The Story of Village Palampur Class 9 Free Study Material PDF
renal failure En1.pptx
1. 1
Illustrations are from Robbins Pathologic basis of disease. V. Kumar,
A.K. Abbas, S.N. Fausto, 7th , 8th , 9th edition, 2007, 2010, 2013;
Harrison’s Principles of internal medicine; Stephen J. McPhee
Pathophysiology of Disease and internet resources. Frolov V.A
Porth Carol, Gaspard Kathryn J. Essentials of Pathophysiology
2. The main functions of kidneys
REGULATION OF
ELECTROLYTE BALANCE
REGULATION OF
WATER BALANCE
REGULATION OF ABB
CONTROL OF NITROGEN BALANCE
REGULATION OF HEMOPOIESIS
REGULATION OF
BLOOD PRESSURE
EXCRETION OF
WASTE PRODUCTS
4. Antigenes are not of glomerular origin
endogenous (SLE),
exogenous - bacterial (streptococci), viral
(hepatitis B), parasitic (Plasmodium
falciparum malaria), and spirochetal
(Treponema pallidum) infections.
1. Damage to glomeruli by immune
complexes.
5. Immune complexes are formed in circulation then
captured by glomeruli
Renal hemodynamics,
mesangial cells
function, charge of
basement membrane
The charge and size of
particles
• Large positively charged
particles cross
basement membrane
and localize
subepithelially (acute
glomerulonephritis)
Localization is depend on:
7. • Neutral charged
particles are localized
within mesangium
• Localization of
complexes within
basement membrane
gives membranous
nephropathy
• Large complexes are
phagocytosed by
macrophages
8. Antigen-antibody complexes deposited in
the glomeruli elicit a local inflammatory reaction
that produces injury.
• engagement of Fc receptors on leukocytes,
glomerular mesangial or other cells
• Activation of complement system
The glomerular lesions may exhibit leukocytic
infiltration and proliferation of mesangial and
endothelial cells.
9. 2. In Situ Formation of Immune Complexes
• Antibodies Against Planted Antigens
Immune complexes are formed
locally by antibodies that react with intrinsic
tissue antigen or with extrinsic antigens
"planted" in the glomerulus from the circulation
(cationic molecules, DNA, bacterial products,
nuclear proteins, the aggregated large proteins,
immune complexes themselves, since they
continue to have reactive sites for further
interactions with free antibody, free antigen, or
complement.
• .
10. 2. In Situ Formation of Immune Complexes
• Antibodies Directed Against Normal
Components of the Glomerular Basement
Membrane
Antigens are normal components of the
Glomerular Basement Membrane.
11. Antibodies bind to intrinsic
antigens homogeneously distrib-
uted along the entire length of the
GBM, resulting in a diffuse linear
pattern of staining for the
antibodies by immunofluorescence
techniques.
Anti-GBM antibodies may cross-
react with basement membranes of
lung alveoli, resulting in
simultaneous
lung and kidney lesions
(Goodpasture syndrome).
12. 3. Cell - mediated mechanism (type IV)
Damage by sensitized Т-lymphocytes
Sensitized T cells cause glomerular
injury and are involved in the
progression of some
glomerulonephritides.
14. proteases, ROSs alteration
Cytokines (IL-1, TNF) local and
systemic responce
Chemokines leukocyte emigration
tissue infiltration
Growth factors: PDGF mesangial cell
proliferation; TGF, connective tissue growth
factor, and fibroblast growth factor
ECM deposition and hialinization leading to
glomerulosclerosis in chronic injury.
VEGF maintain endothelial integrity and may
help regulate capillary permeability.
•
16. • Clotting system
• Fibrinogen (procoagulants activity of
macrophages fibrin formation within
the Boumen’s space stimulation of
endothelial cells proliferation (formation of
crescent-shaped mass).
• Inhibitor of plasminogen activator
thrombi formation, fibrosis
17. Clearance tests determine
the quantity of glomerular filtrate formed
each minute in all nephrons of both kidneys
- glomerular filtration rate (GFR)
Clearance – is the volume of plasma cleared
from any substance per minute
C = (U/P) x V
С – clearance; U - concentration of the test -
substance in urine
P - concentration of the test - substance in
plasma; V - minute diuresis
GFR at the healthy person is 80 - 120 ml / min
(clearance of endogenous creatinine)
18. The filtration occurs under the influence
of Effective filtration pressure
EFP = HP - (OP+ CP)
HP - hydrostatic
pressure of
blood in glomerular
capillaries
OP - oncotic pressure of
blood in glomerular
capillaries
CP - hydrostatic
pressure of ultrafiltrate
in Bowman’s space
19. Reduction in glomerular filtration
а) Decreased effective filtration pressure
Decreased hydrostatic pressure in
glomerular capilaries (hypotension, systolic
pressure less than 80 mm Hg, renal
ischemia, etc.)
Increased blood oncotic pressure
Increased intracapsule hydrostatic pressure
(difficulty of urine outflow)
21. Increase in glomerular filtration
а) Increased effective
filtration pressure
Increased hydrostatic
pressure in glomerular
capillaries
increased glomerular
efferent arterioles tone
(catecholamines,
angiotensin,
vasopressin)
Decreased glomerular afferent arterioles tone
(kinins, prostaglandins A, E)
Decreased oncotic pressure in glomerular
capillaries
b) Increase in permeability of the filtering
membrane
24. • Hyperaminoaciduria (cystinuria)
• Syndrome de Toni – Debre –
Fanconi: the main pathogenetic
factor —enzymatic defect in
Krebs cycle of mitochond.
• Impaired reabsorption of glucose,
phosphates, bicarbonates, amino
acids, proximal tubular acidosis
(loss of hydrocarbonates)
• Renal water diabetes (lack of
response to ADH)
• Pseudohypoaldosteronism
25. Acquired tybulopathy
• Damage of tubular epithelium (toxins, hypoxia,
obturation by casts (cylinders), hemoglobin,
myoglobin)
• Decreased activity of transport proteins
(participating in reabsorption and secretion)
• Decreased energy supply of tubular
transmembrane transport processes
• Overload of reabsorption processes (more than
renal threshold)
• Disorders of hormonal regulation of
reabsorption processes (aldosterone,
vasopressin, atrial peptide)
26. • Mechanisms of chronic tubulointerstitial injury in
glomerulonephritis Various components of the protein-rich
filtrate and cytokines derived from leukocytes cause tubular cell
activation and secretion of cytokines, growth factors, and other
mediators. These, together with products of macrophages, incite
interstitial inflammation and fibrosis. ET-1, endothelin-1, PAI-1,
plasminogen activator inhibitor-1; TIMP-1, tissue inhibitor of
metalloproteinases.
29. *Manifestations of excretory function disorders
signs
Diuresis
abnormalities
hematuria
leukocyturia
cylinderuria
Urine syndrome
13
proteinuria crystalluria
30. Quantitative changes of diuresis
Diuresis – is urine excretion within 24 hours
• Polyuria more than 2 L
• Oliguria less than 0.5 L
• Anuria less than 50 (100) mL
31. POLYURIA
Is increase in diuresis
(more than 2 liters)
Types of polyuria according to origin
Prerenal Renal
Pathogenesis
• increased glomerular filtration
• reduction in glomerular reabsorption
(water or osmotic diuresis)
32. а Physiological (after reception of
plenties of water)
b) Pathological
initial stage of arterial hypertension
(vasoconstriction of efferent arterioles)
hypervolemia
endocrinopathy (diabetes mellitus,
diabetes insipidus)
Prerenal polyuria
33. Renal failure (increased permeability of the
filtering membrane, impairment of renal
countercurrent multiplier system
functioning )
Renal polyuria
34. OLIGURIA
is reduction in daily diuresis less than
500ml
ANURIA - (absence of urine)
Absence of urine formation and
urination (diuresis is less than 50 ml)
PATHOGENESIS
reduction of glomerular filtration
increased tubular reabsorption of sodium
and water
mechanical obstruction for urine passage
35. Types of oliguria and anuria
according to origin
Prerenal
Renal
Postrenal
36. Prerenal oligo-anuria
THE REASONS
reduction of the systolic arterial
pressure less than 80 mm Hg.
hypovolemia
increase in blood oncotic pressure
(transfusions of great volumes of
albumin solutions)
38. • Pollakiuria – is frequent urination (at
cystitis, prostate adenoma)
• Nocturia is predominant night diuresis
(at renal diseases and heart failure)
39. QUALITATIVE CHANGES OF URINE
Proteinuria – is protein in urine
Under normal conditions there are
traces of protein in urine (150 mg per
24 hours):
60 % albumins, 40 % uroprotein
(Tamm Horsefall protein)
40. Types of proteinuria according to
significance for organism
Physiological
(functional)
(for healthy kidneys,
proteinuria is less
than 1 g/day)
orthostatic
at heavy physical
work
Pathological
(at pathological
processes)
42. Glomerular proteinuria
marked excretion of plasma proteins (from
4.0 – 5.0 g up to 50 g per 24 hours)
(the greatest proteinuria is observed at
nephrotic syndrome:
Pathogenesis: increased permeability of
glomerular filtering membrane
43. Types of proteinuria according to
appearance of different proteins in urine
Not selective
Increase in
permeability of
glomerular filter
albumins,
transferrin +
high molecular
proteins (IgG) in
urine
Selective
is observed at
nephrotic syndrome
(minimal change
disease) loss of
a negative charge of
glomerular filter
albumins and
transferrin in urine
(more than 90 %
children of 1- 6 years)
45. lEUKOCYTURIA – leukocytes in urine
(urinalysis –6-8 /HPF)
PYURIA is pus in urine
Is large number of leukocytes in urine
More than 200 /HPF
Shtergeimer- Malbin Cells - Active alive segmented
neutrophils, increased in size with pale-blue, segmented
nuclei, uncolored cytoplasm, they appear in acute
inflammation
Urocytograms:
neutrophils— infection, pyelonephritis, tbc
mononuclears — glomerulonephritis, interstitial nephritis
lymphocytes— SLE, rheumatoid arthritis
Eosinophils — allergy
46. Changes of specific gravity of urine
• Specific gravity of urine reflects renal
concentrating ability
• It is proportional to concentration of the
dissolved substances (urea, uric acid, salts,
creatinine and other organic and nonorganic
products)
• It is provided by the work of countercurrent
mechanism
• Under usual conditions it is 1.018 – 1.025
• Changes in specific gravity are due to
decreased renal tubules functional capacity.
47. Hyposthenuria
is decreased specific gravity of
urine less than 1.010 in all portions
of Zimnitzky’s test
Hypersthenuria
is increased specific gravityof urine
(is observed at diabetes mellitus)
48. Isosthenuria
is constant specific gravity and equal
the specific gravity of the primary
urine (ultrafiltrate) – 1.010- 1.012.
Isosthenuria reflects the failure of
renal concentration ability.
