypertensive therapy
• If the target level of blood pressure was not achieved
by ACE inhibitors and BRA it’s necessary to add the
hypotensive medicine of other pharmacological
groups and/or diuretics
38. The hypotensive effectiveness of RAAS inhibitors in
children with progressive kidney disease
(Nephrology department of Research Institute of Pediatrics & Children surgery,
Moscow, Russia)
100
80
75,0
60
71,4
66,7
63,6
58,3
40
20
0
37,5
SRNS
SA
SRNS – steroid resistant nephrotic syndrome
AS – Alport syndrome
AD PKD – autosomal-dominant polycystic kidney disease
Sapr
ADPKD
TMAP(HUS)
RN
ТМАP (HUS) – thrombotic microangiopathy (hemolytic uremic syndrome)
RN – reflux nephropathy
39. Antihypertensive therapy
• Clinical predictor of renoprotective efficacy of the
drugs is partial (daily proteinuria <2.5 g / day) or
total (daily proteinuria <0.5 g / day) remission of
proteinuria in a few weeks or months after starting of
treatment
40. Dynamics of proteinuria in children with
Alport's syndrome
(Nephrology department of Research Institute of Pediatrics & Children surgery,
Moscow, Russia)
on the therapy with ACE-inhibitors
(n = 14)
without ACE-inhibitors
(n = 8)
12,5%
28,6%
7,1%
50%
50%
37,5%
14,3%
- decreased proteinuria
- proteinuria didn’t increase
- deceleration of the rate of increasing of proteinuria
- stable proteinuria
- increased proteinuria
Конькова Н..Е., 2011
41. Dynamics of GFR in children with progressive course
of Alport's syndrome
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
on the therapy with ACE-inhibitors
(n = 9)
33,3%
22,2%
33,3%
without ACE-inhibitors
(n = 3)
100%
11,1%
- increasing of GFR
- stable GFR
- deceleration of the rate of reduction of GFR
- reduction of GFR
Конькова Н.Е, 2011
42. Frequency of blood hypertension in children with
SRNS receiving different immunosuppressive
therapy
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow,
Russia)
Prograf+Pred
Prograf
Cyph+Pred
MMF+Pred
MMF
CsA+Pred
CsA
Pred maxD
Pred
0
20
40
60
80
100
43. The effectiveness of antihypertensive therapy in children with SRNS
in dependence of the number of antihypertensive drugs
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
100
90
80
70
60
50
40
30
20
10
0
1 medicine
2 medicines
hypotensive effect
3 medicines
44. Principles of antihypertensive therapy in kidney
diseases in children
BH
MONOTHERAPY
(ACE-inibitors, calcium channel blockers, BRA II)
CHRONOTHERAPY
COMBINATION THERAPY
ACE-inibitors + diuretics, ACE-inibitors + calcium channel blockers, ACEinibitors + beta-adrenoblockers, calcium channel blockers + diuretics, etc.
45. CHRONOTHERAPY
ABPM allows:
to identify the peaks of blood pressure rises
to calculate:
Т/Р - duration of antihypertensive action of the drug
N/D - uniformity of drug’s action in the daytime and night hours
IND - uniformity of drug’s action during a day
to optimize therapy
to reduce the risk of target organ’s damage
46. CHRONOTHERAPY
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
• Hypotensive therapy of capoten without individual choice
of time giving was effective in 57% of children with
glomerulonephritis (n = 13).
• The uniformity of the drug’s action during the daytime and
nighttime periods was achieved in 45% of children. The
uniformity of drug’s action during the day was seen in
<25% and a sufficient duration of antihypertensive action
of the drug - in 33% of children.
Burgall А., 2002
47. Effectivenes of hypotensive therapy individualized on the
base of ABPM in children with glomerulonephritis
(Nephrology department of Research Institute of Pediatrics & Children surgery, Moscow, Russia)
100
90
80
70
60
50
40
30
20
10
0
deterioration
no changes
improvement
2 weeks
4 weeks
6 weeks
8 weeks
Burgall А., 2002
49. Conclusion
Preventing initiation and progression of CKD:
• correction of common modifiable risk factors for the
development and progression of renal and cardiovascular
disease;
• primary and secondary prevention of CKD (factors increasing
susceptibility to CKD, factors of initiation of CKD and factors
of progression of CKD);
• nephroprotective and cardioprotective early therapy;
• SMBP control