KIDNEY PATHOLOGY (non-neoplastic renal diseases) www.pathedu.eu

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KIDNEY PATHOLOGY (non-neoplastic renal diseases) www.pathedu.eu by Mind Map: KIDNEY PATHOLOGY (non-neoplastic renal diseases) www.pathedu.eu

1. GLOMERULOPATHIES

1.1. CLASSIFICATIONS

1.1.1. PATHOGENESIS

1.1.1.1. PODOCYTOPATHIES

1.1.1.2. GLOMERULONEPHRITIS - glomerular injury is mediated by immune responses (ICs, Abs) or abnormalities of the complement system

1.1.1.3. NON-IMMUNOLOGICAL GLOMERULOPATHIES

1.1.1.4. THROMBOTIC MICROAGIOPATHY

1.1.1.5. MISCELLANOUS

1.1.2. ETIOLOGICAL

1.1.2.1. PRIMARY/IDIOPATHIC - MANIFEST CLINICALLY AS GLOMERULAR DISEASE (SEE CLINICS) IN THE ABSENCE OF MULTISYSTEMIC DISORDER & ANY IDENTIFIED CAUSE

1.1.2.2. SECONDARY

1.1.2.2.1. SYSTEMIC DISEASES

1.1.2.2.2. NOT ASSOCIATED WITH SYSTEMIC DISEASE

1.1.2.3. HEREDITARY

1.1.2.3.1. COLLAGEN TYPE IV NEPHROPATHIES

1.1.2.3.2. OTHER GBM PROTEIN AND SLIT DIAPHRAGM PROTEIN MUTATIONS

1.1.2.3.3. STORAGE DISEASES

1.1.2.3.4. OTHER

1.1.3. MORPHOLOGICAL

1.1.3.1. LM PATTERNS OF GLOMERULAR REACTION TO INJURY

1.1.3.1.1. BASIC TERMINOLOGY (LM findings)

1.1.3.1.2. MINIMAL LESIONS

1.1.3.1.3. SCLEROSING

1.1.3.1.4. PROLIFERATIVE

1.1.3.1.5. GBM THICKENING

1.1.3.1.6. DISEASES WITH NO PREDOMINANT/MULTIPLE POSSIBLE PATTERNS

1.1.3.2. IF FINDINGS

1.1.3.2.1. IMMUNE DEPOSITS

1.1.3.3. EM FINDINGS

1.1.3.3.1. IMMUNE DEPOSITS

1.1.3.3.2. ABNORMALITIES OF BASEMENT MEMBRANE

1.2. CLINICAL SYNDROMES

1.2.1. ISOLATED PROTEINURIA

1.2.1.1. ANY GLOMERULOPATHY

1.2.1.2. exclude other etiologies of proteinuria

1.2.2. ISOLATED HEMATURIA

1.2.2.1. ALPORT, Thin basement membrane disease (TBMD)

1.2.2.2. IgA

1.2.2.3. exclude other etiologies of hematuria

1.2.3. NEPHROTIC SYNDROME -proteinuria>3,5g/day

1.2.3.1. MCD

1.2.3.2. FSGS

1.2.3.3. MN

1.2.3.4. MPGN

1.2.3.5. SYSTEMIC

1.2.3.5.1. LUPUS NEPHRITIS (CLASS V)

1.2.3.5.2. DIABETES

1.2.3.5.3. AMYLOIDOSIS

1.2.4. NEPHRITIC SYNDROME -hematuria -hypertension -decreased GFR- transient, mild -active urine sediment (ERY, LEU, CASTS)

1.2.4.1. POSTSTREPTOCOCCAL

1.2.4.2. IgA, PROLIFERATIVE

1.2.4.3. MPGN

1.2.4.4. SYSTEMIC

1.2.4.4.1. LUPUS (CLASS III, IV)

1.2.4.4.2. SMALL VESSEL VASCULITIS

1.2.4.4.3. CRYO

1.2.4.4.4. TMA, ACUTE

1.2.5. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS -nephritic syndrome -subacute loss of GFR

1.2.5.1. CLASSIFIED BY IMMUNOFLUORESCENCE

1.2.5.1.1. ANTI-GBM DISEASE

1.2.5.1.2. ANCA VASCULITIS

1.2.5.1.3. IMMUNE COMPLEX GLOMERULONEPHRITIS

2. BIOPSY

2.1. TISSUE CORES

2.1.1. LIGHT MICROSCOPY

2.1.1.1. HISTOLOGY

2.1.1.1.1. KIDNEY

2.1.1.1.2. GLOMERULUS

2.1.2. IMMUNOFLUORESCENT MICROSCOPY IgG,IgA,IgM,C3,kappa,lambda

2.1.2.1. MESANGIAL

2.1.2.1.1. MESANGIAL granular deposits

2.1.2.2. CAPILLARY WALL

2.1.2.2.1. CAPILLARY WALL DEPOSITS -FINELY GRANULAR

2.1.2.2.2. CAPILLARY WALL DEPOSITS - LINEAR

2.1.3. ELECTRON MICROSCOPY

2.1.3.1. SCANNING EM

2.1.3.1.1. PODOCYTES

2.2. CLINICO-LABORATORY DATA: - CLINICAL SYNDROME - DURATION, COEXISTING DISEASES - DRUGS - ANA, ANCA, ANTY-GBM - HIV, HBV, HCV, ASO - C3, C4

2.3. BIOPSY + CLINICO-LABORATORY DATA = DIAGNOSIS

3. TUBULOINTERSTITIAL NEPHROPATHIES

3.1. CLASSIFICATION

3.1.1. ETIOPATHOLOGICAL

3.1.1.1. NON-INFLAMMATORY

3.1.1.1.1. ACUTE TUBULAR INJURY/NECROSIS (ATI/ATN)

3.1.1.2. TUBULOINTERSTITIAL NEPHRITIS (TIN)

3.1.1.2.1. INFECTIOUS TIN

3.1.1.2.2. NON-INFECTIOUS

3.1.2. CLINICAL

3.1.2.1. ACUTE

3.1.2.1.1. Acute renal failure/Acute kidney injury

3.1.2.1.2. Fever, sepsis

3.1.2.2. CHRONIC

3.1.2.2.1. In chronic symptoms depend on the involvement of tubules and secondary loss of parenchyma:

3.2. PATHOLOGY

3.2.1. MICRO

3.2.1.1. TUBULES

3.2.1.1.1. DAMAGE/DEGENERATION

3.2.1.1.2. ATROPHY

3.2.1.1.3. TUBULITIS

3.2.1.2. INTERSTITIUM

3.2.1.2.1. EDEMA

3.2.1.2.2. INFLAMMATORY INFILTRATE

3.2.1.2.3. FIBROSIS

3.2.1.2.4. INTRACANNALICULAR AND INTERSTITIAL CRYSTALS/CASTS

4. VASCULAR DISEASES

4.1. BENIGN/HYPERTENSIVE NEPHROSCLEROSIS

4.1.1. Kidney – culprit & victim of arterial hypertension

4.1.1.1. on LM one can see typical associated lesions of hypertensive nephrosclerosis

4.1.1.1.1. THE CAUSAL RELATIONSHIP CAN NOT BE ESTABLISHED

4.1.1.2. CULPRIT

4.1.1.2.1. Nephrogenic hypertension – renal parenchymal diseases

4.1.1.2.2. Renovascular hypertension – renal artery stenosis

4.1.1.2.3. Some cases of essential hypertension

4.1.1.3. VICTIM

4.1.1.3.1. Some cases of essential hypertension

4.1.2. CLINICAL

4.1.2.1. progressive renal failure in a patient with long-standing hypertension, moderate proteinuria, and no evidence suggesting an alternative diagnosis

4.1.3. PATHOLOGY

4.1.3.1. MACRO

4.1.3.1.1. SMALL WITH GRANULAR SURFACE

4.1.3.2. MICRO

4.1.3.2.1. REMODELING OF ARTERIES

4.1.3.2.2. HYALINE ARTERIOLOSCLEROSIS

4.1.3.2.3. CHRONIC ISCHAEMIC LESIONS (subcapsular)

4.2. THROMBOTIC MICROANGIOPATHY

4.2.1. Non-inflammatory, thrombotic vaculopathies (DDg. vasculitis!!!) – endovascular endothelial injury and thrombosis

4.2.2. CLINICAL PRESENTATION

4.2.2.1. 1. thrombocytopenia + 2. haemolytic anaemia + 3. organ dysfunction (usually kidneys(ARF or nephritic syndrome) and/or CNS )

4.2.2.1.1. HAEMOLYTIC-UREMIC SYNDROME (HUS)

4.2.2.1.2. THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)

4.2.2.1.3. ECLAMPSIA/HELLP SYNDROME

4.2.2.1.4. DIC

4.2.2.1.5. MALIGNANT HYPERTENSION

4.2.2.1.6. SYSTEMIC DISEASES

4.2.3. PATHOLOGY

4.2.3.1. MICRO

4.2.3.1.1. CONSTELLATION OF FINDINGS DIFFERS BETWEEN ENTITIES

4.2.3.1.2. Glomerular changes: endothelial swelling , fibrin thrombi,

4.2.3.1.3. Arteriols and small arteries changes: MYXOID DEGENERATION -> MYOINTIMAL HYPERPLASIA (ONION-SKINNING) ->FIBROINTIMAL SCLEROSIS

4.2.3.1.4. Microhemorrhages/microinfarcts/ ischaemic glomeruli->cortical necrosis

4.2.3.2. MACRO

4.3. RENAL ARTERY STENOSIS

4.4. RENAL INFARCTS

4.4.1. ACUTE RENOVASCULAR DISEASES

4.4.1.1. RENAL VEIN THROMBOSIS

4.4.1.2. RENAL ARTERY EMBOLISM

5. RENAL FAILURE

5.1. ACUTE KIDNEY INJURY

5.1.1. PRERENAL, RENAL, POSTRENAL

5.1.2. Abrupt loss of kidney filtration - decrease GFR - increased azotemia absolute/>50% - oliguria anuria

5.1.3. AT RISK OR ESTABLISHED ACUTE RENAL FAILURE OF DIFFERENT SEVERITY

5.2. CHRONIC KIDNEY DISEASE

5.2.1. Progressive loss of ALL renal functions due to decrease in absolute number of nephrons-kidney damage (USG,lab tests) or -decrease of GFR of less than 60ml/min/1,73m2

5.2.2. AT RISK OR ESTABLISHED CHRONIC RENAL FAILURE OF DIFFERENT SEVERITY

5.2.2.1. END-STAGE KIDNEY DISEASE

5.2.2.2. UREMIA

6. LABORATORY STUDIES

6.1. URINALYSIS (ROUTINE OR REAGENT STRIPS)

6.1.1. GENERAL

6.1.1.1. SPECIFIC GRAVITY (1,002-1,035)

6.1.1.2. COLOR

6.1.2. CHEMICAL

6.1.2.1. pH (4,5-8,0)

6.1.2.2. PROTEINS (<150mg/24h)

6.1.2.2.1. ETIOLOGY?

6.1.2.2.2. Proteinuria - a key biomarker of kidney dysfunction

6.1.2.3. GLUCOSE

6.1.2.4. OTHER

6.1.3. SEDIMENT

6.1.3.1. CELLS

6.1.3.1.1. RBCs (haematuria,erytrocyturia) (<1,2/HPF)

6.1.3.1.2. NEUTROPHILS

6.1.3.2. CASTS

6.1.3.3. CRYSTALS

6.2. RENAL FUNCTION TESTS - GFR estimation

6.2.1. - SERUM BLOOD UREA NITROGEN (BUN) - SERUM CREATININE (07-1,2 mg/mml) (Cr)

6.2.1.1. ESTIMATION OF SEVERITY AND DYNAMICS OF ACUTE KIDNEY INJURY

6.2.2. CREATININE CLEARANCE (CCr)

6.2.2.1. CALCULATED

6.2.2.1.1. formulas based on serum creatinine - eGFR

6.2.2.2. MEASURED

6.2.2.2.1. based on serum and plasma Cr and 24-hour urine collection

6.3. INVESTIGATION OF ABNORMAL TESTS

6.3.1. PROTEINURIA QUANTIFICATION

6.3.1.1. 24H URINE COLLECTION

6.3.1.2. urine PROTEIN/Cr ratio in URINE SAMPLE

6.3.2. ORIGIN OF HAEMATURIA

6.3.2.1. DYSMORPHIC ERYTROCYTES (hallmark of glomerular origin)

6.3.3. SEROLOGICAL STUDIES

6.3.3.1. AUTOANTIBODIES (ANA, ANCA, Anty-GBM)

6.3.3.2. INFECTIONS (pathogen-specific antibodies+ ASO)

6.3.4. COMPLEMENT FACTORS (C3,C4)

6.3.5. CBC