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Renal Pathology Tutorial

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Information about Renal Pathology Tutorial
Education

Published on March 8, 2014

Author: shalaree

Source: slideshare.net

Description

A tutorial of renal/kidney pathology for 5th year medical students at Cambridge University.
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Histopath Tutorial 2: Renal Pathology Christiane Riedinger 6/3/14

Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure (acute kidney INJURY, chronic renal DISEASE) ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities

Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities

Overview of Renal Pathology ● many different ways of organising this topic ● mnemonic ● hereditary vs. acquired ● structure/anatomy ● outcome: acute vs. chronic

Overview of Renal Pathology ctnd. ● mnemonic - surgical sieve: (e.g. A vitamin CDE) ● Acquired: Diabetic kidney disease ● Vascular: Particularly susceptible, renal artery stenosis, arterionephrosclerosis, hypertension ● Infectious: nephritis (glomeruli vs. tubules, potentially post-infectious), TB, abscesses ● Trauma: shock ● Autoimmune: Particularly susceptible, SLE, vasculitides, amyloidosis ● Malignant: benign tumours, tubular or transitional cell carcinoma, nephroblastoma ● Idiopathic: many glomerulonephritides, e.g. minimal change ● Neoplastic: renal carcinoma, Wilm’s tumour, multiple myeloma ● Congenital: PKD, Alport’s, Fabry’s, von Hippel-Lindau ● Drugs: toxicity

Overview of Renal Pathology ctnd. ● structure/anatomy tubule glomerulus macroscopic systemic collecting system vessels http://www.sclerodermasociety.co. uk/Theheartandscleroderma1.php tubulointerstitial http://www.baileybio. com/plogger/? level=picture&id=1486

Overview of Renal Pathology ctnd. ● outcome: acute vs. chronic kidney failure

Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities

1* Symptoms of Renal Pathology ● ● ● ● ● ● haematuria ○ with or without symptoms ○ microscopic or macroscopic proteinuria ○ via leakage - glomerular damage ○ defective reabsorption in tubules ■ heavy metal damage ■ Fanconi syndrome ■ Hartnup disease AA absorption disease ○ overflow ■ haemolysis ■ intravascular haemolysis NEPHRITIC (both) vs NEPHROTIC syndrome (prOtein Only) oligo/anuria renal pain endocrine changes

1* Symptoms of Renal Pathology ctnd. ● ● ● always also think about what is happening in the blood, not just the urine! nephritic syndrome ○ haematuria ○ proteinuria ○ in blood: azotemia ○ oedema, hypertension nephrotic syndrome ○ proteinuria ○ lipiduria ○ in blood: hypoalbuminuria, hyperlipidaemia ○ oedema ○ increased clotting ○ risk of infection

Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities

Kidney Failure: Definitions Acute deterioration in kidney function (over <48h) with increase in creatinine (>0.3mg/dL) and decrease in urine output (<0.5mL/kg/h). Long-term degeneration of kidney function defined by persistently low or decreasing GFR or abnormal structural or functional findings.

Kidney Failure: Causes (acute) ● ● pre-renal ○ all vascular + contents of vessels ○ low blood volume ○ low BP ○ CHF ○ renal artery stenosis ○ ischaemia ○ renal vein thrombosis renal ○ glomerulonephritis (deposition, vasculitis) ○ acute tubular necrosis (toxins, antibiotics, contrast) ○ acute interstitial nephritis (distal obstruction)

Kidney Failure: Causes (acute) ctnd. ● post-renal: ○ ○ ○ ○ ○ ○ think OBSTRUCTION! again many ways to organise e.g. extrinsic vs intrinsic, here: structural parenchyma ■ clot ■ mass ■ papillary necrosis ureters ■ kidney stones ■ AAA ■ retroperitoneal fibrosis bladder ■ bladder stone, tumour, clot ■ neurogenic bladder prostate ■ BPH ■ prostate carcinoma urethra ■ stone ■ stricture

Kidney Failure: Causes (acute) ctnd. ● summary: 80% pre-renal and tubular necrosis (other statistics: 85% ATN, 10% interstitial nephritis, 5% GN)

Kidney Failure: Causes (chronic) ● ● ● diabetes mellitus 30% hypertension 15% glomerulonephritis 25% ● ● ● ● ● ● ● together 75%!!!!! vascular: renal artery stenosis, vasculitis, HUS infectious: HIV nephropathy, parasites toxins congenital: Alport’s syndrome, Fabry’s disease, Polycyst. kidney d. (5%) systemic (see earlier slide) post-renal obstruction (see earlier slide)

Kidney Failure: Causes (chronic) ctnd. ● summary: 75% diabetes, hypertension, GN

Kidney Failure: Acute v. chronic summary

Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities

Sites of Renal Pathology The Glomeruli: Glomerulonephritis

Glomerular Pathogenesis Think DEPOSITION and VASCULAR!

Glomerular Pathogenesis: DEPOSITION ● immune complexes ● glycoprotein deposition, glycation ● amyloid deposition ● paraprotein deposition (MM)

Glomerular Pathogenesis: IMMUNE COMPLEXES ● whole immune complexes get trapped ○ 3 locations: ■ mesangium ■ between endothelium and GBM ■ between GBM and podocytes ○ (GRANULAR PATTERN) ● in situ reaction ○ ABs attack “planted’ non-glomerular antigens ■ SLE nucleosomal complexes, bact. products, protein aggregates ○ ABs attack glomerular AGs (LINEAR PATTERN) ■ anti-GBM, anti-podocyte

Glomerular Pathogenesis: IMMUNE COMPLEXES

Glomerulonephritis: DISTINGUISH ● global vs. segmental (entire glomerulus or part) ● diffuse vs. focal (all glomeruli or patches) ● proliferative vs. non-proliferative (proliferation of endothelial and/or mesangial cells, often a result of inflammation, but does not have to be. I don’t think BM thickening counts as proliferative) ● nephrotic, nephritic syndrome or both? (how big are the holes?) ● pathological entity vs. clinical syndrome!

Glomerulonephritis The following slide is the way I have organised GNs to memorise them more easily - it may not be the best/most correct way as different books group them differently. For resources used see my Histopath notes.

(post-) infectious GN

global, diffuse!

global, diffuse!

global, diffuse!

global, diffuse!

Histology of Glomerulonephritis ● note: For an excellent overview, also see Wheater’s Basic Pathology Chapter 15 page 180ff post-infectious GN membranous GN membranoprolif. GN crescenteric GN

note: GN can cause ischaemia which then causes tubular injury!

Sites of Renal Pathology The Tubules: (Acute) Tubular Necrosis

Pathogenesis of Tubular Necrosis f

Sites of Renal Pathology The Interstitium

Tubulointerstitial Pathology

Sites of Renal Pathology The Collecting System: Kidney Stones

Path. of the Collecting System: STONES! ● ● ● ● ● ● 80% Calcium oxalate - absorptive hypercalcinuria 10% Magnesium/Ammonium phosphate - alkaline urine from UTIs <10% uric acid or cystine - urate from gout - cystine from defect in transport all stones contain 2.5% mucoprotein stone formation around nidus, e.g. bacterial debris or desquamated epithelium blockage of urine flow => hydronephrosis: compression => tubules affected => can’t concentrate urine => even more urine!! Therefore polyuria if partial obstruction Anuria if complete and bilateral (80% of stones unilateral)

Today’s Contents ● ● ● ● ● organising renal pathology major symptoms of renal pathology kidney failure ○ acute vs. chronic ○ causes, clinical phases sites of renal pathology ○ glomeruli ○ tubules ○ interstitium ○ collecting system biochemical abnormalities

Biochemistry of Renal Disease ● ● think about what kidney does and then derive it! In general potential abnormalities in the following tests ○ blood ■ FBC ■ U&E ■ BUN ■ LFTs ■ ■ ■ ESR/CRP clotting screen CK ○ urine ■ output ■ urinalysis ■ electrolytes ■ creatinine ■ osmolality ■ Bence-Jones ■ culture ○ ○ ○ ○ ○ special ■ GFR ■ tubular function imaging ■ US, CT, MRI ■ radioisotope scan pathology ■ biopsy immunology ECG!

Biochemistry of Renal Disease: prerenal INADEQUATE PERFUSION = ACCUMULATION/RETENTION ● ● ● ● ● ● ● urea creatinine H+ compounds containing N anuria/oliguria/polyuria changes in GFR activation of RAAS => uraemia => acidosis => azothemia => Na+ retention => U&E’s => U&E’s+ => U&E’s, ABG? => BUN, BUN/Cr => urine output => GFR => U&E’s, urine blood: hi Na+,also hi K+? urine: low Na+

Biochemistry of Renal Disease: renal REDUCED FUNCTION => ELECTROLYTE IMBALANCE AND LEAKAGE ● => Hyponatraemia (Na+ loss) ● opposite of RAAS hyperkalaemia retention of H+ => metabolic acidosis => ABG => hyperphosphataemia => U&E’s => hypermagnesaemia => U&E’s => urinalysis => urinalysis => urine output retention of phosphate ● ● ● ● retention of Mg2+ proteinuria haematuria anuria/oliguria/polyuria => U&E’s

Biochemical abnormalities: chronic kidney d. ● ● ● ● ● initially compensated one nephron hypothesis of Bricker 1960: ○ as nr of nephrons decrease, remaining nephrons must perform greater fraction of total renal excretion disturbances we mentioned in previous slides starts with polyuria endocrine effects ○ hyperphosphataemia/hypocalcaemia => renal osteodystrophy ○ decreased calcitriol cynthesis ○ decreased T, Oe ○ thyroid abnormalities ○ disorders of glu metabolism ○ anaemia ○ dyslipidaemia

The end.

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