pathogenesis of acute and chronic renal...
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Pathophysiology
of renal system
Pathogenesis of acute and chronic
renal failure
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KIDNEY STRUCTURE and FUNCTIONS
Filtration Reabsorption Secretion Excretion Incretion
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proximal tubule
Bowman’s space
Basal membrane
Visceral Epithelium podocytes
Mesangial cell
Endothelium
JGA
The structure of nephron
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Epithelial Podocyte
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Major functions of the kidney
EXCRETORY - Maintain plasma osmolality near 285 mosm by varying the excretion of water - Maintain plasma concentration of each electrolyte with normal range -Maintain the plasma pH (7.35-7.45) eliminating excess H+ or reabsorption HCO3
-Excrete the nitrogeeous and products of protein metabolism: -Urea, uremic acid, creatinine
NONEXCRETORY -Produce renin - regulation of blood pressure -Produce erythropoietin – stimulation of erythropoiesis -Metabolize vitamin D -Degrade insulin (20%)
--Produce prostaglandin
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Normal blood chemistry levels
Substance Normal value
Blood urea nitrogen (BUN) 8.0-25.0 mg/dl Creatinine 0.7-1.5 mg/dl Sodium 135 – 147 meq/l Chloride 100 – 106 meq/l Potassium 4.2 - 5 meq/l Carbon dioxide 24 – 29 meq/l Calcium 8.5 – 10/3 mg/dl Phosphate 3 – 4.5 mg/dl Uric acid 2.6 – 7.2 mg/dl pH 7.35 – 7.45
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concentration of urine descending loop reabsorption of water NaCL diffloses in Ascending loop Na reabsorps ,water stays in Urea secretion in thin segment
reabsorption of: Nacl H 2 O (ADH ) HCO3
SECRETION of: K H NH3 some drugs
reabsorption of water (ADH) reabsorption or secretion : Na, K, H, NH3
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Renal investigations 1. Examination of urine evaluation of color, turbidity (clear), pH, specific gravity (1.016-1.022), sediments 2. Blood urea 3. Serum creatinine 4. Glomerular filtration rate (GFR) 5. Blood urea nitrogen (BUN) 6. Radiology, isotopic studies computerized tomography 7. Ultrasound 8. Renal biopsy PROTEINURIA - up to 150 mg/day Trace < 30 mg/100ml in urin HEAVY PROTEINURIA ≥ 3.5 g/day ( up to 20-30 g/day)
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Calculation of clearance GFR (renal filtration velocity )
a x (creatinine in serum : b) x (0,993) age
sex a b
Women 144 61,9
Men !$$ 79,6
GFR = (140-age) x body mass Kg x (1,23 for men or 0,5 for women) creatinine in serum (mkmol/l)
GFR = 39,1 x [height/creatinine] 0516 x [1,8/cystitis] 0,294 x x [30/BUN]0,169 x 1099 male x [height/1.4]0188
Cystain C in serum can secrets by all nucleated cells and appears in blood , is filtrated freely and reabsorbed completly
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CASTS in urine
red cell casts
hyaline casts
waxy casts
epithelial casts
granular casts
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Daily DIURESIS
Normal diuresis - 1.0 – 1.5 l ( diet dependent)
Oliguria less then 1.0 l up to 300 ml (hypotension,
hypovolemia, intrinsic renal diseases
Polyuria more then 1.5 l up to 10 – 20 l
(usually with nocturia) - excessive intake of water - ↑ excretion of solute (hyperglycemia) - ↓ ADH production - intake diuretics - ↓ osmolality of blood
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Classification of Renal failure
ACUTE: - abrupt of onset
- often is reversible ( if recognized early)
CHRONIC: - develops slowly
- end – result of irreparable damage to the kidneys
DUE TO PATHOGENESIS: PRERENAL failure RENAL failure POSTRENAL failure
DUE TO ETIOLOGY: infectious, autoimmune, ets.
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PRERENAL FAILURE (ARF)
impaired blood flow
↓ GFR, ↑ BUN
tubular necrosis
hypovolemia dehydration septicemia, shock, heart failure, surgery, (ets.)
CAUSES:
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Intrarenal failure (ARF)
Glomerular : - acute GN acute pyielonephritis Tubular (most common) - Ischemia, - toxic agents -obstruction
Interstitial Tubular obstruction (casts, myoglobin, cellular debris Hb)
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Postrenal failure
Obstruction of urine output from the kidney ureter (calculi, stridures) bladder (tumor, neurogenic) urehtra (prostatic hypertrophy / hyperplasia)
kidney stone, scar tissue
pregnancy, abnormal growth
bladder outflow obstruction
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Examples of kidney pathology
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Acute renal failure (ARF)
ARF is an abrupt reduction in renal function. - is usually associated with oliguria - sufficient to increase nitrogenous wastes - impaired fluid and electrolyte balance - ↓ GFR - Azotemia - ↑ blood levels of nitrogenous wastes: urea, uric acid, creatinine
RISK FACTORS FOR ARF: impaired renal blood flow - diabetes, - administration of nephrotic drugs, which alter intrarenal hemodynamic, -elderly age
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ACUTE RENAL FAILURE
pre renal causes renal causes (intrinsic)
postrenal causes
tubular necrosis interstitial necrosis ( 10% of cases)
acute glomerulonephritis (5% of cases)
ischemia ( 50% of cases)
toxins ( 35 % of cases)
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CAUSES of ARF: • intravascular volume depletion and hypotension due to GI, renal, dermal losses, hemorrhage, shock, congestive heart failure, cirrhosis, nephrosis • Medications : cyclosporine, radiocontrast agents • Hepato -renal syndrome
• Large-vessel renal vascular disease: renal arterial thrombosis or embolism , renal artery stenosis • Small – vessel renal vascular disease: vasculitis, arterioembolism, sclerodermia hemolytic-uremic syndrome, sickle cell anemia, hypocalcemia • Sepsis
•Generalized or localized reduction in renal blood flow
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To control acute renal failure – monitoring of:
- urine osmolality - urine concentration Na ( Na reabsorbtion is maintained in prerenal azotemia, is lost in acute tubular necrosis ) - proteinuria - hemoglobinuria - casts in the urine - blood creatinine, BUN – blood urea nitrogen
STAGES of ARF: - initial, - oliguria, - poyiuri (restoration of diuresis), -recovery
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ACUTE RENAL INJURY
STAGES: 1) Risk 2) Injury 3) Renal failure 4) Loss of functions 5) End stage of renal disease (terminal)
chronic renal diseases = Chronic renal failure
The main criteri0ns for ARI are decreased diuresis and decreased GFR less then 60 ml/min.
The stages of chronic renal disease define due to GFR but Not to concentration of plasma creatinine.
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TYPICAL urine finding in ARF CONDITION DIPSTICK TEST SEDIMENT urine Fractional analysis osmol excretion
Prerenal Trace or no A few hyaline > 500 < 1% Azotemia proteinuria casts possible mosm/kg
Renal azotemia Tubular injury Mild to Pigmented < 350 > 1% Ischemia moderate granular mosmol/kg proteinuria casts Acute intrstinal + hemoglobin RBC, > 500 < 1% nephritis leukocytes RC casts ACUTE Glomerular- Nephritis +hemoglobin -- “ -- POSTRENAL Trace or no Crystal <350 >1% Azotemia proteinuria RBC, WBC
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Mechanism of oliguria in ARF ischemia or nephrotoxins
glomerular injure
tubula r injure
vasoconstriction
decreased permeability decreased surface area
cellular cast formation
decreased GFR
OLIGURIA
obstruction
increased untraluminal pressure
tubular back leak
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Symptoms and signs of ARF
• Diminished urinary output – urine may be dark from concentration of BR or presence of free Hb • Total anuria – no urine at all suggest postrenal obstruction • Thirst and dry mouth – dehydration, i.e. Prerenal • Hiccough, drowsiness from acute uremia • Dyspnea due to pulmonary edema from over hydration
ARF complicatons: -hyperkaliemic cardiac asystole, -pulmonary edema and respiratory failure, - secondary sepsis, - DIC-syndrome, - hypophosphatemia and hypokalemia during diuretic recovery stage
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CHRONIC RENAL FAILURE -
progressive and irreversible loss of renal function
Causes: -uncontrolled hypertension, - urinary tract obstruction and infection - disorders of the glomeruli - systemic diseases (diabetes mellitus)
4 stages for progression: 1) diminished renal reserve 2) renal insufficiency 3) renal failure 4) end-stage-renal disease (terminal)
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4 stages for progression
number of nephrons in %
months or years
1-00 - 75 - 50 - 25 - 0
1--↑ risk of azotemia 2 – hypertrophy of remainding nephrons. Isostenuria. 3 – The kidney cannot regulate volume and solute composition ; - edema - metabolic acidosis; - hypercalcemia 4 - ↓ renal capillaries; - scaring in the glomeruli; - atrophy and fibrosis in the tubules; - ↓ kidney mass
1
2
3
4
TO control renal function they find out: - GFR
- creatinine clearance - Creatinine in serum - Cystatin C
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Chronic renal failure • Body fluid changes
• Inability to concentrate and dilute urine
• ↓ ammonia synthesis, ↓HCO3 conservation
• ↓ potassium excretion
• hyperphosphatemia and inability to activate vitamin D
• ↓ synthesis of erythropoietin, uremic toxins
• impaired platelet formation
• Manifestations
• fixed specific gravity of urine, polyuria, nocturia
• Metabolic acidosis
• Hyperkalemia
• hypocalcemia, ↑parathyroid hormone
• Anemia
• Bleeding tendencies epistaxis, hemorrhagia, gastrointestinal bleeding bruising of the skin
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CHRONIC RENAL DISEASE
STAGES: 1. Symptoms and signs of renal injury (nephropathy) with
normal GFR ≥ 90 ml/min/1,73 m3 2. Nephropathy (Renal injury) with initial decreased GFR GFR < 60 – 89 ml/min 3. Moderate nephropathy decreased GFR Bb = 30 – 59 ml/min 4. Severe decreased GFR = 15 – 29 ml/min 5. Terminal renal failure
Chronic renal failure – from decreased GFR Less then 30 -59 ml/min/m3
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Chronic renal disease STAGES: 1) the features of renal injury GFR ≥ 90 ml/min /1,73 m 2 2) renal injury with initial ↓GFR (60 – 89) 3) moderate decrease d GFR (30 – 59) 4) SEveare decreased GFR ( 15- 20) 5) Terminal renal failure
Stages base on the changes of GFR, but not on the concentration of plasma creatinine
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CHRONIC RENAL FAILURE Systemic effect of uremia
• Cardiovascular function
- Activation of RAAS
- ↑ vascular volume
- ↓ vasodilator proataglandins
- Metabolic toxins
- Fluid retention, hypoalbuminemia
- ↑ extracellular fluid volume
- Gastrointestinal function
- Increased metabolic wastes:
- decomposition of urea by intestinal flora → ↑NH3 ,
- ↑ gastric acid secretion
• Manifestations
• Hypertension
• Uremic pericarditis
• Edema
• Congestive heart failure, pulmonary edema
• Anorexia, nausea, vomiting;
• Ulceration and bleeding of GI mucosa
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CHRONIC RENAL FAILURE • Altered immune function
• Impaired cellular and humoral
immunity
• Impaired skin and mucosal barriers
• Neurologic function
• Uremic toxins → atrophy and demyelination of nerve fibers
• Fluid and electrolyte imbalance ↑ metabolic acids and other small, diffusible particles (urea)
• Manifestations
• Infections
• Peripheral neuropathy
• Headache
• Encephahlopathy: loss of recent memory, lethargy ,coma, seizures, asterixis, muscle twitching
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RENAL OSTEODYSTROPHY
CRF →↓ P excretion→↑ P plasma levels →↓ Ca +2 → ↑ PTH (parathormon)
→bone tissue → ↑Ca+2 reabsorbtion from bone tissue
additional factors: cytokines, persistent hypogonadism
CRF→ ↓vitamin D → → ↓Ca +2 absorbtion in intestine ↓*Ca+2 ] in plasma Hyperparathyroidism
↓ vitamin D
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Renal syndromes and symptoms CHANGES IN DIURESIS: Polyuria - increased daily diuresis more then 1,5 liter Loss of tubular function; Conn’s syndrome; pyelonephritis
Olygouria - decreased daily diuresis low then 1 liter
Decreased number of functional nephrons; sclerosis or thrombosis of renal vessels; obstruction of collecting duct, ureter,
ANuria - daily diuresis not more then 30 -50 ml
Decreased Arterial blood pressure low then 50 mm Hg, ARF; CRF Creatinine cLearance provides a good mesure of GFR . GFRcr = ( Ucr x V) : Pcr. GFR = 100 -120 ml/min. CREATININE - a substance ,produced by muscles, is measured in plasma and urine to calculate GFR. Plasma creatinine concentration = 0,7 – 1,2mg/dl
Blood urea nitrogen - normal range = 10- 20 mg/ dl of blood
BUN increases when ↓ GFR Changes of specific gravity and pH of urine: normal SG = 1.016 –1.022 pH < 6 Urine sediment - casts, red blood cells, white blood cells, crystalls,
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Renal syndromes and symptoms
Uremic syndrome -occur the most frequently in patients with renal
pathology. Characterized by protenuria, hematuria, leukocyturia
Proteinuria - loss of proteins with urine more then 300 mg/daily.
Selective proteinuria - in urine appear protein s with molecular mass less then 70000 (albumins) IS = 15 30% Unselective proteinuria - in urine appear proteins with molecular mass more then 70000. IS > 30% Index selectivity (IS) =( clearance IgG : clearance alb) x 100% Hematuria – increased number of red blood cells in urine. ( Normal: 1 ml of urine - not more then 1000 erythrocytes) Renal ← glomerulonephritis, tuberculesis. Postrenal ← cistitis, urethritis, trauma.
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EXTRA renal syndromes
AZOTEMIA - blood urea nitrogen > 30 mmol/l (urea >6 mmol/l, creatitine > 0,1 mmol/l )
EDEMA - disturbance of water –electrolyte balance
NEPHROTIC syndrome - secondary aldosteronism,
↓ oncotic pressure in blood lymphtic failure
RENAL ARTERIAL HYPERTANSION - activation of RAAS
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Nephritic syndrome
Causes: -acute proliferative glomerulonephritis Ig A nephropathy Rapidly progressive glomerulonephritis
Primary Secondary disease of the glomeruli effect of systemic vasculitis SYNDROME can be initiated by: -Immune complexes, -Antiglomerular BM-antibodies, -Leukocytes
Clinical manifestations : - Hematuria with red blood cells - ↓ GFR -Azotemia, -Oliguria -Hypertension
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Pathophysiology of nephrotic syndrome
Altered glomerular permeability and loss of negative charge
increased function of plasma protein
proteinuria
hypoalbuminemia
edema hepatic synthesis of lipoproteins
hyperlipoproteinemia
lipiduria
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NEPHROSIS Primary disorder Secondary to systemic diseases: (mainly in children younger then 15 year0s Diabetes Mellitus -Minimal change disease -Focal sclerosis -- Membranous glomerulopathy --Membranoproliferative glomerulonephritis
1) diffuse loss of processes from epithelial layer 2) sclerosis of some glomeruli 3) diffuse thickening of BM due to deposition of immune complexes 4) BM thickening + cellular proliferation ( primarily of mesangium cells)
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Pathophysiology of nephrotic syndrome Glomerular damage
↑ permeability of glomerular capillaries
PROTEINURIA ( ≥ 3,59g/24 hr)
HYPOPROTEINEMIA (albumin < 3g/d )
↓ plasma oncotic pressure Compensatory ↑ synthesis of proteins and lipoproteins by liver
HYPERLIPIDEMIA
↓ plasma volume
↓ GFR Fluid escapes into tissue
EDEMA ↑ aldosteron secretion
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Nephrotic syndrome shows the total damage of kidney
Nephrotic syndrome is characterized by proteinuria -hypoproteinemia - edema
Nephritic syndrome shows the inflammation in nephrons
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UREMIC syndrome
The main features of UREMIC SYNDROME are proteinuria and hematouria. Some times leukocytemia and casts.
Characterized by increased blood urea and creatinine levels accompanied by systemic effects.
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Glomerulonephritis
Glomerulonephritis is a number of renal disorders in which proliferation and inflammation of the glomeruli are secondary to immune mechanism.
GLOMERULAR INJURY: immune origin: antibody, AB-Ag complexes Antigens: endogenous (DNA in epithel .cells) exogenous ( hemolytic streptococci )
GLOMERULAR DISEASES: -proliferative - sclerotic -membranous: diffuse, focal, segmental, mesangial
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PATHOGENESIS OF GLOMERULONEPHRITIS
sensibilation t o infections
Ag-AB complexes in blood
deposition of immune complexes in glomeruli
AB –synthesis to Ag of glomerular basal membrane
Ag-AB complexes on glomerular basal membrane
complement activation
proliferation of macrophages and mesangial cells
release , mediators, proteases, oxidants
thrombosis in capillaries
↓ renal blood flow
activation of RAAS ↑ Art. blood pressure edema
↑ permeability
uremic syndrom
↓ GFR
↓ diuresis, azotemia
renal failure
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Acute pyelonephritis
CAUSES: microorganisms: E coli, proteus, pseudomonas. Fungus, virus. RISK Factors: Urinary obstruction and reflux of urine from the bladder Neurogenic bladder, female sexual trauma
The infection is spread by ascending microorganisms along Ureters ( by bloodstream, lymphstream)
CLINICAL MANIFESTAIONS: fever, chills, pain, dysuria , polikuria, may be nausea, vomiting as a result of toxicity. IN BLOOD : NP leukocytosis, ↑ESR, anemia. IN URINE CULTURE : microorganisms