Normal kidney
Ultrasructure of normal Ultrasructure of normal kidneykidney
Clinical presentationsClinical presentations
AzotemiaAzotemia UremiaUremia Nephritic syndromeNephritic syndrome Nephrotic syndromeNephrotic syndrome HematuriaHematuria ProteinuriaProteinuria Acute renal failureAcute renal failure Chronic renal failureChronic renal failure
Nephrotic syndromeNephrotic syndrome
S/SS/S– Heavy proteinuria (3.5 gm%) and hypoalbuminemiaHeavy proteinuria (3.5 gm%) and hypoalbuminemia– EdemaEdema– InfectionsInfections– ThrombosisThrombosis– Hyperlipidemia and lipiduria.Hyperlipidemia and lipiduria.
Disorders with thickening of BM and mesangium.Disorders with thickening of BM and mesangium. Associated common glomerular diseasesAssociated common glomerular diseases
– Membranoproliferative glomerulonephritisMembranoproliferative glomerulonephritis– Membranous glomerulonephritisMembranous glomerulonephritis– Minimal changeMinimal change
Nephritic syndromeNephritic syndrome
Sudden onsetSudden onset S/S: S/S:
– Hematuria, RBC casts.Hematuria, RBC casts.– Proteinuria, mild to moderate, not nephrotic Proteinuria, mild to moderate, not nephrotic
range.range.– HypertensionHypertension
Glomerular diseases with cellular Glomerular diseases with cellular proliferation.proliferation.
Hallmark disease: post streptococcal Hallmark disease: post streptococcal glomerulonephritisglomerulonephritis
Acute Renal failureAcute Renal failure
Kidney stops working.Kidney stops working. Oliguria to anuria.Oliguria to anuria. ReversibleReversible Common cause- acute perfusion failureCommon cause- acute perfusion failure Gross and M/E – Renal cortical necrosisGross and M/E – Renal cortical necrosis Lab Data: increased BUN and Serum CrLab Data: increased BUN and Serum Cr
Hyperkalemia, metabolic acidosis, urinary sodium Hyperkalemia, metabolic acidosis, urinary sodium loss, same plasma and urine osmolality. loss, same plasma and urine osmolality.
Chronic renal failureChronic renal failure
IrreversibleIrreversible Slow progressionSlow progression S/S Uremia, polyuria, bone disease, S/S Uremia, polyuria, bone disease,
anemia. Metabolic compensation.anemia. Metabolic compensation. Common causes: hypertension and Common causes: hypertension and
diabetes.diabetes. Leads to end-stage renal disease. Leads to end-stage renal disease.
End stage renal diseaseEnd stage renal disease
Small, shrunken and Small, shrunken and granulargranular
Misnomer-chronic Misnomer-chronic glomerulonephritisglomerulonephritis
D/D Chronic D/D Chronic pyelonephritispyelonephritis
M/E hyalanized M/E hyalanized glomeruli, tubular glomeruli, tubular atrophy and interstitial atrophy and interstitial fibrosis.fibrosis.
Congenital DisordersCongenital Disorders
Renal agenesis- usually unilateralRenal agenesis- usually unilateral HypoplasiaHypoplasia Ectopic KidneysEctopic Kidneys Horseshoe kidneyHorseshoe kidney
Horse shoe kidney Double ureter
Cystic diseases of kidneyCystic diseases of kidney
Simple cystSimple cyst Adult polycystic kidney diseaseAdult polycystic kidney disease Childhood polycystic kidney diseaseChildhood polycystic kidney disease
Simple renal cyst Adult Polycystic kidney
Adult polycystic kidney Adult polycystic kidney diseasedisease Autosomal dominantAutosomal dominant BilateralBilateral Does not produce symptoms until the 4Does not produce symptoms until the 4thth
decadedecade Slowly progressiveSlowly progressive Associated findingsAssociated findings
– Liver cystsLiver cysts– berry aneurysms.berry aneurysms.
Autosomal recessive kidney disease
Autosomal recessive
Presents early
Bilateral
Liver cysts with proliferation of bile ducts
Renal pathologyRenal pathology
Diseases of the following:Diseases of the following:
Glomeruli- glomerulonephritisGlomeruli- glomerulonephritis( classified on the basis of histopathology)( classified on the basis of histopathology)
VesselsVessels InterstitiumInterstitium TubulesTubules
Pathogenesis of glomerular Pathogenesis of glomerular diseasesdiseases
Immunological:Immunological:– Antibodies reacting with glomerular antigensAntibodies reacting with glomerular antigens
Trapped circulating agent (Membranous)Trapped circulating agent (Membranous) Anti GBM antibodies (Good pasture's disease)Anti GBM antibodies (Good pasture's disease)
– Circulating immune complexes (Post streptococcalCirculating immune complexes (Post streptococcal VascularVascular
– HypertensionHypertension– DiabetesDiabetes
Foreign materialForeign material– AmyloidosisAmyloidosis
Glomerular response to Glomerular response to damagedamageHistological changesHistological changes
HypercellularityHypercellularity BM thickeningBM thickening Hyalinization and sclerosisHyalinization and sclerosis TerminologyTerminology
– Diffuse/focalDiffuse/focal– Global/segmentalGlobal/segmental
Acute glomerulonephritisAcute glomerulonephritis
Acute proliferative(poststreptococcal) Acute proliferative(poststreptococcal) glomerulonephritisglomerulonephritis
Rapidly progressive (crescentric) Rapidly progressive (crescentric) glomerulonephritis.glomerulonephritis.– Reaction to severe glomerular damageReaction to severe glomerular damage– Leakage of fibrin, leading to epithelial cell Leakage of fibrin, leading to epithelial cell
proliferation and crescent formationproliferation and crescent formation– Poor prognosis Poor prognosis
Acute diffuse proliferative Acute diffuse proliferative glomerulonephritisglomerulonephritis 1-2 wks post streptococcal1-2 wks post streptococcal Usually in childrenUsually in children Usually mild and transientUsually mild and transient Clinical presentation- nephritic syndromeClinical presentation- nephritic syndrome DiagnosisDiagnosis
– Histology- increased cellularityHistology- increased cellularity– IF: IgG and C3IF: IgG and C3– EM- granular subepithelial depositsEM- granular subepithelial deposits
Rx supportiveRx supportive
Crescentric Crescentric glomerulonephritisglomerulonephritis
Minimal change diseaseMinimal change disease
In childrenIn children CPCP -Nephrotic syndrome-Nephrotic syndrome HistologyHistology
– H and EH and E NormalNormal– EMEM Fusion of foot processFusion of foot process– IFIF
Rx steroidsRx steroids
Membranous nephropathyMembranous nephropathy Usually adultsUsually adults CP- nephrotic CP- nephrotic
syndromesyndrome Etiology- idiopathic/ Etiology- idiopathic/
secondary to multiple secondary to multiple causescauses– InfectiveInfective– DrugsDrugs– TumorsTumors– SLESLE
DiagnosisDiagnosis H and E- diffuse and H and E- diffuse and
global, BM and global, BM and mesangial thickeningmesangial thickening
IF- IgG and IF- IgG and complementcomplement
EM- Subepithelial EM- Subepithelial deposits (spikes)deposits (spikes)
Membranoproliferative Membranoproliferative glomerulonephritisglomerulonephritis Children and adultsChildren and adults CP- mixed nephrotic and nephriticCP- mixed nephrotic and nephritic Etiology- idiopathic or secondary e.g. SLEEtiology- idiopathic or secondary e.g. SLE Histology- Type 1 and Type 2Histology- Type 1 and Type 2
Type I- increased lobularity of the glomeruli, because of Type I- increased lobularity of the glomeruli, because of mesangial proliferation ( mesangial interposition-tram track mesangial proliferation ( mesangial interposition-tram track appearance)appearance)
EMEM Subendothelial deposits Subendothelial deposits IFIF IgG/ IgM and C3IgG/ IgM and C3
Type II- mesangial proliferation not that prominentType II- mesangial proliferation not that prominent EMEM dense deposit diseasedense deposit disease IFIF C3C3
Course: progressive, poor prognosisCourse: progressive, poor prognosis
Focal glomerulosclerosisFocal glomerulosclerosis
Children and adultsChildren and adults CP- nephrotic syndromeCP- nephrotic syndrome Etiology- Idiopathic/ secondary e.g. Etiology- Idiopathic/ secondary e.g.
HIV.HIV. Poor prognosisPoor prognosis
Kidney and vascular diseaseKidney and vascular disease
Central perfusion failureCentral perfusion failure Large vessel disease e.g. atherosclerosis-Large vessel disease e.g. atherosclerosis-
thromboembolic, renal artery stenosisthromboembolic, renal artery stenosis Small vessel disease e.g. hypertension, Small vessel disease e.g. hypertension,
diabetes and vasculitisdiabetes and vasculitis Pathogenesis- affects glomerular infiltration Pathogenesis- affects glomerular infiltration
and ischemic tubular atrophyand ischemic tubular atrophy Course- usually chronicCourse- usually chronic
Renal infarctsRenal infarcts
Causes:Causes:– accelerated accelerated
hypertensionhypertension– VasculitisVasculitis– EmboliEmboli
Hypertension and kidneyHypertension and kidney
Benign hypertensive nephrosclerosisBenign hypertensive nephrosclerosis– Granular kidneyGranular kidney– Arteriolar hyalinizationArteriolar hyalinization
Malignant hypertensionMalignant hypertension– Flea bitten kidneyFlea bitten kidney– Fibrinoid necrosis of the vesselsFibrinoid necrosis of the vessels
Granular kidney
Hyalanized arterioles
Malignant HypertensionMalignant Hypertension
Fibrinoid necrosis Hyperplastic arteriopathy
Diabetes and kidneyDiabetes and kidney
Diabetes most common cause of end Diabetes most common cause of end stage renal failure.stage renal failure.
Diabetic vascular disease- AS/hyaline Diabetic vascular disease- AS/hyaline arteriosclerosis.arteriosclerosis.
Diabetic glomerulosclerosisDiabetic glomerulosclerosis– Mesangial matrix formationMesangial matrix formation
Diffuse glomerulosclerosisDiffuse glomerulosclerosis Nodular glomerulosclerosis (Kimmelstiel-Nodular glomerulosclerosis (Kimmelstiel-
wilson disease)wilson disease)– BM thickeningBM thickening– Exudative lesions- fibrin capExudative lesions- fibrin cap
Increased infection- PyelonephritisIncreased infection- Pyelonephritis Papillary necrosisPapillary necrosis
Diseases of renal tubules Diseases of renal tubules and interstitiumand interstitium
– Pyelonephritis- acute and chronicPyelonephritis- acute and chronic– Acute tubular necrosisAcute tubular necrosis– Interstitial nephritisInterstitial nephritis
acute and chronicacute and chronic interstitial inflammationinterstitial inflammation Drugs like analgesics and antibioticsDrugs like analgesics and antibiotics
– Metabolic damage to tubules for eg Metabolic damage to tubules for eg calcium and uratecalcium and urate
– Functional tubular abnormalityFunctional tubular abnormality
Acute tubular necrosisAcute tubular necrosis
Reversible acute renal Reversible acute renal failure.failure.
CausesCauses– IschemiaIschemia– DrugsDrugs
Clinical stagesClinical stages– Initiating- oliguriaInitiating- oliguria– Maintenance- polyuriaMaintenance- polyuria– Recovery Recovery
Acute PyelonephritisAcute Pyelonephritis
Bacterial infectionBacterial infection Routes – ascending infection and hematogenousRoutes – ascending infection and hematogenous Predisposing factors: pregnancy, DM, stones, Predisposing factors: pregnancy, DM, stones,
tumor, vesicoureteral refluxtumor, vesicoureteral reflux S/S – pain, fever, often with lower urinary S/S – pain, fever, often with lower urinary
symptoms.symptoms. Gross: small cortical abscessGross: small cortical abscess M/E: neutrophils presentM/E: neutrophils present Course:Course: septicemia, papillary necrosis, peri and septicemia, papillary necrosis, peri and
pyonephrosis.pyonephrosis.
Chronic PyelonephritisChronic Pyelonephritis
Reflux associated/ obstructive.Reflux associated/ obstructive. Gross: irregular cortical scarring, Gross: irregular cortical scarring,
distorted renal calyxdistorted renal calyx M/E: chronic inflammation, fibrosis M/E: chronic inflammation, fibrosis
and tubular atrophy.and tubular atrophy. Specific – Tuberculous pyelonephritis Specific – Tuberculous pyelonephritis
Chronic pyelonephritisChronic pyelonephritis
HYDRONEPHROSISHYDRONEPHROSIS
Dilatation of renal Dilatation of renal pelvis and calyces pelvis and calyces and parenchymal and parenchymal atrophy due to atrophy due to urinary tract urinary tract obstruction.obstruction.
Renal stonesRenal stones FactorsFactors
– Increased conc. of solutesIncreased conc. of solutes– change in urinary Phchange in urinary Ph– decreased urinary volumedecreased urinary volume– infectioninfection
TypesTypes– Calcium (hypercalcinuria, hypercalcemia, excess)Calcium (hypercalcinuria, hypercalcemia, excess)– Magnesium ammonium phosphate stones Magnesium ammonium phosphate stones
(alkaline urine due to infection)(alkaline urine due to infection)– Uric acid stones ( gout, leukemias, acidic urine) Uric acid stones ( gout, leukemias, acidic urine)
Renal tumorsRenal tumors
Benign tumors common.Benign tumors common. Common malignant tumors:Common malignant tumors:
– Renal adenocarcinoma in adults (90%)Renal adenocarcinoma in adults (90%)– Wilm’s tumor in children.Wilm’s tumor in children.
CP- hematuria, pain, mass, metastasis, CP- hematuria, pain, mass, metastasis, paraneoplastic. paraneoplastic.
Prognosis depends on the stage.Prognosis depends on the stage. EtiologyEtiology - cytogenetic abnormalities- cytogenetic abnormalities
Renal Cell CarcinomaRenal Cell Carcinoma
66thth to 7 to 7thth decade decade Male predominance 3:1Male predominance 3:1 Yellow round mass, 3-15 cmYellow round mass, 3-15 cm Often invade renal vein and extend Often invade renal vein and extend
into the inferior vena cavainto the inferior vena cava Chromosome 13Chromosome 13
Wilm’s tumorWilm’s tumor
Childhood tumor composed of Childhood tumor composed of primitive tissue.primitive tissue.
Chromosome 1-loss of cancer Chromosome 1-loss of cancer suppression gene WT-1suppression gene WT-1
Combination of radiotherapy, Combination of radiotherapy, nephrectomy and chemotherapy –nephrectomy and chemotherapy –good results good results