- •Kidney:
- •Kidney functions
- •Nephron - functional unit of the kidney
- •Electronic microscopy: glomerular capillary loops
- •Scheme of glomerulus structur
- •Investigation methods of kidneys and urinary tract
- •Complains
- •Anamnesis
- •Anamnesis
- •Laboratory methods
- •Laboratory methods
- •Proteinuria
- •erythrocytes in 1 ml
- •Haematuria
- •Haematuria
- •CAUSES OF RED OR DARK URINE
- •Dysmorphic erythrocytes on electronic microscopy (A – normal erythrocyte)
- •Leucocyturia - more then 2000 cells in 1 ml
- •Crystalluria
- •Measurement of the glomerular filtration rate
- •Markers of renal functional state
- •Calculation of GFR with Cokroft- Gault formula
- •MDRD formula
- •Image investigations of kidney and urinary tract
- •Эхоангиография правой почки
- •Пиелоуретероэктазии справа (экскреторная урография)
- •Аплазия правой почки (КТ)
- •Нефрокальциноз
- •Опухоль почки (ангиография)
- •Проходимость артерии восстановлена после стентирования
- •Scintigraphy of female patient of
- •Female patient of 67
- •RENAL BIOPSY
- •Normal glomerulus
- •Electronic microscopy
- •Poststreptococcal glomerulonephritis: immunofluorecent staining of deposits
- •Creschendic nephritis with “demilunes” of proliferating cells with rapture of Bowman capsule
- •Creschendic nephritis: immunofluorecent staining shows the lineal deposition of antibodies to basal membrane
- •RENAL SYNDROMS
- •Urinary syndrome
- •Nephritic syndrome
- •Clinical case 1
- •Nephrotic syndrome
- •Edema (nephrotic syndrome)
- •COMMOM CAUSES OF NEPHROTIC SYNDROME
- •CONSEQUENCES AND COMPLICATIONS
- •Hypertensive syndrome
- •Hypertensive syndrome
- •Tubular abnormalitis
- •Incidence of AKI*
- •Staging of AKI
- •Conceptual model for AKI
- •Causes of AKI and diagnostic tests
- •Exposure and susceptibility risk factors for non-specific AKI
- •Classification of AKI
- •Intrinsic Renal Damage
- •Post-renal
- •Natural history of AKI
- •Principles of AKI
- •Management of AKI
- •Chronic renal failure
- •Causes of chronic renal failure
- •Signs of chronic renal failure
- •Mechanisms of progression
- •REVERSIBLE FACTORS IN CHRONIC RENAL FAILURE
- •Markers of activity of renal disease
Intrinsic Renal Damage
•Glomerular and small vessel diseases
•Rapidly progressive GN, endocarditis, post-strep GN, vasculitides, scleroderma/malignant HTN, HUS, PET, DIC
•Interstitial nephritis
•Infection-related, inlammation, drug-induced, infiltrative (lymphoma, leukemia, sarcoidosis)
•Tubular Lesions
•Post-ishemia, nephrotoxic (drugs, contrast, anesthetics, heavy metals), pigment nephropathy, light chain, hypercalcemia
Post-renal
•Bladder flow obstruction
•Urethral, bladder neck (BPH), neurogenic bladder
•Ureteral obstruction (bilateral or of single kidney)
•Stones, clots, tumours, papillary necrosis, retroperitoneal fibrosis, surgical ligation
Natural history of AKI
Cerda et al. cJASN. 2008;
Principles of AKI
Management
•Identify AKI
•Avoid further nephrotoxic injury
•Optimize renal hemodynamics
•Treat complications
•Fluid balance, electrolytes, uremia
•Nutritional support
•Renal Support (RRT)
•Monitoring after AKI
Management of AKI
Chronic renal failure
(Chronic kidney disease stage 3-5)
•Constant and progressive decrease of all kidney functions
•Kidneys are incompetent to support normal homeostasis
Causes of chronic renal failure
Chronic glomerulonphritisSystemic hypertension
Diabetes mellitus with nephropathyChronic obstructive uropathyPolycystic of the kidneysAnalgesic nephropathy
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Signs of chronic renal failure
Sallow complection
Anaemia (normocytic, normochromic)Uraemic fetor
Deep acidotic breathing (Kussmaul respiration)Hypertension
Mental clouding
Uraemic encephalopathy (flapping tremor)Pleural and pericardial effusionPericardial rub (pericarditis)
Evidence of fluid overload or depletionRenal masses (polycystic kidneys)
Large bladder (chronic bladder outlet obstruction)
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Mechanisms of progression
•Activity of disease
•Hemodinamic changes
•Hyperfiltration and intraglomerular hypertension
•Systemic hypertension
•Metabolic factors
•↑ phosphorus
•↑ calcium
•↑ lipids
•↑ glucose
•↑ uric acid
•Provoking factors
infections, UT obstruction, pregnancy, allergic reactions, nephrotoxic drugs, hypovolemia, dehydration, bleeding
REVERSIBLE FACTORS IN CHRONIC RENAL FAILURE
HypertensionReduced renal perfusion
Renal artery stenosis
Hypotension due to drug treatment Sodium and water depletion
Poor cardiac treatmentUrinary tract obstructionUrinary tract infection
Other infections: increased catabolism and urea productionNephrotoxic medications
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