nephrology for dentist students 1., 2. lecture. how to evaluate renal diseases? in a case suspicious...
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NEPHROLOGYfor dentist students
1., 2. lecture
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How to evaluate renal diseases?
In a case suspicious for renal disease the usual steps are:1) to evaluate diagnosis
– clinical– pathological– etiological
2) what is the renal function?– glomerular– tubulointerstitial
3) what kind of therapy may be useful– specific– non specific
4) follow- up of the patients
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MAIN TYPE OF RENAL DISEASES
Renal parenchymal diseases:
I. GLOMERULAR DISEASES
II. TUBULOINTERSTITIAL DISEASES
III. VASCULAR DISEASES
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The glomerular structure
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I. GLOMERULAR DISEASES
difficulties in classification of glomerular nephropathies (NP)
A) Clinical picture:
1) acute nephritic syndrome
2) rapidly progressive glomerulonephritis (GN)
3) nephrotic syndrome
4) asymptomatic urinary abnormalities
(isolated PU and/or HU)
5) macrohaematuria with/without acute renal
insufficiency
6) chronic glomerulonephritis with chronic renal
insufficiency
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B) Pathological picture and
pathophysiological approach:
glomerulus is a target that can
be attacked by different
pathogenic mechanisms
1.) immunologic mechanisms
immune complexes
antibodies against renal structures
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Immune complexes in the glomerulus
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B) Pathological picture and
pathophysiological approach:
glomerulus is a target that can
be attacked by different
pathogenic mechanisms
1.) immunologic mechanisms
immune complexes
antibodies against renal structures
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Glomerular basement membrane antibodies
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2.) non-immunologic mechanisms
systemic alteration of capillary basement
membranes
(diabetic nephropathy)
glomerular hyperfiltration (hypertension)
chr. intravascular coagulation (nephropathy of
pregnancy)
deposition of immunoglobulin light chains
secreted
inappropriately by plasma cells (amyloidosis,
light chain disease etc.)
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C) C) Etiological picture:Etiological picture: "Primary" - unknown etiology
"Secondary" - a likely cause is known
1. Systemic disease: SLE, diabetes etc
2. Infections: bacteria (streptococcus ...) parasites: malaria ... viruses: hepatitis B ...
3. Toxins
gold, penicillamine, heroin ...
4. Neoplasms: carcinoma, lymphoproliferative
disorders ...
5. Familiar and hereditary diseases
Alport syndrome
6. Pregnancy
toxemia of pregnancy with NP
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MAIN TYPE OF RENAL DISEASES
Renal parenchymal diseases:
I. GLOMERULAR DISEASES
II. TUBULOINTERSTITIAL DISEASES
III. VASCULAR DISEASES
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Tubulointerstitial nephritis (TIN)
Inflammatory disease of the renal interstitium with tubular damage.
Acute - chronic
IncidenceAcute TIN: in 11-14 % of acute renal failure
Chronic TIN: in approximately 15 % of chronic renal failure
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Acut TINEtiology1) Drug – induced acut TIN
2) Infections
- bacteria: Brucella
Leptospira etc.
- viruses: Hanta virus etc.
- parazites: Toxoplasma etc.
- others: Chlamydia etc.
3) Systemic diseases
- Sjögren’s syndome
- SLE etc.
4) Idiopathic
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Acut drug – induced TIN
Etiology 1. Antibiotics
β-Lactam antibiotics (ampicilline, methicilline etc.)
Sulfonamides Trimethoprim-sulfamethoxazole Ciprofloxacin etc
2. Diuretics 3. Non-steroid antiinflammatory drugs (NSAID) 4. Others
Phenytoin, Cimetidin, Omeprazol Allopurinol etc
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Clinical features of acute drug-induced TIN
Sign and Symptoms Laboratory Findings
Urine:fever (85-100 %) haematuria (95 %)maculopapular rash (25-50 %) sterile pyuriaarthralgias low grade
proteinuria
acute renal failure
Serum: eosinophilia (80 %)
decreased GFR
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Therapy
- elimination of the drug
- steroid? (useful, but only uncontrolled studies proved it)
- acute dialysis treatment if necessary
Prognosis
complete recovery within 1 yr
rarely: irreversible renal damage
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Chronic TINEtiology
1) Drugs
- analgesics
- NSAID etc.
2) Toxins
- heavy metals (lead etc.)
- Balkan nephropathy (ochratoxin A)
- Chinese herbal nephropathy
(aristolochialic acid) etc.
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3) Metabolic
- se K+ ↓ se Ca++ ↑
- uric – acid nephropathy etc.
4) Immune – mediated
- SLE, Sjögren’s disease etc.
5) Haematological diseases
- myeloma kidney etc.
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Analgesic nephropaty
Characteristic features:
• a chronic TIN with slow progression to end-stage renal failure• one of the few preventable renal diseases!
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Etiology• prolonged daily use of 1. phenacetin alone 2. analgesic mixtures containing: phenacetin (or paracetamol?) + phenazone or salicylic acid (aspirin) + caffeine and/or codeine• caffeine and codeine are addicitive subtances (mood-altering effect)
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Causes of chronic drug abuse:Causes of chronic drug abuse:• chronic headache• chronic joint pain etc.• every other chronic pain
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Pathological alterations
1) Papillary necrosis
2) Chronic TIN
3) Uroepithelial tumours 6 %
4) Renovascular atherosclerosis 4 %
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Clinicopathological picture
1. Papillary necrosis
rupture steril pyuria UTI of the papilla
renal colic HU (micro/macro)
2. Chronic TIN• hypertension• „early” anaemia (EPO)• slow progression to ESRD
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3. Uroepithelial tumours ▪ micro/macro HU ▪ abnormality with imaging techniques
4. Renovascular atherosclerosis ▪ atheromatous renal artery stenosis/trombosis
Clinicopathological picture (cont.)
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DiagnosisDiagnosis
1. Significant history of analgesic abuse
2. Non - sepecific clinical picture renal colic! macro HU! (tumour ?!) „early” anaemia! chronic renal failure (with unknown origin)
3. Imaging techniques US CT
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1. Renal volume depletion
2. Bumpy contours
3. Papillary calcification
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Therapy
Specific• total avoidance of phenacetin and combined analgesics (single analgesics?) (paracetamol?)• to find the etiology of chronic pain and to treat it
Non-specific non-specific renal protective therapy (treatment of hypertension, anaemia etc.)
Prevention !!
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Classifications, definitions:
1. Localisation of UTI a) - upper UTI - acute bacterial pyelonephritis (PN) - chronic bacterial pyelonephritis (PN)
Urinary tract infections Urinary tract infections (UTI)(UTI)
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b) - lower UTI - cystitis - urethritis - prostatitis
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2. Symptoms of UTI a) symptomatic b) asymptomatic
3. a) complicated UTI - with obstruction, functional or
anatomic abnormalities of urinary tract
(e.g. nephrolithiasis, VUR etc), - with recent urological
instrumentation (catheterization etc.)
b) uncomplicated UTI
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Etiology and pathogenesis1. ascending UTI - bacteria migrate from the patients own interstinal flora to the urethra pili of
bact. (e.g. Type I of E. Coli) adhere to the uroepithelial cells of urethra and
bladder colonisation of bacterium urethra bladder ureter kidney
parenchyma prostata
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2. haematogen UTI originating from the blood
UTI are most common in females in age group of 15-40 yrs: ♂ : ♀ =
1:8 with increasing age the incidence
in males rises (prostata hypertrophy!)
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Risk factors1.) age and sex2.) diabetes mellitus3.) immunosuppressive th. 4.) factors that alter urinary flow a) obstruction to urine flow
● Intraluminal - ureteral stones, blood clot,
necrotic papilla - ureteral or urethral
strictures
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● Extraluminal - prostate hypertrophy - retroperitoneal fibrosis - pelvis tumours etc. b) vesicoureteral reflux (VUR) c) residual urine in bladder - neurogenic bladder etc. d) instrumentation of UT - catherization - cystoscopy etc.
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Laboratory diagnosisI. Detection of pyuria: 1. Donne probe 2. microscopic examination of centrifuged urine sedimentfrom properly collected and processed
midstream specimens!(presence of squamous epithelial cells and
mixed bacterial flora = suspect for contamination!)II. Detection of bacteriuria: Urine culture Collection of urine specimens for culture
(into a steril container!)
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MAIN TYPE OF RENAL DISEASES
Renal parenchymal diseases:
I. GLOMERULAR DISEASES
II. TUBULOINTERSTITIAL DISEASES
III. VASCULAR DISEASES
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III. VASCULAR DISEASES renal artery stenosis with/without
thrombosis (chronic) or embolism (acute)
nephrosclerosis acute (malignant)
malignant HTN-caused chronic (benign)
benign HTN-caused systemic vasculitis (ANCA pos/neg)
PAN (polyarteritis nodosa) progressive systemic sclerosis Wegener's granulomatosis etc.
renal vein thrombosis
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1) Excretion of metabolic end products and
foreign substances (e.g. urea, creatinin,
toxins, drugs etc.) with the urine
2) Regulation of body fluid volume
osmolality, electrolyte content, fluid content
(concentration – dilutions) and acidity
FUNCTIONS OF THE KIDNEY
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3) Production and secretion of enzymes and hormonesa) renin
catalyzes the formation of AT I
angiotensinogen AT I AT II. blood pressure regulation
b) erythropoietinstimulates the maturation of erythrocytes in the bone
marrow
c) 1,25 - dihydroxyvitamin D3, the biologically mostactive form of vitamin D3regulation of body Ca and P balance
4) Production of vasoactiv mediators NO etc.
renin ACE
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EXAMINATION OF RENAL FUNCTION
For screening: serum creatinine and CN For correct glomerular filtration rate (GFR)
measurement:
creatinine clearance (ml/min)
GFR = UV U = urine creatinine
P P = plasma creatinine
V = urine volume/min
GFR may estimate from se creatinine using the
following 2 formula:
Urine collection!
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1. Cockroft formula:
if se creatinine is in mg/dl: USA
(140 - age in yrs) x weight in kg men GFR = 72 x serum creatinine (in mg/dl)
”-” ”-” ”-” x 0.85 women
if se creatinine is in μmol/l: Europe
1.23 x (140 - age in yrs) x weight in kg men
GFR = se creatinine
”-” ”-” ”-” x 0.85
women
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2. MDRD-175 formula with 4 variable
GFR =
175 (serum creatinine/88,4) -1,154
X age (years) -0,203
(men)
175 (serum creatinine/88,4) -1,154
X age (years) -0,203
X 0,742
(women)
Normal range: men 125 ± 25 ml/min
women 95 ± 20 ml/min