1 / 49

NEPHROLOGY for dentist students

NEPHROLOGY for dentist students. 1., 2. lecture. How to evaluate renal diseases?. In a case suspicious for renal disease the usual steps are: to evaluate diagnosis clinical pathological etiological what is the renal function? glomerular tubulointerstitial

larrykholmes
Download Presentation

NEPHROLOGY for dentist students

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. NEPHROLOGYfor dentist students 1., 2. lecture

  2. How to evaluate renal diseases? In a case suspicious for renal disease the usual steps are: • to evaluate diagnosis • clinical • pathological • etiological • what is the renal function? • glomerular • tubulointerstitial • what kind of therapy may be useful • specific • non specific • follow- up of the patients

  3. MAIN TYPE OF RENAL DISEASES Renal parenchymal diseases: I. GLOMERULAR DISEASES II. TUBULOINTERSTITIAL DISEASES III. VASCULAR DISEASES

  4. The glomerular structure

  5. 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

  6. 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

  7. Immune complexes in the glomerulus

  8. 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

  9. Glomerular basement membrane antibodies

  10. 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.)

  11. C) 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

  12. MAIN TYPE OF RENAL DISEASES Renal parenchymal diseases: I. GLOMERULAR DISEASES II. TUBULOINTERSTITIAL DISEASES III. VASCULAR DISEASES

  13. Tubulointerstitial nephritis (TIN) Inflammatory disease of the renal interstitium with tubular damage. Acute - chronic Incidence AcuteTIN: in 11-14 % of acute renal failure Chronic TIN: in approximately 15 % of chronic renal failure

  14. Acut TIN Etiology 1) 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

  15. 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

  16. Clinical features of acute drug-induced TIN Sign and SymptomsLaboratory Findings Urine: fever (85-100 %) haematuria (95 %) maculopapular rash (25-50 %) sterile pyuria arthralgias low grade proteinuria acute renal failure Serum: eosinophilia (80 %) decreased GFR

  17. 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

  18. Chronic TIN Etiology 1) Drugs - analgesics - NSAID etc. 2) Toxins - heavy metals (lead etc.) - Balkan nephropathy (ochratoxin A) - Chinese herbal nephropathy (aristolochialic acid) etc.

  19. 3) Metabolic - se K+ ↓ se Ca++ ↑ - uric – acid nephropathy etc. 4) Immune – mediated - SLE, Sjögren’s disease etc. 5) Haematological diseases - myeloma kidney etc.

  20. Analgesic nephropaty Characteristic features: • a chronic TIN with slow progression to end-stage renal failure • one of the few preventable renal diseases!

  21. 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)

  22. Causes of chronic drug abuse: • chronic headache • chronic joint pain etc. • every other chronic pain

  23. Pathological alterations 1) Papillary necrosis 2) Chronic TIN 3) Uroepithelial tumours 6 % 4) Renovascular atherosclerosis 4 %

  24. Clinicopathological picture • 1. Papillary necrosis • rupture steril pyuria UTI • of the papilla • renal colicHU • (micro/macro) • 2. Chronic TIN • hypertension • „early” anaemia (EPO) • slow progression to ESRD

  25. Clinicopathological picture (cont.) • 3. Uroepithelial tumours • ▪ micro/macro HU • ▪ abnormality with imaging techniques • 4. Renovascular atherosclerosis • ▪ atheromatous renal artery stenosis/trombosis

  26. Diagnosis 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

  27. 1. Renal volume depletion 2. Bumpy contours 3. Papillary calcification

  28. 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 !!

  29. Urinary tract infections (UTI) Classifications, definitions: 1. Localisation of UTI a) - upper UTI - acute bacterial pyelonephritis (PN) - chronic bacterial pyelonephritis (PN)

  30. b) - lower UTI - cystitis - urethritis - prostatitis

  31. 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

  32. Etiology and pathogenesis 1. 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

  33. 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!)

  34. Risk factors 1.) age and sex 2.) diabetes mellitus 3.) immunosuppressive th. 4.) factors that alter urinary flow a) obstruction to urine flow ● Intraluminal - ureteral stones, blood clot, necrotic papilla - ureteral or urethral strictures

  35. ●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.

  36. Laboratory diagnosis I. Detection of pyuria: 1. Donne probe 2. microscopic examination of centrifuged urine sediment from 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!)

  37. MAIN TYPE OF RENAL DISEASES Renal parenchymal diseases: I. GLOMERULAR DISEASES II. TUBULOINTERSTITIAL DISEASES III. VASCULAR DISEASES

  38. 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

  39. FUNCTIONS OF THE KIDNEY • Excretion of metabolic end productsand foreign substances (e.g. urea, creatinin, toxins, drugs etc.) with the urine • Regulation of body fluid volume osmolality, electrolyte content, fluid content (concentration – dilutions) and acidity

  40. Production and secretion of enzymes and hormones • renin catalyzes the formation of AT I angiotensinogen AT I AT II. blood pressure regulation • erythropoietin stimulates the maturation of erythrocytes in the bone marrow • 1,25 - dihydroxyvitamin D3, the biologically most active form of vitamin D3 regulation of body Ca and P balance 4) Production of vasoactiv mediators NO etc. renin ACE

  41. 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!

  42. 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

  43. 2. MDRD-175 formulawith 4 variable GFR = 175 (serum creatinine/88,4) -1,154X age (years) -0,203 (men) 175 (serum creatinine/88,4) -1,154X age (years) -0,203X 0,742 (women) Normal range: men 125 ± 25 ml/min women 95 ± 20 ml/min

More Related